American Journal of Diseases of Children

GIARDINO, ANGELO;GIARDINO, EILEEN

1991 American Journal of Diseases of Children

doi: 10.1001/archpedi.1991.02160080017002pmid: 1858712

Abstract Sir.—In recent issues of AJDC, Bedrick 12 and Winter3 address the issue of residency work demands and the overburden in terms of hours and responsibility that hinder the effectiveness and humanity of the physician education process. They suggest that to hire more house staff to limit the number of resident working hours is not the answer to the problem. Likewise, expanding the number of residents in a given program to meet the ever-increasing service demands of the current tertiary and quaternary care centers will not meet service needs or optimize a resident's educational experience. Other practical ways are needed to address the problems associated with resident overwork and hospital care needs. The use of nonphysician primary care providers in the inpatient hospital setting bears further comment. Before a solution is implemented, physicians should analyze the available data to ensure that quality of patient care is maintained. It is References 1. Bedrick AD. The eighty-hour workweek: residency friend or foe? AJDC . 1990;144:857. 2. Bedrick AD. In reply to: Winter RJ. Neonatology and residency training . AJDC . 1990;144:953-954. 3. Winter RJ. Neonatology and residency training . AJDC . 1990;144:953. 4. Sox HC. Quality of patient care by nurse practitioners and physician's assistants . Ann Intern Med . 1979;91:459-468.Crossref 5. Honigfeld L, Perloff J, Barzansky B. Replacing the work of pediatric residents . Pediatrics . 1990;85:969-976. 6. Silver HK, McAtee P. On the use of nonphysician 'associate residents' in overcrowded specialty-training programs . N Engl J Med . 1984;311:326-328.Crossref 7. Silver HK, McAtee P. Should nurses substitute for house staff? Am J Nurs. 1988;88:1671-1673. 8. Silver HK, Ott JE, Dungy CI, Fine LL, Moore VM, Krugman RD. Assessment and evaluation of child health associates . Pediatrics . 1981;67:47-52. 9. Silver HK, Murphy MA, Gitterman BA. The hospital nurse practitioner in pediatrics: a new expanded role for staff nurses . AJDC . 1984;138:237-239.

PIDCOCK, FRANK S.

1991 American Journal of Diseases of Children

doi: 10.1001/archpedi.1991.02160080017001pmid: 1858711

Abstract Sir.—The problem of infants requiring prolonged hospitalization for lack of appropriate discharge placements has resulted in a new population of children receiving medical care. These children have been called "boarder babies," and their numbers are steadily increasing. On a given day in Philadelphia, Pa, 70 boarder babies are in hospitals awaiting discharge. They limit access to medical care for other children by occupying beds and increasing the hospitals' operating costs. This is one of the most insidious side effects of the current crack cocaine epidemic, resulting in the abandonment of numerous infants in hospitals. It has resulted in what one author describes as "the youngest of the homeless."1 A June 1989 survey1 by the Child Welfare League of America of hospitals in five American cities identified 304 boarder babies in the 54 hospitals reporting cases. At least 69% of the identified babies showed signs of impairment due References 1. Munns JM. The youngest of the homeless: characteristics of hospital boarder babies in five cities. Presented at the Child Welfare League of America; August 2, 1989. 2. Philadelphia, Pa, City Council Operating Budget Hearings, April 23, 1990 (testimony of Joan M. Reeves, commissioner of the Department of Human Services, Philadelphia).

JACOBS, STEPHEN E.

1991 American Journal of Diseases of Children

doi: 10.1001/archpedi.1991.02160080019003pmid: 1858713

Abstract Sir.—I found it interesting to read Goetzman's comments1 in the December 1990 issue of AJDC concerning the effects of selecting a new department head. As a practicing physician, I had no insight into some of what he mentioned. I was struck, however, by the comment that junior faculty members are said to "sacrifice" their careers if they are to "keep clinical programs afloat." In other words, caring for the sick will interfere with the need to publish. In the editorial by Bier et al2 in the same issue, several editors discuss their methods for dealing with "selfplagiarism." The motivation for this activity is to enlarge the physician's list of publications. In reality, the cause of "self-plagiarism" is the mind-set evidenced by Goetzman's comments. I have no quarrel with research. All of what I do is based on what researchers have done before me. However, I have a References 1. Goetzman B. The editorial board speaks: appointment vs anointment . AJDC . 1990;144:1291. 2. Bier DM, Fulginiti VA, Garfunkel JM, et al. Duplicate publication and related problems . AJDC . 1990;144:1293-1294.

LUBICKY, JOHN P.

1991 American Journal of Diseases of Children

doi: 10.1001/archpedi.1991.02160080019005pmid: 1858714

Abstract Sir.—Because my oldest son was a thumb-sucker who also carried a blanket and now needs orthodontic correction of malaligned teeth, I was particularly interested in the recent article by Friman.1 Thumb-sucking seems to be fairly common, yet Friman studied only eight patients. This seems like a very small sample size considering the prevalence of this problem. The eight patients who were followed up seem to have been preselected in a sense, not only because of the general inclusion criteria, but also because of the apparent motivation to stop thumbsucking exhibited by both the children and their parents. Thumbsucking, with or without other object attachment, is a very common problem. Therefore, it seems to me that Friman could have studied a much larger patient group and reached much more valid conclusions. Similar problems occur in studies in orthopedic surgery, especially those in which the natural history of a disease References 1. Friman PC. Concurrent habits: what would Linus do with his blanket if his thumb-sucking were treated? AJDC . 1990;144:1316-1318.

GOETZMAN, BOYD W.

1991 American Journal of Diseases of Children

doi: 10.1001/archpedi.1991.02160080019004

This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables. Abstract In Reply.—The development of special academic series for faculty members heavily involved in patient care is becoming widespread in academic medical centers in this country. Faculty in such series must make creative contributions in the clinical arena, but the pressure on them is significantly reduced in recognition of their major time commitment to patient care. It is hoped that this will help alleviate the problem that Jacobs addresses. In this age of medical specialization and subspecialization, it has taken quite a while to recognize that faculty members also become more expert at one of the traditional academic modes of university service, ie, teaching, research, and public service, when clinical activities are a central part of these duties. Thus, it is becoming more and more rare in academic medicine for an individual to be excellent in all three roles. As the pendulum swings, let us hope that it swings far

FRIMAN, PATRICK C.

1991 American Journal of Diseases of Children

doi: 10.1001/archpedi.1991.02160080019006

Abstract In Reply.—I appreciate Dr Lubicky's interest in my study of concurrent habits, but he has misunderstood it in two ways. First, it was not a study of thumb-sucking per se, but rather of covariation between chronic thumb-sucking and object attachment (ie, the "Linus" syndrome). To study this covariation, I treated thumb-sucking and measured, but did not treat, attachment. I followed guidelines derived from a thorough literature review for treatment of thumb-sucking.1,2 These guidelines recommend that only children aged 5 years or older be treated to reduce thumb-sucking, and then only if the habit is chronic (ie, occurs in more than one environment, such as at home and at school). Thumb-sucking is common in young children, but chronic thumb-sucking in children aged 5 years and older is not. No incidence figures are available, but my estimate, based on 9 years of research on thumb-sucking, is that about 5% to References 1. Friman PC, Schmitt BD. Thumb sucking in childhood: pediatrician's guidelines . Clin Pediatr . 1989;28:438-440.Crossref 2. Friman PC, Leibowitz JM. An acceptable and effective treatment alternative for chronic thumb and finger sucking . J Pediatr Psychol . 1990;15:57-65.Crossref 3. Johnston JM, Pennypacker HS. Strategies and Tactics of Human Behavioral Research . Hillsdale, NJ: Lawrence Erlbaum; 1980. 4. Kratochwill TR. Single Subject Research: Strategies for Evaluating Change . Orlando, Fla: Academic Press Inc; 1978.

BEDRICK, ALAN D.

1991 American Journal of Diseases of Children

doi: 10.1001/archpedi.1991.02160080020007pmid: 1858715

Abstract Sir.—AJDC recently published two commentaries by me concerning the educational goals (vs service needs) of resident rotations in the neonatal intensive care unit1 and the implications of an 80-hour workweek for pediatric residents.2 In these pieces, I reflected on the potential impact of these issues on the educational curricula of pediatric postgraduate programs. Now, after several months of "lively discussion," not only in AJDC, but with residents and faculty at my own institution, it is appropriate now for me to present some additional thoughts and "closing arguments." Concerns that excess workloads result in overstressed physicians and ensuring that residents go home to sleep after a rigorous night on call are important as we design optimal residency educational curricula. However, dwelling on these topics at the expense of the learning process may sidestep some of the more pressing issues about postgraduate residency training. The long working hours References 1. Bedrick AD. Neonatology in residency curricula: how much is too much? AJDC . 1990;144:159. 2. Bedrick AD. The eighty-hour workweek: residency friend or foe? AJDC . 1990;144:857.

GUTMAN, LAURA T.;CLAIRE, KAREN ST;HERMAN-GIDDENS, MARCIA;MCKINNEY, Ross E.

1991 American Journal of Diseases of Children

doi: 10.1001/archpedi.1991.02160080021009

Abstract In Reply.—Dr Monteleone has made several points worthy of reply. First, he notes that the incidence rate of sexual abuse in the general population is 17%. Studies that lead to prevalence rates of that level define sexual abuse broadly (a definition we endorse). However, many of the abusive activities are only minimally physically invasive, such as viewing, fondling, kissing, rubbing, photographing, and so forth. These activities would not cause the traumatic injuries that resulted in the genital physical findings that were described in 13 of the 14 children in the present study. This is in contrast to the situation for the majority of sexually abused children in whom significant physical findings resulting from the abuse are not found. Therefore, compared with other groups of abused children, and as was noted in the original article, the abuse of the children in our study was unusually severe. We were not prospectively References 1. National HIV Seroprevalence Surveys: Summary of Results . DHHS publication HIV/CID 9-90/006. Atlanta, Ga: Centers for Disease Control; 1990. 2. Gellert G, Berkowitz C, Durfee M. Situational and sociodemographic characteristics of children infected with HIV from pediatric sexual abuse. Presented at the Seventh International Congress on AIDS; Florence, Italy. June 15-21, 1991.

MONTELEONE, JAMES A.

1991 American Journal of Diseases of Children

doi: 10.1001/archpedi.1991.02160080021008pmid: 1858716

Abstract Sir.—The article by Gutman et al1 on human immunodeficiency virus (HIV) transmission by child sexual abuse in the February 1991 issue of AJDC can be misleading. The authors found that the incidence of sexual abuse among the 96 children who tested positive for HIV was 14.6%. The accepted incidence of sexual abuse in the general population is one in six, or 17%.2 If one were to examine any group of children for signs of sexual abuse, leukemia, or the common cold, one would expect to come up with a similar figure. It appears that HIV-positive children are at no increased risk of abuse. I agree with the authors that it is important to identify those children who are HIV positive and have been sexually abused, because some immediate and delayed behavioral sequelae of child sexual abuse may put the child and adult survivor at increased risk of References 1. Gutman LT, St Claire KK, Weedy C, et al. Human immunodeficiency virus transmission by child sexual abuse . AJDC . 1991;145:137-141. 2. Greenwood CL, Tangalos EG, Maruta T. Prevalence of sexual abuse, physical abuse, and concurrent traumatic life events in a general medical population . Mayo Clinic Proc . 1990;65:1067-1071.Crossref 3. Centers for Disease Control. HIV prevalence estimates and AIDS case projections for the United States . MMWR . 1990;39:1-31.

BAKER, ROBERT B.

1991 American Journal of Diseases of Children

doi: 10.1001/archpedi.1991.02160080022010pmid: 1858717

Abstract Sir.—The article by Bays and Jenny1 in the December 1990 issue of AJDC is a valuable review of the many physical findings that can be confused with sexual abuse. The authors stated that forceful abduction of the legs may cause splitting injuries of midline structures. I would like to report a case in which forceful abduction of the buttocks coupled with misrecognition of a normal structure led to a false assumption of sexual abuse. Report of a Case.—A 12-month-old white girl was brought to the office by her mother. The mother gave a specific history that the father, who had only weekend custody, had had rectal intercourse with her daughter. The mother stated that the child had difficulty with bowel movements after a weekend visitation. The child had already been examined by an emergency department physician and another local pediatrician. Without prompting, the mother then suddenly demonstrated References 1. Bays J, Jenny C. Genital and anal conditions confused with child sexual abuse trauma . AJDC . 1990;144:1319-1322. 2. Paradise JE, Rosatain AL, Nathanson M. Substitution of sexual abuse charges when parents dispute custody or visitation . Pediatrics . 1988;81:835-839. 3. Fay RE. Allegations of sexual abuse . Pediatrics . 1990;86:488-489.

FAIGEL, HARRIS C.

1991 American Journal of Diseases of Children

doi: 10.1001/archpedi.1991.02160080023012pmid: 1858718

Abstract Sir.—I am writing in regard to the Radiological Case of the Month on retropharyngeal abscess published in the December 1990 issue of AJDC.1 Although Fig 2 of this article is a very nice exhibit of an abscess, I fail to see the necessity of computed tomography as part of the evaluation and treatment of a peritonsillar or retropharyngeal abscess. In the discussion, the computed tomographic scan adds little to the diagnosis or treatment. I can assure you, it adds much to the high cost of medical care. The publication of such photos can be easily misinterpreted as a demonstration of the proper procedure in handling such cases. It is not. It is, in fact, an abuse of the available technology. It is abuses such as this that bring such strong reactions to control medical practice as a means of controlling medical costs. References 1. Grosso J, Myer CM, Wood BP. Retropharyngeal abscess . AJDC . 1990;144: 1349-1350.

MYER, CHARLES M.;GROSSO, JOHN

1991 American Journal of Diseases of Children

doi: 10.1001/archpedi.1991.02160080023013

This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables. Abstract In Reply.—We certainly agree with Dr Faigel that in many situations there is abuse of advanced technology in the form of "overtesting." This particular infant, however, was suspected of having retropharyngeal abscess (RPA) several days before otolaryngologic consultation was obtained. A delay in treatment of an RPA leads to an increased risk that the infectious process may spread not only within the retropharyngeal space, but also to the parapharyngeal space, carotid sheath, and mediastinum. The surgical procedure for a complicated RPA is much different from that for an uncomplicated one. Most RPAs are incised and drained with a transoral approach. If there is spread of the abscess to the parapharyngeal space or within the retropharyngeal space below the hyoid bone, for example, an external neck approach is best. As discussed in our article, a complete medical history, physical examination, and lateral neck roentgenography are the best tools for diag-nosing

BAYS, JAN;JENNY, CAROLE

1991 American Journal of Diseases of Children

doi: 10.1001/archpedi.1991.02160080022011

Abstract In Reply.—The case described by Baker is unfortunate. It is intrusive and even abusive for a child to be taken to multiple examiners for repetitive genital examinations. Herman-Giddens and Berson1 have described parents who focus excessively on their child's genitalia, including parents who performed genital inspections or took the child for multiple examinations or procedures by professionals. Many physicians have not been trained to perform detailed genital examinations,2 and further confusion arises if the examiner is unsure or mistaken in interpreting physical findings. It is unfortunate that the mother in the case described by Baker, and apparently the child protective authorities, "remained convinced that abuse had occurred" even after being informed that the "bruise" was a venous plexus. Regardless of whether a child is being molested, unresolved allegations of sexual abuse in the context of a divorce or custody dispute create additional stress for the child. These References 1. Herman-Giddens ME, Berson NL. Harmful genital care practices in children: a type of child abuse . JAMA . 1989;261:577-579.Crossref 2. Ladson S, Johnson, CJ, Doty RE. Do physicians recognize sexual abuse? AJDC . 1987;141:411-415.

LEWY, JOHN E.

1991 American Journal of Diseases of Children

doi: 10.1001/archpedi.1991.02160080025014

This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables. Abstract In every field of endeavor, only a limited number of people make a major impact. Jack Metcoff has had such an influence in the fields of pediatric nephrology and body fluid physiology. On June 11, 1990, a symposium and dinner was held in his honor. Several of the articles in this issue of the Journal were presented at the symposium. Approximately 100 of his colleagues and students attended the event. Seventeen presented synopses of their experiences working with Dr Metcoff or their current research in pediatrics. Some of the presentations were submitted to and reviewed by AJDC, and those that were accepted appear in this issue. Jack Metcoff was honored as an outstanding and visionary scientist, teacher, and leader. His scientific contributions include an early description of an experimental model of the nephrotic syndrome produced in the rat by injection of an aminonucleoside of puromycin and an elegant exposition of

1991 American Journal of Diseases of Children

doi: 10.1001/archpedi.1991.02160080026015

Abstract Peggy has been a workhorse for AJDC. She has reviewed hundreds of manuscripts for us, suggested new features and procedures for AJDC, and recently implemented one of these, "Pediatric Legal Medicine." In addition, she has faithfully handled our "Book Review" section for the past 8 years. In her contribution this month, she details a change in professional life-style she has recently undergone. Having worked with Peggy during her full-time activities, I can attest to her dedication to hard work, to completion of all of her duties, no matter what she was asked to do, and to her professionally competent performance. I have no doubt that her "reduced" activity will not alter the way in which she performs, for academe and for AJDC. Even a brief glance at her curriculum vitae reveals continued high-level activity locally, regionally, and nationally. AJDC, pediatrics, and pediatric neurology have benefited from her energy, intelligence, and References 1. AAMC Data Book . Washington, DC: Association of American Medical Colleges; 1991. 2. Eisenberg C. Medicine is no longer a man's profession: or, when the men's club goes coed, it's time to change the regs . N Engl J Med . 1989;321:1542-1544.Crossref

Sandstead, Harold H.

1991 American Journal of Diseases of Children

doi: 10.1001/archpedi.1991.02160080029016pmid: 1858720

Abstract • Zinc deficiency occurs in individuals and populations whose diets are low in sources of readily bioavailable zinc such as red meat, and high in unrefined cereals that are rich in phytate and dietary fibers. Dietary zinc deficiency was described nearly three decades ago among the poor of the Middle East. It is now known to occur in children and adolescents from widely diverse areas including Egypt, Iran, Turkey, China, Yugoslavia, Canada, and the United States; and among pregnant women from Iran, Turkey, the United Kingdom, Australia, and the United States. Major manifestations include retarded growth and development and an increased incidence of pregnancy complications. Other manifestations may include suppressed immunity, poor healing, dermatitis, and impairments in neuropsychological functions. Precise information as to the numbers of people affected by dietary zinc deficiency is not available. Even so the nature of diets associated with zinc deficiency suggests that mild deficiency is common in some populations. (AJDC. 1991;145:853-859) References 1. Prasad AS, Miale A Jr, Farid Z, Sandstead HH, Schulert AR, Darby WJ. Biochemical studies on dwarfism, hypogonadism and anemia . Arch Intern Med . 1963;111:407-428.Crossref 2. Prasad AS, Miale A Jr, Farid Z, Sandstead HH, Schulert AR. Zinc metabolism in patients with syndrome of iron deficiency anemia, hepatosplemomegaly, dwarfism and hypogonadism . Lab Clin Med . 1963;61:537-549. 3. Sandstead HH, Prasad AS, Farid Z, et al. Human zinc deficiency, endocrine manifestations, and response to treatment . Am J Clin Nutr . 1967;20:422-442. 4. Halsted JA, Ronaghy HA, Abadi P, et al. Zinc deficiency in man: the Shiraz experiment . Am J Med . 1972;53:277-284.Crossref 5. Minnich V, Okçuoǧlu A, Tarcon Y, et al. Pica in Turkey, II: effect of clay on iron absorption . Am J Clin Nutr . 1968;21:78-86. 6. Sommer AL, Lipman CB. Evidence on the indispensable nature of zinc and boron for higher green plants . Plant Phys . 1926;1:231-249.Crossref 7. Todd WR, Elvehjem CA, Hart EB. Zinc in the nutrition of the rat . Am J Physiol . 1934;107:146-156. 8. Hove E, Elvehjem CA, Hart EB. Further studies on zinc deficiency in rats . Am J Physiol . 1938;124:750-758. 9. O'Dell BL, Newberne PM, Savage JE. Significance of dietary zinc for the growing chicken . J Nutr . 1958;65:503-523. 10. Tucker HF, Salmon WD. Parakeratosis or zinc deficiency in the pig . Proc Soc Exp Biol Med . 1955;88:613-616.Crossref 11. O'Dell BL, Savage JE. Effect of phytic acid on zinc availability . Proc Soc Exp Biol Med . 1960;103:304-306.Crossref 12. Lieberman L, Abrams R, Hunt N, Ove P. Levels of enzyme activity and deoxyribonucleic acid synthesis in mammalian cells cultured from the animal . J Biol Chem . 1963;238:3955-3962. 13. Sandstead HH, Rinaldi RA. Impairment of deoxyribonucleic acid synthesis by dietary zinc deficiency in the rat . J Cell Physiol . 1969;73:81-83.Crossref 14. Dreosti IE, Gray PC, Wilkins PJ. Deoxyribonucleaic synthesis, protein synthesis, and teratogenisis in zinc deficient rats . So Afr Med J . 1972;46:1585-1588. 15. Hsu JM, Woosley RL. Metabolism of L-methionine 35S in zinc deficient rats . J Nutr . 1972;102:1181-1186. 16. Terhune MW, Sandstead HH. Decreased RNA polymerase activity in mammalian zinc deficiency . Science . 1972;177:68-69.Crossref 17. Duerre JA, Ford KM, Sandstead HH. Effects of zinc deficiency on protein synthesis in brain and liver of suckling rats . J Nutr . 1977;107:1082-1093. 18. Prasad AS, Oberleas D. Thymidine kinase activity and incorporation of thymidine into DNA in zinc-deficient tissue . J Lab Clin Med . 1974;83:634-639. 19. Hicks SE, Wallwork JC. Effect of dietary zinc deficiency on protein synthesis in cell-free systems isolated from rat liver . J Nutr . 1987;117:1234-1240. 20. Fosmire GJ, Al-Ubaidi YY, Halas ES, Sandstead HH. Some effects of postnatal zinc deficiency on developing rat brain . Pediatr Res . 1975;9:89-93.Crossref 21. Fosmire GJ, Fosmire MA, Sandstead HH. Zinc deficiency in the weanling rat: effects on liver composition and polysomal profile . J Nutr . 1976;106:1152-1158. 22. Hanas JS, Hazuda DJ, Wu CW. Xenopus transcription factor A promotes DNA reassociation . J Biol Chem . 1985;260:13 316-13 220. 23. Somers M, Underwood EJ. Ribonuclease activity and nucleic acid and protein metabolism in the testes of zinc deficient rats . Aust J Biochem Sci . 1969;22:1277-1282. 24. Prasad AS, Rabbani P. Nucleoside phosphorylase in zinc deficiency . Trans Assoc Am Physicians . 1981;94:314-321. 25. Sandstead HH. Zinc in human nutrition . In: Bronner F, Coburn J, eds. Disorders of MineralMetabolism-2 . Orlando, Fla: Academic Press Inc; 1981:93-157. 26. Hambidge KM, Casey CE, Krebs NF. Zinc . In: Mertz W, ed. Trace Elements in Human and Animal Nutrition . Orlando, Fla: Academic Press Inc; 1986:1. 27. Cousins RJ, Hempe JM. Zinc . In: Brown ML, ed. Present Knowledge in Nutrition . Washington, DC: International Life Science Institute (ILSI), Nutrition Foundation; ) 1990:251-260. 28. Sandstead HH, Darnell LS, Wallwork JC. Role of zinc and the contribution of meat to human nutrition . In: Pearson AM, Dutsoin TR, eds. Meat and Health, Advances in Meat Research . Amsterdam, the Netherlands: Elsevier Science Publishers; 1990:237-274. 29. United States Department of Agriculture, Food and Consumer Services. Nutrition Monitoring in the United States: A Progress Report from the Joint Nutrition Monitoring Evaluation Committee . Hyattsville, Md: US Dept of Health and Human Services Public Health Service; 1986.National Center for Health Statistics, Human Nutrition Information Service publication PHS 1255. 30. Welsh SO, Marston RM. Zinc levels of the US food supply 1909-1980 . Food Technol . 1982;36:70-76. 31. Anderson BM, Gibson RS, Sabry JH. The iron and zinc status of long-term vegetarian women . Am J Clin Nutr . 1981;34:1042-1048. 32. Reinhold JG, Faradji B, Abadi P, Ismail-Beigi F. Binding of zinc to fiber and other solids of wholemeal bread . In: Prasad AS, ed. Trace Elements in Human Health and Disease . Orlando, Fla: Academic Press Inc; 1976;1:163-180. 33. Solomons NW, Pineda O, Viteri F, Sandstead HH. Studies on the bioavailability of zinc in humans: mechanism of the intestinal interaction of non-heme iron and zinc . J Nutr . 1983;113:337-349. 34. Harzer G, Kauer H. Binding of zinc to casein . Am J Clin Nutr . 1982;35:981-990. 35. Mills CF. Dietary interactions involving the trace elements . Annu Rev Nutr . 1985;5:173-193.Crossref 36. Sandstead HH. Requirements and availability of dietary zinc for humans . In: Prasad AS, ed. Clinical and Public Health Significance of Trace Elements in the World Population . New York, NY: Alan R Liss Inc; 1982:83-102. 37. Sandstead HH. Requirement of zinc in human subjects . J Am Coll Nutr . 1985;4:73-82.Crossref 38. Evans GW, Johnson PE. Characterization and quantitation of a zinc binding ligand in human milk . Pediatr Res . 1980;14:847-880.Crossref 39. Oestreicher P, Cousins RJ. Influence of intraluminal constituents on zinc absorption by isolated, vascularly perfused rat intestine . J Nutr . 1982;112:1978-1982. 40. Seal CJ, Heaton FW. Chemical factors affecting the intestinal absorption of zinc in vitro and in vivo . Br J Nutr . 1983;50:317-324.Crossref 41. Wapnir RA, Khani DE, Bayne MA, Lifshitz F. Absorption of zinc by the rat ileum: effects of histidine and other low molecular-weight ligands . J Nutr . 1983;113:1346-1354. 42. Oberleas D, Muhrer ME, O'Dell BL. Dietary metalcomplexing agents and zinc availability in the rat . J Nutr . 1966;90:56-62. 43. Reinhold JG, Hedayati H, Lahimgarzadeh A, Nasr K. Zinc, calcium, phosphorus, and nitrogen balances of Iranian villages following a change from phytate rich to phytate poor diets . Ecol Food Nutr . 1973;2:157-161.Crossref 44. Pecoud A, Donzel P, Schelling JL. Effect of foodstuffs on the absorption of zinc sulfate . Clin Pharmacol Ther . 1975;17:469-473. 45. Turnland JR, King JC, Keyes WR, Gong B, Michel MC. A stable isotope study of zinc absorption in young men: effects of phytate and alpha-cellulose . Am J Clin Nutr . 1984;40:1071-1077. 46. Sandstrom B, Almgren A, Kivisto B, Cederblad Å Zinc absorption in humans from meals based on rye, barley, oatmeal, triticale and whole wheat . J Nutr . 1987;117:1898-1902. 47. Navert B, Sandström B, Cederblad Å. Reduction of the phytate content of bran by leavening in bread and its effect on zinc absorption in man . Br J Nutr . 1985;53:47-53.Crossref 48. Sandström B, Almgren A, Kivistö B, Cederblad Å. Effect of protein level and protein source on zinc absorption in humans . J Nutr . 1989;119:48-53. 49. Sandstead HH, Dintzis FR, Bogyo TP, Milne DA, Jacob RA, Klevay LM. Dietary factors that can impair calcium and zinc nutriture of the elderly . In: Prinsley DM, Sandstead HH, eds. Nutrition and Aging . New York, NY: Alan R Liss Inc; 1990:241-262. 50. Solomons NW, Jacob RA, Pineda O, Viteri F. Studies on the bioavailability of zinc in man, II: absorption of zinc from organic and inorganic sources . JLab Clin Med . 1979;94:335-343. 51. Brune M, Rossander L, Hallberg L. Iron absorption: no intestinal adaptation to a high-phytate diet . Am J Clin Nutr . 1989;49:542-545. 52. Lykken Gl,Johnson PE,Mahalko J, etal. Effect of browned and unbrowned corn products intrinsically labeled with zinc on absorption of zinc in humans . J Nutr . 1986;116:795-801. 53. World Health Organization (WHO). Zinc . WHO Tech Rep Ser . 1973;532:9-16. 54. Waslien CA. Human intake of trace elements . In: Prasad AS, ed. Trace Elements in Human, Health and Disease . Orlando, Fla: Academic Press Inc; 1976:347-370. 55. Sandström BM, King J, Chandra R, et al. Human zinc requirements. WHO Tech Rep Ser. 1991. In press. 56. White HS. Inorganic elements in weighted diets of girls and young women . J Am Diet Assoc . 1969;55:38-43. 57. Holden JM, Wold WR, Mertz W. Zinc and copper in selfselected diets . J Am Diet Assoc . 1979;75:23-28. 58. Gibson RS, Scythes CA. Trace element intakes of women . Br J Nutr . 1982;48:241-248.Crossref 59. Arcasoy A, Cavdar AO, Babacan E. Decreased iron and zinc absorption in Turkish children with iron deficiency and geophagia . Acta Hematol . 1978;60:76-84.Crossref 60. Xue-Cun C, Tai-An Y, Jin-Sheng H, Giu-Yan M, Zhi-Min H, Li-Xiang L. Low levels of zinc in hair and blood, pica, anorexia, and poor growth in Chinese preschool children . Am J clin Nutr . 1985;42:694-700. 61. Buzina R, Jusic M, sapunar J, Milanovic N. Zinc nutrition and taste acuity in school children with impaired growth . Am J clin Nutr . 1980;33:2262-2267. 62. Udomkesmalee E, Dhanamitta S, Yhoung-Aree J, Rojroongwasinkul N, Smith JC Jr. Biochemical evidence suggestive of suboptimal zinc and vitamin A status in schoolchildren in Northeast Thailand . Am J clin Nutr . 1990;52:564-567. 63. Hambidge KM, Hambidge C, Jacobs M, Baum JD. Low levels of zinc in hair, anorexia, poor growth and hypogeusia in children . Pediatr Res . 1972;6:868-874.Crossref 64. Walravens PA, Krebs NF, Hambidge KM. Linear growth of low income preschool children receiving a zinc supplement . Am J clin Nutr . 1983;38:195-201. 65. Pilch SM, Senti FR. Analysis of zinc data from the Second National Health and Nutrition Examination Survey (NHANES II) . J Nutr . 1985;115:1393-1397. 66. Gibson RS, Vanderkooy PDS, MacDonald AC, Goldman A, Ryan BA, Berry M. A growth-limiting mild zinc deficiency syndrome in some Southern Ontario boys with low height percentiles . Am J clin Nutr . 1989;49:1266-1277. 67. Vanderkooy PDS, Gibson RS. Food consumption patterns of Canadian preschool children in relation to zinc and growth status . Am J clin Nutr . 1987;45:609-616. 68. Scoular FL. A quantitative study by means of spectrographic analysis of zinc in nutrition . J Nutr . 1939;17:103-113. 69. Engle RW, Miller RF, Price NO. Metabolic patterns in peradolescent children, XIII: zinc balance . In: Prasad AS, ed. Zinc Metabolism . Springfield, Ill: Charles C Thomas Publisher; 1966:326-337. 70. Price NO, Bunce GE, Engel RW. Copper, manganese and zinc balance in preadolescent girls . Am J clin Nutr . 1970;23:258-260. 71. Sandstead HH. Zinc nutrition in the United States . Am J clin Nutr . 1973;26:1251-1260. 72. Hambidge KM, Chavez MN, Brown RM, Walravens PA. Zinc nutritional status of young middle-income children and effects of consuming zinc-fortified breakfast cereal . Am J clin Nutr . 1979;37:2532-2539. 73. Jameson S. Effects of zinc deficiency in human reproduction . Acta Med Scand Suppl . 1976;593:4-89. 74. Blamberg DL, Blackwood WB, Supplee WC, Combs CF. Effect of zinc deficiency in hens on hatchability and embryonic development . Proc Soc Exp Biol Med . 1960;104:217-220.Crossref 75. Hurley LS, Swenerton H. Congenital malformation resulting from zinc deficiency in rats . Proc Soc Exp Biol Med . 1966;123:692-696.Crossref 76. Apgar J. Effect of zinc deprivation from day 12,15,18 of gestation on parturition in the rat . J Nutr . 1972;102:343-348. 77. Hurley LS, Shrader RE. Abnormal development of preimplantation rat eggs after three days of maternal dietary zinc deficiency . Nature . 1974;254:427-429.Crossref 78. Mckenzie JM, Fosmire GJ, Sandstead HH. Zinc deficiency during the later third of pregnancy: effects on fetal rat brain, liver, and placenta . J Nutr . 1975;105:1466-1475. 79. Sandstead HH. Zinc: essentiality for brain development and function . Nutr Rev . 1985;43:129-137.Crossref 80. Sever LE, Emanuel I. Is there a connection between maternal zinc deficiency and congenital malformations of the central nervous system in man? Teratology . 1973;7:117-118.Crossref 81. Cavdar AO, Babacan E, Asik S, et al. Neural tube defects and zinc . Nutr Res Suppl . 1985:331-334. 82. Mukherjee MD, Sandstead HH, Ratnaparkhi MV, Johnson LK, Milne DB, Stelling HF. Maternal zinc, iron, folic acid, and protein nutriture and outcome of human pregnancy . Am J clin Nutr . 1984;40:496-507. 83. Meadows NJ, Ruse W, Smith MF, et al. Zinc and small babies . Lancet . 1981;2:1135-1136.Crossref 84. Favier M, Yacoub M, Racinet C, Marka C, Chambert P, Benbassa A. Les ions metalliques dans le liquide amniotique au cours du troisiem trimetre de la gestation . Rev Frn Gynecol Obstet . 1972;67:707-714. 85. Jameson S, Bertröm M, Hellsing K. Zinc status in pregnancy, the effect of zinc therapy on perinatal mortality. Presented at the 7th International Symposium on Trace Elements in Man and Animals; May 20,1990; Dubrovnik, Yugoslavia. Abstract. 86. Neggers YH, Cutter GR, Acton RT, et al. A positive association between maternal serum zinc concentration and birth weight . Am J Clin Nutr . 1990;51:678-684. 87. Cherry FF, Sandstead HH, Rojas P,Johnson LK, Batson HK, Wang XB. Adolescent pregnancy: associations among body weight, zinc nutriture, and pregnancy outcome . Am J Clin Nutr . 1989;50:945-954. 88. Jameson S. Zinc status and pregnancy outcome in humans . In: Prasad AS, Dreosti IE, Hetzel BS, eds. Clinical Application of Recent Advances in Zinc Metabolism . New York, NY: Alan R Liss Inc; 1982:39-52. 89. Hunt IF, Murphy NJ, Cleaver AE, et al. Zinc supplementation during pregnancy . Am J Clin Nutr . 1984;40:508-521. 90. MacDonald LD, Gibson RS, Miles JE. Changes in hair zinc and copper concentration of breast fed and bottle fed infants during the first six months . 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[Phytate] [calcium]/[zinc] ratios in Asian immigrant lacto-ovo vegetarian diets and their relationship to zinc nutriture . Nutr Res . 1986;6:475-483.Crossref

Kallen, Ronald J.

1991 American Journal of Diseases of Children

doi: 10.1001/archpedi.1991.02160080036017pmid: 1858721

Abstract •Urinary tract infections, in association with ureteral reflux or dysperistalsis, may lead to invasive renal parenchymal infection and residual scarring (reflux nephropathy). Such infections in infants are often not diagnosed during the acute phase. Late sequelae of reflux nephropathy include hypertension, proteinuria, or chronic renal failure. The latter may eventuate in the subset of patients with urinary tract infection and unilateral reflux extending to a solitary kidney or bilateral reflux. Proteinuria may herald the inexorable progression of glomerular sclerosis in patients destined to progress to end-stage renal disease, despite the absence of further recurrences of urinary tract infections. The mechanism of progression is probably similar to that occurring in other forms of chronic, diffuse parenchymal renal disease, which all have similar alterations in glomerular hemodynamics (an increase in glomerular capillary flow, pressure, and filtration). The consequent hyperfiltration per nephron may be related to the level of dietary protein intake or to some derivative of the protein load. Hyperfiltration appears to recapitulate the presumed renal hemodynamic response to the relatively high level of episodic meat consumption by paleolithic hunter-gatherers. A prudent therapeutic intervention in children with progressive reflux nephropathy may be a proportional reduction in protein intake. (AJDC. 1991;145:860-864) References 1. Goldraich NP, Barratt TM. Vesicoureteric reflux and renal scarring . In: Holliday MA, BarrattTM, Vernier RL, eds. Pediatric Nephrology . 2nd ed. Baltimore, Md: Williams & Wilkins; 1986:647-666. 2. Savage JM, Koh CT, Shah V, Barratt TM, Dillon MJ. Five year prospective study of plasma renin activity and blood pressure in patients with longstanding reflux nephropathy . Arch Dis Child . 1987;62:678-682.Crossref 3. Arant BS, Sotelo-Avila C, Bernstein J. Segmental 'hypoplasia' of the kidney (Ask-Upmark) . J Pediatr . 1979;95:931-939.Crossref 4. Roberts JA. Pathogenesis of nonobstructive urinary tract infections in children . J Urol . 1990;144( (pt 2) ):475-479. 5. Winberg J, Bollgren I, Kallenius G, Mollby R, Svenson SB. Clinical pyelonephritis and focal renal scarring: a selected review of pathogenesis, prevention, and prognosis . Pediatr Clin North Am . 1982;29:801-814. 6. Marild S, Heilstrom M, Jacobsson B, Jodal U, Eden CS. Influence of bacterial adhesion on ureteral width in children with acute pyelonephritis . J Pediatr . 1989;115:265-268.Crossref 7. Ransley PG, Risdon RA. The renal papilla, intrarenal reflux, and chronic pyelonephritis . In: Hodson CJ, Kincaid-Smith P, eds. Reflux Nephropathy . New York, NY: Masson Publishing USA Inc; 1979. 8. Jacobson SH, Eklof O, Eriksson CG, Lins L-E, Tidgren B, Winberg J. Development of hypertension and uraemia after pyelonephritis in childhood: 27 year followup . BMJ . 1989;299:703-706.Crossref 9. Lerner GR, Fleischmann LE, Perlmutter AD. Reflux nephropathy . Pediatr Clin North Am . 1987;34:747-770. 10. Dunn BR, Anderson S, Brenner BM. The hemodynamic basis of progressive renal disease . Semin Nephrol . 1986;6:122-138. 11. Brenner BM, Meyer TW, Hostetter TH. Dietary protein intake and the progressive nature of kidney disease: the role of hemodynamically mediated glomerular injury in the pathogenesis of progressive glomerular sclerosis in aging, renal ablation, and intrinsic renal disease . N Engl J Med . 1982;307:652-659.Crossref 12. Brenner BM, Garcia DL, Anderson S. Glomeruli and blood pressure: less of one, more of the other? Am J Hypertens . 1988;1( (pt 1) ):335-347.Crossref 13. Pelayo JC, Quan AG. Pathophysiology of glomerular hemodynamic adaptations to nephron loss . Semin Nephrol . 1989;9:10-13. 14. White RHR. Vesicoureteric reflux and renal scarring . Arch Dis Child . 1989;64:407-412.Crossref 15. Brenner BM. Hemodynamically mediated glomerular injury and the progressive nature of kidney disease . Kidney Int . 1983;23:547-655.Crossref 16. El-Khatib M, Becker GJ, Kincaid-Smith PS. Reflux nephropathy and primary vesicoureteric reflux in adults . Q J Med . 1990:77(New Series):1241-1253.Crossref 17. Krensky AM, Reddish JM, Teele RL. Causes of increased renal echogenicity in pediatric patients . Pediatrics . 1983;72:840-846. 18. Enriquez G, Lucaya J, Nieto J, Aso C. Hyperechogenic renal hypertrophy in glomerulosclerosis . Pediatr Radio! . 1989;19:441.Crossref 19. Avni EF, Van Sinoy ML, Hall H, Stallenberg B, Matos CL. Hypothesis: reduced renal mass with glomerular hyperfiltration, a cause of renal hyperechogenicity in children . Pediatr Radiol . 1989;19:108-110.Crossref 20. Anderson S, Brenner BM. Progressive renal disease: a disorder of adaptation . Q J Med. 1989;70(New Series):185-189. 21. Klahr S, Schreiner G, Ichikawa I. The progression of renal disease . N Engl J Med . 1988;318:1657-1666.Crossref 22. Fogo A, Ichikawa I. Evidence for the central role of glomerular growth promoters in the development of sclerosis . Semin Nephrol . 1989;9:329-342. 23. Lafferty HM, Brenner BM. Are glomerular hypertension and 'hypertrophy' independent risk factors for progression of renal disease? Semin Nephrol . 1990;10:294-304. 24. Eaton SB, Konner M. Paleolithic nutrition: a consideration of its nature and current implications . N Engl J Med . 1985;312:283-289.Crossref 25. Hill K. Hunting and human evolution . J Hum Evolut . 1982;11:521-544.Crossref 26. Foley R. A reconsideration of the role of predation on large mammals in tropical hunter-gatherer adaptation . Man . 1982;17:393-402.Crossref 27. Klahr S, Tripathy K. Evaluation of renal function in malnutrition . Arch Intern Med . 1966;118:322-325.Crossref 28. Hostetter TH. Human renal response to meat meal . Am J Physiol . 1986;250:F613-F618. 29. Herrera J, Rodriguez-lturbe B, Parra G, etal. Urinary prostaglandin E and kallikrein activity in glomerular hyperfiltration induced by a meat meal in man . Clin Nephrol . 1988;30:151-157. 30. BroeckerWS, Denton GH. What drives glacial cycles? Sci Am . 1990;262:48-56.Crossref 31. Bronowski J. The Ascent of Man . Boston, Mass: Little Brown & Co lnc; 1973:65-68. 32. ltskovitz HD. The renin-angiotensin system . In: Kurtzman NA, Martinez-Maldonado M, eds. Pathophysiology of the Kidney . Springfield, lll: Charles CThomas Publisher; 1977:391-445. 33. Giebisch G, Malnic G, Berliner RW. Renal transport and control of potassium excretion . In: Brenner BM, Rector FC Jr, eds. The Kidney . 3rd ed. Philadelphia, Pa: WB Saunders Co; 1986:177-205. 34. Meyer TW, Anderson S, Brenner BM. Dietary protein intake and progressive glomerular sclerosis: the role of capillary hypertension and hyperperfusion in the progression of renal disease . Ann Intern Med . 1983;98( (pt 2) ):832-838.Crossref 35. Thorner PS, Arbus GS, Celermajer DS, Baumal R. Focal segmental glomerulosclerosis and progressive renal failure associated with a unilateral kidney . Pediatrics . 1984;73:806-810. 36. Nomura S, Osawa G. Focal glomerular sclerotic lesions in a patient with unilateral oligomeganephronia and agenesis of the contralateral kidney: a case report . Clin Nephrol . 1990; 33:7-11. 37. Wikstad I, Celsi G, Larsson L, Herin P, Aperia A. Kidney function in adults born with unilateral renalagenesis agenesisornephrectomized in childhood . Pediatr Nephrol . 1988;2:177-182.Crossref 38. Klahr S. The modification of diet in renal disease study . N Engl J Med . 1989;320:864-866.Crossref 39. Metcoff J, Kelsey WM, Janeway CA. The nephrotic syndrome in children: an interpretation of its clinical, biochemical, and renal hemodynamic features as a variation of a single type of nephron disease . J Clin Invest . 1951;30:471-491.Crossref 40. Garcia DL, Rennke HG, Brenner BM, Anderson S. Glucocorticoids amplify glomerular injury in rats with renal ablation . Am J Hypertens . 1988;1:54-57. 41. Friedman AL. Dietary manipulation and progression of renal disease: strategies for the growing animal . Semin Nephrol . 1989;9:14-18. 42. Fine LG. Preventing the progression of human renal disease: have rational therapeutic principles emerged? Kidney Int . 1988;33:116-128.Crossref 43. Hunsicker LG. Studies of therapy of progressive renal failure in humans . Semin Nephrol . 1989;9:380-394. 44. Acchiardo SR, Moore LW, Cockrell S. Does low protein diet halt the progression of renal insufficiency? Clin Nephrol . 1986;25:289-294. 45. Ihle BU, Becker GJ, Whitworth JA, Charlwood RA, Kincaid-Smith PS. The effect of protein restriction on the progression of renal insufficiency . N Engl J Med . 1989;321:17731777.Crossref 46. Zeller K, Whittaker E, Sullivan L, Raskin P, Jacobson HR. Effect of restricting dietary protein on the progression of renal failure in patients with insulin-dependent diabetes mellitus . N Engl J Med . 1991; 324:78-84.Crossref 47. Uauy R, Hogg RJ, Holliday M. Protein-energy requirements of children with chronic renal insufficiency: report from the Southwest Pediatrie Nephrology Study Group and the Infant Diet Protein Study Group . Semin Nephrol . 1989;9:24-30. 48. Keane WF, Andersons, Aureli M, de ZeeuwD, NarinsRG, Povar G. Angiotensin converting enzyme inhibitors and progressive renal insufficiency. 1989;111:503-516. 49. Trachtman H, Gauthier B. Effect of angiotensinconverting enzyme inhibitor therapy on proteinuria in children with renal disease . J Pediatr . 1988;112:295-298.Crossref 50. Miller IJ, Suthanthiran M, Rigio RR, et al. Impact of renal donation: long-term clinical and biochemical follow-up of living donors in a single center . Am J Med . 1985;79:201-208.Crossref 51. Anderson CF, Velosa JA, Frohnert PP, et al. The risks of unilateral nephrectomy: status of kidney donors 10 to 20 years postoperatively . Mayo Clin Proc . 1985;60:367-374.Crossref 52. Chavers BM, Michael AF, Weiland D, Najarian JS, Mauer SM. Urinary albumin excretion in renal transplant donors . Am J Surg . 1985;149:343-346.Crossref 53. Williams SL, Oler J, Jorkasky DK. Long-term renal function in kidney donors: a comparison of donors and their siblings . Ann Intern Med . 1986;105:1-8.Crossref 54. Talseth T, Fauchald P, Skrede S, et al. Long-term blood pressure and renal function in kidney donors . Kidney Int . 1986;29:1072-1076.Crossref 55. BayWH, Hebert LA. The living donor in kidney transplantation . Ann Intern Med . 1987;106:719-727.Crossref

Hanna, James D.;Niimi, Kazuhiko;Chan, James C. M.

1991 American Journal of Diseases of Children

doi: 10.1001/archpedi.1991.02160080041018pmid: 1858722

Abstract • X-linked hypophosphatemia is a hereditary form of rickets that results from an isolated renal tubular wasting of phosphate. The clinical features unique to this disorder, and the recent advances in our understanding of vitamin D metabolism and molecular genetics in X-linked hypophosphatemia are reviewed. Finally, a succinct critique of the controversial treatment modalities round up this review. (AJDC. 1991;145:865-870) References 1. Davis M, Stanbury SW. The rheumatic manifestation of metabolic bone disease . Clin Rheum Dis . 1981;7:595-646. 2. Rasmussen H, Tenenhouse HS. Hypophosphatemias . In: Scriver CR, Beaudet AC, Sly W, Valle D, eds. Metabolic Basis of Inherited Disease . 6th ed. New York, NY: McGraw-Hill International Book Co; 1989:2581-2604. 3. Engfeldt B, Zetterstrom R, Winberg J. Primary vitamin D—resistant rickets, III: biophysical studies of skeletal tissues . J Bone Joint Surg Am . 1956;38:1323-1334. 4. Frost HM. A unique histological feature of vitamin D—resistant rickets observed in four cases . Acta Orthop Scand . 1963;33:220-226.Crossref 5. Steendijk R, van den Hooff A, Nielsen HKL, Jowsey J. Lesion of bone matrix in vitamin D—resistant rickets . Nature . 1965;207:426-427.Crossref 6. Ecarot-Charrier B, Glorieux FH, Travers R, Desbarats M, Bouchard F, Huick A. Defective bone formation by transplanted Hyp mouse bone cells into normal mice . Endocrinology . 1988;123:768-773.Crossref 7. Hardy DC, Murphy WA, Siegel BA, Reid IR, Whyte MP. X-linked hypophosphatemia in adults: prevalence of skeletal radiographic and scintigraphic features . Radiology . 1989;171: 403-414.Crossref 8. Chan JCM, Alon U, Hirschman GM. Renal hypophosphatemic rickets . J Pediatr . 1985;106:533-544.Crossref 9. Brickman AS, Coburn JW, Kurokawa K, Bethune JE, Harrison HE, Norman AW. Actions of 1,25-dihydroxycholecalciferol in patients with hypophosphatemic, vitamin D—resistant rickets . N Engl J Med . 1973;289:495-498.Crossref 10. Glorieux FH, Scriver CR, Reade TM, Goldman H, Roseborough A. Use of phosphate and vitamin D to prevent dwarfism and rickets in X-linked hypophosphatemia . N Engl J Med . 1972;287:481-487.Crossref 11. Hirschman GH, DeLuca HF, Chan JCM. Hypophosphatemic vitamin D—resistant rickets: metabolic balance studies in a child receiving 1,25-dihydroxyvitamin-D3, phosphate and ascorbic acid . Pediatrics . 1978;61:451-457.Crossref 12. Glorieux FH, Marie PJ, Pettifor JM, Delvin EE. Bone response to phosphate salts, ergocalciferol, and calcitriol in hypophosphatemic vitamin D—resistant rickets . N Engl J Med . 1980;303:1023-1031.Crossref 13. Kristiansen JH, Pedersen VF. Hypophosphatemic vitamin D-resistant rickets treated with 1 alpha-hydroxyvitamin D3 . Int J Pediatr Nephrol . 1981;2:245-247. 14. Chesney RW, Mazess RB, Rose P, Hamstra AJ, DeLuca HF, Breed AL. Long-term influence of calcitriol (1,25-dihydroxyvitamin D) and supplemental phosphate in X-linked hypophosphatemic rickets . Pediatrics . 1983;71:559-567. 15. Rasmussen H, Pechet M, Anast C, Mazur A, Gertner J, Broadus AE. Long-term treatment of familial hypophosphatemic rickets with oral phosphate and 1 alpha-hydroxyvitamin D3 . J Pediatr . 1981;99:16-25.Crossref 16. Chesney RW, Mazess RB, Rose P, Hamstra AJ, DeLuca HF. Supranormal 25-hydroxyvitamin D and subnormal 1,25-dihydroxyvitamin D: their role in x-linked hydrophosphatemic rickets . AJDC . 1980;134:140-143. 17. Lyles KW, Clark AG, Drezner MK. Serum 1,25-dihydroxyvitamin D levels in subjects with X-linked hypophosphatemic rickets and osteomalacia . Calcif Tissue Int . 1982; 34:125-130.Crossref 18. Lyles KW, Clark AG, Drezner MK. Parathyroid hormone effects on serum 1,25-dihydroxyvitamin D levels in patients with X-linked dominant hypophosphatemic rickets: evidence for abnormal 25-hydroxyvitamin D-1-hydroxylase activity . J Clin Endocrinol Metab . 1982;54:638-644.Crossref 19. Mason RS, Rohl PG, Lissner D, Posen S. Vitamin D metabolism in hypophosphatemic rickets . AJDC . 1982;136:909-913. 20. Meyer RA Jr, Gray RW, Meyer MH. Abnormal vitamin D metabolism in the X-linked hypophosphatemic mouse . Endocrinology . 1980;107:1577-1581.Crossref 21. Tenenhouse HS. Abnormal mitochondrial 25-hydroxyvitamin D3-1-hydroxylase activity in the vitamin D and calcium deficient X-linked Hyp mouse . Endocrinology . 1983;113:816-818.Crossref 22. Chan JCM, Lovinger RD, Mamunes P. Renal hypophosphatemic rickets: growth acceleration after long-term treatment with 1,25-dihydroxyvitamin D3 . Pediatrics . 1980;66:445-454. 23. Balsan S, Tieder M. Linear growth in patients with hypophosphatemic vitamin D—resistant rickets: influence of treatment regimen and parental height . J Pediatr . 1990;116:365-370.Crossref 24. Alon U, Chan JCM. Effects of hydrochlorothiazide and amiloride in renal hypophosphatemic rickets . Pediatrics . 1985;75:754-763. 25. Alon U, Costanzo LS, Chan JCM. Additive hypocalciuric effects of amiloride and hydrochlorothiazide in patients treated with calcitriol . Miner Electrolyte Metab . 1984;10:379-386. 26. Alon U, Brewer WH, Chan JCM. Nephrocalcinosis: detection by ultrasonography . Pediatrics . 1983;71:970-973. 27. Tanner JM, Whitehouse RH, Marshall WA, Carter BS. Prediction of adult height, bone age, and occurrence of menarche at ages 4 to 6 with allowance for midparent height . Arch Dis Child . 1975;50:14-26.Crossref 28. Wilson DM, Lee PDK, Marcus R, et al. Growth hormone therapy in familial hypophosphatemia . PediatrRes . 1990;27:195. 29. Alon U, Newsome H, Chan JCM. Hyperparathyroidism in patients with X-linked dominant hypophosphatemic rickets: application of the calcium infusion test as an indication for parathyroidectomy . Int J Pediatr Nephrol . 1984;5:39-43. 30. Goodyer PR, Kronick JB, Jequier S, Reade TM, Scriver CR. Nephrocalcinosis and its relationship to treatment of hereditary rickets . J Pediatr . 1987;111:700-704.Crossref 31. Moncrieff MW, Change GW. Nephrotoxic effect of vitamin D therapy in vitamin D refractory rickets . Arch Dis Child . 1969;44:571-579.Crossref 32. Weber G, Cazziffo MA, Frisone F, et al. Nephrocalcinosis in children and adolescents: sonographic evaluation during long-term treatment with 1,25-dihydroxycholecalciferol . Child Nephrol Urol . 1988-1989;9:273-276. 33. Stickler GB, Morgenstern BZ. Hypophosphataemic rickets: final height and clinical symptoms in adults . Lancet . 1989;2:902-905.Crossref 34. Stickler GB, Jowsey J, Bianco AJ Jr. Possible detrimental effect of large doses of vitamin D in familial hypophosphatemic vitamin D—resistant rickets . J Pediatr . 1971;79:68-71.Crossref 35. Reid IR, Hardy DC, Murphy WA, Teitelbaum SL, Bergfield MA, Whyte MP. X-linked hypophosphatemia: a clinical, biochemical, and histopathologic assessment of morbidity in adults . Medicine . 1989;68:336-352.Crossref 36. Slatopolsky E, Weerts C, Thielan R, Horst R, Harter H, Martin K. Marked suppression of secondary hyperparathyroidism by intravenous administration of 1,25-dihydroxy-cholecalciferol in uremic patients . J Clin Invest . 1984;74: 2136-2143.Crossref 37. Silver J, Naveh-Many T, Mayer H, Schmelzer H, Popovtzer M. Regulation by vitamin D metabolites of parathyroid hormone gene transcription in vivo in the rat . J Clin Invest . 1986;78:1296-1301.Crossref 38. Burmester JK, Weise RJ, Maeda N, DeLuca HF. Structure and regulation of the rat 1,25-dihydroxyvitamin D3 receptor . Proc Natl Acad Sci USA . 1988;85:9499-9502.Crossref 39. Minghetti PP, Norman AW. 1,25(OH)2-vitamin D3 receptors: gene regulation and genetic circuitry . FASEB J . 1988;2:3043-3053. 40. DeLuca HF. The vitamin D story: a collaborative effort of basic science and clinical medicine . FASEB J . 1988;2:224-236. 41. Kainer G, Bell NH, Chan JCM. Disorders of calcium metabolism . In: Chan JCM, Gill JR Jr, eds. Kidney Electrolyte Disorders . New York, NY: Churchill Livingstone Inc; 1990:171-222. 42. Rasmussen H, Anast C. Familial hypophosphatemic and vitamin D dependent rickets . In: Stanbury JB, Wyngaarden JB, Frederickson DS, Goldstein JL, Brown MS, eds. Metabolic Basis of Inherited Disease . 5th ed. New York, NY: McGraw-Hill International Book Co; 1983:1743-1773. 43. Clarke GD, Kainer G, Conway WF, Chan JCM. Intramyocellular phosphate metabolism in X-linked hypophosphatemic rickets . J Pediatr . 1990;116:288-292.Crossref 44. Smith R, Newman RJ, Radda GK, Stokes M, Young A. Hypophosphatemic osteomalacia and myopathy: studies with nuclear magnetic resonance spectroscopy . Clin Sci . 1984;67:505-509. 45. Meyer RA Jr, Meyer MH, Gray RW. Parabiosis suggests a humoral factor is involved in X-linked hypophosphatemia in mice . J Bone Miner Res . 1989;4:493-500.Crossref 46. Meyer RA Jr, Conway GD, Chan JCM. X-linked hypophosphatemia . Semin Nephrol . 1989;9:56-61. 47. Lyon MF, Scriver CR, Baker LRT, Tenenhouse HS, Kronick J, Mandla S. The Gy mutation: another cause of hypophosphatemia in mouse . Proc Natl Acad Sci USA . 1986;83:4899-4903.Crossref 48. Reade AP, Thakker RV, Davis KE, et al. Mapping of human X-linked hypophosphatemic rickets by multilocus linkage analysis . Hum Genet . 1986;73:267-270.Crossref 49. Machler M, Frey D, Gal A, et al. X-linked dominant hypophosphatemia is closely linked to DNA markers DX 41 and DX 43 at Xp22 . Hum Genet . 1986;73:271-275.Crossref 50. Kainer G, Clarke GD, Spence JE, Chan JCM. X-linked hypophosphatemia: an 'experiment of nature' on phosphate transport . In: Strauss J, ed. Growth Immunosuppression and Renal Disorders in Neonates and Children . Coral Gables, Fla: University of Miami Press; 1989:59-66. 51. Spence JE, Kainer G, Chan JCM. Genetics of vitamin D resistant rickets . In: Spitzer A, Avner E, eds. Inheritance of Kidney and Urinary Tract Disease . Boston, Mass: Kluwer Academic Publishers; 1989:167-176. 52. Boneh A, Reade TM, Scriver CR, Rishikof E. Audiometric evidence for two forms of X-linked hypophosphatemia in humans, apparent counterpoints of Hyp and Gy mutations in mouse . Am J Med Genet . 1987;27:997-1003.Crossref 53. Kainer G, Spence JE, Chan JCM. X-linked hypophosphatemia: progress in characterization of genetic and metabolic defects . Nephron . 1989;51:449-453.Crossref

Crosby, Warren M.

1991 American Journal of Diseases of Children

doi: 10.1001/archpedi.1991.02160080047019pmid: 1858723

Abstract • Fetal malnutrition, a worldwide problem, is accompanied by varying degrees of lifelong morbidity for the child. Only 25% of fetal malnutrition is accomplished by maternal risk factors known to cause intrauterine growth retardation (ie, chronic hypertension, advanced diabetes mellitus, or severe preeclampsia). If the malnourished fetus could be detected early in pregnancy, nutritional intervention might be successful in improving fetal growth rate and in avoiding the morbidity due to malnutrition. This communication reviews the almost 40 years of studies by Jack Metcoff, MD, and coworkers to unravel the causes of fetal malnutrition and their efforts to prevent it. (AJDC. 1991;145:871-876) References 1. Metcoff J. Intrauterine detection of fetal malnutrition . In: Hake ESE, ed. The Mammalian Fetus: Comparative Biology and Methodology . Springfield, Ill: Charles C Thomas Publisher; 1975:213-235. 2. Lubchenko LO. The High Risk Infant . Philadelphia, Pa: WB Saunders Co; 1976. 3. Cruise MD. A longitudinal study of the growth of low birth weight infants . Pediatrics . 1973;51:260-268. 4. Rosso P, Winick M. The effect of severe malnutrition on weight, cholesterol, phospholipid and DNA content of the developing human brain . Fed Proc . 1970;29:495. 5. Chase HP. Alterations in human brain biochemistry following intrauterine growth retardation . Pediatrics . 1972;50:403. 6. Drillien CM. The small for date infant: etiology and prognosis . Pediatr Clin North Am . 1970;17:9-24. 7. Fitzhardinge PM, Steven EN. The small for date infant, II: neurological and intellectual sequelae . Pediatrics . 1972;50:50-57. 8. Fancourt R, Campbell S, Harvey D, Norman AP. Follow up study of small for dates babies . BMJ . 1976;1:1435-1437.Crossref 9. Metcoff J. Biochemical effects of protein-calorie malnutrition in man . Annu Rev Med . 1967;18:377-422.Crossref 10. Altshuler G, Russell P, Ermocilla R. The placental pathology of small-for-gestational age infants . Am J Obstet Gynecol . 1975;121:351-359. 11. Metcoff J, Frank S, Yoshida T, Torres-Pineda R, Kaiser E, Hansen JDL. Cell composition and metabolism in kwashiorkor (severe protein-calorie malnutrition in children) . Medicine . 1966;45:365-390.Crossref 12. Metcoff J, Wikman-Coffelt, Yoshida T, et al. Energy metabolism and protein synthesis in human leukocytes during pregnancy and in placenta related to fetal growth . Pediatrics . 1973;51:866-877. 13. Yoshida T, Metcoff J, Frank S, de la Pena C. Intermediary metabolites and adenine nucleotides in leukocytes of children with protein calorie malnutrition . Nature . 1967;214:525-526.Crossref 14. Krebs HA, Eggleston LV. The role of pyruvate kinase in the regulation of gluconeogenesis . Biochem J . 1965;94:3C-4C. 15. Crosby WM, Metcoff J, Costiloe JP, et al. Fetal malnutrition: an appraisal of correlated factors . Am J Obstet Gynecol . 1977;128:22-31. 16. McClain PE, Metcoff J, Crosby WM, Costiloe JP. Relationship of maternal amino acid profiles at 25 weeks gestation to fetal growth . Am J Clin Nutr . 1978;31:401-407. 17. Metcoff J. Maternal nutrition and fetal development . J Early Hum Dev . 1980;4:99-120.Crossref 18. Metcoff J, Cole TJ, Luff R. Fetal growth retardation induced by dietary imbalance of threonine and dispensable amino acids with adequate energy and protein-equivalent intakes in pregnant rats . J Nutr . 1981;111:1411-1424. 19. Metcoff J, Costiloe JP, Crosby WM, et al. Maternal nutrition and fetal outcome . Am J Clin Nutr . 1981;34:708-721. 20. Metcoff J, Costiloe JP, Crosby WM, et al. Effect of food supplementation (WIC) during pregnancy on birth weight . Am J Clin Nutr . 1985;41:933-947. 21. Metcoff J, Costiloe JP, Crosby WM, Sandstead H, Milne D. Smoking in pregnancy: relation of birth weight to maternal plasma, carotene and cholesterol levels . Obstet Gynecol . 1989;74:302-309.

Kooh, Sang Whay;Binet, Ann

1991 American Journal of Diseases of Children

doi: 10.1001/archpedi.1991.02160080053020pmid: 1858724

Abstract •We encountered three children who had neonatal hypocalcemia followed by a period of normocalcemia and recurrence of hypocalcemia later in childhood. They were full-term infants with normal birth weights who developed hypocalcemia within the first 48 hours after birth. The hypocalcemia resolved in 1 week, 3 months, and 14 months in the three patients. The recurrences of hypocalcemia occurred at 4, 7, and 12 years of age. Their plasma parathyroid hormone concentrations were consistently low but detectable. We suggest that partial hypoparathyroidism is the underlying abnormality in these patients and that neonatal hypocalcemia in otherwise healthy infants indicates the need for calcium measurements during childhood and adolescence. (AJDC. 1991;145:877-880) References 1. Senterre J, Salle B. Problems in homeostasis of calcium, phosphorus and magnesium . In: Stern L, Vert P, eds. Neonatal Medicine . New York, NY: Masson Publishing USA Inc; 1987:836. 2. Fanconi A, Prader A. Transient congenital idiopathic hypoparathyroidism . Helv Paediatr Acta . 1967;22:342-359. 3. Rosenbloom AL. Transient congenital idiopathic hypoparathyroidism . South Med J . 1973;66:666-670.Crossref 4. Bainbridge R, Maghai Z, Mimouni F, Tsang RC. Transient congenital hypoparathyroidism: how transient is it? J Pediatr . 1987;111:866-868.Crossref 5. Tsang RC, Kleinman LI, Sutherland JM, Light IJ. Hypocalcemia in infants of diabetic mothers: studies in Ca, P, and Mg metabolism and in parathormone responsiveness . J Pediatr . 1972;80:384-395.Crossref 6. Tsang RC, Chen IW, Friedman MA, Chen I. Neonatal parathyroid function: role of gestational and post-natal age . J Pediatr . 1973;83:728-738.Crossref 7. Tsang RC, Chen IW, Hayes W, Atkinson W, Atherton H, Edwards N. Neonatal hypocalcemia in birth asphyxia . J Pediatr . 1974;84:428-433.Crossref 8. Tsang RC, Chen IW, Friedman MA, et al. Parathyroid function in infants of diabetic mothers . J Pediatr . 1974;86:399-404. 9. Conley ME, Beckwith JB, Mancer JF, Tenckhoff L. The spectrum of the DiGeorge syndrome . J Pediatr . 1979;94:883-890.Crossref 10. Gidding SS, Minciotti AL, Langman CB. Unmasking of hypoparathyroidism in familial partial DiGeorge syndrome by challenging with disodiumedetate . Nfng/y Med . 1988; 319:1589-1591. 11. Müller W, Peter HH, Wilken M, et al. The DiGeorge syndrome, I: clinical evaluation and course of partial and complete form of the syndrome . Eur J Pediatr . 1988;147:496-502.Crossref 12. Mallette LE, Cooper JB, Kirkland JL. Transient congenital hypoparathyroidism: possible association with anomalies of the pulmonary valve . J Pediatr . 1982;101:928-931.Crossref 13. Blind E, Schmidt-Gayle H, Scharia S, et al. Two-site assay of intact parathyroid hormone in the investigation of primary hyperparathyroidism and other disorders of calcium metabolism compared with amid region assay . J Clin Endocrinol Metab . 1988;67:353-360.Crossref 14. Nussbaum SR, Zahradnik RJ, LavigneJR, etal. Highly sensitive two-site immunoradiometric assay of parathyrin, and its clinical utility in evaluating patients with hypercalcemia . Clin Chem . 1987;33:1364-1367.

Needlman, Robert;Fried, Lise E.;Morley, Debra S.;Taylor, Sunday;Zuckerman, Barry

1991 American Journal of Diseases of Children

doi: 10.1001/archpedi.1991.02160080059021pmid: 1858725

Abstract •Educational research has shown that children become literate more easily if their parents read to them. A clinic-based program was designed to encourage early book use among parents of children at risk. It included (1 ) waiting room readers, (2) guidance about literacy development, and (3) provision of children's books at each visit. Seventy-nine parents of children aged 6 to 60 months were interviewed. Parents who had previously received a book were more likely to report looking at books with their children or that looking at books was a favorite activity (adjusted odds ratio, 4.05). This association was strongest among parents receiving Aid to Families With Dependent Children (odds ratio, 7.8). This preliminary study suggests that pediatricians can play a role in enriching children's early literacy environments, especially for children at high risk of school failure. (AJDC. 1991;145:881-884) References 1. Anastasiou N, HanesML, Hanes M. Language and Reading Strategies for Poverty Children . Baltimore, Md: University Park Press; 1982. 2. Teale W, Sulzby E. Emergent literacy as a perspective for examining howyoung children become writers and readers . In: Teale W, Sulzby E, eds. Emergent Literacy: Writing and Reading . Norwood, NJ: Ablex Publishing Corp; 1986. 3. Anderson AB, Stokes SJ. Social and institutional influences and the development and practice of literacy . In: Goelman H, Oberg A, Smith F, eds. Awakening to Literacy . Exeter, NH: Heinemann; 1984:23. 4. Goldfield BA, Snow C. Reading books with children: the mechanics of parental influence on children's reading achievement . In: Flood J, ed. Promoting Reading Comprehension . Newark, Del: International Reading Association; 1984. 5. Hiebert EH. Issues related to home influences on young children's print-related development . In: YadenDB,Templeton S, eds. Metalinguistic Awareness and Beginning Literacy . Portsmouth, NH: Heinemann Educational Books; 1986. 6. Durkin D. Children Who Read Early: Two Longitudinal Studies . New York, NY: Teachers College Press; 1966. 7. McCormickC, Mason J. Intervention procedures for increasing preschool children's interest in and knowledge about reading . In: Teale W, Sulzby E, eds. Emergent Literacy: Writingand Reading . Norwood, NJ: Ablex Publishing Corp; 1986:90-116. 8. BettelheimB,ZelanK. On LearningtoRead . NewYork,NY: Random House; 1982 9. Heath SB. Ways With Words: Language Life and Work in Communities and Classrooms . Cambridge, Mass: Cambridge University Press; 1983. 10. Brown DR, Ottinger DR. The Perceptual Basis of Developing Reading Skill: Final Report . Washington, DC: Office of Education, Bureau of Research; 1970. US Department of Health, Education, and Welfare publication RMQ66004. 11. Lewis C, Gregory S. Parents' talk to their infants: the importance of context . First Language . 1987;7:201-216.Crossref 12. Ninio A, Bruner JS. The achievement and antecedents of labelling . J Child Lang . 1978;5:1-15.Crossref 13. SnowC, Ninio A. The contracts of literacy: what children learn from learning to read books . In: Teale W, Sulzby E, eds. Emergent Literacy: Writing and Reading . Norwood, NJ: Ablex Publishing Corp.; 1986:116-138. 14. Heath SB, Branscombe A. The book as narrative prop in language acquisition . In: Schieffelin B, Gilmore P, eds. The Acquisition of Literacy: Ethnographic Perspectives . Norwood, NJ: Ablex Publishing Corp.; 1986:16-34. 15. Kleinbaum DG, Kupper LL, Morgenstern H. Epidemiologie Research . New York, NY: Van Nostrand Reinhold; 1982. 16. Locke J. Pittsburgh's Beginning With Books Project . School Library J . (February) 1988:22-24. 17. Ninio A. Picture-book reading in mother-infant dyads belonging to two subgroups in Israel . Child Dev . 1980;51:587-590.Crossref 18. Parker S, Greer S, Zuckerman B. Double jeopardy: the impact of poverty on early child development . Pediatr Clin North Am . 1988;45:1227-1240

Ridgway, Derry;Wolff, Lawrence J.;Deforest, Adamadla

1991 American Journal of Diseases of Children

doi: 10.1001/archpedi.1991.02160080065022pmid: 1858726

Abstract • Twenty-four children receiving maintenance chemotherapy for acute lymphoblastic leukemia were given booster doses of tetanus-diphtheria combined toxoids. One month later, 19 of the 24 children were given Haemophilus influenzae B oligosaccharide-cross-reacting material conjugate vaccine. Following immunization, all patients had protective antibody titers against tetanus, 92% had protective antidiphtheria titers, and 84% had protective titers against H influenzae. Preimmunization titers, postimmunization titers, and response to immunization varied according to the intensity of therapy. There was no correlation with duration of therapy or quantitative hematologie values in the peripheral blood. These observations support the recommendation that children treated for acute lymphoblastic leukemia should be immunized against H influenzae B. (AJDC. 1991;145:887-891) References 1. Kung FH, Orgel HA, Wallace WW, Hamburger RN. Antibody production following immunization with diphtheria and tetanus toxoids in children receiving chemotherapy during remission of malignant disease . Pediatrics . 1984;74:86-89. 2. Feldman S, Giglioni F, ShenepJL, Roberson PK, LottL. Risk of Haemophilus influenza type b disease in children with cancer and response of immunocompromised leukemic children to a conjugate vaccine . J Infect Dis . 1990;161:926-931.Crossref 3. Nyerges G, Zimonyi I, Nyerges G, Meszner Z, Marosi A. Efficiency of tetanus toxoid booster in leukemic children . Acta Paediatr Acad Scientiarum Hung . 1981;22:237-241. 4. van der Does-van den Berg A, Hermans J, Nagel), van Steenis G. Immunity to diphteria, pertussis, tetanus, and poliomyelitis in children with acute lymphocytic leukemia after cessation of chemotherapy . Pediatrics . 1981;67:222-229. 5. Feldman S, Giglioni F, Bockhold C, NaegeleR. Measles and rubella antibody status in previously vaccinated children with cancer . Med Pediatr Oncol . 1988;16:308-311.Crossref 6. Weisman SJ, Cates KL, Allegretta GJ, Quinn JJ, Altman AJ. Antibody response to immunization with Haemophilus influenza type B polysaccharide vaccine in children with cancer . / Pediatr . 1987;111 -.727-729.Crossref 7. Lange B, jakacki R, Nasab AH, Luevy N. Immunization of leukemic children with Haemophilus conjugate vaccine . J Pediatr Infect Dis . 1989;8:883-884.Crossref 8. Gaynon PS, Steinherz PG, Reaman GH, Bleyer WA, Sather H, Hammond GD. Strategies for the treatment of children with acute lymphoblastic leukemia and unfavorable presenting features . Haematol Blood Transfus . 1987;30:167-172. 9. Deforest A, Long SS, Lischner HW, etal. Simultaneous administration of measles-mumps-rubella vaccine with booster doses of diphtheria-tetanus-pertussis and poliovirus vaccines . Pediatrics . 1988;81:237-246. 10. Hardegree MC, Barile MF, Pittman M, Maloney CJ, Schofield F, Maclennan R. Immunization against neonatal tetanus in NewGuinea, IV: comparison oftetanus antitoxin titres obtained by haemagglutination and toxin neutralization in mice . Bull WHO . 1970;43:461-468. 11. MiyamuraK, NishioS, Ito A, Murata R, Kono R. Micro cell culture method for determination of diphtheria toxin and antitoxin titres using VERO cells, I: studies on factors affecting the toxin and antitoxin titration . J Biol Stand . 1974;2:189-201.Crossref 12. Farr RS. A quantitative immunochemical measure of the primary interaction between l*BSA and antibody . J Infect Dis . 1958;103:239-262.Crossref 13. Anderson P. Intrinsic tritium labeling of the capsular polysaccharide antigen of Haemophilus influenza type B . J Immunol . 1978;120:866-870. 14. Orenstein WA, Weisfeld JS, Halsey NA. Diphtheria and Tetanus Toxoids and Pertussis Vaccine, Combined . Washington, DC: Pan American Health Organization, World Health Organization; 1983. Publication 451:30-51. 15. Saarinen UM. Severe infections in childhood leukemia: a follow-up study of 100 consecutive ALL patients . Acta Paediatr Scand . 1984;73:515-522.Crossref 16. SiberGR. Bacteremias due to Haemophilus influenza and Streptococcus pneumonia: their occurrence and course in children with cancer . AJDC . 1980;134:668-672. 17. Immunization Practices Advisory Committee. Update: prevention of Haemophilus influenza type B disease . AJDC . 1988;142:419-420.

Ing, Donna J.;Glass, Roger I.;Woods, Patricia A.;Simonetti, Murri;Pallansch, Mark A.;Wilcox, Wallace D.;Davidson, Bruce L.;Sievert, Alan J.

1991 American Journal of Diseases of Children

doi: 10.1001/archpedi.1991.02160080070023pmid: 1650128

Abstract • Between January and November 1989, we studied 174 infants aged 6 to 16 weeks in a randomized clinical trial to (1) determine the immunogenicity of a single dose of tetravalent rhesus rotavirus vaccine (RRV-TV) when administered with three different buffer regimens: no antacid buffer and small-volume (2.5-mL) and large-volume (30-mL) antacid buffer; and (2) examine the potential interference of RRV-TV on the immune response to oral polio vaccine. Immunogenicity of RRV-TV, measured as a fourfold rise in antibody titers to rotavirus, was similar in the groups receiving small- and large-dose buffer (45% and 49%, respectively) and significantly less in the group that received RRV-TV alone (23%). Administration of RRV-TV with oral polio vaccine did not significantly interfere with the neutralization response of oral polio vaccine poliovirus serotypes 1, 2, or 3, and overall, 29%, 87%, and 24% of the infants had a fourfold rise in titer to each serotype, respectively. (AJDC. 1991;145:892-897) References 1. Kapikian AZ. Approaches to immunization of infants and young children against gastroenteritis due to rotaviruses . Rev Infect Dis . 1980;2:459-469.Crossref 2. De Zoysa I, Feachem RG. Interventions for the control of diarrhoeal diseases among young children: rotavirus and cholera immunization . Bull WHO . 1985;63:569-583. 3. Institute of Medicine. Prospects for immunizing against rotavirus . In: New Vaccine Development: Establishing Priorities . Washington, DC: National Academy Press; 1985;1:410-423. 4. Kapikian AZ, Flores J, HoshinoY, etal. Rotavirus: the major etiologic agent of severe infantile diarrhea may be controllable by a 'Jennerian' approach to vaccination . J Infect Dis . 1986;153:815-822.Crossref 5. Gothefors L, Wadell G, Juto P, et al. Prolonged efficacy of rhesus rotavirus vaccine in Swedish children . J Infect Dis . 1989;159:753-757.Crossref 6. Flores J, Perez-Schael I, Gonzalez M, et al. Protection against severe rotavirus diarrhoea by rhesus rotavirus vaccine in Venezuelan infants . Lancet . 1987;1:1882-1884. 7. Clark HF, Borian FE, Plotkin SA. Immune protection of infants against rotavi rus gastroenteritis by a serotype 1 reassortant of bovine rotavirus WC-3 . J Infect Dis . 1990;161:1099-1104.Crossref 8. Clemens J, Jertborn M, Sack D, et al. Effect of neutralization of gastric acid on immune responses to oral B-subunit killed whole-cell cholera vaccine . J Infect Dis . 1986;154:175-178.Crossref 9. Ho MS, Floyd RL, Glass RI, et al. Simultaneous administration of rhesus rotavirus vaccine and oral poliovirus vaccine: immunogenicity and reactogenicity . Pediatr Infect Dis J . 1989;8:692-696.Crossref 10. Giammanco G, DeGrandi V, Lupo L, et al. Interference of oral poliovirus vaccine on RIT 4237 oral rotavirus vaccine . Eur J Epidemiol . 1988;4:121-123.Crossref 11. Hanlon P, Marsh V, Shenton F, etal. Trial of an attenuated bovine rotavirus vaccine (RIT 4237) in Cambian infants . Lancet . 1987;1:342-345. 12. Vodopija I, BaklaicZ, Vlatkovic R. Combined vaccination with live oral poliovirus vaccine and the bovine rotavirus RIT 4237 strain . Vaccine . 1988;4:233-236.Crossref 13. Wulff H, Anderson LJ, Pallansch MA, et al. Diagnosis of enterovirus 70 infection by demonstration of IgM antibodies . J Med Virol . 1987;21:321-327.Crossref 14. Schmidt NJ. Diagnostic procedures for viral, rickettsial and chlamydial infections . In: Lennette EH, Schmidt NJ, eds. Cell Culture Techniques for Diagnostic Virology . 5th ed. Washington, DC: American Public Health Association; 1979:65-139. 15. Weiss C, Clark HF. Rapid inactivation of rotaviruses by exposure to acid buffer or acidic gastric juice . J Gen Virol . 1985;66:2725-2730.Crossref 16. Jalil F. Immunogenicity and reactogenicity rhesus rotavirus vaccine given in combination with oral or inactivated poliovirus vaccine and diptheria tetanus and pertussis vaccine. Trans R Soc Trop Med Hyg. In press.

Rothstein, Edward P.;Schiller, Ruth P.;Girone, Joseph A. C.;Hipp, Thomas J.;Souder, Ronald L.;Bernstein, Henry H.;Madore, Dace V.;Johnson, Cynthia L.;Smith, David H.

1991 American Journal of Diseases of Children

doi: 10.1001/archpedi.1991.02160080076024pmid: 1858727

Abstract • Objective. —To evaluate the immunologie potential of infants 7 to 15 months of age to respond to Haemophilus influenzae type b polysaccharide vaccine following immunization with H influenzae b oligosaccharide-CRM197 conjugate vaccine. Study Design. —One hundred seventy-one infants, aged 7 to 15 months, were consecutively and alternatively assigned to one of three immunization protocols. Group 1 (n = 71) received three doses of H influenzae b oligosaccharideCRM197 conjugate vaccine, group 2 (n = 47) received two doses of H influenzae b oligosaccharide-CRM197 conjugate vaccine followed by one dose of H influenzae type b polysaccharide vaccine, and group 3 received one dose of H influenzae b oligosaccharide-CRM197 conjugate vaccine followed by two doses of H influenzae type b polysaccharide vaccine. Immunizations were given on day 0 and at 2 months and 6 months. Anti-H influenzae type b polysaccharide antibody levels were measured on day 0 and 2, 3,6, 7, and 12 months after the study began. Results. —Haemophilus influenzae type b polysaccharide vaccine given as a second dose stimulated an antibody rise but did so less effectively than H influenzae b oligosaccharideCRM197 conjugate vaccine. Two doses of H influenzae b oligosaccharide-CRM197 conjugate vaccine were highly immunogenic; geometric means were 31 and 35 γg/mL in the 7to 11-month and 12- to 15-month age groups, respectively. Following two doses of H influenzae b oligosaccharide-CRM197 conjugate vaccine, both immunization protocols resulted in (1) equally high geometric mean antibody levels 1 month after immunization and (2) similar geometric mean antibody levels 6 months after immunization. Conclusions. —Haemophilus influenzae b oligosaccharide-CRM197 conjugate vaccine induces antibody levels that would be expected to protect infants from initial invasion and primes the immune system for an anamnestic response. Our data indicate that if a booster immunization is needed, H influenzae type b polysaccharide vaccine could be an alternative to H influenzae b oligosaccharide-CRM197 conjugate vaccine.(AJDC. 1991;145:898-900) References 1. Granoff DM, Cates KL. Haemophilus influenzae type b polysaccharide vaccines . J Pediatr . 1985;107:330-335.Crossref 2. KäyhtyH, Karanko V, Peltola H, Mäkelä PH. Serumantibodies after vaccination with Haemophilus influenzae type b capsular polysaccharide and responses to reimmunization . Pediatrics . 1984;74:857-865. 3. Anderson P, Pichichero M, Edwards K, Porch CR, Insel RA. Priming and induction of Haemophilus influenzae type b capsular antibodies in early infancy by Dpo20, an oligosaccharideprotein conjugate vaccine . J Pediatr . 1987;111:644-650.Crossref 4. Ward J. Newer Haemophilus influenzae type b vaccines and passive prophylaxis . Pediatr Infect Dis J . 1987;6:799-803.Crossref 5. Centers for Disease Control. Food and Drug Administration approval of use of a Haemophilus b conjugate vaccine for infants . MMWR . 1990;39:925-926. 6. Centers for Disease Control. Food and Drug Administration approval of use of a Haemophilus b conjugate vaccine in infants . MMWR . 1990;39:698-699. 7. Madore DV, Johnson CL, Phipps DC, et al. Safety and immunologie response to Haemophilus influenzae type b oligosaccharide-CRM197 conjugate vaccine in 1- to 6-month-old infants . Pediatrics . 1990;85:331-337. 8. Käyhty H, Peltola H, Karenko V, Mäkelä PH. The protective level of serum antibodies to the capsular polysaccharide of Haemophilus influenzae type b . J Infect Dis . 1983;147:1100.Crossref

Strauss, Ronald G.

1991 American Journal of Diseases of Children

doi: 10.1001/archpedi.1991.02160080082025pmid: 1858728

Abstract • Infants, particularly those who were very small premature neonates, are among the most common of all patient groups to undergo extensive transfusion. It is estimated that approximately 300000 neonates undergo transfusions annually. Most infants who undergo transfusion are exposed to multiple blood donors, and although each exposure poses only a small risk, the potential for adverse effects of multiple transfusions is not trivial. Transfusion practices for neonates are controversial, variable, and based on scanty scientific information. For the most part, controlled scientific studies have not been performed to clearly establish the indications for the transfusion of blood components to neonates. Considering these limitations, guidelines are offered for the transfusion of red blood cells, platelets, and neutrophils into neonates. (AJDC. 1991;145:904-911) References 1. Wegman WE. Annual summary of vital statistics—1988 . Pediatrics . 1989;84:943-955. 2. Guyer B, Wallach LA, Rosen SL. Birth-weight-standardized neonatal mortality rates and prevention of low birth weight: how does Massachusetts compare with Sweden? N Engl J Med . 1982;306:1230-1233.Crossref 3. Kim HC. Red blood cell transfusion in the neonate . Semin Perinatal . 1983;7:159-174. 4. Sacher RA, Luban NLC, Strauss RG. Current practice and guidelines for the transfusion of cellular blood components in the newborn . Transfusion Med Rev . 1989;3:39-54.Crossref 5. Floss AM, Strauss RG, Goeken N, Knox L. Multiple transfusions fail to provoke antibodies against blood cell antigens in human infants . Transfusion . 1986;26:419-422.Crossref 6. Brown MS, Berman ER, Luckey D. Prediction of the need for transfusion during anemia of prematurity . J Pediatr . 1990;116:773-778.Crossref 7. Council on Scientific Affairs. Autologous blood transfusions . JAMA . 1983;256:2378-2380. 8. CzajaAJ, DavisGL. Hepatitis non-A, non-B: manifestations and implications of acute and chronic disease . Mayo Clin Proc . 1982;57:639-652. 9. Rogers MF, Thomas PA, Starcher ET, Noa MC, Bush TJ, Jaffe HW. Acquired immunodeficiency syndrome in children: report of the Centers for Disease Control national surveillance, 1982 to 1985 . Pediatrics . 1987;79:1008-1014. 10. Strauss RG. Safety of Iowa's blood supply . Iowa Med . 1990;80:195-198. 11. Blajchman MA, Sheridan D, Rawls WE. Risks associated with blood transfusion in newborn infants . Clin Perinatol . 1984;2:403-415. 12. Howell RR. The diagnostic value of serum enzyme measurements . 7 Pediatr . 1966;68:121-134.Crossref 13. Alter HJ, Pu reell RH, Shih JW, et al. Detection of antibody to hepatitis C virus in prospectively following transfusion recipients with acute and chronic non-A, non-B hepatitis . N Engl J Med . 1989;321:1494-1500.Crossref 14. Tegtmeier GE. The use of cytomegalovirus-screened blood in neonates . Transfusion . 1988;28:201-203.Crossref 15. Adler SP. Transfusion-acquired CMV infection in premature infants . Transfusion . 1989;29:278-279.Crossref 16. American Association of Blood Banks. 13th ed. Standards for Blood Banks and Transfusion Services . Arlington, Va: American Association of Blood Banks; 1989:31-35. 17. Strauss RG, Barnes A, Blanchette VS, et al. Directed and limited-exposure blood donations for infants and children . Transfusion . 1990;30:68-72.Crossref 18. Sanders MR, Graeber JE. Posttransfusion graft-versushost disease in infancy . J Pediatr . 1990;117:159-163.Crossref 19. Shaw JCL. Iron absorption by the premature infant: the effect of transfusion and iron supplements on the serum ferritin levels . Acra Paediatr Scand . 1982;299( (suppl) ):83-89.Crossref 20. Adamkin DH, Shott RJ, Cook LN, Andrews BF. Nonhyperoxic retrolental fibroplasia . Pediatrics . 1977;60:828-830. 21. Sjoberg POI, Bondesson UG, Sedin EG, Gustafsson JP. Exposure of newborn infants to plasticizers . Transfusion . 1985;25:424-428.Crossref 22. Williams RA, Brown EF, Hurst D, Franklin LC. Transfusion of infants with activation of erythrocyte T antigen . J Pediatr . 1989;115:949-953.Crossref 23. Pahwa S, Sia C, Harper R, Pahwa R. T lymphocyte subpopulations in high-risk infants: influence of age and blood transfusions . Pediatrics . 1985;76:914-917. 24. Sullivan JL. Iron, plasma antioxidants, and the Oxygen radical disease of prematurity.' AJDC . 1988;142:1341-1344. 25. Strauss RG. Current issues in neonatal transfusions . Vox Sang . 1986;51:1-9.Crossref 26. Blanchette VS,Zipursky A. Assessment of anemia in newborn infants . Clin Perinatol . 1984;11:489-510. 27. Strauss RG, Sacher RA, Blazina JF, et al. Commentary on small-volume red cell transfusions for neonatal patients . Transfusion . 1990;30:565-570.Crossref 28. Lenes BA, Sacher RA. Blood component therapy in neonatal medicine . Clin Lab Med . 1981;1:285-309. 29. Stockman JA. Anemia of prematurity. Current concepts in the issue of when to transfuse . Pediatr Clin North Am . 1986;33:111-128. 30. Alverson DC, Isken VH, Cohen RS. Effect of booster blood transfusions on oxygen utilization in infants with bronchopulmonary dysplasia . J Pediatr . 1988;113:722-726.Crossref 31. Lister G, Hellenbrand WE, Kleinman CS, Talner NS. Physiologic effects of increasing hemoglobin concentration in leftto-right shunting in infants with ventricular septal defects . N Engl J Med . 1982;306:502-506.Crossref 32. Rosenthal A. Hemodynamics in physiologic anemia of infancy . N Engl J Med . 1982;306:538-540.Crossref 33. Kattwinkel J. Neonatal apnea: pathogenesis and therapy . J Pediatr . 1977;90:342-347.Crossref 34. Joshi A, Gerhardt T, Shandloff P, Bankalari E. Blood transfusion effect on the respiratory pattern of preterm infants . Pediatrics . 1987;80:79-84. 35. KeyesWG,DonohuePK, SpivakJL, Jones MD Jr, Oski FA. Assessingthe need fortransfusion of premature infants and role of hematocrit, clinical signs, and erythropoietin level . Pediatrics . 1989;84:412-417. 36. Kurzner SI, Garg M, Gautista DB, et al. Growth failure in infants with bronchopulmonary dysplasia: nutrition and elevated resting metabolic expenditure . Pediatrics . 1988;81:379384. 37. Stockman JA, Clark DA. Weight gain: a response to transfusion in selected preterm infants . AJDC . 1984;138:828-830. 38. Blank JP, Sheagren TG, Vajaria J, Mangurten HH, Benawra RS, Puppala BL. The role of RBC transfusion in the premature infant . A7DC . 1984;138:831-833. 39. Ross MP, Christensen RD, Rothstein G, et al. A randomized trial to develop criteria for administering erythrocyte transfusions to anemic preterm infants 1 to 3 months of age . J Perinatol . 1989;9:246-253. 40. Luban NLC, Strauss RG, Hume HA. Commentary on the safety of red blood cells preserved in extended storage media for neonatal transfusions . Transfusion . 1990;31:229-235.Crossref 41. Strauss RG. The risks of thrombocytopenia and the standard uses of platelet transfusions . Plasma Ther Transfusion Technol . 1986;7:279-285. 42. Strauss RG. Perinatal platelet and granulocyte transfusions . In: Kennedy MS, Wilson S, Kelton J, eds. Perinatal Transfusion Medicine . Arlington, Va: American Association of Blood Banks; 1990:123-144. 43. Gibson B. Neonatal haemostasis . Arch Dis Child . 1989;64:503-506.Crossref 44. Andrew M, Castle V, Saigal S, Carter C, Kelton JG. Clinical impart of neonatal thrombocytopenia . J Pediatr . 1987;110:457464. 45. Lupton BA, Hill A, Whitfield MR, Carter CJ, Wadsworth LD, Roland EH. Reduced platelet count as a risk factor for intraventricular hemorrhage . AJDC . 1988;142:1222-1224. 46. Moroff G, Friedman A, Robkin-Kline L, Gautier G, Luban NLC. Reduction of the volume of stored platelet concentrates for use in neonatal patients . Transfusion . 1984;24:144-146.Crossref 47. Simon TL, Sierra ER. Concentration of platelet units into small volumes . Transfusion . 1984;24:173-175.Crossref 48. Strauss RG. Granulopoiesis and neutrophil function in the neonate . In: Stockman JA, Pochedly C,eds. Developmental and Neonatal Hematology . New York, NY: Raven Press; 1988:88-101. 49. Cairo MS. Neonatal neutrophil host defense . AJDC . 1989;143:40-46. 50. Christensen RD, Rothstein G, Anstall HB, Bybee B. Granulocyte transfusions in neonates with bacterial infection, neutropenia and depletion of mature marrow neutrophils . Pediatrics . 1982;70:1-6. 51. Laurenti F, Ferro R, Isacchi G, et al. Polymorphonuclear leukocyte transfusion for the treatment for sepsis in the newborn infant . J Pediatr . 1981;98:118-123.Crossref 52. Cairo MS, RuckerR, Bennetts GA, etal. Improved survival of newborns receiving leukocyte transfusions for sepsis . Pediatrics . 1984;74:887-892. 53. Cairo MS, Worcester C, RuckerR, et al. Role of circulating complement and polymorphonuclear leukocyte transfusion in treatment and outcome in critically ill neonates with sepsis . J Pediatr . 1987; 110:935-941.Crossref 54. DeCurtin M, Romano G, Scarpato N, D'Antonia F, Paludetto R, Ciccimara F. Transfusions of polymorphonuclear leukocytes (PMN) in an infant with necrotizing enterocolitis (NEC) and a defect of phagocytosis . J Pediatr . 1981;99:665-668. 55. Christensen RD,Anstall H, Rothstein G. Neutrophil transfusion in septic neutropenic neonates . Transfusion . 1982;22:151-154.Crossref 56. Laing IA, Boulton FE, Hume R. Polymorphonuclear leukocyte transfusion in neonatal septicemia . Arch Dis Child . 1983;58:1003-1005.Crossref 57. Laurenti F, LaGreca G, Ferro R, Bucci G. Transfusion of polymorphonuclear neutrophils in premature infant with Klebsiella sepsis . Lancet . 1978;2:111-112.Crossref 58. Baley JE, Stork EK, Warkentin PI, Shurin SB. Buffy coat transfusions in neutropenic neonates with presumed sepsis: a prospective, randomized trial . Pediatrics . 1987;80:712-720. 59. Wheeler JC, Chauvenet AR, Johnson CA, etal. Buffy coat transfusions in neonates with sepsis and neutrophil storage pool depletion . Pediatrics . 1987;97:422-425. 60. Newman RS, Waffarn F, Simmons GE, Goldsticker RD, Pcariz JA. Questionable value of saline prepared granulocytes in the treatment of neonatal septicemia . Transfusion . 1988;28:196-197.Crossref 61. Strauss RG. Current status of granulocyte transfusions to treat neonatal sepsis . J Clin Apheresis . 1989;5:25-29.Crossref 62. Halpern DS, Wacher P, LacourtG, etal. Effects of recombinant human erythropoietin in infants with the anemia of prematurity: a pilot study . J Pediatr . 1990;116:779-786.Crossref 63. Shannon KE, Mentzer WC, Abels RI, et al. Recombinant human erythropoietin (r-Hu-EPO) in anemia of prematurity (ACP): preliminary results of a double-blind placebo controlled pilot study . Pediatr Res . 1990;27:269A. 64. Strauss RG. Directed and limited-exposure donor programs for children . In: Sacher RA, Strauss RG, eds. Contemporary Issues in Pediatrie Transfusion Medicine . Arlington, Va: American Association of Blood Banks; 1989:1-11. 65. Elbert C, Strauss RG, Barrett F, Goeken NE, Pittner B, Cordie D. Biological mothers may be dangerous donors for their neonates. Acfa Haematol. 1991. In press.

Gonzalez-Heydrich, Joseph;Kerner, John Alan;Steiner, Hans

1991 American Journal of Diseases of Children

doi: 10.1001/archpedi.1991.02160080091026pmid: 1858729

Abstract • We treated four patients with chronic vomiting during childhood in whom a tentative diagnosis of psychogenic vomiting was made after an extensive evaluation. In each case, the diagnosis was reconsidered during the course of treatment, as observations about the patients and their response to interventions accumulated. In three instances, these observations did not fit those expected if the diagnosis of psychogenic vomiting was correct. This led to a reexamination of the organic evaluation and the discovery of an undiagnosed organic contribution to the vomiting. In the fourth patient, gastric emptying studies confirmed that there was a strong psychological contribution to the vomiting, and helped to more carefully define this contribution. Family and individual psychotherapy and treatment were aided by the greater clarity in diagnosis. (AJDC. 1991;145:913-916) References 1. Malagelada JR, Camilleri M. Unexplained vomiting: a diagnostic challenge . Ann Intern Med . 1984;101:211-218.Crossref 2. Hill WH. Psychogenic vomiting . Gut . 1968;9:348-352.Crossref 3. Clarke DJ, Salmons PH, Harrison T. Psychogenic vomiting among female Asian migrants to the United Kingdom . Int J Soc Psychiatry . 1988;34:221-229.Crossref 4. Leibovich MA. Psychogenic vomiting . Psychother Psychosom . 1973;22:263-268.Crossref 5. Reinhart JB. Disorders of the gastrointestinal tract in children: consultation-liaison experience . Psychiatr Clin North Am . 1982;5:387-397. 6. Rosenthal RH, Webb WL, Wruble LD. Diagnosis and management of persistent psychogenic vomiting . Psychosomatics . 1980;21:722-730. 7. Wruble LD, Rosenthal RH, Webb WL. Psychogenic vomiting: a review . Am J Gastroenterol . 1982;77:318-321. 8. Stacher G. Differentialdiagnose psychosomatischer Schluckstorungen . Wien Klin Wochenschr . 1986;98:658-663. 9. Abell TL, Kim CH, Malagelada JR. Idiopathic cyclic nausea and vomiting: a disorder of gastrointestinal motility? Mayo Clin Proc . 1988;63:1169-1175.Crossref 10. Camilleri M. Organic basis for symptoms in functional gastrointestinal disease? Mayo Clin Proc . 1988;63:1256-1257.Crossref 11. Smart HL, Atkinson M. Abnormal vagal function in irritable bowel syndrome . Lancet . 1987;2:475-478.Crossref 12. Camilleri M, Fealey RD. Idiopathic autonomic denervation (AD): an unrecognized cause of dysmotility in patients with apparently functional bowel disorders . Gastroenterology . 1988;95:858.

Freed, Gary L.;Landers, Susan;Schanler, Richard J.

1991 American Journal of Diseases of Children

doi: 10.1001/archpedi.1991.02160080095027pmid: 1858730

Abstract • It is often difficult for new mothers to know whom to approach for the necessary guidance and practical problem solving required for successful long-term lactation. Although obstetricians are familiar with the care of the breast, they may not maintain the degree of postpartum follow-up necessary to ensure its proper function nor is it their responsibility to ensure that the infant receives proper nourishment. Pediatricians are expected to offer advice and information regarding not only the advantages and disadvantages of breastfeeding but also practical management of this art. We provide a guide for practitioners who wish to assist breast-feeding mothers and their infants. (AJDC. 1991;145:917-921) References 1. Neifert M, Secat J. Medical management of successful breastfeeding . Pediatr Clin North Am . 1986;30:743-762. 2. Koop CE, Brannin ME. Breastfeeding—the community norm: report of a workshop . Public Health Rep . 1984;99:550-558. 3. Sarett P, Bain KR, O'Leary JC. Decisions on breastfeeding or formula feeding and trends in infant feeding practices . AJDC . 1983;137:719-725. 4. Palti H, Mansbuck I, Pridan H, et al. Episodes of illness in breastfed and bottle-fed infants in Jerusalem . Isr J Med Sci . 1984;20:395-399. 5. Cunningham AS. Morbidity in breastfed and artificially-fed infants . J Pediatr . 1977;90:726-729.Crossref 6. Cunningham AS. Morbidity in breastfed and artificially-fed infants, II . J Pediatr . 1979;95: (5) :685-689.Crossref 7. Fergusson DM, Horwood LJ, Shannon FT, Taylor B. Breast-feeding, gastrointestinal and lower respiratory illness in the first two years . Aust Pediatr J . 1981;17:191-195. 8. Habicht JP, DaVanzo J, Butz WP. Does breastfeeding really save lives, or are apparent benefits due to biases . Am J Epidemiol . 1986;123:279-290. 9. Beske E, Garvis M. Important factors in breastfeeding success . Matern Child Nurs J . 1982;7:174-149.Crossref 10. Hill R. A Passage Into Life: Breastfeeding . Houston, Tex: Texas Children's Hospital Press; 1981:2. 11. Hoffman JB. A suggested treatment for inverted nipples . Am J Obstet Gynecol . 1953;66:346-348. 12. Brown MS, Hurlock JT. Preparation of the breast for breastfeeding . Nurs Res . 1975;24:448-451.Crossref 13. American Academy of Pediatrics. Breastfeeding . Evanston, Ill: American Academy of Pediatrics Publications Department; 1984. 14. Lawrence RA. Breastfeeding: a guide for the medical profession . St Louis, Mo: CV Mosby Co; 1980:123. 15. Lascari A. 'Early' breastfeeding jaundice: clinical significance . J Pediatr . 1986;108:156-158.Crossref 16. DeCarvalho MD, Hall M, Harvey D. Effects of water supplementation on physiological jaundice in breastfed babies . Arch Dis Child . 1989;56:568-569.Crossref 17. Gartner LM, Auerbach KG. Breastfeeding and human milk: their association with jaundice in the neonate . Clin Perinatol . 1987;14:89-107. 18. Winfield CR, MacFaul R. Clinical study of prolonged jaundice in breast and bottle-fed babies . Arch Dis Child . 1978;53:506-507.Crossref 19. Maisels MJ. Hyperbilirubinemia . In: Nelson NM, ed. Current Therapy in Neonatal-Perinatal Medicine, 1985-86 . St Louis, Mo: CV Mosby Co; 1985. 20. Neifert MR, Seacat JM. Contemporary breast-feeding management . Clin Perinatol . 1985;12:319-342.

Rutstein, Richard M.

1991 American Journal of Diseases of Children

doi: 10.1001/archpedi.1991.02160080100028pmid: 1677526

Abstract • Effective prophylaxis exists against Pneumocystis carinii pneumonia, a major cause of illness and death among human immunodeficiency virus—infected children and adults. While adults with CD4 counts less than 0.2 × 109/L are at highest risk for Pneumocystis carinii, clinical or laboratory markers of high risk in children infected with the human immunodeficiency virus have not yet been established. A chart review of 13 infants with perinatally acquired human immunodeficiency virus infection and children with Pneumocystis carinii pneumonia revealed that infants younger than 12 months developed Pneumocystis carinii pneumonia despite CD4 counts that were normal by adult standards. In contrast to the markedly increased serum IgG levels seen in most children infected with the human immunodeficiency virus, five children with Pneumocystis carinii pneumonia had IgG levels less than 3.0 g/L. Twelve patients had preexisting symptoms consistent with human immunodeficiency virus infection before the episode of Pneumocystis carinii pneumonia. In addition to clinical symptoms, low IgG levels and CD4 counts adjusted for age may serve to identify those children who are most at risk for Pneumocystis carinii pneumonia and therefore candidates for prophylaxis. Prophylaxis should be offered to all infants under age 12 months with proven, or clinical symptoms compatible with, human immunodeficiency virus infection. For children older than 12 months, CD4 counts less than 0.3 × 109/L appear to be predictive of risk for Pneumocystis carinii pneumonia, and these children should also receive prophylaxis. (AJDC. 1991;145:922-924) References 1. Centers for Disease Control. AIDS Weekly Surveillance Report . (January 30) , 1989;1-5. 2. Scott GB, Hutto C, Makuch RW, et al. Survival in children with perinatally acquired human immunodeficiency virus type 1 infection . N Engl J Med . 1989;321:1791-1796.Crossref 3. Hughes WT, KuhnS, Chaudhary S, et al. Successfulchemoprophylaxis for Pneumocystis carinii pneumonia . N Engl J Med . 1977;297:1419-1426.Crossref 4. Hughes WF, Rivera GK, Schell MJ, Thornton D, Lott L. Successful intermittent chemoprophylaxis for Pneumocystis carinii pneumonitis . N Engl J Med . 1987;316:1627-1632.Crossref 5. Leoung GS, Montgomery AB, McGinty E, Feigal DW, LymphoMed Consortium Investigators. Double-blinded randomized trial of aerosol pentamidine for secondary prophylaxis of Pneumocystis carinii pneumonia. Proceedings of the Fifth International Conference on AIDS; June 4-9, 1989; Montreal, Canada 6. Fischl MA, Dickinson GM, La Voie L. Safety and efficacy of sulfamethoxazole and trimethoprin chemoprophylaxis for Pneumocystis carinii pneumonia in AIDS . JAMA . 1988;259:1185-1189.Crossref 7. Kovacs JA, Masur H. Prophylaxis of Pneumocystis carinii pneumonia: an update . J Infect Dis . 1989;160:882-886.Crossref 8. Phair JP, Munoz A, Detels R, et al. The risk of Pneumocystis carinii pneumonia among men infected with human immunodeficiency virus type 1 . N Engl J Med . 1990;322:161-165.Crossref 9. Centers for Disease Control. Guidelines for prophylaxis against Pneumocystis carinii pneumonia for persons infected with human immunodeficiency virus . MMWR . 1989;38:1-9. 10. Bernstein LA, Bye MR, Rubinstein A. Prognostic factors and life expectancy in children with acquired immunodeficiency syndrome and Pneumocystis carinii pneumonia . AJDC . 1989;143:775-778. 11. Sanders-Laufer D, Burroughs M, Marshall F, et al. Pneumocystis carinii pneumonia in "low risk" HIV-infected children . Pediatr Res . 1990;27:183. 12. Bagarazzi ML, Connor E, McSherry GD, Oleske JM. PCP among HIV infected children: ten years experience . Pediatr Res . 1990;27:166. 13. Leibovitz E, Riguard M, Pollack H, et al. Pneumocystis carinii pneumonia in infants with the human immunodeficiency virus with more than 450 CD4 lymphocytes per cubic millimeter . N Engl J Med . 1990;323:531-533.Crossref 14. Centers for Disease Control. Classification system for human immunodeficiency virus (HIV) in children under 13 years of age . MMWR . 1987;36:225-230. 15. O'Rouke S, Plaeger-Marshall S, Gillespie S, et al. T cell parameters by age in normal and HIV-infected children. Presented at the Sixth International Conference on AIDS; June 1990; San Francisco, Calif. 16. Denn TN, Niven P, Skuia C, et al. Age related changes of lymphocyte phenotypes in healthy children . Pediatr Res . 1990;27:155. 17. Rubinstein A. Pediatric AIDS . Curr Probl Pediatr . 1986; 26:387-392. 18. Blanche S, Le Deist F, Fischer A, et al. Longitudinal study of 18 children with perinatal LAV/HTLV III infection . J Pediatr . 1986;109:965-970.Crossref 19. Johnson JP, Nair P, Hines SF, et al. Natural history and serologic diagnosis of infants born to human immunodeficiency virus infected women . AJDC . 1989;143:1147-1153. 20. Rao CP, Gelfand EW. Pneumocystis carinii pneumonitis in patients with hypogammaglobunemia and intact T cell immunity . J Pediatr . 1983;103:410-412.Crossref 21. Gordin FM, Simon GL, Wofsky CB, Mills J. Adverse reactions to trimethoprin-sulfamethoxazole in patients with acquired immunodeficiency syndrome . Ann Intern Med . 1984;100:495-499.Crossref 22. Sattler FR, Cowan R, Nielsen DM, Ruskin J. Trimethoprin-sulfamethoxazole compared with pentamidine for treatment of Pneumocystis carinii pneumonia in the acquired immunodeficiency syndrome . Ann Intern Med . 1988;109:280-287.Crossref

Glasser, Lewis;Duncan, Burris R.;Corrigan, James J.

1991 American Journal of Diseases of Children

doi: 10.1001/archpedi.1991.02160080103029pmid: 1713405

Abstract • A 12-month-old boy with Kostmann's syndrome was admitted with cavitary pulmonary disease. He had also had bacterial conjunctivitis, periorbital cellulitis, pneumonitis, and otitis media since the age of 10 days. His umbilical cord had not fallen off until he was 3 weeks old. Neutropenia was diagnosed at 4 weeks of age. Antineutrophil antibody studies were negative. A bone marrow aspirate showed granulocytic hypoplasia and a maturation arrest at the promyelocyte stage. Hematopoietic cell culture showed normal numbers of colony-forming units—granulocyte macrophage. Serum granulocyte-macrophage colony-stimulating factor level, was 0.24 ng/mL (normal, >0.05 ng/mL). Serum granulocyte colony-stimulating factor levels, measured by enzyme immunoassay, were undetectable. The patient was successfully treated with filgrastim (granulocyte colony-stimulating factor), with an increase in the absolute neutrophil count to 10.0×109/L. Thus, our case of Kostmann's syndrome appears to represent a defect in regulation or production of granulocyte colony-stimulating factor. (AJDC. 1991;145:925-928) References 1. Watari K, Shigetaka A, Shirafuji N, et al. Serum granulocyte colony-stimulating factor levels in healthy volunteers and patients with various disorders as estimated by enzyme immunoassay . Blood . 1989;73:117-122. 2. Kostmann R. Infantile agranulocytosis: a review with presentation of ten new cases . Acta Paediatr Scand . 1975;64:362-368.Crossref 3. Welte K, Zeidler C, Reiter A, et al. Differential effects of granulocyte-macrophage colony-stimulating factor and granulocyte colony-stimulating factor in children with severe congenital neutropenia . Blood . 1990;75:1056-1063. 4. Lalezari P, Pryce SC. Detection of neutrophil and platelet antibodies in immunologically induced neutropenia and thrombocytopenia . In: Rose NR, Friedman H, eds. Manual of Clinical Immunology . Washington, DC: American Society for Microbiology; 1980:744-749. 5. Kurland JI. Granulocyte-monocyte progenitor cells . In: Golde DW, ed. Methods in Hematology, 11: Hematopoiesis . New York, NY: Churchill Livingstone; 1984:87-122. 6. Iscove NN, Sieber F, Winterhalter KH. Erythroid colony formation in cultures of mouse and human bone marrow: analysis of the requirement for erythropoietin by gel filtration and affinity chromatography on agarose-concavalin A . J Cell Physiol . 1974;83:309-320.Crossref 7. Ogawa M, Leary AG. Erythroid progenitors . In: Golde DW, ed. Methods in Hematology, 11: Hematopoiesis . New York, NY: Churchill Livingstone; 1984:123-132. 8. Tsu TT, Hertzenberg LA. Solid-phase radioimmune assays . In: Mishell BB, Shiigi SM, eds. Selected Methods in Cellular Immunology . San Francisco, Calif: WH Freeman; 1980:373-397. 9. Motojima H, Kobayashi T, Shimane M, Kamachi S, Fukushima M. Quantitative enzyme immunoassay for human granulocyte colony stimulating factor (G-CSF) . J Immunol Methods . 1989;118:187-192.Crossref 10. Cantrell MA, Anderson D, Cerretti DP, et al. Cloning, sequence, and expression of a human granulocyte/macrophage colony stimulating factor . Proc Natl Acad Sci U S A . 1985; 82:6250-6254.Crossref 11. Groopman JE, Molina JM, Scadden DT. Hematopoietic growth factors . N Engl J Med . 1989;321:1449-1459.Crossref 12. Bonilla MA, Gillio AP, Ruggeiro M, et al. Effects of recombinant human granulocyte-stimulating factor on neutropenia in patients with congenital agranulocytosis . N Engl J Med . 1989;320:1574-1580.Crossref 13. Sonoda Y, Arai N, Ogawa M. Humoral regulation of eosinophilopoiesis in vitro: analysis of the targets of interleukin-3, granulocyte/macrophage colony-stimulating factor (GM-CSF), and interleukin-5 . Leukemia . 1989;3:14-18. 14. Kawaguchi Y, Kobayashi M, Tanabe A, et al. Granulopoiesis in patients with congenital neutropenia . Am J Hematol . 1985;20:223-234.Crossref 15. Pietsch T, Buhrer C, Mempel K, et al. Blood mononuclear cells from patients with severe congenital neutropenia are capable of producing granulocyte colony-stimulating factor . Blood . 1991;77:1234-1237.

1991 American Journal of Diseases of Children

doi: 10.1001/archpedi.1991.02160080110030

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Trustees, Board of

1991 American Journal of Diseases of Children

doi: 10.1001/archpedi.1991.02160080111031

Abstract • Infant walkers are used by many parents because of the convenience they provide in keeping children occupied. Unfortunately, parents may develop a false sense of security that leads to diminished vigilance over the safety of their infant. Although most injuries that result from walkers are minor, serious trauma from head injuries, lacerations, and burns does occur occasionally. The American Medical Association recommends that physicians counsel parents on the risk of injury that can occur from the use of infant walkers and inform parents that these devices do not either promote bipedal ambulation or offer a substitute for careful parental supervision. (AJDC. 1991;145:933-934) References 1. US Consumer Product Safety Commission. Baby Walker Injuries: Hazard Analysis . Washington DC: US Bureau of Epi demiology; 1974. 2. US Consumer Product Safety Commission. Baby Walkers . Washington DC: US Bureau of Epidemiology; 1975. US Consumer Product Safety Commission Fact Sheet 66. 3. US Consumer Product Safety Commission. Baby Walkers . Washington DC: US Bureau of Epidemiology; 1980. US Consumer Product Safety Commission Fact Sheet 66 Revised. 4. Fazen LF, Felizberto PI. Baby walker injuries . Pediatrics . 1982;70:106-109. 5. Kavanagh CA, Banco L. The infant walker: a previously unrecognized health hazard . AJDC . 1982;136:205-206. 6. Stoffman JM, Bass MJ, Fox AM. Head injuries related to the use of baby walkers . Can Med Assoc J . 1984;131:573-575. 7. Greensher J, Mofenson HC. Injuries at play . Pediatr Clin North Am . 1985;32:136-139. 8. Rieder MJ, Schwartz C, Newman J. Patterns of walker use and walker injury . Pediatrics . 1986;78:488-493. 9. Kauffman IB, Ridenour M. Influences of infant walker on onset and quality of walking pattern of locomotion: an electromyographic investigation . Percept Mot Skills . 1977;45:1323-1329.Crossref 10. Holm VA, Harthun-Smith L, Tada WL. Infant walkers and cerebral palsy . AJDC . 1983;137:1189-1190.

Mota-Hernández, Felipe;Bross-Soriano, Daniel;Pérez-Ricardez, Maria L.;Velásquez-Jones, Luis

1991 American Journal of Diseases of Children

doi: 10.1001/archpedi.1991.02160080115032pmid: 1858732

Abstract • We sought to determine the efficacy of three different types of treatment in children with acute diarrhea who, during the oral rehydration period, had high stool output (>10 mL/kg per hour). Sixty-six children, aged 1 to 18 months, with an average stool output of 22.6 mL/kg per hour were randomly distributed into three groups: group 1 received a rice flour solution, group 2 received the World Health Organization rehydration solution by gastric infusion, and group 3 continued to receive this solution orally. In all three groups, a decrease in stool output was observed, with the higher decrease observed in group 1 patients. Such a decrease facilitated rehydration of all 22 patients in group 1 (100%) in 3.3±1.5 hours, 16 (73%) in group 2 in 4.3±2.1 hours, and 15 (69%) in group 3 in 4.9±2.0 hours. No complications were observed. These data indicate that the rice flour solution is effective in children with high stool output diarrhea. (AJDC. 1991;145:937-940) References 1. World Health Organization. A Manual for the Treatment of Acute Diarrhea: For Use by Physicians and Other Senior Health Workers . Geneva, Switzerland: Program for Control of Diarrhoeal Diseases, World Health Organization; 1984. WHO/CDD/SER/80.2, Rev 1. 2. Santosham M, Daum RS, Dillman L, et al. Oral rehydration therapy of infantile diarrhea . N Engl J Med . 1982;306:1070-1076.Crossref 3. Velásquez JL, Llausás ME, Mota HF, Quiroz RB. Tratamiento ambulatorio del ninõ deshidratado por diarrea aguda . Bol Med Hosp Infant Mex . 1985;42:220-225. 4. Pizarro D, Posada G, Mahalanabis D, Sandi L. Comparison of efficacy of a glucose/glycine/glycil-glycine electrolyte solution versus the standard WHO/ORS in diarrheic dehydrated children . J Pediatr Gastroenterol Nutr . 1988;7:882-888.Crossref 5. Mahalanabis D. Development of an Improved Formulation of Oral Rehydration Salts (ORS) With Antidiarrhoeal and Nutritional Properties: A 'Super ORS.' Geneva, Switzerland: World Health Organization; 1985. WHO/CDD/DDM/85.3. 6. Murtaza A, Zulbigan I, Khan S, Lindblod BS, Sahlgren BA, Aperia A. The benefits of the very early introduction of powdered rice and dried edible seeds (Dal moong) in the oral rehydration solution during the treatment of acute infectious diarrhoea of infancy . Acta Paediatr Scand . 1987;76:861-864.Crossref 7. Carpenter CH, Greenough WB, Pierce N. Oral-rehydration therapy: the role of polymeric substrates . N Engl J Med . 1988;319:1346-1348.Crossref 8. Velasquez JL. Nuevas soluciones de hidratación oral en diarrea aguda . Bol Med Hosp Infant Mex . 1988;45:781-786. 9. Wong HB. Rice water in the treatment of infantile infectious gastroenteritis . Lancet . 1981;2:102-103.Crossref 10. Molla AM, Sarker SA, Holssain M, Greenough WB. Rice powder electrolyte solution as oral therapy in diarrhea due to Vibrio cholerae and Escherichia coli . Lancet . 1982;1:1317-1319.Crossref 11. Mehta MN, Subramanian S. Comparison of rice water, rice eletrolyte solution, and glucose electrolyte solution in the management of infantile diarrhoea . Lancet . 1986;1:843-845.Crossref 12. Bhan MK, Ghut OP, Knoshoo V, et al. Efficacy of mungbean (lentil) and pop rice based rehydration solutions in comparison with the standard glucose electrolyte solution . J Pediatr Gastroenterol Nutr . 1987;6:392-399.Crossref 13. World Health Organization. Oral Rehydration Salts (ORS) Formulation Containing Trisodium Citrate . Geneva, Switzerland: Program for Control of Diarrhoeal Diseases, World Health Organization; 1984. World Health Organization/Control Diarrhoeal Diseases/SER/84.7. 14. Pocock SJ. Clinical trials: a practical approach . New York, NY: John Wiley & Sons Inc; 1983:123. 15. Mota HF. Diagnóstico en Pediatría: Interpretación Clínica de Exámenes de Laboratorio y Gabinete . México, D.F.: Ed. Méndez Cervantes; 1985. 16. Brown G. Sample size . AJDC . 1988;142:1213-1215. 17. Bradford H. Principios de Estadística Médica . 3rd ed. Buenos Aires, Argentina: Ed. El Ateneo; 1965. 18. Velásquez JL, Mota HF. Procedimientos médicos para la hidratación oral en ninõs con diarrea . Bol Med Hosp Infant Mex . 1984;41:505-511. 19. Velásquez JL, Mota HF, Kane QJ, Puente TME, Llausás ME. Frecuencia de vómitos en ninõs con diarrea hidratados por vía oral . Bol Med Hosp Infant Mex . 1986;43:353-358. 20. Lifshitz F, Wapnir RA. Oral hydration solutions: experimental optimization of water and sodium absorption . J Pediatr . 1985;106:383-386.Crossref 21. Rahman ASMM, Bari A, Molla AM, Greenough WB. Mothers can prepare rice and use rice-salt oral rehydration solution in rural Bangladesh . Lancet . 1985;2:539-541.Crossref 22. De Vizia B, Ciccimarra F, DeCicco N, Auricchio S. Digestibility of starches in infants and children . J Pediatr . 1975;86:50-55.Crossref

Specker, Bonny L.;Tsang, Reginald C.;Ho, Mona L.;Landi, Theresa M.;Gratton, Teresa L.

1991 American Journal of Diseases of Children

doi: 10.1001/archpedi.1991.02160080119033pmid: 1858733

Abstract • We previously suggested that "late" neonatal hypocalcemia is related to a low calcium-phosphorus ratio of current cow's milk—based formula compared with human milk. However, there are no longitudinal studies of ionized calcium and parathyroid hormone concentrations in neonates receiving formulas with varying Ca/P ratios. Sixty-nine term neonates were studied through 2 weeks of age, and formula-fed neonates were randomized at birth to receive formula with molar ratios of 0.9,1.2, or 1.4. Serum phosphate concentrations on days 2 and 6 of age were higher, and ionized calcium levels lower on days 6 and 14, in formula-fed vs human milk—fed neonates. Serum intact parathyroid hormone level increased between days 2 and 6 in formula-fed neonates compared with a decrease in human milk—fed neonates. Serum parathyroid hormone level on day 6 correlated with phosphorus intake among formula-fed neonates. No differences were noted in serum mineral or hormone levels among formula-fed groups. We speculate that the lowering of serum ionized calcium concentrations in neonates fed a modern "humanized" cow's milk formula may be a factor in late neonatal hypocalcemia. (AJDC. 1991;145:941-945) References 1. Venkataraman PS, Tsang RC, Greer FR, Noguchi A, Laskarzewski P, Steichen JJ. Late infantile tetany and secondary hyperparathyroidism in infants fed humanized cow's milk formula: longitudinal follow-up . AJDC . 1985;139:664-668. 2. Specker BL, Lichtenstein P, Mimouni F, Gormley C, Tsang RC. Calcium-regulating hormones and minerals from birth to 18 months of age: a cross-sectional study, II: effects of sex, race, age, season, and diet on serum minerals, parathyroid hormone, and calcitonin . Pediatrics . 1986;77:891-896. 3. Lichtenstein P, Specker BL, Tsang RC, Mimouni F, Gormley C. Calcium-regulating hormones and minerals from birth to 18 months of age: a cross-sectional study, I: effects of sex, race, age, season, and diet on vitamin D status . Pediatrics . 1986;77:883-890. 4. Arnaud C, Tsao J, Littledike T. Radioimmunoassay of human parathyroid hormone in serum . J Clin Invest . 1971;50:21.Crossref 5. Hicks CR. Fundamental Concepts in the Design of Experiments . 2nd ed. New York, NY: Holt Rinehart & Winston; 1973. 6. Bakwin H. Tetany in newborn infants . AJDC . 1937;54:1211-1226. 7. Baum D, Cooper L, Davies PA. Hypocalcemic fits in neonates . Lancet . 1968;1:598-599.Crossref 8. Lealman GT, Logan RW, Hutchinson JH, Kerr MM, Fulton AM, Brown CW. Calcium, phosphorus and magnesium concentrations in plasma during first week of life and their relation to type of milk feed . Arch Dis Child . 1976;51:377-384.Crossref 9. Bagnoli F, Bruchi S, Sardelli S, et al. Calcium homeostasis in the first days of life in relation to feeding . Eur J Pediatr . 1985;144:41-44.Crossref 10. Allen LH. Calcium bioavailability and absorption: a review . Am J Clin Nutr . 1982;35:783-808. 11. Mulroney SE, Lumpkin MD, Haramati A. Antagonist to GH-releasing factor inhibits growth and renal Pi reabsorption in immature rats . Am J Physiol . 1989;257:F29-F34. 12. Johnson A, Spitzer A. Renal reabsorption of phosphate during development: whole-kidney events . Am J Physiol . 1986;251:F251-F256. 13. Loughead JL, Mimouni F, Tsang RC. Serum ionized calcium concentrations in normal neonates . AJDC . 1988;142:516-518.

GROOTHUIS, JESSIE R.

1991 American Journal of Diseases of Children

doi: 10.1001/archpedi.1991.02160080123034

This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables. Abstract This is a clear, well-written book that walks the reader through a clinical research project. It begins with defining the research question and ends with critiquing the published project description. The author has consulted respected clinical researchers in writing this text, and her introduction is an excellent précis of the journey from the beginning to the end of a research project. Chapter 1, which discusses the scientific method, is the most difficult chapter to understand and could be simplified in the next edition. Chapters 2 and 3 review the definition of the research question and selection of subjects. Chapter 4 ("Types of Research Models and Methods") is particularly good. It clarifies such difficult concepts as varied study designs by using excellent tables and figures. Chapter 5 discusses data collection, management, and analysis; like chapter 4, its clarification of topics such as statistical tests of significance and data collection methods is

Jaimovich, David G.;Kumar, Ashir;Francom, Steve

1991 American Journal of Diseases of Children

doi: 10.1001/archpedi.1991.02160080124035pmid: 1858734

Abstract • Objectives. —To compare intraosseous vs intravenous routes of administration and their effects on serum levels of four antibiotics in an animal model. Design. —Prospective controlled study comparing two routes of drug administration. Setting. —Research laboratories of a large pharmaceutical company. Participants. —Twenty male and female domestic swine weighing 10 to 20 kg. Interventions. —The animals were anesthetized and treated with controlled ventilation. The animals were divided into one of four groups: (1) intravenous and intraosseous cefotaxime sodium (50 mg/kg), (2) intravenous and intraosseous chloramphenicol sodium succinate (25 mg/kg), (3) intravenous and intraosseous vancomycin hydrochloride (15 mg/kg), or (4) intravenous and intraosseous tobramycin sulfate (2.5 mg/kg). There was a 24-hour clearance period for groups 1 and 2 and a 48-hour clearance period for groups 3 and 4. Serum drug levels were measured at 115,30,45, 60, 90, and 120 minutes after intravenous and intraosseous administration of the respective antibiotics. Control and treated tibias were sampled for drug levels at the end of the experiment. Measurements and Main Results. —Peak serum concentrations for intravenously administered antibiotics were within the therapeutic range. Peak serum levels after intravenous and intraosseous administration were 102 and 82 mg/L, respectively for cefotaxime; 13.9 and 6.3 mg/L, respectively, for chloramphenicol; 24.5 and 3.8 mg/L, respectively, for vancomycin; and 7.1 and 1.3 mg/L, respectively, for tobramycin. Conclusions. —Cefotaxime may be administered intraosseously when intravenous access is not possible. We cannot recommend chloramphenicol or vancomycin for intraosseous administration, because serum levels were not comparable with those following intravenous administration. Findings with tobramycin suggested a lack of achievement of serum levels comparable with those following intravenous administration.(AJDC. 1991;145:946-949) References 1. Gotoff SP, Behrman RE. Neonatal septicemia . J Pediatr . 1970;76:142-153.Crossref 2. Hodes HL. Care of the critically ill child: endotoxic shock . Pediatrics . 1969;44:248-260. 3. Spivey WH, Unger HD, Lathers CM, McNamara RM. Intraosseous diazepam suppression of pentylenetetrazol-induced epileptogenic activity in pigs . Ann Emerg Med . 1987;16:156-158.Crossref 4. Spivey WH, Lathers CM, Malone DR, et al. Comparison of intraosseous, central, and peripheral routes of sodium bicarbonate administration during CPR in pigs . Ann Emerg Med . 1985;14:1135-1140.Crossref 5. Berg RA. Emergency infusion of catecholamines into bone marrow . AJDC . 1984;138:810-811. 6. Rosetti VA,Thompson BM, Miller J, Mateer JR, Aprahamian C. Intraosseous infusion: an alternative route of pediatric intravascular access . Ann Emerg Med . 1985;14:885-888. 7. Spivey WH. Intraosseous infusions . J Pediatr . 1987;111: 639-643. 8. Jaimovich DC, Shabino CL, Ringer TV, Peters GR. Comparison of intraosseous and intravenous routes of anticonvulsant administration in a porcine model . Ann Emerg Med . 1989;18:842-846. 9. McCracken CH, Nelson JD. Clinical pharmacology and dosage . In: McCracken GH, Nelson JD, eds. Antimicrobial Therapy for Newborns: Practical Application of Pharmacology to Clinical Usage . New York, NY: Grune & Stratton; 1977:5-68. 10. Orlowski JP, Porembka DT, Gallagher JM, van Lente F. Comparison study of intraosseous, central intravenous, and peripheral intravenous infusions of emergency drugs . AJDC . 1990;144:112-117

1991 American Journal of Diseases of Children

doi: 10.1001/archpedi.1991.02160080128036

This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables.