American Journal of Diseases of Children

LUKENS, JOHN N.

1972 American Journal of Diseases of Children

doi: 10.1001/archpedi.1972.02110170017001pmid: 5085476

Abstract Physicians attentive to the preventive aspects of medical practice have long recognized the importance of vitamin K prophylaxis in the prevention of hemorrhagic disease of the newborn. Pathologic bleeding due to vitamin K deficiency in older infants and children is generally approached with less familiarity. In a paper published 26 years ago in this journal, Rapoport and Dodd1 reported observations made on a group of seven infants, 2 to 12 months of age, with chronic diarrhea. Each of the infants was hypoprothrombinemic and four experienced symptomatic bleeding. Both clinical and laboratory manifestations of the coagulopathy were effectively corrected with vitamin K. The paper seems to have attracted little attention, and the subject of vitamin K deficiency in older infants with intestinal disturbances lay dormant for two decades. In recent years, reports such as that by Walters and Koch in this issue (page 641) have served to rekindle interest in References 1. Rapoport S, Dodd K: Hypoprothrombinemia in infants with diarrhea . Am J Dis Child 71:611-617, 1946. 2. Vitamin K supplementation for infants receiving milk substitute infant formulas and for those with fat malabsorption, Committee on Nutrition, American Academy of Pediatrics . Pediatrics 48:483-487, 1971. 3. Goodnight SH, et al: Factor VII antibody-neutralizing material in hereditary and acquired factor VII deficiency . Blood 38:1-8, 1971. 4. Josso F, et al: Differents etats moleculaires du facteur II (prothrombine): Leur étude a l'aide de la staphylocoagulase et d'anticorps anti-facteur II . Thromb Diath Haemorrh 20:88-98, 1968. 5. Larrieu MJ, Meyer D: Abnormal factor IX during anticoagulant treatment . Lancet 2:1085, 1970.Crossref 6. Hemker HC, Muller AD: Kinetic aspects of the interaction of blood-clotting enzymes: VI. Localization of the site of blood-coagulation inhibition by the protein induced by vitamin K absence . Thromb Diath Haemorrh 20:78-87, 1968.

Walters, Thomas R.;Koch, Col H. Frederick

1972 American Journal of Diseases of Children

doi: 10.1001/archpedi.1972.02110170019002pmid: 5085477

Abstract Four infants, 1 to 4 months of age, with cystic fibrosis, had severe bleeding caused by vitamin K deficiency and hypoprothrombinemia. The decreased prothrombin activity was attributed to poor dietary intake, malabsorption caused by pancreatic disease, and decreased synthesis following the administration of antibiotics. Second stage coagulation defects can be responsible for the presenting symptom of cystic fibrosis in early infancy. In infants with unexplained prolongation of the prothrombin time, the possibiliity of cystic fibrosis should be evaluated. Supplemental vitamin K should be administered to infants with cystic fibrosis. References 1. Gibson LE, Cooke RE: A test for concentration in sweat in cystic fibrosis of the pancreas utilizing pilocarpine by iontophoresis . Pediatrics 23:545-549, 1959. 2. Quick AJ: Hemorrhagic Diseases and Thrombosis , ed 2. Philadelphia, Lea & Febiger 1966, pp 391-395. 3. Nye SW, Graham JB, Brinkhous KM: The partial thromboplastin time as a screening test for the detection of latent bleeders . Am J Med Sci 243:279-287, 1962.Crossref 4. Schwachman H, Redmond A, Khaw KT: Studies in cystic fibrosis: A report of 130 patients diagnosed under 3 months of age over a 20 year period . Pediatrics 46:335-343, 1970. 5. Tortenson OL, et al: Cystic fibrosis presenting with severe hemorrhage due to vitamin K malabsorption: A report of three cases . Pediatrics 45:857-861, 1970. 6. Goldman HI, Deposito F: Hypoprothrombinemic bleeding in young infants: Association with diarrhea, antibiotics, and milk substitutes Am J Dis Child 111:430-432, 1966.Crossref 7. Moss MH: Hypoprothrombinemic bleeding in a young infant: Association with a soy protein formula Am J Dis Child 117:540-542, 1969.Crossref 8. Goldman HI, Amadio P: Vitamin K deficiency after the newborn period . Pediatrics 44:745-749, 1969. 9. Nammacher MA, et al: Vitamin K deficiency in infants beyond the neonatal period . J Pediatr 76:549-554, 1970.Crossref 10. Oppenheimer EH: Focal necrosis of striated muscle in an infant with cystic fibrosis of the pancreas and evidence of lack of absorption of fat-soluble vitamins . Bull Johns Hopkins Hosp 98:353-359, 1956.

Joshi, Vijay V.;Mandavia, Sharad G.;Stern, Leo;Wiglesworth, Fredrick W.

1972 American Journal of Diseases of Children

doi: 10.1001/archpedi.1972.02110170024003pmid: 5085478

Abstract Clinical charts, autopsy records, and slides of the larynx, trachea, and bronchi in 172 cases of newborn infants with respiratory distress syndrome (RDS) were reviewed for acute lesions induced by endotracheal intubation. Mild lesions (mucosal or submucosal necrosis) were seen in 63.3% and relatively severe lesions showing inflammatory changes in 15.8% of the cases. No lesions were seen in the remaining cases. Vocal cords with or without the subglottic region of larynx and trachea were the commonest lesion sites. Lesion severity was directly related to duration of intubation and subsequent bacterial infection. In seven (4.3%) cases Pseudomonas pneumonia with or without septicemia extending from acute diffuse laryngotracheobronchitis was a major factor in infant death. Comparable focal lesions in RDS survivors may result in residual permanent damage to upper respiratory tract. References 1. Daily WJR, Cave-Smith P: Mechanical ventilation of the newborn infant . Current Problems in Pediatrics . Chicago, Year Book Medical Publishers, 1971, vol 1. 2. Donnelly WH: Histopathology of endotracheal intubation: An autopsy study of 99 cases . Arch Pathol 88:511-520, 1969. 3. Stein AA, et al: A postmortem evaluation of laryngotracheal alterations associated with intubation . Ann Surg 151:130-138, 1960.Crossref 4. Way WL, Sooy FA: Histologic changes produced by endotracheal intubation . Ann Otol Rhinol Laryngol 74:799-812, 1965. 5. Blanc WA: Complications of treatment, catheter disease , in Dancis J (ed): Idiopathic Respiratory Distress Syndrome . Public Health Service, National Institutes of Health, Bethesda, Md, 1969, pp 103-110. 6. Symchych PS, Cadotte M: Squamous metaplasia and necrosis of the trachea complicating prolonged nasotracheal intubation of small newborn infants . J Pediatr 71:534-541, 1967.Crossref 7. Barson AJ: Fatal Pseudomonas aeruginosa bronchopneumonia in a children's hospital . Arch Dis Child 46:55-60, 1971.Crossref 8. Striker TW, Stool S, Downes JJ: Prolonged nasotracheal intubation in infants and children . Arch Otolaryngol 85:106-109, 1967.Crossref 9. Lu AT, Tamura Y, Koobs DH: The pathology of laryngotracheal complications: Lesions of the larynx and trachea after intubation anesthesia . Arch Otolaryngol 74:105-114, 1961.Crossref 10. Pinkham JR, Beckwith JB: Vocal cord lesions in the sudden infant death syndrome , in Bergman AB, Beckwith JB, Ray CG (eds): Sudden Infant Death Syndrome . Seattle, University of Washington Press, 1970, pp 104-106. 11. Harrison V, et al: Prolonged endotracheal intubation in the new born infant . Br J Anaesth 39:645-646, 1967.Crossref 12. Fishman NH, et al: Post intubation tracheal stenosis . Ann Thorac Surg 8:47-56, 1969.Crossref 13. Hatch DJ: Prolonged nasotracheal intubation in infants and children . Lancet 1:1272-1275, 1968.Crossref 14. Wigger HJ, Tang P: Fatal laryngeal obstruction by iatrogenic subglottic cyst . J Pediatr 72:815-820, 1968.Crossref 15. Choffat D, Goumaz CF, Guex JC: Laryngotracheal damage after prolonged endotracheal intubation in the newborn infant , in Stetson J (ed): Proceedings of the Strora Korno Conference on Intensive Care in the Newborn . Springfield, Ill, Charles C Thomas Publisher, to be published. 16. Guess WL, Stetson JB: Tissue reactions to organotin stabilized polyvinyl chloride (PVC) catheters . JAMA 204:118-122, 1968.Crossref 17. Stetson JB, Guess WL: Causes of damage to tissues by polymers and elastomers used in the fabrication of tracheal devices . Anesthesiology 33:635-652, 1970.Crossref 18. Stern L: Description and utilization of the negative pressure apparatus . Biol Neonate 16:24-29, 1970.Crossref 19. Stern L, et al: Negative pressure artificial ventilation: Use in treatment of respiratory failure of the newborn . Can Med Assoc J 102:595-601, 1970.

Aur, Rhomas J. A.;Westbrook, H. Wade;Riggs, Webster

1972 American Journal of Diseases of Children

doi: 10.1001/archpedi.1972.02110170031004pmid: 4508099

Abstract The purpose of this study was to determine whether initial skeletal roentgenographic findings correlated with subsequent clinical course in children with previously untreated acute lymphocytic leukemia. Findings that were considered definitely attributable to leukemia included prominent transverse metaphyseal lucent bands, intramedullary osteolytic mottling, and periosteal reaction. One or more of these roentgenographic findings was observed in 41 of the 191 children (21%). The median durations of remission induction time, complete remission, hematological remission, and survival in children with such findings were compared to those in children who had none. The data demonstrated that the presence of initial bone involvement by roentgenography bore no significant relationship to clinical outcome in childhood acute lymphocytic leukemia. References 1. Hustu HO, Pinkel D: Lymphosarcoma, Hodgkin's disease and leukemia in bone . Clin Orthop 52:83-93, 1967.Crossref 2. Silverman FN: The skeletal lesions in leukemia: Clinical and roentgenographic observations in 103 infants and children . Amer J Roentgenol Radium Ther Nucl Med 59:819-845, 1948. 3. Thomas LB, Forkner CE Jr, Frei E III, et al: The skeletal lesions of acute leukemia . Cancer 14:608-621, 1961.Crossref 4. George P, Hernandez K, Hustu O, et al: A study of "total therapy" of acute lymphocytic leukemia in children . J Pediatr 72:399-408, 1968.Crossref 5. Pinkel D, Hernandez K, Borella L, et al: Drug dosage and remission duration in childhood lymphocytic leukemia . Cancer 27:247-256, 1971.Crossref 6. Aur RJA, Simone J, Hustu HO, et al: Central nervous system therapy and combination chemotherapy of childhood lymphocytic leukemia . Blood 37:272-281, 1971. 7. Aur RJA, Simone JV, Hustu HO, et al: A comparative study of central nervous system irradiation and intensive chemotherapy early in remission of childhood acute lymphocytic leukemia . Cancer 29:381-391, 1972.Crossref 8. Pinkel D: Five-year follow-up of "total therapy" of childhood lymphocytic leukemia . JAMA 216:648-652, 1971.Crossref 9. Simmons CR, Harle TS, Singleton EB: The osseous manifestations of leukemia in children . Radiol Clin N Am 6:115-130, 1968. 10. Willson JKV: The bone lesions of childhood leukemia: A survey of 140 cases . Radiology 72:672-680, 1959.Crossref 11. Silverstein MN, Kelly PJ: Leukemia with osteoarticular symptoms and signs . Ann Intern Med 59:637-645, 1963.Crossref

Wedemeyer, Anne L.;Edson, J. Roger;Krivit, William

1972 American Journal of Diseases of Children

doi: 10.1001/archpedi.1972.02110170034005pmid: 5085479

Abstract A comprehensive study of the hemostatic status of 33 patients with cyanotic congenital heart disease and nine patients with acyanotic heart disease was undertaken to define the types of coagulation abnormalities present in cardiac patients prior to surgery. Evidence of disseminated intravascular coagulation was sought, but never found. Thrombocytopenia was the most frequent abnormality and was directly related to the degree of polycythemia. Abnormalities of many coagulation factors existed in patients having hematocrit values above 60%. Because of the variability in the coagulation factor levels in patients with similar hematocrit readings, each child must be studied and considered separately prior to surgery. The therapeutic success of surgery can be compromised by complications of postoperative hemorrhage or thrombosis or both. References 1. Bahnson HT, Ziegler RF: A consideration of the causes of death following operation for congenital heart disease of the cyanotic type . Surg Gynec Obstet 90:60-76, 1950. 2. Hartmann RC: A hemorrhagic disorder occurring in patients with cyanotic congenital heart disease . Bull Johns Hopkins Hosp 91:49-67, 1952. 3. Jackson DP: Hemorrhagic diathesis in patients with cyanotic congenital heart disease: Preoperative management . Ann NY Acad Sci 115:235-251, 1964.Crossref 4. Somerville J, McDonald L, Edgill M: Postoperative hemorrhage and related abnormalities of blood coagulation in cyanotic congenital heart disease . Brit Heart J 27:440-448, 1965.Crossref 5. Kontras SB, Sirak HD, Newton WA: Hematologic abnormalities in children with congenital heart disease . JAMA 195:611-615, 1966.Crossref 6. Dennis LH, Stewart JL, Conrad ME: A consumption coagulation defect in congenital cyanotic heart disease and its treatment with heparin . J Pediat 71:407-410, 1967.Crossref 7. Ekert H, Gilchrist GS: Coagulation studies in congenital heart disease . Lancet 2:280, 1968.Crossref 8. Johnson CA, Abildgaard CF, Schulman I: Absence of coagulation abnormalities in children with cyanotic congenital heart disease . Lancet 2:660-662, 1968.Crossref 9. Kontras SB, Bodenbender JG, Craemen JO, et al: Hyperviscosity in congenital heart disease . J Pediat 76:214-220, 1970.Crossref 10. Ekert H, Gilchrist GS, Stanton R, et al: Hemostasis and cyanotic congenital heart disease . J Pediat 76:221-230, 1970.Crossref 11. Komp DM, Sparrow AW: Polycythemia in cyanotic heart disease: A study of altered coagulation . J Pediat 76:231-236, 1970.Crossref 12. Biggs R, MacFarlane RG: Human Blood Coagulation and Its Disorders , ed 3. Philadelphia, FA Davis Co, 1962, p 385. 13. Proctor RR, Rapaport SI: The partial thromboplastin time with kaolin . Amer J Clin Path 36:212-219, 1961. 14. Ratnoff OD, Menzie C: A new method for the determination of fibrinogen in small samples of plasma . J Lab Clin Med 37:316-320, 1951. 15. Gaston LW, Mack BF, Beck WW: Hemophilia A and concurrent factor VII deficiency . New Eng J Med 264:1078-1082, 1961.Crossref 16. Bachman F, Duckert F, Koller F: The Stuart-Prower factor and its clinical significance . Thromb Diath Haemorrh 2:24-38, 1958. 17. Rapaport SI, Schiffman S, Patch MJ, et al: A simple specific one-stage assay for plasma thromboplastin antecedent activity . J Lab Clin Med 57:771-780, 1961. 18. Lucia SP, Aggeler PM, Hamlin LM: Blood clot retraction . Amer J Med Sci 204:507-516, 1942.Crossref 19. Buckell M: The effect of citrate on euglobulin methods of estimating fibrinolytic activity . J Clin Path 11:403-405, 1958.Crossref 20. Stiehm ER, Clatanoff DV: Split products of fibrin in the serum of newborns . Pediatrics 43:770-780, 1969. 21. Komp DM, Sparrow AW: Fibrinolysis in cyanotic heart disease . J Pediat 77:679-682, 1970.Crossref 22. Dennis LH, Stewart JL, Conrad ME: Heparin treatment of haemorrhagic diathesis in cyanotic congenital heart disease . Lancet 1:1088-1089, 1967.Crossref 23. Gross S, Keefer V, Liebman J: The platelets in cyanotic congenital heart disease . Pediatrics 42:651-658, 1968. 24. Paul M, Currimbhoy Z, Miller RA, et al: Thrombocytopenia in cyanotic congenital heart disease . Circulation 24:1013, 1961. 25. Gross S, Newman AJ, Keefer V: The platelets in iron deficiency anemia . Pediatrics 34:315-323, 1964.

Dunkle, Lisa M.;Rowe, Richard D.

1972 American Journal of Diseases of Children

doi: 10.1001/archpedi.1972.02110170044006pmid: 5085480

Abstract The incidence of a transient murmur resembling that of pulmonary arterial stenosis in healthy premature infants during the first six weeks of life was 67% (ten of 15) whereas only 5% of term infants (three of 61) were noted to have such a murmur during the few days spent in hospital. None of 25 term infants examined at home during the first four weeks of life had the murmur. The murmur was most frequently seen in babies with a birth weight below 2,200 gm (5 lb). Hypoplasia of the pulmonary artery branches or unusual alignment of the main pulmonary artery with its branches in premature infants are postulated as causes of the murmur which disappears as the infant grows. References 1. Eldridge F, Selzer A, Hultgren H: Stenosis of a branch of the pulmonary artery: An additional cause of continuous murmurs over the chest . Circulation 15:865-874, 1957.Crossref 2. Keith JD, Rowe RD, Vlad P: Heart Disease in Infancy and Childhood . New York, Macmillan Co, 1967, pp 584-597. 3. Wasserman WB, Varghese PJ, Rowe RD: The evolution of pulmonary artery stenosis associated with congenital rubella . Am Heart J 76:638-644, 1968.Crossref 4. Danilowicz DA, et al: Physiologic pressure differences between main and branch pulmonary arteries in infants . Circulation 45:410-419, 1972.Crossref 5. Patten BM: The changes in the circulation following birth . Am Heart J 6:192-205, 1930.Crossref 6. Rowe RD, Mehrizi A: The Neonate with Congenital Heart Disease . Philadelphia, WB Saunders Co, 1968, p 26. 7. Braudo M, Rowe RD: Auscultation of the heart—early neonatal period . Am J Dis Child 101:575-586, 1961. 8. Craige E, Harned HS Jr: Phonocardiographic and electrocardiographic studies in normal newborn infants . Am Heart J 65:180-189, 1963.Crossref 9. Hallidie-Smith KA: Some auscultatory and phonocardiographic findings observed in early infancy . Br Med J 1:756-759, 1960.Crossref 10. Naeye RL: Arterial changes during the perinatal period . Arch Path 71:121-128, 1961.

Shuler, Stanton E.;Aprill, Charles N.;Weiss, Thomas E.

1972 American Journal of Diseases of Children

doi: 10.1001/archpedi.1972.02110170051007pmid: 5085481

Abstract Peripheral joint imaging is a useful tool in evaluation of children with peripheral bone or joint disease since it is simple and associated with a low radiation dose. The pattern of isotope localization provides the clinician with documentation of synovitis in order that he may follow the course of an illness or, in some instances, have an aid in differential diagnosis. Peripheral joint imaging has been used as an aid in early diagnosis of bone or joint infection. Changes appearing in imaging have antedated radiographic changes by up to one week. A characteristic pattern of isotope localization is seen in the epiphyseal area of normal joints; however, normal localization may be obscured in some children with inflammatory joint conditions because of the intense isotope localization in the diseased joint. The finding of decreased epiphyseal localization in children receiving large doses of prednisone may be a related factor in their poor growth response. References 1. Weiss TE, Maxfield WS, Murison PJ, et al: Iodinated human serum albumin (I131) localization studies of rheumatoid arthritis joints by scintillation scanning . Arthritis Rheum 8:976-987, 1965.Crossref 2. Weiss TE, Maxfield WS, Murison PJ, et al: Scintillation scanning in rheumatoid arthritis . Southern Med J 59:484-488, 1966.Crossref 3. Maxfield WS, Weiss TE, Murison PJ, et al: Scintillation scanning of the rheumatoid joint , in Croll MN, Brady LW (eds): Recent Advances in Nuclear Medicine . New York, Appleton-Century-Crofts, 1966, pp 224-234. 4. Alarcon-Segovia D, Trujeque M, Tovar E, et al: Scintillation scanning of joints with technetium99m , abstracted. Arthritis Rheum 10:262, 1967.Crossref 5. Whaley K, Pack AI, Boyle JA, et al: The articular scan in patients with rheumatoid arthritis: A possible method of quantitating joint inflammation using radio-technetium . Clin Sci 35:547-552, 1968. 6. Maxfield WS, Weiss TE, Murison PJ, et al: Joint scanning with labeled albumin , in Hidalgo JV, Turiel SN (eds): Symposium on Computers and Scanning . New York, Society of Nuclear Medicine, 1968, pp 143-159. 7. Maxfield WS, Weiss TE, Tutton RH, et al: Detection of arthritis by joint scanning , in Medical Radioisotope Scintigraphy , monograph of the International Atomic Energy Agency. Salzburg, Austria, (August 6) -15, 1968, pp 307-323 8. McCarty DJ, Polcyn R, Gottschalk A, et al: 99mTechnetium (99mTc) scintiphotography: Clinical applications . Arthritis Rheum 11:831-832, 1968. 9. Maxfield WD, Weiss TE: Technetium-99m joint images . Radiology 92:1461-1466, 1969.Crossref 10. McCarty DJ, Polcyn RE, Collins PA: Experience with joint scanning using 99mTc-pertechnetate , abstracted. J Nucl Med 10:356, 1969. 11. Sholkoff SD, Glickman MG: Scintiphotographic evaluation of arthritis activity . Invest Radiol 4:207-214, 1969.Crossref 12. Glickman MG, Sholkoff SD, Gilbert RJ: Appearance of normal peripheral joints by scintiphotography . Invest Radiol 5:50-58, 1970.Crossref 13. Aprill CN III, Shuler SE, Weiss TE: Peripheral joint imaging: Variations in normal children . J Nucl Med 13:367-372, 1972. 14. Cohen MB, Lorber A: Reliability and accuracy of various joint scanning agents , abstracted. J Nucl Med 11:308, 1970. 15. Sholkoff SD, Glickman MG, Schachter J, et al: External counting and scintiphotography in rabbits with arthritis . Arthritis Rheum 12:220-227, 1969.Crossref

Collipp, Platon J.;Sharma, Raj K.;Thomas, Joseph;Maddaiah, Vaddanahally T.;Chen, Sliang Y.

1972 American Journal of Diseases of Children

doi: 10.1001/archpedi.1972.02110170060008pmid: 5085482

Abstract Oral glucose tolerance tests on 24 children with achondroplasia showed glucose intolerance in 16 of them. They were also found to have significantly elevated levels of plasma free fatty acids after an overnight fast, which rose still higher following human growth hormone administration. Plasma insulin levels were normal, but growth hormone levels were significantly below normal at 8 am, and tended to remain low during the day. These data are consistent with the concept that children with achondroplasia have a defect in peripheral glucose utilization. References 1. Johnston FE: Some observations on the roles of achondroplastic dwarfs through history . Clin Pediatr 2:703-709, 1963.Crossref 2. Zellweger H, Taylor B: Genetic aspects of achondroplasia . J Lancet 85:8-16, 1965. 3. Silverman FN: A differential diagnosis of achondroplasia . Radiol Clin North Am 6:223-235, 1968. 4. Shepard TH, Bass GO: Organ culture of limb buds from riboflavin deficient and normal rat embryos in normal and riboflavin deficient media . Teratology 3:163-170, 1970.Crossref 5. Shepard TH, Moffet BC, Fry LR: A metabolic defect in glucose utilization by achondroplastic cartilage . Soc Pediatric Res 38:21, 1968. 6. Dole VP: A simplified method for determination of plasma free fatty acids . J Clin Invest 35:150-156, 1956.Crossref 7. Satoh K, Price GM: Fluorometric determination of xanthurenic acid and kynurenic acid in human urine . J Biol Chem 230:781-789, 1958. 8. Rimoin DL, Hughes GN, Kaufman RL, et al: Enchondral ossification in achondroplastic dwarfism . N Engl J Med 283:728-735, 1969.Crossref 9. Luft R, Cerasi E, Anderson B: Obesity as an additional factor in the pathogenesis of diabetes . Acta Endocrinol . 59:344-351, 1968. 10. Stanesio V, Bona C, Ionesco V, et al: Recherches histochimiques et histoenzymologiques sur le cartilage de croissance tibial de l'achondroplasie humaine . Rev Franc Etud Clin Biol 11:600-608, 1966. 11. Gershberg H, Mari S, Hulse M: Long-term treatment of hypopituitary and of achondroplastic dwarfism with human growth hormone . Metabolism 13:152-156, 1964.Crossref 12. Taylor L, Blackard WG: Effect of lipids on growth hormone synthesis by isolated pituitaries . Proc Soc Exp Biol Med 137:1026-1028, 1971.Crossref 13. Blackard WG, Boylen CT, Hinson TC, et al: Effect of lipid and ketone infusions on insulin induced growth hormone elevations rhesus monkeys . Endocrinology 85:1180-1185, 1969.Crossref 14. Hazelwood RL: Growth hormone, plasma glucose, and ketone bodies as determinants of cardiac glycogen in normal and diabetic rats . Proc Soc Exp Biol Med 127:45-48, 1968.Crossref 15. Friedman M, Byers SD, Elek SR: Pituitary growth hormone essential for regulation of serum cholesterol . Nature 225:464-466, 1970.Crossref 16. Kotake Y Jr, Inada T: Studies on xanthurenic acid: Preliminary report on xanthurenic acid diabetes . J Biochem 40:291-296, 1953. 17. Sharma RK, Collipp PJ, Thomas J[ill] et al: Abnormal glucose metabolism in diastrophic dwarfism. JAMA, to be published. 18. Gyorgy P: Developments leading to the metabolic value of vitamin B6 . Am J Clin Nutr 24:1250-1255, 1971.

Sperling, Mark A.;Bacon, George;Kenny, Frederick M.;Drash, Allan L.

1972 American Journal of Diseases of Children

doi: 10.1001/archpedi.1972.02110170068009pmid: 4628604

Abstract Acute changes in adrenocortical function were assessed by a method which permits simultaneous determination of cortisol and short-term cortisol secretion rates from specific activities in serum. Four children were studied during the first two hours of their initial hospitalization for impending ketoacidosis. Three were acidotic (plasma bicarbonate [unk] 19 mEq/liter); two of these were restudied one week later following stabilization of their disease. In all six studies cortisol secretion rate was directly correlated to the degree of acidosis (r =.96), being high in the presence of, but normal in the absence or following correction of, acidosis. These studies document the magnitude of adrenal response to the stress of diabetic ketoacidosis. The consistent presence of normal cortisol secretion rate in diabetic children without acidosis argues against the contention that increased cortisol secretion is a factor in the pathogenesis of juvenile diabetes mellitus. References 1. Bookman JJ, Drachman SR, Schaefer LE, et al: Steroid diabetes in man: The development of diabetes during treatment with cortisone and corticotropin . Diabetes 2:100-111, 1953. 2. Conn JW, Fajans SS: Influence of adrenal cortical steroids in carbohydrate metabolism in man . Metabolism 5:114-127, 1956. 3. Boshell BR, Chaudalia HB: Hormonal interrelationships , in Ellenberg M, Rifkin H (eds): Diabetes Mellitus: Theory and Practice . New York, McGraw Hill Book Co Inc, 1970, pp 96-111. 4. Rifkin HS, Solomon S, Lieberman S: Adrenal cortical function in diabetic retinopathy and nephropathy . Diabetes 7:9-14, 1958. 5. Lentle BC, Thomas JP: Adrenal function and the complications of diabetes . Lancet 2:544-549, 1964.Crossref 6. Garces LY, Kenny FM, Drash A, et al: Cortisol secretion in acidotic and non-acidotic juvenile diabetes mellitus . J Pediat 74:517-522, 1969.Crossref 7. Petersen RE, Wyngaarden JB: The miscible pool and turnover rate of hydrocortisone in man . J Clin Invest 35:552-561, 1956.Crossref 8. Murphy BEP: Some studies of the protein binding of steroids and their application to the routine micro and ultra-micro measurement of various steroids in body fluids by competitive protein-binding radioassay . J Clin Endocr 27:973-990, 1967.Crossref 9. Kenny FM, Malvaux D, Migeon CJ: Cortisol production rates in newborn babies, older infants and children . Pediatrics 31:360-373, 1963. 10. Pfeiffer EF: Recognized diabetogenic hormones and diabetes in man , in Leibel BS, Wrenshall GA (eds): On the Nature and Treatment of Diabetes . Amsterdam, Excerpta Medica Foundation, 1965, pp 368-386. 11. McArthur JW, Smart GA, McLachlan EA, et al: Studies concerning the role of adrenal cortex in the pathologic physiology of diabetic acidosis: Temporal relations between the metabolic events of experimental diabetic acidosis and the level of adrenocortical function . J Clin Invest 33:420-436, 1954.Crossref 12. Wieland RE, Schachner SH, Kruger FA, et al: False elevation of plasma 17-OHCS in diabetic ketosis . Diabetes 14:744-745, 1965. 13. Klein R, Weigand FA, Iunnes M, et al: Corticoids in serum of children with treated diabetes mellitus . Pediatrics 17:214-220, 1956. 14. Lundquist I, Norden A, Schersten B: Studies in subjects with positive postprandial clinistix (R) test . Acta Med Scand 187:163-168, 1970.Crossref 15. Espiner EA, Beaven DW: Cortisol metabolism in diabetes mellitus . Clin Sci 24:383-389, 1963. 16. Hellman L, Fujimori N, Curti J, et al: Cortisol is secreted episodically by normal man . J Clin Endocr 30:411-422, 1970.Crossref

Kleinman, Leonard I.;Sell, John E.;Petering, Harold G.

1972 American Journal of Diseases of Children

doi: 10.1001/archpedi.1972.02110170074010pmid: 4628605

Abstract Blood obtained from umbilical cords of 106 preterm infants was analyzed for carbonic anhydrase (CA) activity. Carbonic anhydrase isoenzymes were measured in red blood cells from five adults, eight full-term newborn infants, and 16 premature infants. Carbonic anhydrase activity increased progressively with gestation. Infants with respiratory distress syndrome (RDS) had lower cord blood CA activity than infants without RDS. Carbonic anhydrase B (CA-B), carbonic anhydrase C (CA-C), and total carbonic anhydrase protein (CA-B + CA-C) were highest in adults, then full-term newborns, premature newborns without RDS, and infants with RDS. The ratio of CA-B/CA-C was the same for all newborn groups and lower than the adult ratio. All enzyme activity in newborns could be accounted for by CA-B and CA-C. No inhibitors or abnormal enzymes were present. Importance of findings to RDS pathogenesis is discussed. References 1. Maren TH: Carbonic anhydrase: Chemistry, physiology and inhibition . Physiol Rev 47:595-781, 1967. 2. Stevenson SS: Carbonic anhydrase in newborn infants . J Clin Invest 22:403-409, 1943.Crossref 3. Altschule MD, Smith CA: Blood carbonic anhydrase activity in newborn infants and their mothers . Pediatrics 6:717-720, 1950. 4. Berfenstam R: Studies on carbonic anhydrase activity in children . Acta Paediat Scand 41:32-52, 1952.Crossref 5. Mazzeo G: L'attività carbo-anidrasica nell' immaturo, nel bambino a varie età e suo comportamento in corso di ossigenoterapia . Lattante 30:310-332, 1959. 6. Kleinman LI, Petering HG, Sutherland JM: Blood carbonic anhydrase activity and zinc concentration in infants with respiratory distress syndrome . N Engl J Med 277:1157-1161, 1967.Crossref 7. Tashian RE, Shreffler DC, Shows TB: Genetic and phylogenetic variation in the different molecular forms of mammalian erythrocyte carbonic anhydrases . Ann NY Acad Sci 151:64-77, 1968.Crossref 8. Sell JE: A Biochemical Study of Erythrocyte Carbonic Anhydrase in Neonatal Infants, dissertation submitted to the Division of Graduate Studies, University of Cincinnati, 1971, to be published. 9. Liljestrand G: Chemical control of distribution of pulmonary blood flow . Acta Physiol Scand 44:216-240, 1958.Crossref 10. Chu J, Clements JA, Cotton EK, et al: Neonatal pulmonary ischemia: I. Clinical and physiological studies . Pediatrics 40( (suppl) ):704-782, 1967. 11. Gluck L, Sribney M, Kulovich MV: The biochemical development of surface activity in mammalian lung: II. The biosynthesis of phospholipids in the lung of the developing rabbit fetus and newborn . Pediatr Res 1:247-265, 1967.Crossref