Archives of Dermatology

1991 Archives of Dermatology

doi: 10.1001/archderm.1991.01680020017001

Abstract In November 1990, a physician in New Jersey reported two cases of imported vivax malaria to the New Jersey State Department of Health. Both of these patients were among five patients who had been diagnosed with late-stage Lyme disease and referred by the physician to sources in Mexico for intramuscular injections of blood containing Plasmodium vivax parasites. The malaria donors reportedly had been screened for serologic evidence of syphilis, hepatitis B, and human immunodeficiency virus infection. On return to New Jersey, the two patients were diagnosed with parasitemia 3 days and 14 days after the injection, respectively. Approximately 3 weeks after onset of malaria, the patients were treated with chloroquine with satisfactory response. Reported by: K Mertz, MD, KC Spitalny, MD, State Epidemiologist, New Jersey State Dept of Health. Bacterial Zoonoses Br, Div of Vector-Borne Infectious Diseases and Malaria Br, Div of Parasitic Diseases, Center for Infectious Diseases, CDC (MMWR References 1. Steere AC. Lyme disease . N Engl J Med 1989;321:586-96.Crossref 2. Miller GL, Craven RB, Bailey RE, Tsai TF. The epidemiology of Lyme disease in the United States 1987-1988 . Laboratory Medicine 1990;21: 285-9. 3. Luft BJ, Dattwyler RJ. Treatment of Lyme borreliosis . Rheum Dis Clin North Am 1989;15: 747-55. 4. Logigian EL, Kaplan RF, Steere AC. Chronic neurologic manifestations of Lyme disease . N Engl J Med 1990;323:1438-44.Crossref 5. Preac-Mursic V, Weber K, Pfister HW, et al. Survival of Borrelia burgdorferi in antibiotically treated patients with Lyme borreliosis . Infection 1989;17:355-9.Crossref 6. Dattwyler RJ, Luft BJ. Immunodiagnosis of Lyme borreliosis . Rheum Dis Clin North Am 1989; 15:727-34. 7. Heimlich HJ. Should we try malariotherapy for Lyme disease? (Letter) . N Engl J Med 1990;322: 1234-5.Crossref 8. Becker FT. Induced malaria as a therapeutic agent . In: Boyd MF, ed. Malariology . Philadelphia: WB Saunders Co, 1949:1145-57. 9. Mayne B. A review of selected papers contributing to the progress of malaria therapy during the past year . Southern Med J 1936;29:755-7.Crossref 10. Maldonado YA, Nahlen BL, Roberto RR, et al. Transmission of Plasmodium vivax malaria in San Diego County, California, 1986 . Am J Trop Med Hyg 1990;42:3-9.

Coldiron, Brett M.;Manders, Steven M.

1991 Archives of Dermatology

doi: 10.1001/archderm.1991.01680020021002

Abstract A 48-year-old woman with noninsulin dependent diabetes and controlled schizophrenia was initially seen in the emergency department for a groin rash of 1 year's duration. She was given clotrimazole cream, to be used topically twice a day, and discharged. Two weeks later she returned to the emergency department with an exacerbation of her eruption. She was seen by the dermatology service, and was noted to have extensive erythema and maceration of the vulva, perineum, and inner thighs. Satellite pustules were noted and potassium hydroxide preparation revealed pseudohyphae. Her serum glucose concentration was elevated at 17.6 mmol/L (normal, 3.3 to 5.5 mmol/L). She was admitted to the hospital because of her worsening skin condition and elevated blood glucose level. She was treated with oral ketoconazole, 200 mg twice a day, topical soaks, and aeration. Her blood glucose level was gradually brought under control using insulin on a sliding scale. She improved References 1. Saag MS, Dismukes WE. Azole antifungals agents: emphasis on new triazoles . Antimicrob Agents Chemother. 1988;32:1-8.Crossref 2. Graybill JR. The long and the short of antifungal therapy . Infect Dis Clin North Am. 1988;2:805-825. 3. Hay RJ. New oral treatments for dermatophytosis . Ann N Y Acad Sci. 1988;54:580-585.Crossref

Dusing, C.

1991 Archives of Dermatology

doi: 10.1001/archderm.1991.01680020031003

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 (Internat. Centralbl. f. d. Physiol. und Patholog. der Harn- und Sexual-Organe, Band ii., Heft 3 und 4.) The relation of the number of males to the number of females born is a constant one as regards man, animals, and plants. In man the numerical relation of male to female is 106 to 100. In horses, male and female, it is 100 to 98. This relationship in man is subject to variation to a certain extent. For example, during war male births predominate. The absence of a considerable number of men exerts this certain influence. In favorable times not alone are a greater number of children born, but girls preponderate. In unfavorable times fewer female children are born and more boys. Among the first births in the human species there are relatively many males. This excess is especially seen in the children of those mothers who are advanced in age when they become pregnant, and is attributable to the nutrition of the mother not being up to normal. From the author's foregoing explanations, it is concluded that the sex is not inherited, but results from a combined action of causes. These factors act not only at the time of impregnation, but at various times after. From the beginning the ovule has a tendency to the development of a certain sex, and the semen possesses the same tendency; both combine at the time of impregnation to constitute one tendency, which determines the sex. Long after impregnation, when the embryo is already developed, the nutrition is still of influence, and can cause a change of tendency even if the sexual organs have begun to develop: as for example the occurrence in the mother of a poor state of nutrition may arrest the development of the female and bring about the development of the male organs. When this late reactionary influence remains absent or is not exerted strongly enough to cause a change in the development of the sexual organs, then the sex is definitely decided. F. Tilden Brown J Cutan Genito-Urin Dis. February 1891;9:73.

1991 Archives of Dermatology

doi: 10.1001/archderm.1991.01680020044004

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 Dermatology Visiting Fellowship.— New York (NY) University Medical Center is offering a dermatopathology visiting fellowship that is designed to prepare dermatologists and pathologists for careers in dermatopathology in a medical center environment. This is accomplished by full participation in an active dermatopathology laboratory functioning within a department of clinical dermatology. Under supervision, the registrant learns the optimal handling of specimens and studies microscopically the more than 400 skin specimens processed daily in the laboratory. At the conclusion of the program, the fellow is expected to be expert in diagnostic dermatopathology, to be proficient in teaching the subject effectively, and to be capable of advancing the field through new observations and new concepts. The duration of the course will be 1 year and will be taught at the Dermatology Office, New York University Medical Center, Suite 7J, 530 First Ave, New York, NY. There will be 1 hour of Category 1

Guzzo, Cynthia;Lavker, Robert;Roberts, L. Jackson;Fox, Kevin;Schechter, Norman;Lazarus, Gerald

1991 Archives of Dermatology

doi: 10.1001/archderm.1991.01680020059005

Abstract † Nine patients with adult-onset urticaria pigmentosa were studied for the incidence of extracutaneous mast cell involvement and the efficacy of potent topical corticosteroid therapy for cutaneous lesions. Seven of the nine patients had increased mast cells in the marrow biopsy specimens, and five patients had focal aggregates of mast cells. The bone scan was abnormal in one patient. Liver-spleen scans revealed a shift of colloid uptake from liver to spleen in four patients. No abnormal gastrointestinal tract roentgenograms were obtained. Urinary histamine metabolites correlated with nodular bone marrow involvement, but not with other parameters. Results of the psychoneurologic testing revealed significant deviation from the norm with a verbal memory deficit in all nine patients and abnormalities on the Minnesota Multiphasic Personality Inventory in four patients. All nine patients were treated with 0.05% betamethasone dipropionate ointment under occlusion over half of the body nightly for 6 weeks. Seven of nine patients treated responded with almost complete resolution of their lesions. Hypothalamic pituitary adrenal axis suppression was evaluated with intramuscular cosyntropin stimulation and metyrapone administration during treatment. Only two patients, both of whom used the medication improperly, developed transient abnormalities. Slow return of lesions was noted 6 months after completion of therapy. Remissions could be lengthened with single weekly applications of topical steroids. Systemic involvement is frequent in patients with cutaneous mast cell disease and it is best demonstrated by bone marrow biopsy. Mast cell lesions can be safely and effectively treated with topical steroids in motivated patients. (Arch Dermatol. 1991;127:191-196) References 1. Caplan RM. The natural course of urticaria pigmentosa . Arch Dermatol. 1983;87:146-157.Crossref 2. Sagher F, Even-Paz Z. Mastocytosis and the Mast Cell . Chicago, Ill: Year Book Medical Publishers Inc; 1967:4-242. 3. Ridell B, Olafsson JH, Roupe G, et al. The bone marrow in urticaria pigmentosas and systemic mastocytosis . Arch Dermatol. 1986;122:422-427.Crossref 4. Barton J, Lavker RM, Schecter NM, Lazarus GS. Treatment of urticaria pigmentosa with corticosteroids . Arch Dermatol. 1985;121:1516-1523.Crossref 5. Keyzer JJ, De Monchy JGR, Van Doormaal JJ, Van Voorst Vader PC. Improved diagnosis of mastocytosis by measurement of urinary histamine metabolites . N Engl J Med. 1983;309:1603-1605.Crossref 6. Roberts LJ, Oates JA. Accurate and efficient method for quantification of urinary histamine by gas chromatography negative ion chemical ionization mass spectrometry . Anal Biochem. 1984;136: 258-263.Crossref 7. Morrow JD, Parsons WJ, Roberts LJ. Release of markedly increased quantities of PGD2 in vivo in humans following the administration of nicotinic acid . Prostaglandins . 1989;38:263-274.Crossref 8. Calnan CD. Use and abuse of topical steroids . Dermatologica . 1976;152:247-251.Crossref 9. Ehrlich P. Bertrage zur Kenntnis der Anilinfarbungen und ihrer Verwendung in der mikroskopischen Technik . Arch Mikros Anat. 1877;13:263-277.Crossref 10. Nettleship E, Tay W. Rare forms of urticaria . BMJ. 1869;2:323-324.Crossref 11. Unna PG. Beitrage zur Anatomie und Pathogenese der Urticaria simplex und pigmentosa . Mschr Prakt Dermatol. 1887;3H:1.1. 12. Touraine A, Solente G, Renault P. Urticaire pigmentaire avec réaction splènique et myelèmique . Bull Soc Franc Dermatol Syphilol . 1933;40:1691. 13. Ellis JM. Urticaria pigmentosa: report of a case with autopsy . Arch Pathol. 1949;48:426-435. 14. Lennert K, Parwaresch MR. Mast cells and mast cell neoplasias: a review . Histopathology . 1979;3:349-365.Crossref 15. Webb TA, Lin CY, Yan LT. Systemic mast cell disease: a clinical and hematopathologic study of 26 cases . Cancer . 1982;49:927-938.Crossref 16. Bendel WL, Race GJ. Urticaria pigmentosa with bone involvement . J Bone Joint Surg. 1963;45:1043-1056. 17. Sostre S, Handler HL. Bony lesions in systemic mastocytosis . Arch Dermatol. 1977;113:1245-1247.Crossref 18. Bieler EU, Wohlenberg H, Utech C. Skeletal manifestations of generalized mastocytosis in the skeletal scintigram compared with roentgen findings . ROFO . 1985;142:552-558.Crossref 19. Ammann RW, Vetter D, Deyhle P, Tschen H, Sulser H, Schmid M. Gastrointestinal involvement in systemic mastocytosis . Gut. 1976;17:107-112.Crossref 20. Fishman RS, Fleming CR, Li CY. Systemic mastocytosis with review of gastrointestinal manifestations . Mayo Clin Proc. 1979;54:51-54. 21. Clenentt AR, Fishbone G, Levine J, James AE, Janower M. Gastrointestinal lesions in mastocytosis . AJR Am J Roentgenol. 1968;103:405.Crossref 22. Katsuda S, Okada Y, Oda Y. Systemic mastocytosis without cutaneous involvement . Acta Pathol Jpn. 1987;37:167-177. 23. Roberts LJ, Oates JA. Disorders of vasodilator hormones: the carcinoid syndrome and mastocytosis . In: Wilson JD, Foster DW, eds. Williams Textbook of Endocrinology . Philadelphia, Pa: WB Saunders Co; 1985:1363-1378. 24. Roberts LJ II. Carcinoid syndrome and disorders of systemic mast cell activation including systemic mastocytosis . Endocrinol Metab Clin North Am. 1988;17:415-436. 25. Wilson GA, Keyes W. The significance of the liver-spleen uptake ratio in liver scanning . J Nucl Med. 1974;15:593-597. 26. Dermis DJ. The mastocytosis syndrome: clinical and biological studies . Ann Intern Med. 1963;59:194-206.Crossref 27. Soter NA, Austen KF, Wasserman SL. Oral disodium cromoglycate in the treatment of systemic mastocytosis . N Engl J Med. 1979;301:465-469.Crossref 28. Rogers MP, Bloomingdale K, Murawski BJ, Soter NA, Reich P, Austen KF. Mixed organic brain syndrome as a manifestation of systemic mastocytosis . Psychosom Med. 1986;48:437-447.Crossref 29. Gerrard JW, Ko C. Urticaria pigmentosa: treatment with cimetidine and chlorpheniramine . J Pediatr. 1979;9:843-844.Crossref 30. Simon RA. Treatment of mastocytosis . N Engl J Med. 1980;302:231.Crossref 31. Hirschowitz BI, Groarka MB. Effect of cimetidine on gastric hypersecretion and diarrhea in systemic mastocytosis . Ann Intern Med. 1979;90:769-771.Crossref 32. Roberts LJ, Sweetman BJ, Lewis RA, et al. Increased production of prostaglandin D2 in patients with systemic mastocytosis . N Engl J Med. 1980;303:1400-1404.Crossref 33. Fairley JA, Pentland AP, Voorhees JJ. Urticaria pigmentosa responsive to nifedipine . J Am Acad Dermatol. 1984;11:740-743.Crossref 34. Christophers E, Honigsmann H, Wolff K, Langner A. PUVA treatment of urticaria pigmentosa . Br J Dermatol. 1978;98:701-702.Crossref 35. Granerus G, Roupe G, Swanbeck G. Decreased urinary histamine metabolite after successful PUVA treatment of urticaria pigmentosa . J Invest Dermatol. 1981;76:1-3.Crossref 36. Vaatainen N, Hannuksela M, Karvonen J. Trioxsalen baths plus UVA in the treatment of lichen planus and urticaria pigmentoasa . Clin Exp Dermatol. 1981;6:133-138.Crossref 37. Nella Briffa D, Eady RA, James MP. Photochemotherapy (PUVA) in the treatment of urticarial pigmentosa . Br J Dermatol. 1983;109:67-75.Crossref 38. Dolde G, Frosch PJ, Czarmetzke BM. Response of cutaneous mast cells to PUVA in patients with urticaria pigmentosa: histomorphometric, ultrastructural and biochemical investigations . J Invest Dermatol. 1984;83:175-178.Crossref 39. Aso M. The effects of potent topical corticosteroids on adrenocortical function . J Dermatol. 1983;10:145-149. 40. Gomez EC, Kaminester L, Frost P. Topical halcinonide and betamethasone valerate effects on plasma cortisol . Arch Dermatol. 1977;113:1196-1202.Crossref 41. Munro DD. The effect of percutaneously absorbed steroids on hypothalamic-pituitary adrenal function after intensive use in inpatients . Br J Dermatol. 1976;94( (suppl 12) ):67-76.Crossref 42. Carr RD, Tarnowski WM. Percutaneous absorption of corticosteroids . Acta Derm Venereol. 1968;48:417-428. 43. Katz HI, Hien NT, Prawer SE, Mastbaum LI, Mooney JJ, Samson CR. Superpotent topical steroid treatment of psoriasis vulgaris: clinical efficacy and adrenal function . J Am Acad Dermatol. 1987;16:804-811.Crossref

Olsen, Elise A.

1991 Archives of Dermatology

doi: 10.1001/archderm.1991.01680020065006

Abstract • Six generic formulations of five topical steroids were compared for bioequivalence with their trade-name counterparts using an in vivo vasoconstriction assay. Two of six generic formulations were found to show significantly less vasoconstriction than the respective trade-name topical steroids. The issue of generic equivalence of topical steroids is discussed, with particular emphasis on the vagaries of the vasoconstriction assay. (Arch Dermatol. 1991;127:197-201) References 1. Strom BL. Generic drug substitution revisited: special article . N Engl J Med. 1987;316:1456-1462.Crossref 2. Stoughton RB. Are generic formulations equivalent to trade name topical glucocorticoids? Arch Dermatol. 1987;123:1312-1314.Crossref 3. Jackson DB, Thompson C, McCormack JR, Guin JD. Bioequivalence (bioavailability) of generic topical corticosteroids . J Am Acad Dermatol. 1989;20:791-796.Crossref 4. Shah VP, Peck CC, Skelly JP. `Vasoconstriction'—skin blanching—assay for glucocorticoids—a critique . Arch Dermatol. 1989; 125:1558-1561.Crossref 5. Burdick KH. Various vagaries of vasoconstriction . Arch Dermatol. 1974;110:238-242.Crossref 6. Poulsen J, Rorsman H. Ranking of glucocorticoid creams and ointments . Acta Dermatovener (Stockh) . 1980;60:57-62. 7. Barry BW, Woodford R. Comparative bio-availability of proprietary topical corticosteroid preparations: vasoconstrictor assays on thirty creams and gels . Br J Dermatol. 1974;91:323-338.Crossref 8. Kirsch J, Gibson JR, Darley CR, Barth J, Burke CA. Forearm site variation with the corticosteroid vasoconstrictor assay . Br J Dermatol. 1982;106:495.Crossref 9. Barry BW, Woodford R. Activity and bioavailability of topical steroids: in vivo/in vitro correlations for the vasoconstrictor test . J Clin Pharmacol. 1978;3:43-65. 10. Moore-Robinson M, Christie GA. Vasoconstrictor activity of topical corticosteroids: methodology and results . Br J Dermatol. 1970;82:86-92.Crossref 11. Gibson JR, Kirsch JM, Darley CR, Harvey SG, Burke CA, Hanson ME. An assessment of the relationship between vasoconstrictor assay findings, clinical efficacy, and skin thinning effects of a variety of undiluted and diluted corticosteroid preparations . Br J Dermatol. 1984;111:204-212.Crossref 12. Cornell RC, Stoughton RB. Correlation of the vasoconstriction assay and clinical activity in psoriasis . Arch Dermatol. 1985;121:63-67.Crossref 13. McKenzie AW. Percutaneous absorption of steroids . Arch Dermatol. 1962;86:611-614.Crossref 14. Place VA, Velazquez JG, Burdick KH. Precise evaluation of topically applied corticosteroid potency . Arch Dermatol. 1970; 101:532-537.Crossref 15. Poulsen BJ, Burdick K, Bessler S. Paired comparison vasoconstrictor assays . Arch Dermatol. 1974;109:367-371.Crossref 16. Burdick KH, Haleblian JK, Poulsen BJ, Cobner SE. Corticosteroid ointments: comparison by two human bioassays . Curr Ther Res. 1973;15:233-242. 17. Stoughton RB, Wullich K. The same glucocorticoid in brandname products. Does increasing the concentration result in greater topical biologic activity? Arch Dermatol. 1989;125:1509-1511.Crossref 18. McKenzie AW, Atkinson RM. Topical activities of betamethasone esters in man . Arch Dermatol. 1964;89:741-746.Crossref 19. Sefton J, Loder JS, Kyriakopoulos AA. Clinical evaluation of hydrocortisone valerate 0.2% ointment . Clin Ther. 1984;6;282-293. 20. Coldman MF, Lockerbie L, Laws EA. The evaluation of a novel corticosteroid formulation, fluocinonide in `FAPG' base, in the blanching test . Br J Dermatol. 1971;85:573-576.Crossref 21. Stoughton RB, Cornell RC. Review of super-potent topical corticosteroids . Semin Dermatol. 1987;6:72-76.

Ashinoff, Robin;Geronemus, Roy G.

1991 Archives of Dermatology

doi: 10.1001/archderm.1991.01680020070007

Abstract • Strawberry, or capillary, hemangiomas are common vascular neoplasms, with an incidence of approximately 2.6% in neonates. They usually develop in the first few weeks of life, so that between 1 month and 1 year the incidence rises to between 8.7% and 10.1%. These lesions may grow quite large in the first year of life, and they may ulcerate or obstruct a vital organ or function. The great majority will spontaneously regress after the first year of life. Parents are often alarmed at the sight of these hemangiomas and need reassurance that the great majority will regress spontaneously. Treatments such as cryosurgery, irradiation, radium instillation, corticosteroid therapy, or surgical excision are often ineffective or cause significant morbidity. We describe 10 children with capillary hemangiomas treated with the flash lamp—pumped pulsed dye laser. The patients ranged in age from 7 weeks to 5.5 years at the beginning of laser therapy. The patients underwent 3.1 ± 1 (mean ± SD) laser treatments, with a mean regression of the lesions of 69.9% ±4.5%. All patients demonstrated some diminution in the size and color of their hemangiomas after the treatments, and there were no ill effects, such as ulceration, hemorrhage, infection, or scarring. There was no evidence of hyperpigmentation or hypopigmentation. Pulsed dye laser therapy should be considered as an option in the treatment of capillary hemangiomas, preferably prior to their full evolution. It is also a useful therapeutic approach in those hemangiomas that are slow to regress in older children. (Arch Dermatol. 1991;127:202-205) References 1. Jacobs AH, Walton RG. The incidence of birthmarks in the neonate . Pediatrics . 1976;58:218-222. 2. Bivings L. Spontaneous regression of angiomas in children: twenty-two years' observation covering 236 cases . J Pediatr. 1954;45:643-647.Crossref 3. Jacobs AH. Strawberry hemangiomas: the natural history of the untreated lesion . Calif Med. 1957;86:8-10. 4. Margileth AM, Museles M. Cutaneous hemangiomas in children . JAMA . 1965;194:523-526.Crossref 5. Baker ER, Manders E, Whitney CW. Growth of cavernous hemangioma with puberty . Clin Pediatr. 1985;24:596-598.Crossref 6. Lister WA. The natural history of strawberry naevi . Lancet . 1938;1:1429-1434.Crossref 7. Apfelberg DB, Greene RA, Maser MR, Lash H, Rivers JL, Laub DR. Results of argon laser exposure of capillary hemangiomas of infancy: preliminary report . Plast Reconstr Surg. 1981;67:188-193.Crossref 8. Bowers RE, Graham EA, Tomlinson KM. The natural history of the strawberry nevus . Arch Dermatol. 1960;82:667-680.Crossref 9. Hobby LW. Further evaluation of the potential of the argon laser in the treatment of strawberry hemangiomas . Plast Reconstr Surg. 1983;71:481-485.Crossref 10. Noe JM, Barsky SH, Geer DE, Rosen S. Portwine stains and the response to argon laser therapy: successful treatment and the predictive role of color, age and biopsy . Plast Reconstr Surg. 1988;65:130-136.Crossref 11. Dixon JA, Huether S, Rotering RH. Hypertrophic scarring in argon laser treatment of portwine stains . Plast Reconstr Surg. 1984;73:771-780.Crossref 12. Mulliken JB. Diagnosis and natural history of hemangiomas . In: Mulliken JB, Young AE, eds. Vascular Birthmarks: Hemangiomas and Malformations . Philadelphia, Pa: WB Saunders Co; 1988:41-62. 13. Tan OT, Gilchrest BA. Laser therapy for selected cutaneous vascular lesions in the pediatric population: a review . Pediatrics . 1988;82:652-662. 14. Mulliken JB. Treatment of hemangiomas . In: Mulliken JB, Young AE, eds. Vascular Birthmarks: Hemangiomas and Malformations . Philadelphia, Pa: WB Saunders Co; 1988:89. 15. Friedman M, Strang LB. Effect of long-term corticosteroids and corticotropin on the growth of children . Lancet . 1966;2:568-572.Crossref 16. Anderson RR, Parrish JA. Selective photothermolysis: precise microsurgery by selective absorption of pulsed irradiation . Science . 1983;220:524-527.Crossref 17. Tan OT, Sherwood KA, Gilchrest BA. Treatment of children with portwine stains using the flashlamp pulsed tunable dye laser . N Engl J Med. 1989;320:416-421.Crossref 18. Dover JS, Arndt KA, Geronemus RG, Olbright SM, Noe JM, Stern RS. Dye lasers . In: Illustrated Cutaneous Laser Surgery: A Practitioner's Guide . East Norwalk, Conn: Appleton & Lange; 1990:108-120. 19. Reyes B, Geronemus RG. Flashlamp pumped pulsed dye laser treatment of portwine stains in children . J Am Acad Dermatol. 1990;23:1142-1148.Crossref 20. Tan OT, Murray S, Kurban AK. Action spectrum of vascular specific injury using pulsed irradiation . J Invest Dermatol. 1989;92:868-871.Crossref 21. Sherwood KA, Tan OT. Treatment of a capillary hemangioma with the flashlamp pumped-dye laser . J Am Acad Dermatol. 1990;22:136-137.Crossref

Rosenthal, David;LeBoit, Philip E.;Klumpp, Lesley;Berger, Timothy G.

1991 Archives of Dermatology

doi: 10.1001/archderm.1991.01680020074008

Abstract • We studied 13 patients with human immunodeficiency virus (HIV) infection and a chronic pruritic folliculitis that was unresponsive to systemic treatment with bactericidal antistaphylococcal antibiotics. The skin eruption was characterized by multiple urticarial follicular papules scattered on the trunk (100%), the head and neck (85%), and the proximal aspect of the extremities (62%). Absolute peripheral eosinophil counts were increased in six of 13 patients; a relative peripheral eosinophilia was present in 10 of 13 patients. Serum IgE levels were elevated in all seven patients tested (range, 88 to 9050 IU). Histopathologic features included a folliculitis with eosinophils. Pathogenic bacteria were not consistently found by routine bacterial skin cultures, cultures of skin biopsy specimens, or histopathologic evaluation. CD4 counts were decreased in all of the 12 patients tested (<300 cells per cubic millimeter) and were below 250 cells per cubic millimeter in 10 patients. A clinical response was noted to astemizole, to ultraviolet light in the B range, and to topical clobetasol propionate. These observations demonstrate that HIV-associated eosinophilic folliculitis is a unique HIV-related cutaneous disorder that is characterized by a culture-negative, chronic, pruritic folliculitis and a characteristic histopathologic picture. Of special importance, because it is associated with CD4 counts of less than 250 to 300 cells per cubic millimeter, eosinophilic folliculitis appears to be an important clinical marker of HIV infection and, particularly, of patients at increased risk of developing opportunistic infections. We suggest that the term eosinophilic pustular folliculitis (Ofuji's disease), previously used to describe this dermatosis in HIV-infected patients, should be discarded. (Arch Dermatol. 1991;127:206-209) References 1. Kaplan M, Sadick N, McNutt S, Meltzer M, Sarngadharan MG, Pahwa S. Dermatologic findings and manifestations of acquired immunodeficiency syndrome (AIDS) . J Am Acad Dermatol . 1987; 16:485-506.Crossref 2. Goodman DS, Teplitz ED, Wishner A, Klein RS, Burk PG. Prevalence of cutaneous disease in patients with acquired immunodeficiency syndrome (AIDS) or AIDS-related complex . J Am Acad Dermatol . 1987;17:210-220.Crossref 3. Fisher BK, Warner LC. Cutaneous manifestations of the acquired immunodeficiency syndrome . Int J Dermatol . 1987;26: 615-630.Crossref 4. Duvic M, Johnson T, Rapini RP. Acquired immunodeficiency syndrome—associated psoriasis and Reiter's syndrome . Arch Dermatol . 1987;123:1622-1632.Crossref 5. Ofuji S, Atsuhiko 0, Horio T, Ohseko T, Uehara M. Eosinophilic pustular folliculitis . Acta Derm Venereol (Stockh) . 1970;50:195-203. 6. Soeprono FF, Schinella RA. Eosinophilic pustular folliculitis in patients with acquired immunodeficiency syndrome . J Am Acad Dermatol . 1986;14:1020-1022.Crossref 7. Jenkins D Jr, Fisher BK, Chalvardjian A, Adam P. Eosinophilic pustular folliculitis in a patient with AIDS . Int J Dermatol . 1988;27:34-35.Crossref 8. Centers for Disease Control. CDC classification system for HIV infections . MMWR . 1986;35:334-339. 9. Scully M, Berger TG. Pruritus, Staphylococcus aureus, and human immunodeficiency virus infection . Arch Dermatol . 1990; 126:684-685.Crossref 10. Takematsu H, Nakamura K, Igarashi M, Tagami H. Eosinophilic pustular folliculitis . Arch Dermatol . 1985;121:917-920.Crossref 11. Buchness MR, Gregory N, Lim HW, Soter NA. The role of mast cells and eosinophils in eosinophilic pustular folliculitis of the acquired immunodeficiency syndrome . J Invest Dermatol . 1989; 92:408. 12. Buchness MR, Lim HW, Hatcher VA, Sanchez M, Soter NA. Eosinophilic pustular folliculitis in the acquired immunodeficiency syndrome . N Engl J Med . 1988;318:1183-1186.Crossref 13. Stanley SK, Folks TM, Fauci AS. Induction of expression of human immunodeficiency virus in a chronically infected promonocytic cell line by ultraviolet irradiation . AIDS Res Hum Retroviruses . 1989;5:375-384.Crossref 14. Valerie K, Delers A, Bruck C, et al. Activation of human immunodeficiency virus type 1 by DNA damage in human cells . Nature . 1988;333:78-81.Crossref 15. Greenspan D, Greenspan JS, de Souza Y, et al. Oral hairy leukoplakia in an HIV-negative renal transplant recipient . J Oral Pathol Med . 1989;18:32-34.Crossref 16. Cockerell CJ, Bergstresser PR, Myrie-Williams C, Tierno PM. Bacillary epithelioid angiomatosis occurring in an immunocompetent individual . Arch Dermatol . 1990;126:787-790.Crossref 17. Masur H, Ognibene FP, Yarchoan R, et al. CD4 counts as predictors of opportunistic pneumonias in human immunodeficiency virus (HIV) infection . Ann Intern Med . 1989;111:223-231.Crossref

Lucky, Anne W.;Biro, Frank M.;Huster, Gertrude A.;Morrison, John A.;Elder, Nancy

1991 Archives of Dermatology

doi: 10.1001/archderm.1991.01680020078009

Abstract • To assess the prevalence and severity of acne vulgaris in young adolescent boys, we studied 219 black and 249 white boys in fifth through ninth grades in Cincinnati, Ohio. The mean age was 12.2 ± 1.4 years, with a range of 9 to 15 years. Pubertal maturation was scored as Tanner pubic hair stages (PH I to V) and pubertal stages (PS I to IV) that included testicular volume assessment. Acne was scored by number of comedonal (open plus closed comedones) and inflammatory (papules plus pustules) lesions. Comedonal and inflammatory lesions were analyzed separately and evaluated both as numerical scores and as grades (1, ≤10 lesions; 2,11 to 25 lesions; and 3, ≥26 lesions). Grades 2 and 3 were considered clinically significant acne. Acne became progressively more severe with advancing maturity. Mean acne scores correlated better with PS and pubic hair than with age. Black subjects were more mature than white subjects. Black boys in PS I and II had significantly more comedones than white boys; white boys had significantly more inflammatory lesions at PS I and III. Clinically significant comedonal acne was already present in PS I and occurred in 100% of boys in PS IV. In contrast, no boys at PS I and only 50% at PS IV had significant inflammatory acne. Midfacial acne dominated. We concluded that acne prevalence and severity correlate well with advancing pubertal maturation in young adolescent boys. Comedonal acne was more frequent and severe than inflammatory disease. Awareness of the extent and severity of acne in preadolescents and young adolescents may ultimately provide rationale for early intervention and thus prevention of severe acne vulgaris. (Arch Dermatol. 1991;127:210-216) References 1. Bloch B. Metabolism, endocrine glands and skin-diseases, with special reference to acne vulgaris and xanthoma . Br J Dermatol . 1931;43:61-87.Crossref 2. Hinrichsen J, Ivy AC. Incidence in the Chicago region of acne vulgaris . Arch Dermatol Syphilol . 1938;37:975-982.Crossref 3. Hamilton J, Terada H, Mestler GE. Greater tendency to acne in white Americans than in Japanese populations . J Clin Endocrinol Metab . 1964;24:267-272.Crossref 4. Munro-Ashman D. Acne vulgaris in a public school . Trans St John's Hosp Dermatol Soc . 1963;49:144-148. 5. Burton L, Cunliffe WJ, Stafford I, Suster S. The prevalence of acne vulgaris in adolescence . Br J Dermatol . 1971;85:119-126.Crossref 6. Pochi PE, Strauss JS, Downing DT. Skin surface lipid composition, acne, pubertal development, and urinary excretion of testosterone and 17-ketosteroids in children . J Invest Dermatol . 1977; 69:485-489.Crossref 7. Lee PA. Normal ages of pubertal events among American males and females . J Adolesc Health Care . 1980;1:26-29.Crossref 8. Fellowes HM, Billewicz WZ, Thompson AM. Is acne a sign of normal puberty? A longitudinal study . J Biol Sci . 1981;13:401-407. 9. Cunliffe WJ, ed. Acne . Chicago, Ill: Year Book Medical Publishers Inc; 1989:2-10. 10. Marshall WA, Tanner JM. Variations in the pattern of pubertal changes in boys . Arch Dis Child . 1970;45:13-23.Crossref 11. Software Solutions Inc. DataEase Reference Manual . Milford, Conn: Software Solutions Inc; 1984. 12. SAS Institute Inc. SAS User's Guide: Basics . 5th ed. Cary, NC: SAS Institute Inc; 1985:171-254,403-432. 13. Cochran WG. Some methods for strengthening the χ2 tests . Biometrics . 1954;10:417-451.Crossref 14. Mantel N. Chi-square tests with one degree of freedom: extensions of the Mantel-Haenszel procedure . J Am Stat Assoc . 1963; 58:690-700. 15. Birch MW. The detection of partial association, II: the general case . J R Stat Soc . 1965;27:111-124. 16. Landis RJ, Heyman ER, Koch GG. Average partial association in three-way contingency tables: a review and discussion of alternative tests . Int Stat Rev . 1978;46:237-254.Crossref 17. Grizzle JE, Stammer CF, Koch GG. Analysis of categorical data by linear models . Biometrics . 1969;25:489-504.Crossref 18. Tanner JM. Growth at Adolescence . Boston, Mass: Blackwell Scientific Publications Inc; 1962. 19. Kligman AM. An overview of acne . J Invest Dermatol . 1974;62:268-287.Crossref

Gordon, Marsha L.;Lebwohl, Mark G.;Phelps, Robert G.;Cohen, Steven R.;Fleischmajer, Raul

1991 Archives of Dermatology

doi: 10.1001/archderm.1991.01680020085010

Abstract • Recently, the ingestion of tryptophan has been associated with eosinophilia-myalgia syndrome, which is characterized by eosinophilia, myalgias, and several less consistently reported findings. We treated 13 patients who exhibited clinical features of eosinophilic fasciitis who were taking high-dose tryptophan before the onset of clinical symptoms. Twelve patients exhibited eosinophilia, with eosinophil counts ranging from 0.13 to 0.88. The remaining patient was taking oral corticosteroids when her eosinophil count was determined. Eight patients complained of myalgias. Other symptoms included arthralgias, pruritus, cutaneous burning, weakness, fever, rashes, malaise, edema, muscle spasms, and alopecia. 5-Hydroxyindoleacetic acid levels were elevated in four of the eight urine specimens that were tested. Our findings suggest that previously diagnosed cases of eosinophilic fasciitis may represent variants of tryptophan-associated eosinophilia-myalgia syndrome. Derangements in the metabolism of tryptophan may play a role in sclerotic diseases. (Arch Dermatol. 1991;127:217-220) References 1. Centers for Disease Control, Center for Environmental Health and Injury Control. Interim Information and Guidance for Physicians on Eosinophilia-Myalgia Syndrome . Atlanta, Ga: Centers for Disease Control; (November 22) , 1989. 2. Back EE, Melius JM. Summary of New York State Cases Affected With the Eosinophilia-Myalgia Syndrome . New York, NY: Department of Health; (November 26) ,1989. 3. Centers for Disease Control. International notes: eosinophilia-myalgia syndrome—Canada . MMWR . 1990;39:326-327. 4. Centers for Disease Control. Eosinophilia-myalgia syndrome and L-tryptophan-containing products—New Mexico, Minnesota, Oregon, and New York, 1989 . MMWR . 1989;38:785-788 5. Udenfriend S, Titus E, Weissbach H. Identification of 5-hydroxy-3-indoleacetic acid in normal urine and a method for its assay . J Biol Chem. 1955;216:499-505. 6. Oates JA. 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Jaffe I, Kopelman R, Baird R, Grossman M, Hays A. Eosinophilic fasciitis associated with the eosinophilia-myalgia syndrome . Am J Med. 1990;88:542-546.Crossref 20. Tuffanelli DL. Urinary 5-hydroxyindoleacetic acid excretion in scleroderma . J Invest Dermatol. 1963;41:139-140.Crossref 21. Crawford MA. Excretion of 5-hydroxyindoleacetic acid in East Africans . Lancet . 1962;1:352-353.Crossref 22. Sternberg EM, Van Woert MH, Young SN, et al. Development of a scleroderma-like illness during therapy with L-5-hydroxytryptophan and carbidopa . N Engl J Med. 1980;303:782-787.Crossref 23. Graham JR. Cardiac and pulmonary fibrosis during methysergide therapy for headache . Am J Med Sci. 1967;254:1-12.Crossref 24. MacDonald RA, Robbins SL, Mallory AK. Dermal fibrosis following subcutaneous injections of serotonin creatinine sulfate . Proc Soc Exp Biol Med. 1958;97:334-337.Crossref 25. Price JM, Yess N, Brown RR, Johnson SAM. Tryptophan metabolism: a hitherto unreported abnormality occuring in a family . Arch Dermatol. 1967;95:462-472.Crossref 26. McConnell RB, Cheltham HD. Acute pellagra during isoniazid therapy . Lancet . 1952;2:959-960.Crossref 27. Stachow A, Jablonska S, Skiendzielewska A. 5-Hydroxytryptamine and tryptamine pathways in scleroderma . Br J Dermatol. 1977;97:147-154.Crossref 28. Analysis of L-tryptophan for the etiology of eosinophilia-myalgia syndrome . Arch Dermatol. 1990;126:1274.Crossref