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. Measurement of urinary tryptamine, tyramine and serotonin . Methods Med Res. 1961;9:169-174. 7. Weissbach H, King W, Sjoerdsma A, Udenfriend S. Formation of indole-3-acetic acid and tryptamine in animals . J Biol Chem. 1959;234:81-86. 8. Fleischmajer R, Pollock JL. Progressive systemic sclerosis: pseudoscleroderma . Clin Rheum Dis. 1979;22:243-261. 9. Ligresti DJ. Rash and eosinophilia . In: Lebwohl MG, ed. Difficult Diagnoses in Dermatology . New York, NY: Churchill Livingstone Inc; 1988:187-201. 10. Boman B. L-tryptophan: a rational anti-depressant and a natural hypnotic? Aust N Z J Psychiatry . 1988;22:83-97.Crossref 11. Segura R, Ventura JL. Effect of L-tryptophan supplementation on exercise performance . Int J Sports Med. 1988;9:301-305.Crossref 12. Seltzer S, Stock R, Marcus R, Jackson E. Alteration of human pain thresholds by nutritional manipulation and L-tryptophan supplementation . Pain . 1982;13:385-393.Crossref 13. Demisch K, Bauer J, Georgi K. Treatment of severe chronic insomnia with L-tryptophan and varying sleeping times . Pharmacopsychiatry . 1987;20:245-248.Crossref 14. Demisch K, Bauer J, Georgi K, Demisch L. Treatment of severe chronic insomnia with L-tryptophan: results of a double blind cross-over study . Pharmacopsychiatry . 1987;20:242-244.Crossref 15. Spinweber CL. L-tryptophan administered to chronic sleep-onset insomniacs: late-appearing reduction of sleep latency . Psychopharmacology (Berlin) . 1986;90:151-155.Crossref 16. Schneider-Helmert D, Spinweber CL. Evaluation of L-tryptophan for treatment of insomnia: a review . Psychopharmacology (Berlin) . 1986;89:1-7.Crossref 17. Amor B, Rajzbaum G, Poiraudeau S, Haas C, Kahan A. Eosinophilia-myalgia linked with L-tryptophan . Lancet . 1990;335:420. Letter.Crossref 18. Vionnet-Fuasset M, Sternberg EM. Scleroderma, fasciitis and eosinophilia associated with the ingestion of tryptophan . N Engl J Med. 1990;322:874-881.Crossref 19. 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

Teraki, Yuichi;Amagai, Naoko;Hashimoto, Takashi;Kusunoki, Toshio;Nishikawa, Takeji

1991 Archives of Dermatology

doi: 10.1001/archderm.1991.01680020089011

Abstract • We describe a 7-year-old girl with recurrent pruritic vesiculopustular lesions involving the trunk, extremities, face, and oral mucosa. Histopathologic examination revealed intraepidermal bullae containing neutrophils and eosinophils, and direct immunofluorescence test showed the deposition of IgA in the intercellular space of the epidermis. Circulating IgA anti-intercellular antibodies were also detected by indirect immunofluorescence test. Immunofluorescence studies using monoclonal antibodies to human IgA subclasses showed that these IgA antibodies belonged to IgA1. Antisera against J chain and secretory component did not show any specific intercellular staining. Surface IgA+-B cells were transiently increased in the peripheral blood during the active stage of the disease. These results indicated the extragut origin of these IgA antibodies. Dapsone therapy was shown to be very effective. (Arch Dermatol. 1991;127:221-224) References 1. Wallach D, Foldès C, Cottenot F. Pustulose sous-cornée acantholyse superficielle et IgA monoclonale . Ann Dermatol Venereol. 1982;109:953-963. 2. Tagami H, Iwatsuki K, Iwase Y, Yamada M. Subcorneal pustular dermatosis with vesiculo-bullous eruption: demonstration of subcorneal IgA deposits and a leukocyte chemotactic factor . Br J Dermatol. 1983;109:581-587.Crossref 3. Burrows D, Bingham EA. Subcorneal pustular dermatosis and IgA gammopathy . Br J Dermatol. 1984;111:91-93.Crossref 4. Huff JC, Golitz LE, Kunke KS. Intraepidermal neutrophilic IgA dermatosis . N Engl J Med. 1985;313:1643-1645.Crossref 5. Hashimoto T, Inamoto N, Nakamura K, Nishikawa T. Intercellular IgA dermatosis with clinical features of subcorneal pustular dermatosis . Arch Dermatol. 1987;123:1062-1065.Crossref 6. Nishikawa T, Shimizu H, Hashimoto T. Role of IgA intercellular antibodies: report of clinically and immunologically atypical cases . In: Orfanos CE, Stadler R, Gollnick H, eds. Proceedings of the 17th World Congress of Dermatology . New York, NY: Springer-Verlag NY Inc; 1987:383-384. 7. Gollnick H, Thies W, Taud W, Orfanos CE. Intraepidermale neutrophile und eosinophile IgA-Dermatose . In: Gollnick H, Stadler R, eds. Fallvorstellungen anlässlich des 17. Weltkongresses für Dermatologie, Berlin, 1987 . Stuttgart, Germany: Schattauer; 1987:68-70. 8. Piette W, Burken RR, Ray TL. Intraepidermal neutrophilic IgA dermatosis: presence of circulating pemphigus-like IgA antibody specific for monkey epithelium . J Invest Dermatol. 1987; 88:512. 9. Beutner EH, Chorzelski TP, Wilson RM, et al. IgA pemphigus foliaceus: report of two cases and review of literature . J Am Acad Dermatol. 1989;20:89-97.Crossref 10. Saurat JH, Mérot Y, Salomon D, Didierjean L. Pemphiguslike IgA deposits and vesiculo-pustular dermatosis in a 10-year-old girl . Dermatologica . 1987;175:96-100.Crossref 11. Wright S, Phillips T, Ryan J, Leigh IM. Intraepidermal neutrophilic IgA dermatosis with colitis . Br J Dermatol. 1989;129:113-119.Crossref 12. Conley ME, Kearney JF, Lawton AR III, Cooper MD. Differentiation of human B cells expressing the IgA subclasses as demonstrated by monoclonal antibodies . J Immunol. 1980;125:2311-2316. 13. Leonard JN, Haffenden GP, Unthworth DJ, Ring NP, Holborow EJ, Fly L. Evidence that the IgA in patients with linear IgA disease is qualitatively different from that of patients with dermatitis herpetiformis . Br J Dermatol. 1984;110:315-321.Crossref 14. Wojnarowska F, Delacroix D, Gengoux P. Cutaneous IgA subclasses in dermatitis herpetiformis and linear IgA dermatosis . J Cutan Pathol. 1988;15:272-275.Crossref 15. Nomoto Y, Sakai H, Arimoto S. Increase of IgA-bearing lymphocytes in peripheral blood from patients with IgA nephropathy . Am J Clin Pathol. 1979;71:158-160. 16. Kuno-Sakai H, Sakai H, Nomoto Y, Takakura I, Kimura M. Increase of IgA-bearing lymphocytes in peripheral blood in children with Henoch-Schoenlein purpura . Pediatrics . 1979;64:918-922. 17. Hashimoto T, Ogawa MM, Konohana A, Nishikawa T. Detection of pemphigus vulgaris and pemphigus foliaceus antigens by immunoblot analysis using different antigen sources . J Invest Dermatol. 1990;94:327-331.Crossref

Goeteyn, Marleen;Oranje, Arnold P.;Vuzevski, Vojislav D.;de Groot, Ronald;van Suijlekom-Smit, Lisette W. A.

1991 Archives of Dermatology

doi: 10.1001/archderm.1991.01680020093012

Abstract • The Shwachman syndrome comprises exocrine pancreatic insufficiency, growth retardation, and bone marrow hypoplasia resulting in neutropenia. Clinical, morphological, and ultrastructural studies, as well as hair analysis, were performed in a patient with Shwachman's syndrome and severe ichthyosis. Clinical findings were lamellar ichthyosiform desquamation on the extremities. The hair was scanty and short on the scalp, in the eyelashes, and in the eyebrows. The nails were hyperkeratotic. Morphologic findings were slight, regular acanthosis and severe diffuse hyperkeratosis with variable parakeratosis. The granular layer was thickened. The papillary dermis showed very slight perivascular lymphocyte infiltration. The most prominent ultrastructural finding was the presence of solitary or multiple droplets of varying size in the cytoplasm of the keratinocytes. Hair analysis revealed no abnormalities; the cystine concentration in hair specimens was normal. (Arch Dermatol. 1991;127:225-230) References 1. Shwachman H, Diamond LK, Oski FA, et al. The syndrome of pancreatic insufficiency and bone marrow dysfunction . J Pediatr. 1964;65:645-663.Crossref 2. Shwachman H, Holsclaw D. Some clinical observations on the Shwachman syndrome (pancreatic insufficiency and bone marrow hypoplasia) . Birth Defects . 1972;8:46-49. 3. Aggett PJ, Cavanagh HPC, Matthew DJ, et al. Shwachman's syndrome: a review of 21 cases . Arch Dis Child . 1980;55:331-347.Crossref 4. Aggett PJ, Harries JT, Harvey BAM, et al. An inherited defect of neutrophil mobility in Shwachman syndrome . J Pediatr. 1979;94:391-394.Crossref 5. Savilahti E, Rapola J. Frequent myocardial lesions in Shwachman's syndrome: eight fatal cases among 16 Finnish patients . Acta Paediatr Scand. 1984;73:642-651.Crossref 6. Ruutu P, Savilahti E, Repo H, et al. Constant defect in neutrophil locomotion but with age decreasing susceptibility to infection in Shwachman syndrome . Clin Exp Immunol. 1984;57:249-255. 7. Hill RE, Durie PR, Gaskin KJ, et al. Steatorrhea and pancreatic insufficiency in Shwachman syndrome . Gastroenterology . 1982;83:22-27. 8. Woods WG, Roloff JS, Lukens JH, et al. The occurrence of leukemia in patients with the Shwachman syndrome . J Pediatr. 1981;99:425-428.Crossref 9. Dopfer R, Döring A, Niethammer D. Kombination eines Shwachman-syndroms mit einer komplexen Granulocytenfunktions-störung bei einem Mädchen . Helv Paediatr Acta. 1983;38:351-360. 10. Happle R, Traupe H, Grösse H, et al. The Tay syndrome (congenital ichthyosis with trichothiodystrophy) . Eur J Pediatr. 1984;141:147-152.Crossref 11. Lischka A, Frisch H, Weissenbacher G. Radiologische Veränderungen bei metaphysärer Chondrodystrophie Typ McKusick (Knorpel-Haar-Hypoplasia) . Monatsschr Kinderheilkd. 1984;132: 550-553. 12. Fryns JP, Pedersen JC, Pardon W, et al. Cartilage-hair hypoplasia . Acta Paediatr Belg. 1980;33:265-267. 13. Elias PM, Williams ML. Neutral lipid storage disease with ichthyosis: defective lamellar body contents and intracellular dispersion . Arch Dermatol. 1985;121:1000-1008.Crossref 14. Williams ML, Elias PM. The ichthyoses . In: Thiers BH, Dobson RL, eds. Pathogenesis of Skin Diseases . New York, NY: Churchill Livingstone Inc; 1986:519-548. 15. Prottey C, Hartop PJ, Press M. Correction of the cutaneous manifestations of essential fatty acid deficiency in man by application of sunflower-seed oil to the skin . J Invest Dermatol. 1975; 64:228-234.Crossref 16. Rothbaum RJ, Williams DA, Daugherty CC. An unusual surface distribution of concanavalin A reflects a cytoskeletal defect in neutrophils in Shwachman's syndrome . Lancet . 1982;2:800-801.Crossref 17. Garty BZ, Scalin T, Goldsmith DP, et al. Cutaneous manifestations of cystic fibrosis: possible role of cryoglobulines . Br J Dermatol. 1989;121:655-658.Crossref 18. McLennan TW, Steinbach HL. Shwachman's syndrome: the broad spectrum of bony abnormalities . Pediatr Radiol. 1974;112: 167-173. 19. Hibron D, Filiasteadt D. Le syndrome de Shwachman aspects échographiques et tomodensitometriques: à propos de trois cas . Ann Radiol. 1985;28:469-475. 20. Robberecht E, Nachtegaele P, Van Rattinghe R, et al. Pancreatic lipomatosis in the Shwachman-Diamond syndrome: identification by sonography and CT scan . Pediatr Radiol. 1985;15:348-349.Crossref 21. Labrune M, Dommergues JP, Chaboche CH, et al. Syndrome de Shwachman à manifestations thoraciques néonatales . Arch Fr Pediatr. 1984;41:561-563.

Greenbaum, Steven S.;Varga, John

1991 Archives of Dermatology

doi: 10.1001/archderm.1991.01680020099013

Abstract • Long-term treatment with high doses of corticosteroids leads to the development of truncal obesity and focal fatty deposition. These deposits characteristically are located on the face, the nuchal and truncal areas, and episternally, as well as in the mediastinum and epicardium. We studied a patient with juxta-articular adiposis dolorosa who had L-tryptophan-associated eosinophilia-myalgia syndrome and was treated with high doses of prednisone. This is the first reported case of adiposis dolorosa occurring as a complication of corticosteroid treatment. Alterations of fat metabolism induced by corticosteroid excess may have played a role in the development of this unusual painful syndrome. (Arch Dermatol. 1991;127:231-233) References 1. Dercum FX. Three cases of a hitherto unclassified affection resembling in its grosser aspects obesity, but associated with special symptoms: adiposis dolorosa . Am J Med Sci. 1982;104:521-535.Crossref 2. Bonatus TJ, Alexander AH. Dercum's disease (adiposis dolorosa): a case report and review of the literature . Clin Orthop Rel Res. 1986;205:251-253. 3. Blomstrand R, Juhlin L, Nordenstam H, Ohlsson R, Werner B, Engstrom J. Adiposis dolorosa associated with defects of lipid metabolism . Acta Derm Venereol (Stockh). 1971;51:243-250. 4. Eisman J, Swezey RL. Juxta-articular adiposis dolorosa: what is it? report of two cases . Ann Rheum Dis. 1979;38:479-482.Crossref 5. Steiger WA, Litvin H, Lasche EM, Durant TM. Adiposis dolorosa (Dercum's disease) . N Engl J Med. 1952;247:393-396.Crossref 6. Stallworth JM, Hennigar GR, Jonsson HT, Rodriguez O. The chronically swollen painful extremity . JAMA . 1974;228:1656-1659.Crossref 7. Peterson P, Kastrup J. Dercum's disease (adiposis dolorosa): treatment of the severe pain with intravenous lidocaine . Pain. 1987;28:77-80.Crossref 8. Scheinberg MA, Diniz R, Diamant J. Improvement of juxtaarticular adiposis dolorosa by fat suction . Arthritis Rheum. 1987;30:1435-1437.Crossref 9. Varga J, Peltonen J, Uitto J, Jimenez SA. Development of diffuse fasciitis with eosinophilia during L-tryptophan treatment: demonstration of elevated type 1 collagen gene expression in affected tissues: a clinicopathological study of four patients . Ann Intern Med. 1990;112:344-351.Crossref 10. Centers Control.ase Control. Eosinophilia-myalgia syndrome and L-tryptophan—containing products—New Mexico, Minnesota, Oregon, and New York . MMWR . 1989;38:785-788. 11. Slutsker L, Hoesly FC, Miller LM, Williams LP, Watson JC, Fleming DW. Eosinophilia-myalgia syndrome associated with exposure to tryptophan from a single manufacturer . JAMA . 1990;264: 213-217.Crossref 12. Silver R, Heyes P, Maize J, Querry B, Vionnet-Fuasset M, Sternberg E. Scleroderma, fasciitis, and eosinophilia associated with the ingestion of tryptophan . N Engl J Med. 1990;322:874-888.Crossref 13. Varga J, Heiman-Patterson D, Emery D, et al. Clinical spectrum of the systemic manifestations of the eosinophilia-myalgia syndrome. Semin Arthritis Rheum. 1990;19:313-328.Crossref 14. L-tryptophan: a `natural' sedative? Med Lett Drugs Ther. 1977;19:108. 15. Fries JF, Lindgren JA, Bull JM. Scleroderma-like lesions and the carcinoid syndrome . Arch Intern Med. 1973;131:550-553.Crossref 16. Stachow A, Jablonska S, Kencka D. Tryptophan metabolism in scleroderma and eosinophilic fasciitis . In: Black CM, Myers AR, eds. Current Topics in Rheumatology: Systemic Sclerosis (Scleroderma) . New York, NY: Gower Medical Publishers; 1985:130-134. 17. Cushing H. Basophil adenomas of the pituitary body and their clinical manifestations . Bull Johns Hopkins Hosp. 1932;50:137-195. 18. Seale PS, Compton MR. Side-effects of corticosteroid agents . Med J Aust. 1986;144:139-142. 19. Mayo-Smith W, Hayes CW, Biller BM, Klibanski A, Rosenthal H, Rosenthal D. Body fat distribution measured with CT: correlations in healthy subjects, patients with anorexia nervosa, and patients with Cushing's syndrome . Radiology . 1989;170:515-518.Crossref 20. Horber HH, Xurcher RM, Herren H, Crivelli MA, Robotti G, Frey FJ. Altered body fat distribution in patients with glucocorticoid treatment and in patients on long-term dialysis . Am J Clin Nutr. 1986;43:758-769. 21. Bachow TB, Hesselink JR, Aaron JO, Davis KR, Taveras JM. Fat deposition in the cavernous sinus in Cushing's disease . Radiology . 1984;153:135-136.Crossref 22. Gottlieb NL. Temporal fat pad sign during corticosteroid treatment . Arch Intern Med. 1980;140:1507-1508.Crossref 23. Brythian D, Piette C, Ducervean MN, Robert G, Godeau P, Heitz F. Steroid induced spinal epidural lipomatosis: CT survey . J Comput Assist Tomogr. 1988;12:501-503.Crossref 24. Ettinger WH, Goldberg AP, Appelbaum-Bowden D, Hazzard WR. Dyslipoproteinemia in systemic lupus erythematosus: effect of corticosteroids . Am J Med. 1987;83:503-508.Crossref 25. Zimmerman F, Fainura M, Eisenberg S. The effect of prednisone therapy on plasma lipoproteins and apoproteins: a prospective study . Metabolism. 1984;33:521-526.Crossref 26. Rebuffe-Scrive M. Steroid hormones and distribution of adipose tissue . Acta Med Scand Suppl. 1988;723:143-146.

Shelley, Walter B.;Shelley, E. Dorinda

1991 Archives of Dermatology

doi: 10.1001/archderm.1991.01680020102014

Abstract • A multiple puncture technique using a bifurcated vaccination needle to introduce bleomycin sulfate (1 U/mL sterile saline solution) into warts resulted in elimination of 92% of a random series of 258 warts after a single treatment. Recurrence was not observed during a 6-month follow-up period. Six of the 66 patients required two to seven treatments for wart eradication, and four patients requested alternative therapy after initial failure with a single bleomycin treatment. (Arch Dermatol. 1991;127:234-236) References 1. Bunney MH. Viral Warts: Their Biology and Treatment . New York, NY: Oxford University Press Inc; 1982. 2. Belisario JC. Warts and their treatment . Australas J Dermatol. 1951;1:20-30.Crossref 3. Beutner KR, Conant MA, Friedman-Kien AE, et al. Patient-applied podofilox for the treatment of genital warts . Lancet . 1989;1:831-834.Crossref 4. Lasser AE, Glazer SD. Vehicle effects on comparative irritancy and patient compliance in topical wart therapy . Curr Ther Res. 1986;39:1011-1016. 5. McCarthy JT. Warts . Cutis. 1986;38:87. 6. Fenner F, Henderson DA, Arita I, Jezek Z, Ladnyi ID. Smallpox and Its Eradication . Geneva, Switzerland; World Health Organization; 1988:567-574. 7. Hayes ME, O'Keefe EJ. Reduced dose of bleomycin in the treatment of recalcitrant warts . J Am Acad Dermatol. 1986;15:1002-1006.Crossref 8. Mishima Y, Matunaka M. Effect of bleomycin on benign and malignant cutaneous tumours . Acta Derm Venereol (Stockh) . 1971;52:211-215. 9. Bennett JM, Reich SD. Bleomycin . Ann Intern Med. 1979;90:945-948.Crossref 10. Bremner RM. Warts: treatment with intralesional bleomycin . Cutis. 1976;18:264-266. 11. Shumack PH, Haddock MJ. Bleomycin: an effective treatment for warts . Australas J Dermatol. 1979;20:41-42.Crossref 12. Takigawa M, Oku T, Ginoza M, Yamada M, Yamamoto T, Kobayashi I. Treatment of viral warts with pressure-sensitive adhesive tape containing bleomycin sulfate . Arch Dermatol. 1985;121:1108.Crossref 13. Laffitte F, Chavoin JP, Bonafe JL, Costagliola M. Under heel foot wart . Dermatologica. 1985;171:206-208.Crossref 14. Zaias N. The Nail in Health and Disease . 2nd ed. East Norwalk, Conn: Appleton & Lange; 1990:216-217. 15. Epstein E. Persisting Raynaud's phenomenon following intralesional bleomycin treatment of finger warts . J Am Acad Dermatol. 1985;13: 468-469.Crossref 16. Smith EA, Harper FE, LeRoy EC. Raynaud's phenomenon of a single digit following local intradermal bleomycin sulfate injection . Arthritis Rheum. 1985;28:459-461.Crossref 17. Miller RAW. Nail dystrophy following intralesional injections of bleomycin for a periungual wart . Arch Dermatol. 1984;120:963-964.Crossref 18. González FU, Gil MCC, Martinez AA, Rodriquez PG, de Paz FS, García-Pérez A. Cutaneous toxicity of intralesional bleomycin administration in the treatment of periungual warts . Arch Dermatol. 1986;122:974-975.Crossref 19. Bunney MH. Intralesional bleomycin sulfate in treatment of recalcitrant warts . Clin Dermatol. 1985;3:189-194.Crossref 20. Sayama S, Tagami H. Treatment of keratoacanthoma with intralesional bleomycin . Br J Dermatol. 1983;109:449-452.Crossref

Kirby, Philip K.;Munyao, Titus;Kreiss, Joan;Holmes, King K.

1991 Archives of Dermatology

doi: 10.1001/archderm.1991.01680020105015

Abstract Transmission (HIV) occurs through exposure to infected bodily fluids, including blood, blood products, semen, and genital secretions. Exposure to blood or blood products has been associated with HIV infection among intravenous drug users, persons receiving transfusions, and hemophiliacs. Although the prevalence of infection continues to increase among intravenous drug users, blood products are now safe as a result of blood donor counseling, screening of donors for HIV antibodies, and heat treatment of clotting factor concentrates. Sexual contact, both homosexual and heterosexual, continues to be the predominant mode of HIV transmission among adults. Heterosexual transmission predominates in Africa and the Caribbean and is becoming relatively more important elsewhere as well, as transmission by homosexual contact may be decreasing. Early during the epidemic of acquired immunodeficiency syndrome (AIDS), it was recognized that HIV infection was associated with sexual promiscuity and with a high incidence of other sexually transmitted diseases (STDs) among sexually References 1. Padian N, Marquis L, Francis DP, et al. Male to female transmission of human immunodeficiency virus . JAMA . 1987;258:788-790.Crossref 2. Redfield RR, Markham PD, Salahuddin SZ, et al. Heterosexually acquired HTLV-III/LAV disease: epidemiologic evidence for female to male transmission . JAMA . 1985;254:2094-2096.Crossref 3. Peterman TA, Stoneburner RL, Allen JR, et al. Risk of human immunodeficiency virus transmission from heterosexual adults with transfusion-associated infections . JAMA . 1988;259:55-58.Crossref 4. Johnson AM, Petherick A, Davidson S, et al. Transmission of HIV to sexual partners of infected men and women . AIDS . 1989;3:367-372.Crossref 5. Padian N, Shiboski S, Jewell N. The relative efficiency of female-to-male HIV sexual transmission . In: Program and abstracts of the Sixth International Conference on AIDS; June 20-24,1990; San Francisco, Calif. Abstract Th. C. 101. 6. Holmes KK, Kreiss J. Heterosexual transmission of human immunodeficiency virus: overview of a neglected aspect of the AIDS epidemic . J Acquir Immune Defic Syndr. 1988;1:602-610. 7. Cameron DW, Simonsen JN, D'Costa LJ, et al. Female to male transmission of human immunodeficiency virus type 1: risk factors for seroconversion in men . Lancet . 1989;2:403-407.Crossref 8. Plummer FA, Cameron DW, Simonsen N, et al. Co-factors in male to female transmission of HIV . In: Program and abstracts of the Fourth International Conference on AIDS; June 12-16, 1988; Stockholm, Sweden . Abstract 4554. 9. Laga M, Nzila N, Manoka AT, et al. Non-ulcerative sexually transmitted diseases (STD) as risk factors for HIV infection . In: Programs and abstracts of the Sixth International Conference on AIDS; June 20-24,1990; San Francisco, Calif. Abstract Th. C. 97. 10. Latif AS, Katzenstein DA, Bassett MT, et al. Genital ulcers and transmission of HIV among couples in Zimbabwe . AIDS . 1989;3:519-523.Crossref 11. Holmberg SD, Stewart JA, Gerber AR, et al. Prior herpes simplex virus type 2 as a risk factor for HIV infection . JAMA . 1988;260:1048-1050.Crossref 12. Stamm WE, Handsfield HH, Rompalo AM, et al. The association between genital ulcer disease and acquisition of HIV infection in homosexual men . JAMA . 1988;260:1429-1433.Crossref 13. Kreiss JK, Coombs R, Plummer F, et al. Isolation of human immunodeficiency virus from genital ulcers in Nairobi prostitutes . J Infect Dis. 1989;160:380-384.Crossref 14. Plummer FA, Wainberg MA, Plourde P, et al. Detection of human immunodeficiency virus type 1 (HIV-1) in genital ulcer exudate of HIV-1 infected men by culture and gene amplification . J Infect Dis. 1990;161:810-811.Crossref 15. Sheldon WH, Heyman A. Studies on chancroid, I: observations on the histology with an evaluation of the biopsy as a diagnostic procedure . Am J Pathol. 1985;22:415-422. 16. Lukehart SA, Baker-Zander SA, Lloyd RMC, Sell S. Characterization of lymphocyte responsiveness in early experimental syphilis; II: nature of cellular infiltration and Treponema pallidum distribution in testicular infection . J Immunol. 1980;124:461-467. 17. Goodell SE, Quinn TC, Mrktichian E, et al. Herpes simplex virus proctitis in homosexual men: clinical, sigmoidoscopic and histopathologic features . N Engl J Med. 1983;308:868-871.Crossref 18. Fischl MA, Dickinson GM, Scott GB, et al. Evaluation of heterosexual partners, children and household contacts of adults with AIDS . JAMA . 1987;257:640-644.Crossref 19. Nzila N, Ryder R, Colebunders R, et al. Married couples in Zaire with discordant HIV serology . In: Program and abstracts of the Fourth International Conference on AIDS; June 12-16, 1988; Stockholm . Abstract 4059. 20. Fischl M, Fayne T, Flanagan S, et al. Seroprevalence and risks of HIV infection in spouses of persons infected with HIV . In: Program and abstracts of the Fourth International Conference on AIDS; June 12-16,1988; Stockholm, Sweden . Abstract 4060. 21. Haley C, Anderson P, Freeman A, et al. Relationship of STD history to HIV seropositivity in a cohort of homosexual men in Dallas, Texas . In: Program and abstracts of the Fifth International Conference on AIDS; June 4, 1989; Montreal, Canada . Abstract W.A.P.39. 22. Cameron DW, Plummer FA, D'Costa LJ, et al. Prediction of HIV infection by treatment failure for chancroid, a genital ulcer disease . In: Program and abstracts of the Fourth International Conference on AIDS; June 12-16, 1988; Stockholm, Sweden . Abstract 7637. 23. Seigal FP, Lopez C, Hamer GS, et al. Severe acquired immunodeficiency in male homosexuals manifested by chronic perianal ulcerative herpes simplex lesions . N Engl J Med. 1981;305:1439-1444.Crossref 24. Coombs RW, Collier A, Allain JP, et al. Plasma viremia in human immunodeficiency virus infection . N Engl J Med. 1989;321:1626-1631.Crossref 25. Laga M, Taelman H, Van der Stuyft P, et al. Advanced immunodeficiency as a risk factor for heterosexual transmission of HIV . AIDS . 1989;3:361-366.Crossref 26. Greenblatt RM, Lukehart SA, Plummer FA, et al. Genital ulceration as a risk factor for human immunodeficiency virus infection . AIDS . 1988;2:47-50.Crossref 27. Simonsen JN, Cameron DW, Gakinya MN, et al. Human immunodeficiency virus infection among men with sexually transmitted diseases: experience from a center in Africa . N Engl J Med. 1988;319:274-278.Crossref 28. Bongaarts J, Reining P, Way P, et al. The relationship between male circumcision and HIV infection in African populations . AIDS . 1989;3:373-377.Crossref 29. Conant M, Hardy D, Sernatinger J, et al. Condoms prevent transmission of AIDS associated retrovirus . JAMA . 1986;255:1706.Crossref 30. Mann J, Quinn TC, Piot P, et al. Condom use and HIV infection among prostitutes in Zaire . N Engl J Med. 1987;316:345. 31. Ngugi EN, Plummer FA, Simonsen JN, et al. Prevention of transmission of human immunodeficiency virus in Africa: effectiveness of condom promotion and health education among prostitutes . Lancet . 1988;2:887-890.Crossref 32. Valle SL. Sexually transmitted diseases and the use of condoms in a cohort of homosexual men followed since 1983 in Finland . Scand J Infect Dis. 1988;20:153-161.Crossref 33. Coutinho RA, Schoonhoven FJ, Van den Hoek JA, et al. Influence of special programmes and AIDS on declining incidence of syphilis in Amsterdam . Genitourin Med. 1987;63:210-213. 34. Hessol N, O'Malley P, Lifson A, et al. Incidence and prevalence of HIV infection among homosexual and bisexual men, 1978-1988 . In: Program and abstracts of the Fifth International Conference on AIDS; June 4-9, 1989; Montreal, Canada . Abstract M.A.O.27. 35. Handsfield HH, Krekeler B, Nicola RM. Trends in gonorrhea in homosexually active men—King County, Washington, 1989 . MMWR . 1989;38:762-764. 36. World Health Organization. Consensus statement from consultation on sexually transmitted diseases as a risk factor for HIV transmission . WHO/GPA/INF 89.1 Geneva. (January) 1989. 37. Hicks CB, Benson PM, Lupton GP. Seronegative secondary syphilis in a patient infected with the human immunodeficiency virus (HIV) with Kaposi's sarcoma: a diagnostic dilemma . Ann Intern Med. 1987;107:492-494.Crossref 38. Centers for Disease Control. Recommendations for diagnosing and treating syphilis in HIV infected patients . JAMA . 1988;260:2488-2489.Crossref 39. Felman YM. Recent developments in the diagnosis and treatment of sexually transmitted diseases: infectious syphilis and acquired immunodeficiency syndrome . Cutis . 1989;44:288-289. 40. Lukehart SA, Hook EW, Baker-Zander SA, et al. Invasion of the central nervous system by Trepomena pallidum: implications for diagnosis and therapy . Ann Intern Med. 1988;109:855-862.Crossref 41. New York City Health Department. Genital ulcer disease in New York City . New York City Health Information Newsletter . (March) 1989. 42. Langenberg A, Benedetti J, Jenkins J, et al. Development of clinically recognizable genital lesions among women previously identified as having `asymptomatic' herpes simplex virus type 2 infection . Ann Intern Med. 1989;110:882-887Crossref 43. Stamm WE. Diagnosis of Chlamydia trachomatis genitourinary infections . Ann Intern Med. 1988;108:710-717.Crossref 44. Krieger JN, Tam MR, Stevens CE, et al. Diagnosis of trichomoniasis: comparison of conventional wet mount examination with cytologic studies, cultures and monoclonal antibody staining of direct specimens . JAMA . 1988;259:1223-1227.Crossref 45. Cated W, Meheus A. Strategies for development of sexually transmitted diseases control programs . In: Holmes KK, Mårdh P-A, Sparling PF, Wiesner PJ, eds. Sexually Transmitted Diseases . 2nd ed. New York, NY: McGraw-Hill International Book Co; 1990:1023-1030. 46. Meheus A, Schulz KF, Cates W. Development of prevention and control programs for sexually transmitted diseases in developing countries . In: Holmes KK, Mårdh P-A, Sparling PF, Wiesner PJ, eds. Sexually Transmitted Diseases . 2nd ed. New York, NY: McGraw-Hill International Book Co; 1990:1041-1046. 47. World Health Organization and Pan American Health Organization. Control of sexually transmitted diseases . Geneva, Switzerland: World Health Organization; 1985. 48. World Health Organization. WHO expert committee on venereal diseases and treponematoses: sixth report . Geneva, Switzerland: World Health Organization; 1986. 49. Schmid GP, Sanders LL, Blount JH, Alexander ER. Chancroid in the United States: reestablishment of an old disease . JAMA . 1987;258:3265-3268.Crossref 50. Centers for Disease Control. Continuing increases in infectious syphilis—United States . MMWR . 1988;37:35-38.

Mulliken, John B.

1991 Archives of Dermatology

doi: 10.1001/archderm.1991.01680020111016

Abstract The anguished parents bring their perfect child to you. Now, there is a red facial blemish. The bright hemangioma seems to beckon you to do something— try anything! Over the years, physicians have demonstrated their resourcefulness in assailing hemangiomas by strangulation with sutures, injection of caustics, and freezing. Electromagnetic energy has also been utilized, including electrolysis, thermocautery, radiation, and now, lasers.1 Perhaps focusing the laser on infant hemangiomas was hastened by its efficacy in treating port-wine stains, vascular malformations often mislabeled as "capillary hemangiomas." Apfelberg and coworkers2 and Hobby3 presented preliminary reports on the use of argon laser for the treatment of infant hemangiomas. Achauer and Vander Kam4 compared use of the argon with the Nd:YAG laser in the treatment of hemangioma. Now Ashinoff and Geronemus5 present their experience treating 10 children with cutaneous hemangiomas using the flashlamp-pumped pulsed dye laser. A positive response, ie, decrease in size and lightening, is References 1. Mulliken JB, Young AE. Vascular Birthmarks: Hemangiomas and Malformations . Philadelphia, Pa: WB Saunders Co; 1988:77-82. 2. Apfelberg DB, Greene RA, Maser R, et al. Results of argon laser exposure of capillary hemangiomas of infancy: preliminary report . Plast Reconstr Surg. 1981;67:188-193.Crossref 3. 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 4. Achauer M, Vander Kam VM. Capillary hemangioma (strawberry mark) of infancy: comparison of argon and Nd:YAG laser treatment . Plast Reconstr Surg. 1989;84:60-69.Crossref 5. Ashinoff R, Geronemus RG. Capillary hemangiomas and treatment with the flashlamp-pumped pulsed dye laser . Arch Dermatol. 1991;127:202-205.Crossref 6. Berlien HP, Muller G, Waldschmidt J. Lasers in pediatric surgery . In: Angerpointner TA, Gauderer MWL, Hecker WCH, et al, eds. Progress in Pediatric Surgery . New York, NY: Springer-Verlag NY Inc; 1990;25:6-22. 7. Enjolras O, Riché MC, Merland JJ, Escande JP. Management of alarming hemangiomas in infancy: a review of 25 cases . Pediatrics . 1990;85:491-498. 8. Folkman J. Angiogenesis . In: Verstraete M, Vermylen J, Lijnen HR, Arnout J, eds. Thrombosis and Haemostasis . Leuven, Belgium: Leuven University Press; 1987:583-596. 9. Folkman J, Klagsbrun M. Angiogenic factors . Science . 1987;235:442-447.Crossref 10. Orchard PJ, Smith CM III, Woods WG, et al. Treatment of haemangioendotheliomas with alpha interferon . Lancet . 1989;2: 565-567.Crossref

Oursler, Judith R.;Goldblum, Orin M.

1991 Archives of Dermatology

doi: 10.1001/archderm.1991.01680020115017pmid: 1990993

Abstract REPORT OF A CASE A 65-year-old man presented with a 2-month history of blisters on his legs. The blisters had developed spontaneously and were asymptomatic. They ruptured spontaneously and healed slowly. A course of oral cephalexin, prescribed by his internist, had no effect on the appearance or healing of his lesions. His medical history was pertinent for long-standing type II diabetes mellitus treated with insulin. Major diabetic complications, such as retinopathy, nephropathy, or neuropathy, had not developed.Results from the physical examination showed scattered tense bullae on the lower extremities bilaterally, which ranged from 1.0 to 3.0 cm (Figs 1 and 2). Also revealed were discrete, round ulcerations of a similar size. These were present on the lower extremities bilaterally at the sites of previous bullae. No similar lesions were present elsewhere.Laboratory tests disclosed the following values: white blood cell count, 4.9 × 109/L (normal, 4.8 to References 1. Kramer DW. Early or warning signs of impending gangrene in diabetes . Med J Rec. 1930;132:338-342. 2. Cantwell AR, Martz W. Idiopathic bullae in diabetics: bullosis diabeticorum . Arch Dermatol. 1967;96:42-44.Crossref 3. Toonstra J. Bullosis diabeticorum: report of a case with a review of the literature . J Am Acad Dermatol. 1985;13:799-805.Crossref 4. Bernstein JE, Levine LE, Medenica MM, Yung CW, Soltani K. Reduced threshold to suction-induced blister formation in insulindependent diabetics . J Am Acad Dermatol. 1983;8:790-791.Crossref 5. Bernstein JE, Medenica M, Soltani K, Griem SF. Bullous eruption of diabetes mellitus . Arch Dermatol. 1979;115:324-325.Crossref 6. Kurwa A, Roberts P, Whitehead R. Concurrence of bullous and atrophic skin lesions in diabetic mellitus . Arch Dermatol. 1971; 103:670-675.Crossref

Albers, Sharon E.;Fenske, Neil A.

1991 Archives of Dermatology

doi: 10.1001/archderm.1991.01680020117018

Abstract REPORT OF A CASE The patient, a 62-year-old white woman, was referred to the University of South Florida Medical Clinics, Tampa, for examination of pruritic lesions of her extremities that were present intermittently for a few years. The physical examination disclosed periorbital edema; dry skin over both lower extremities; and a few eczematous, coin-shaped lesions on the extensor aspects of the lower extremities. On careful inspection of the skin, the patient was noted to have waxy, indurated pale areas over the right pretibial region and two large, exuberant tumoral lesions with brawny edema on the dorsum of her left foot (Fig 1). Examination of her nails revealed clubbing (Fig 2). Biopsy specimens were obtained and sent for hematoxylin-eosin (Fig 3) and special staining (Fig 4).What is your diagnosis? DIAGNOSIS: Pretibial myxedema. DISCUSSION Localized myxedema is an infiltrative, metabolic dermopathy with deposition of acid mucopolysaccha-rides in the dermis.1-5 Classically, this process manifests cutaneously as raised, waxy nodules or plaques varying in color from flesh to yellow-brown to red. References 1. Matsuoka L, Wortsman J, Dietrich J, Pearson R. Pretibial myxedema . Arch Dermatol. 1981;117:250-251.Crossref 2. Noppakun N, Bancheun K, Chandraprasert S. Unusual location of localized myxedema in Graves' disease . Arch Dermatol. 1986; 122:85-88.Crossref 3. Truhan A. Pretibial myxedema . Am Fam Physician . 1985; 31:135-138. 4. Elte J, Hensen E. Pretibial myxoedema: report of 17 cases and review of the literature . Neth J Med. 1983;26:220-227. 5. Lever WF, Schaumburg-Lever G. Histopathology of the Skin . ed 6. Philadelphia, Pa: JB Lippincott; 1983:424-426.

Scheinman, Pamela L.;Helm, Klaus F.;Fairley, Janet A.

1991 Archives of Dermatology

doi: 10.1001/archderm.1991.01680020119019

Abstract REPORT OF A CASE A 63-year-old woman with a history of hypertension, diabetes, and end-stage renal disease was admitted with complaints of joint stiffness distally, decreased sensation in a glove-stocking distribution, and pain in her extremities distally. Her renal function had been deteriorating and dialysis was initiated. Results of the physical examination revealed purplish mottling of the skin of her lower extremities. This quickly progressed to painful subcutaneous nodules with eventual ulceration and necrosis. Several digits, as well as the left lateral malleolus and the dorsum of the left foot, became gangrenous with time (Figure). Laboratory studies disclosed the following values: hemoglobin, 77 g/L; hematocrit, 0.25; white blood cell count, 8.7 × 109/L; platelet count and cell differential, normal; erythrocyte sedimentation rate, 126 mm/h; serum urea nitrogen, 21 mmol/L; creatinine, 434 μmol/L; calcium, 2.27 mmol/L; phosphate, 2.49 mmol/L; parathyroid hormone, 9.9 ng/mL (0.16 to 0.96 ng/mL); antinuclear References 1. Gipstein RM, Cobrun JW, Adams DA. Calciphylaxis in man: a syndrome of tissue necrosis and vascular calcification in 11 patients with chronic renal failure . Arch Intern Med. 1976;136:1273-1280.Crossref 2. Fox R, Banowsky LH, Cruz AB. Post-renal transplant calciphylaxis . J Urol. 1983;129:362-363. 3. Conn J, Krumlovsky FA, Del Grecco F, et al. Calciphylaxis: etiology of progressive vascular calcification and gangrene . Ann Surg. 1973;177:206-210.Crossref 4. Massry SG, Gordon A, Coburn JW, et al. Vascular calcification and peripheral necrosis in a renal transplant recipient . Am J Med. 1970;49:416-422.Crossref 5. Selye H. Calciphylaxis . Chicago, Ill: University of Chicago Press; 1962:1-16. 6. Massry SG, Coburn JW, Popovtzer MM, et al. Secondary hyperparathyroidism in chronic renal failure: the clinical spectrum in uremia, during hemodialysis, and after renal transplantation . Arch Intern Med. 1969;124:431-441.Crossref 7. Parfitt AM. Soft-tissue calcification in uremia . Arch Intern Med. 1969;124:544-556.Crossref 8. Richens G, Piepkorn MW, Krueger GG. Calcifying panniculitis associated with renal failure . J Am Acad Dermatol. 1982;6:537-539.Crossref 9. Cooksley WE, Craswell PW. Involvement of the skin and subcutaneous tissue in azotemic hyperparathyroidism . Aust N Z J Med. 1972;2:142-147.Crossref 10. Richardson JA, Herron G, Retiz R, Layzer R. Ischemic ulcerations of skin and necrosis of muscle in azotemic hyperparathyroidism . Ann Intern Med. 1969;71:129.Crossref 11. Taylor LM, Baur GM, Porter JM. Finger gangrene caused by small artery occlusive disease . Ann Surg. 1981;193:453-461.Crossref

Dhawan, Sunil S.;Herbst, Jay S.;Fields, Kenneth W.

1991 Archives of Dermatology

doi: 10.1001/archderm.1991.01680020121020

Abstract REPORT OF A CASE A 49-year-old man was admitted to Mount Sinai Medical Center, Miami Beach, Fla, for epigastric pain radiating to the back that was associated with fever. He had a history of alcohol abuse, recurrent pancreatitis, and pancreatic pseudocysts. Results from the physical examination revealed abdominal tenderness, ascites, and pleural effusions. Laboratory tests disclosed the following findings and values: leukocytosis; erythrocyte sedimentation rate, elevated; liver function tests, normal; serum amylase, 590 U/L (normal, 30 to 110 U/L); and serum lipase, 1694 U/L (normal, 23 to 208 U/L).Ten days after admission, painful nodules on the lower legs, arthralgia involving the ankles, and eosinophilia developed. The eruption consisted of groups of tender, red, 1- to 3-cm nodules with ill-defined borders on the anterior legs (Figs 1 and 2).A hematoxylin-eosin-stained section of an excisional biopsy specimen is shown in Figs 3 and 4. The nodules resolved within 2 weeks, leaving hyperpig-mentation. References 1. Chiari H. Über die sogenannte Fettnekrose . Prager Med Wochenschr. 1883;8:285-286. 2. Szymanski FJ, Bluefarb SM. Nodular fat necrosis and pancreatic diseases . Arch Dermatol. 1961;83:224-229.Crossref 3. Hughes PSH, Apisarnthanarax P, Mullins JF. Subcutaneous fat necrosis associated with pancreatic disease . Arch Dermatol. 1975; 111:506-510.Crossref 4. Bennett RG, Petrozzi JW. Nodular subcutaneous fat necrosis . Arch Dermatol. 1975;111:896-898.Crossref 5. Potts DE, Mass MF, Iseman MD. Syndrome of pancreatic disease, subcutaneous fat necrosis, and polyserositis: case report and review of the literature . Am J Med. 1975;58:417-423.Crossref 6. Swerdlow AB, Berman ME, Gibbel MI, et al. Subcutaneous fat necrosis associated with acute pancreatitis . JAMA . 1960;173:765-769.Crossref 7. Good AE, Schnitzer B, Kawanishi H, et al. Acinar pancreatic tumor with metastatic fat necrosis: report of a case and review of rheumatic manifestations . Dig Dis. 1976;21:978-987.Crossref 8. Cannon JR, Pitha JV, Everett MA. Subcutaneous fat necrosis in pancreatitis . J Cutan Pathol. 1979;6:501-506.Crossref 9. Wilson HA, Askari AD, Neiderhiser DH, et al. Pancreatitis with arthropathy and subcutaneous fat necrosis: evidence for the pathogenicity of lipolytic enzymes . Arthritis Rheum. 1983;26:121-126.Crossref 10. Schrier RW, Melmon KL, Fenster LF. Subcutaneous nodular fat necrosis in pancreatitis . Arch Intern Med. 1965;116:832-836.Crossref 11. Lever WF, Schaumburg-Lever G. Histopathology of the Skin . Philadelphia, Pa: JB Lippincott; 1983. 12. Berman B, Conteas C, Smith B, et al. Fatal pancreatitis presenting with subcutaneous fat necrosis . J Am Acad Dermatol. 1987;17:359-364.Crossref 13. Forstrom L, Winklemann RK. Acute, generalized panniculitis with amylase and lipase in skin . Arch Dermatol. 1975;111:497-502.Crossref 14. Fine RM: Subcutaneous fat necrosis, pancreatitis, and arthropathy . Int J Dermatol. 1983;22:575-576.Crossref

Lazar, Andrew P.;Lazar, Paul

1991 Archives of Dermatology

doi: 10.1001/archderm.1991.01680020135021

Abstract To the Editor.— The cause-and-effect relationship between the exposure to silicone gel prostheses used in augmentation mammoplasty and sclerodermatous changes is still somewhat tenuous. A recent case report1 about the association prompted this article concerning a patient who developed localized morphea 2 months after the implantation of a silicone gel-filled prosthesis. Report of a Case.— A 64-year-old white woman was seen in July 1988, 7 months after undergoing augmentation mammoplasty of the left breast. Other than having had breast cancer, she was generally in good health, taking only captopril (Capoten) for hypertension. She had never taken levotryptophan.Seven weeks after the surgery she noticed a "bruise the size of a quarter." It changed to a reddish firm area with a slightly red rim and a pale center. Our clinical impression was morphea (localized scleroderma) confirmed by microscopic examination. Prior to the surgical implantation, the patient experienced mild arthritic symptoms References 1. Sahn EE, Garen PD, Silver RM, et al. Scleroderma following augmentation mammoplasty . Arch Dermatol. 1990;126:1198-1202.Crossref 2. Varga J, Schumacher HR, Jimenez SA. Systemic sclerosis after augmentation mammoplasty with silicone implants . Ann Intern Med. 1989; 111:277-383.Crossref 3. Spiera F. Scleroderma after silicone augmentation mammoplasty . JAMA . 1988;260:236-238.Crossref

Humbert, Philippe;Agache, Pierre

1991 Archives of Dermatology

doi: 10.1001/archderm.1991.01680020135022pmid: 1990997

Abstract To the Editor.— A variety of dysimmune conditions may be seen in patients with acquired ichthyosis. Among the more common are Hodgkin's disease and sarcoidosis. Font et al1 recently reported a new case of acquired ichthyosis in a patient with systemic lupus erythematosus. Evidence that acquired ichthyosis may be a new reported manifestation of collagenosis was supported by their case report, as well as by the observation we published 1 year ago.2 Our patient was suffering from mixed connective tissue disease that may be considered as a clinical and biological form of systemic lupus erythematosus.3 Acquired ichthyosis was also reported to be associated with dermatomyositis.4 In a recent review of the literature, we were not able to find other cases of collagenosis related to acquired ichthyosis.5 The association of autoimmune conditions with acquired ichthyosis indicates that abnormal host immune response may have a role in References 1. Font J, Bosch X, Ingelmo M, Herrero C, Bielsa I, Mascaro JM. Acquired ichthyosis in a patient with systemic lupus erythematosus . Arch Dermatol. 1990;126:829.Crossref 2. Humbert P, Dupond JL, Carbillet JP, Agache P. L'ichtyose acquise: un nouveau signe cutané des collagénoses . Ann Med Interne . 1989;140:221-222. 3. Reichlin M. Problems in differentiating SLE and MCTD . N Engl J Med. 1976;295:1194-1195.Crossref 4. Urrutia S, Vazquez F, Requena L, Yus ES. Acquired ichthyosis associated with dermatomyositis . J Am Acad Dermatol. 1987;16:627-628.Crossref 5. Humbert P, Dupond JL, Agache P. L'ichtyose acquise . Ann Dermatol Venereol . 1988;115:937-942. 6. Aram H. Acquired ichthyosis and related conditions . Int J Dermatol. 1984;23:458-461. 7. Zwitter M. Hodgkin's disease: five steps from autoimmunity to cancer . Med Hypotheses . 1984;15:399-413.Crossref

van Praag, M. C. G.;Boom, B. W.;van Hees, C. L. M.;Vermeer, B. J.;Scheffer, E.

1991 Archives of Dermatology

doi: 10.1001/archderm.1991.01680020136023

Abstract To the Editor.— One of the clinical variants of lichen planus (LP) is the ulcerative form, which shows bullae, erosions, and ulcerations of the feet and toes, and results in atrophic scarring and permanent loss of toenails. Cicatricial alopecia of the scalp and mucosal lesions may be present.1 The histologic picture of this variant is similar to other forms of LP with lymphocytes dominating the dermal inflammatory infiltrate. Plasma cells, if present, are sparse in number.From the literature we know of only one case of LP with an infiltrate of 40% to 50% plasma cells2 and two cases of lichen nitidus.3 We describe a patient with long-standing classical and ulcerative LP, whose lesions are histologically characterized by an inflammatory infiltrate that predominantly contains plasma cells. Report of a Case.— In January 1989 an 86-year-old woman presented with ulcerations of her feet. In 1940 she developed a References 1. Thormann J. Ulcerative lichen planus of the feet . Arch Dermatol. 1974;110:753-755.Crossref 2. Lupton GP, Goette K. Lichen planus with plasma cell infiltrate . Arch Dermatol. 1981;117:124-125.Crossref 3. Eisen RF, Stenn J, Kahn SM, Bhawan J. Lichen nitidus with plasma cell infiltrate . Arch Dermatol. 1985;121:1193-1194.Crossref 4. Moss ALH, Harman RRM. Surgical treatment of painful lichen planus of the hand and foot . Br J Plast Surg. 1986;39:402-407.Crossref 5. Torres MT, Sanches JL. Cutaneous plasmacytic infiltrates . Am J Dermatopathol. 1988;10:319-329.Crossref

Wright, D. Craig;Lennox, Jeffrey L.;James, William D.;Oster, Charles N.;Tramont, Edmond C.

1991 Archives of Dermatology

doi: 10.1001/archderm.1991.01680020137024

Abstract To the Editor.— Cutaneous and mucocutaneous disorders were some of the earliest recognized complications occurring in persons infected with the human immunodeficiency virus 1 (HIV-1). Oral and vaginal candidiasis, tinea pedis, onychomycosis, and deep mycotic infections have been the fungal infections most frequently reported in these patients.1 These infections occur predominantly in those patients with severe immunologic dysfunction characterized by CD4 lymphocyte depletion and/or anergy. We describe three CD4-deficient, HIV-1-infected patients in whom generalized chronic dermatophytosis developed. Report of Cases.—Case 1.— A 29-year-old man with transfusionacquired HIV-1 infection and central nervous system toxoplasmosis presented with a 2-month history of a pruritic eruption that had appeared initially in his groin and progressively spread downward over both legs and upward onto his abdomen over the next 3 months. On physical examination a raised, erythematous, confluent, scaly eruption extended from his umbilicus to his ankles and involved approximately 30% References 1. Kaplan MH, Sadick N, McNutt NS, 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. Dahl MV. Host defense: fungus . In: Clinical Immunodermatology . Chicago Ill: Year Book Medical Publishers; 1988:173-176. 3. Goodman DS, Teplitz ED, Wishner A, et al. Prevalence of cutaneous disease in patients with acquired immunodeficiency syndrome (AIDS) or AIDS-related complex . J Am Acad Dermatol. 1987;17:21-22. 4. Torssander J, Karlsson A, Mortfeldt-Mason L, Putkonen P, Wasserman J. Dermatophytosis and HIV infection . Acta Derm Venerol (Stockh) . 1988; 68:53-56. 5. Redfield RR, Wright DC, Tramont EC. The Walter Reed Staging classification for HTLV-III/LAV infection . N Engl J Med. 1986;314:313-322.Crossref

Merkle, Tanja;Braun-Falco, Otto;Fröschl, Monika;Ruzicka, Thomas;Landthaler, Michael

1991 Archives of Dermatology

doi: 10.1001/archderm.1991.01680020138025

Abstract To the Editor.— Although Kaposi's sarcoma and non-Hodgkin's lymphomas are the most common neoplasms in human immunodeficiency virus (HIV) infection, other neoplasms have been described, such as colorectal cancer, cancer of the lung, and squamous cell carcinoma of the oral and anal mucosa.In recent years, some authors have reported dysplastic nevi and malignant melanoma in patients with HIV infection,1-3 and Rasokat and coworkers3 theoretically estimated a very high incidence of 100 malignant melanomas per 100 000 HIV-infected patients. This article describes a patient with malignant melanoma in HIV-2 infection running a fulminant course. Report of a Case.— A 39-year-old homosexual man (the case was reported briefly in a publication concerning HIV-1 and HIV-2 distribution in West Germany4) had a 7-year history of a brown lesion on his back, but was unaware of changes in size or pigmentation. The patient had several homosexual contacts in Europe, North References 1. Tindall B, Finlayson R, Mutimer K, et al. Malignant melanoma associated with human immunodeficiency virus in three homosexual men . J Am Acad Dermatol. 1989;20:587-591.Crossref 2. Duvic M, Lowe L, Rapini RP, et al. Eruptive dysplastic nevi associated with human immunodeficiency virus infection . Arch Dermatol. 1989;125:397-401.Crossref 3. Rasokat H, Steigleder GK, Bendick C, et al. Malignes Melanom und HIV Infektion . Z Hautkr. 1989;64:581-587. 4. Enders G, Hartter P, Schäfer B, et al. Epidemiologischer Trend der HIV-1 und HIV-2 Infektion 1987/1988 in Stuttgart und Umgebung . Dtsch Med Wochenschr. 1988;113:1412-1415.Crossref 5. Braun-Falco 0, Landthaler M, Hölzel D, et al. Therapie und Prognose maligner Melanome der Haut . Dtsch Med Wochenschr. 1986;111:1750-1756.Crossref

Tadini, Gianluca;D&apos;Orso, Marco;Cusini, Marco;Alessi, Elvio;Cinque, Paola

1991 Archives of Dermatology

doi: 10.1001/archderm.1991.01680020139026

Abstract To the Editor.— Azidothymidine (zidovudine) is frequently used in the treatment of patients with acquired immunodeficiency syndrome (AIDS) or with AIDS-related complex. Side-effects during azidothymidine treatment are common and different. Bone marrow depression is the most relevant among them.1 Recently, several patients affected by nail pigmentation have been described.2 We describe two patients affected by pigmentation of the oral mucosa that appeared after the beginning of azidothymidine therapy. Report of Cases.—Case 1.— A 47-year-old homosexual man, who was anti-human immunodeficiency virus positive since 1986, began treatment with azidothymidine in March 1989, at a dose of 800 mg/d. After approximately 15 days, he developed three irregularly pigmented macules, ranging from 0.5- to 2-cm wide, on the lateral and upper sides of the tongue. The macules showed irregular borders and their color varied from yellowish to light brown. Neither hyperkeratosis nor infiltration was clinically appreciable. At the same time the patient presented with a single hyperpigmented longitudinal band on the thumbnail of the right hand. References 1. Gelmon K, Montaner JS, Fanning M, et al. Nature, time course and dose dependence of zidovudine-related side-effects: results from the Multicenter Canadian Azidothymidine Trial . AIDS . 1989;3:555-561.Crossref 2. Fisher CA, McPoland PR. Azidothymidine-induced nail pigmentation . Cutis . 1989;43:552-554. 3. Bronner AK, Hood AF. Cutaneous complications of chemotherapeutic agents . J Am Acad Dermatol. 1983;9:645-663.Crossref 4. Barone R, Ficarra G, Gaglioti D, et al. Prevalence of oral lesions among HIV-infected drug abusers and other risk groups . Oral Surg Oral Med Oral Pathol. 1990;69:169-173.Crossref 5. Langford A, Kunze R, Groth A, et al. Oral hyperpigmentation associated with HIV infection . Presented at the Fifth International Conference on AIDS: 'The Scientific and Social Challenge,' Montreal, Quebec, 1989 . Abstract.

Smith, David L.;Wernick, Richard

1991 Archives of Dermatology

doi: 10.1001/archderm.1991.01680020140027

Abstract To the Editor.— Psoriatic arthritis typically consists of psoriatic skin and nail changes concomitant with asymmetrical, pauciarticular joint disease. The primary therapeutic modality advocated for joint involvement is the administration of an anti-inflammatory medication. Many patients with moderate to severe psoriatic arthritis receive a disease-modifying agent such as injectable gold (chrysotherapy). Although dermatitis occurs in 15% to 25% of patients receiving gold therapy,1 the ability of chrysotherapy to exacerbate psoriasis has not been proven; neither a major review of drug-induced psoriasis2 nor a standard textbook of dermatology3 lists gold as a precipitant. We describe a patient with sparsely distributed, long-standing psoriasis who developed diffuse psoriasis shortly after the initiation of intramuscular gold sodium thiomalate, and review the English literature from 1969 to 1990 for reports of possible gold-induced psoriasis, aided by a Medline search. Report of a Case.— A 54-year-old white man was seen with a 14-year References 1. Paulus H. Clinical pharmacology of the antirheumatic drugs . In: Schumacher HR, Klippel JH, Robinson DR, eds. Primer on the Rheumatic Diseases . 9th ed. Atlanta, Ga: Arthritis Foundation; 1988;282-287. 2. Abel EA, DiCicco LM, Orenberg EK, Fraki JE, Farber EM. Drugs in exacerbation of psoriasis . J Am Acad Dermatol. 1986;15:1007-1022.Crossref 3. Christophers E, Krueger G. Psoriasis . In: Fitzpatrick TB, Eisen AZ, Wolff K, Freedberg IM. Austen KF, eds. Dermatology in General Medicine . New York, NY: McGraw-Hill International Book Co; 1987:461-491. 4. Penneys NS, Ackerman A, Gottlieb N. Gold dermatitis: a clinical and histopathological study . Arch Dermatol. 1974;109:372-376.Crossref 5. Dorwart BB, Gall EP, Schumacher HR, Krauser RE. Chrysotherapy in psoriatic arthritis: efficacy and toxicity compared to rheumatoid arthritis . Arthritis Rheum. 1978;21:513-515.Crossref 6. Richter MB, Kinsella P, Corbett M. Gold in psoriatic arthropathy . Ann Rheum Dis. 1980;39:279-280.Crossref 7. Dequeker J, Gevers G. An open study on the efficacy and safety of auranofin in treating psoriatic arthritis . Scand J Rheum. 1986;2( (suppl 63) ):85-95. 8. Carette S, Calin A, McCafferty J, Wallin B, et al. A double-blind placebo-controlled study of auranofin in patients with psoriatic arthritis . Arthritis Rheum. 1989;32:158-165.Crossref 9. Naranjo CA, Busto U, Sellers EM, Sandor P, et al. A method for estimating the probability of adverse drug reactions . Clin Pharmacol Ther. 1981;27:239-245.Crossref 10. Cox AJ, Marich KW. Gold in the dermis following gold therapy for rheumatoid arthritis . Arch Dermatol. 1973;108:655-657.Crossref

Nielsen, Hans Jørgen;Nielsen, Henrik;Georgsen, Jørgen

1991 Archives of Dermatology

doi: 10.1001/archderm.1991.01680020142028

Abstract To the Editor.— Our studies of the effect of the histamine2 (H2) receptor antagonist, ranitidine, in patients with trauma- and blood transfusion-induced immunosuppression, in patients with multiple myeloma, and in patients with human immunodeficiency virus infection,1 have included a few patients with psoriatic lesions. Some of these patients who were treated with the active drug showed improvement in psoriatic disease, but with recurrence within a few weeks after the therapy was discontinued. Based on these observations, and despite previous randomized, placebo-controlled studies of short-term treatment (28 days) with another H2 receptor antagonist, cimetidine, which had shown no beneficial effect,2 an open pilot study of the effect of long-term (4 months) treatment with ranitidine in patients with different forms of psoriasis was initiated. Subjects and Methods.— Six patients were studied in the autumn of 1989 (September 1 through December 31, 1989). All of the patients had References 1. Nielsen HJ, Hammer JH, Moesgaard F, Kehlet H. The potential impact of histamine-2 receptor antagonists as adjuvant therapy in colorectal cancer surgery: review . Acta Chir Scand. In press. 2. Long PR, Miller OF. Cimetidine and psoriasis . Arch Dermatol. 1981;117:523.Crossref 3. Rai GS, Webster SGP. Cimetidine and psoriasis . Lancet . 1979;1:50.Crossref 4. Giacosa A, Farris A, Cheli R. Cimetidine and psoriasis . Lancet . 1978;2:1211.Crossref 5. Merk H, Goerz G, Runne U, et al. Cimetidine and chlorpheniramine in the treatment of psoriasis . Dermatologica . 1983;166:94-96.Crossref

Nickoloff, Brian J.

1991 Archives of Dermatology

doi: 10.1001/archderm.1991.01680020143029

Abstract To the Editor.— During the past several years, the molecular basis for leukocyte trafficking into the skin of psoriasis lesions, as well as other inflammatory and neoplastic cutaneous disorders has begun to be defined.1 The main focus of this work has centered around the β-2 integrin LFA-1, which is expressed by infiltrating leukocytes, and intercellular adhesion molecule-1 (ICAM-1) expressed by the overlying epidermal keratinocytes. There is excellent spatial colocalization and temporal correlation between intraepidermal LFA-1-positive cells and ICAM-1-expressing keratinocytes.1 Much of this in vivo work was derived from our earlier in vitro discovery that normal cultured keratinocytes (which are ICAM-1 negative) do not bind lymphocyte/monocytes, but, after exposure to cytokines such as interferon-γ, there was dramatic increase in binding mediated by induction on the keratinocyte of ICAM-1 that facilitated LFA-1/ICAM-1 interaction. We have recently discovered a second adhesion pathway involving binding between cultured keratinocytes and lymphocytes that is References 1. Nickoloff BJ, Griffiths CEM, Barker JNWN. The role of adhesion molecules, chemotactic factors, and cytokines in inflammatory and neoplastic skin disease: 1990 update . J Invest Dermatol. 1990;94( (suppl) )1515-1575.Crossref 2. DeStrooper B, Van der Schueren B, Jaspers M, et al. Distribution of the β-1 subgroup of the integrins in human cells and tissues . J Histochem Cytochem. 1989;37:299-207.Crossref 3. Peltunen J, Larjava H, Jaakkola S, et al. Localization of integrin receptors for fibronectin, collagen and laminin in human skin . J Clin Invest. 1989;84:1916-1923.Crossref 4. Kajiji S, Tamura RN, Quaranta V. A novel integrin (αEβ4) from human epithelial cells suggest a fourth family of integrin adhesion receptors . Embo J. 1989;8:673-680. 5. Hessle H, Sakai LY, Hollister DW, Burgeson RE, Engvall E. Basement membrane diversity detected by monoclonal antibodies : Differentiation . 1984;26:49.Crossref 6. Konter U, Kellner I, Klein E, Kaufmann R, Mielke V, Sterry W. Adhesion molecule mapping in normal human skin . Arch Dermatol Res. 1989; 281:454-462.Crossref 7. Farber EM, Nickoloff BJ, Recht B, Fraki JE. Stress, symmetry and psoriasis: possible role of neuropeptides . J Am Acad Dermatol. 1986;14:305-311.Crossref 8. Naukkarinen A, Nickoloff BJ, Farber EM. Quantification of cutaneous sensory nerves and their substance P content in psoriasis . J Invest Dermatol. 1989;92:126-129.Crossref

Cooper, Dennis L.;Bolognia, Jean L.;Lin, James T.

1991 Archives of Dermatology

doi: 10.1001/archderm.1991.01680020144031

Abstract To the Editor.— Atrophie blanche (livedoid vasculitis) is characterized by purpura and painful ulcerations of the lower extremities, and can be divided into primary and secondary forms. The latter have been associated with connective tissue diseases and lymphoma, as well as several plasma cell dyscrasias, such as macroglobulinemia and cryoglobulinemia.1 This is a report of a patient with γ—heavy-chain disease and recalcitrant atrophie blanche complicated by Serratia marcescens cellulitis. Report of a Case.— In 1974, a 51-year-old white man was seen who had developed painful purpuric papules and ulcerations on the extensor surfaces of the distal lower extremities. Eight years later he presented to another hospital with fever, abdominal cramps, diarrhea, and worsening of his skin ulcerations. Laboratory abnormalities included a mild anemia (hemoglobin, 1.75 mmol/L), leukopenia (leukocyte count, 3.0 × 109/L), and an occasional plasmacytoid cell in the peripheral smear. Serum protein electrophoresis showed a monoclonal References 1. Shornick JK, Nicholes BK, Bergstresser PR, Gilliam JN. Idiopathic atrophie blanche . J Am Acad Dermatol. 1983;8:792-798.Crossref 2. Fermand JP, Brouet JC, Danon F, Seligmann M. Gamma heavy chain `disease': heterogeneity of the clinicopathologic features: report of 16 cases and review of the literature . Medicine . 1989;68:321-335.Crossref 3. Abrahams C, Pirani CL, Pollak VE. Ultrastructure of the kidney in a patient with multiple myeloma . J Pathol Bacteriol. 1966;92:220-225.Crossref 4. Porush JG, Grishman E, Alter AA, Manderbaum H, Churg J. Paraproteinemia and cryoglobulinemia associated with atypical glomerulonephritis and the nephrotic syndrome . Am J Med. 1969;47:957-964.Crossref 5. Vilpo JA, Irjala K, Viljanen MK, Klemi P, Kouvonen I, Ronnemaa T. γ— Heavy chain disease: a study of a case . Clin Immunol Immunopathol. 1980;17:584-594.Crossref

Wagner, Richard F.;Sanchez, Ramon L.

1991 Archives of Dermatology

doi: 10.1001/archderm.1991.01680020144030pmid: 1991003

Abstract To the Editor.— Intralesional interferon alfa-2b (Schering Corp, Kenilworth, NJ) has generated significant clinical interest for its potential use in the treatment of a variety of benign and malignant skin tumors. The acute side effects of the interferons are well described and are usually transient.1 We report two unusual malignant cutaneous tumors (dermatofibrosarcoma protuberans of the scalp and sebaceous carcinoma of the nasal root) that developed in two of five study patients subsequent to treatment with intralesional interferon alfa-2b for in situ squamous cell carcinoma. Report of Cases.—Case 1.— In May 1989, a 59-year-old white man was enrolled in an interferon alfa-2b (Schering Corp, Kenilworth, NJ) protocol for a primary 2.2 × 1.4-cm squamous cell carcinoma in situ of the left upper arm. After an informed consent was obtained, the patient received 1.5 × 106 IU of intralesional interferon triweekly for 3 consecutive weeks. There References 1. Edwards L, Tucker SB, Perednia D, et al. The effect of an intralesional sustained-release formulation of interferon alfa-2b on basal cell carcinomas . Arch Dermatol. 1990;126:1029-1032.Crossref

Gross, Alexander S.;King, Lloyd E.;Patten, William T.

1991 Archives of Dermatology

doi: 10.1001/archderm.1991.01680020145032

Abstract To the Editor.— In our modern climate of increased awareness of health and personal appearance, a seemingly endless number of special diets have been developed to foster weight loss. Recently, a patient with previously untreated dermatitis herpetiformis had the good fortune of being placed on such a diet to treat coexistent morbid obesity. As the exclusively protein diet contained no gluten, his skin disease resolved rapidly, before dapsone therapy could be initiated. Report of a Case.— A 42-year-old man was referred for evaluation of an asymptomatic elbow rash of several months' duration. The patient weighed 135 kg (296 pounds) but was otherwise in good health and taking no oral medications. Examination of the skin revealed plaques of clustered vesicles on an erythematous base covering both elbows. The clinical diagnosis of dermatitis herpetiformis was confirmed histopathologically with the presence of granular IgA and C3 at the basement membrane zone on immunofluorescent References 1. Reunala T, Blomquist K, Tarpila S, Halme H, Kangas K. Gluten-free diet in dermatitis herpetiformis: clinical response of skin lesions in 81 patients . Br J Dermatol. 1977;97:473-480.Crossref 2. Fry L, Leonard JN, Swain F, et al. Long-term follow-up of dermatitis herpetiformis with and without dietary gluten withdrawal . Br J Dermatol. 1982;108:631-640.Crossref

Baden, Howard P.

1991 Archives of Dermatology

doi: 10.1001/archderm.1991.01680020146033

Abstract To the Editor.— Localized expression of psoriasis can be very difficult to treat, and scalp involvement is a particularly important example that may be resistant to topical therapy. It has the added problems of troublesome pruritus and producing a significant cosmetic defect in the form of scaling. Since potent systemic agents (eg, cyclosporine)1 cannot be justified, we must search for newer effective topical treatments.We have observed that Epilyt with occlusion can be very effective in removing thick scales on the scalp. Use of Epilyt results in rather prompt clearing and is relatively easy for the patient to use.We followed a group of 12 patients with severe scalp involvement who had been referred due to failure to respond to most of the commonly used scalp preparations, including those containing a corticosteroid. Epilyt was applied nightly and then covered with a shower cap for 4 to 8 hours. In References 1. Ellis CN, Gorsulowsky DC, Hamilton TA, et al. Cyclosporine improves psoriasis in a double-blind study . JAMA . 1986;256:3110-3116.Crossref

McDonagh, Andrew J. G.;Wright, Andrew L.;Messenger, Andrew G.

1991 Archives of Dermatology

doi: 10.1001/archderm.1991.01680020146034pmid: 1991006

Abstract To the Editor.— We describe a patient with intractable pain and ulceration of the foot associated with an arteriovenous malformation. Conventional dressing techniques failed, and the possibility of amputation was under consideration when healing was achieved using the recently reported technique of four-layer bandaging.1 Report of a Case.— A 35-year-old previously healthy Bangladeshi woman presented with a 12-month history of painful ulceration over the dorsum of the right foot (Fig 1). Her health was otherwise good. Dilated veins on the dorsum of the foot and a bruit at the ankle suggested a possible underlying arteriovenous malformation. Angiographic studies confirmed this, demonstrating an extensive arteriovenous malformation in the forefoot fed by grossly dilated anterior and posterior tibial arteries (Fig 2). Treatment with various compressive bandages applied regularly over an 8-month period and culminating in a 4-week period of hospitalization, produced no improvement. Complete healing was achieved, however, within 3 weeks References 1. Blair SD, Wright DDI, Backhouse CM, et al. Sustained compression and healing of chronic venous ulcers . BMJ . 1988;297:1159-1161.Crossref 2. Coursely G, Ivins JC, Barker NW. Congenital arteriovenous fistulas in the extremities: an analysis of 69 cases . Angiology . 1956;7:201-217.Crossref 3. Field CL, Vassos GA. Congenital arteriovenous fistulation of the lower limb: report of a case successfully treated by total excision . N Engl J Med. 1951;245:885-888.Crossref 4. Szilagyi DE, Smith RF, Elliott JP, et al. Congenital arteriovenous anomalies of the limbs . Arch Surg. 1976;111:423-429.Crossref 5. Burnand KG. The aetiology of venous ulceration . Acta Chir Scand Suppl. 1988;544:21-24.

McBride, M. E.;Rudolph, A. H.;Tschen, J. A.;Cernoch, P.;Davis, J.;Brown, B. A.;Wallace, R. J.

1991 Archives of Dermatology

doi: 10.1001/archderm.1991.01680020148035

Abstract To the Editor.— Among the nontuberculous species of Mycobacterium isolated from cutaneous lesions, Mycobacterium haemophilum has received the least attention. Since first described in 1978,1 fewer than 20 cases have been reported worldwide. Clinical disease is usually associated with an underlying condition resulting in immunosuppression, and is characterized by cutaneous nodules or plaques on the extremities. The unique features that separate M haemophilum from other Mycobacterium are the requirement of hemin for growth, and an unusual antimicrobial susceptibility pattern. We report a case in a nonimmunosuppressed host where the organism was isolated on routine bacteriologic medium and the patient was successfully treated with ciprofloxacin. Report of a Case.— In August 1988, a 65-year-old white woman was evaluated for a scaly erythematous papular eruption on her right forearm (Fig 1) that developed postoperatively following coronary artery bypass surgery. The rash had been present for 4 months and was unresponsive to References 1. Sompolinsky D, Lagziel A, Naveh D, Yankilevitz T. Mycobacterium haemophilum sp. nov., a new pathogen of humans . Int J Syst Bacteriol. 1978;28:67-75.Crossref 2. Wallace RJ, Swenson JM, Silcox VA. The rapidly growing mycobacteria: characterization and susceptibility testing . Antimicrob Newslett. 1985;2:85-92.Crossref 3. Mezo A, Jennis F, McCarthy SW, Dawson DJ. Unusual mycobacteria in five cases of opportunistic infections . Pathology . 1979;11:377-384.Crossref 4. Rogers PL, Walker RE, Lane HC, et al. Disseminated Mycobacterium haemophilum infection in two patients with the acquired immunodeficiency syndrome . Am J Med. 1988;84:640-642.Crossref 5. Males BM, West TE, Bartholemew WR. Mycobacterium haemophilum infection in a patient with acquired immune deficiency syndrome . J Clin Microbiol. 1987;25:186-190.

Coopman, Serge A.

1991 Archives of Dermatology

doi: 10.1001/archderm.1991.01680020158037

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 therapeutic manual is designed to be an easy to use "how to" book for a broad variety of practitioners who must treat patients with skin problems. The book consists of 187 chapters that review the therapy for a variety of disorders and that are each divided into the following four parts: "Initial Therapy," "Alternative Therapy," "Subsequent Therapy," and "Pitfalls." It is assumed that the correct diagnosis has already been made. The "Initial Therapy" section outlines the first-line treatment of the condition, reflecting the preference of the authors of the San Francisco school. In the "Alternative Therapy" section, other possible standard therapies are discussed, with suggestions for specific subsets of patients. The "Subsequent Therapy" section covers what to do after the initial treatment phase. Under the "Pitfalls" heading, common errors of management are outlined. In the appendixes, the side effects of certain drugs commonly used in dermatology are described. As

Dover, Jeffrey S.

1991 Archives of Dermatology

doi: 10.1001/archderm.1991.01680020158036

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 Neal S. Penneys' Skin Manifestations of AIDS is the fourth book published about the cutaneous manifestations of the syndrome since the acquired immunodeficiency syndrome (AIDS) epidemic began. The other two worthy of mention are A Colour Atlas of AIDS and HIV Disease by Farthing et al and Friedman-Kien's Color Atlas of AIDS, both of which are excellent illustrated atlases of the skin manifestations of AIDS. Penneys has attempted a slightly different approach to the topic. Rather than preparing a compendium of photographs of the various skin manifestations, he has attempted to write a textbook of the manifestations of AIDS, including with it a collection of representative photographs. Each of the subsections of the chapters is introduced with text, followed by photographs making the text and photographs nicely complementary. The book is divided into 13 sections that include chapters on epidemiology, early cutaneous signs of human immunodeficiency virus (HIV), superficial and

1991 Archives of Dermatology

doi: 10.1001/archderm.1991.01680020161038

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