Archives of Dermatology

Basler, Rodney S.W.

1979 Archives of Dermatology

doi: 10.1001/archderm.1979.04010120001001

Abstract To the Editor.— Following the publication of my and Dr Paul W. Kohnen's recent article "Localized Hemosiderosis as a Sequela of Acne" (Arch Dermatol 114:1695-1697, 1978), I have received reports from clinicians commenting on similar conditions in their patients. One consistent finding is that all of the patients had been receiving long-term minocycline therapy for acne. Our patient had been taking 100 mg of minocycline twice daily for nearly three years when the blue-black macules first appeared on her face.Hemosiderin was demonstrated, by electron microscopy, to be the pigment retained in our patient's lesions and was observed within dermal macrophages as well as in extracellular deposits. No membrane-bound intracellular hemosiderin aggregates could be identified, suggesting that the pigment persisted because of an inability of the macrophages to surround the toxic iron compound with protective lysosomal membranes. It is plausible that this defect may, in some way, have been the References 1. Ragucci BD: Green bones and teeth roots: Minocycline? Schoch Letter 29( (No. 1) ):3, 1979. 2. Gretzinger T: Minocycline and thyroid function . Arch Dermatol 113:1302, 1977.Crossref 3. Sauer GC: "Muddy skin" from minocycline? Schoch Letter 29( (No. 3) ):3, 1979.

Mathews-Roth, Micheline M.;Kass, Edward H.;Fitzpatrick, Thomas B.;Pathak, Madhu A.;Harber, Leonard C.

1979 Archives of Dermatology

doi: 10.1001/archderm.1979.04010120001002pmid: 533282

Abstract To the Editor.— Attempts have been made by several groups to assess the photosensitivity of patients with erythropoietic protoporphyria (EPP) by an objective method, ie, phototesting with monochromatic light at several discrete wavelengths. However, many patients have failed to respond at all to this kind of light exposure. We have had more consistent phototest results by irradiating with polychromatic light ranging from 380 to 560 nm and by grading the immediate erythema that developed.1 We suggest that phototesting with this spectral region, as well as with monochromatic light, be used as an objective method of evaluating photosensitivity in EPP, as well as a response to therapy.When we phototested patients with EPP using a xenon arc lamp filtered to transmit 380 to 560 nm,1 immediate erythema developed in every patient tested who was exposed to this light. In addition to erythema, wheals, itching, and burning develop in a References 1. Mathews-Roth MM, Pathak MA, Fitzpatrick TB, et al: Beta-carotene as an oral photoprotective agent in erythropoietic protoporphyria . JAMA 228:1004-1008, 1974.Crossref 2. Krook G, Haeger-Aronsen B: Erythrohepatic protoporphyria and its treatment with betacarotene . Acta Derm Venereol 54:39-44, 1974. 3. Wennersten G, Swanbeck G: Treatment of light sensitivity with carotenoids: Serum concentrations and light protection . Acta Derm Venereol 54:491-499, 1974. 4. Thune P: Chronic polymorphic light eruption: Particular wavebands and the effect of carotene therapy . Acta Derm Venereol 56:127-133, 1976.

1979 Archives of Dermatology

doi: 10.1001/archderm.1979.04010120002004

This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables. Abstract In the article titled "Topical Tretinoin Therapy and Oral Lichen Planus," published in the June Archives (115:716-718, 1979), Fig 2 was transposed, giving the impression that the pretreatment photograph (Fig 1) is of the left bucca and the posttreatment photograph (Fig 2) is of the right bucca. Both Fig 1 and Fig 2 are of the left bucca.

Goldman, Leon

1979 Archives of Dermatology

doi: 10.1001/archderm.1979.04010120002003

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 To the Editor.— It is of interest to review the antiquity of plants that cause dermatitis. A specimen of fossilized poison sumac leaves was obtained that was similar to current poison sumac (Figure). This was identified by paleobotanists as Rhus merrilli Chaney found in central Oregon in the John Day Formation. It is from the early Oligocene period. This makes it approximately 37.5 million years old. So, this plant was present long before any form of man appeared on earth. It is hoped that other members of the famed Anacardiaceae family, such as R toxicodendron and R diversiloba, will be found as fossilized and unchanged markers of skin contactants.

Dahl, Mark V.

1979 Archives of Dermatology

doi: 10.1001/archderm.1979.04010120005005

Abstract Chemotaxis is the locomotion of cells or organisms in response to substances in their environment. In dermatology, chemotaxis ordinarily refers to the directed migration of polymorphonuclear leukocytes to an infected or inflamed area. Detailed studies have been published.1-6 A phagocytic cell, particularly a neutrophil or macrophage, is a major effector cell of the immune response. A number of immunologic events occur, but the actual killing of infectious organisms, engulfing of immune complexes, and other end-stage events are all performed by the phagocyte. To fill these functions, the phagocyte must first arrive at the site of inflammation or infection. Chemotaxis is the process that guides the phagocyte from the blood vessels to this site. A major problem is the lack of totally reliable and reproducible methodology for measuring chemotaxis, both in vivo and in vitro. In the in vivo Rebuck skin window technique, test substances are applied to abraded skin. References 1. Dahl MV: Chemotaxis in cutaneous disease . Int J Dermatol 17:95-104, 1978.Crossref 2. Gammon WR: Phagocyte chemotaxis: A review . Prog Dermatol 13:1-6, 1979. 3. Gallin JI, Quie PG (eds): Leukocyte Chemotaxis: Methods, Physiology, & Clinical Implications . New York, Raven Press, 1978. 4. Wilkinson PC: Chemotaxis and Inflammation . New York, Churchill-Livingstone, 1974. 5. Dahl MV, Cates KL, Quie PG: Disorders of phagocytosis and related disorders , in Safai B, Good R (eds): Immunodermatology . New York, Plenum Press Publishing Corp, to be published. 6. Zigmond SH: Chemotaxis by polymorphonuclear leukocytes . J Cell Biol 77:269-287, 1978.Crossref

Sontheimer, Richard D.;Thomas, Jesse R.;Gilliam, James N.

1979 Archives of Dermatology

doi: 10.1001/archderm.1979.04010120007006

Abstract We have characterized the clinical and laboratory features of 27 patients who had in common a recurring, superficial, nonscarring type of cutaneous lupus erythematosus (LE) that occurred in a characteristic distribution (subacute cutaneous lupus erythematosus [SCLE]). This clinically distinct form of cutaneous LE has not previously been analyzed as a separate entity and thus, its clinical importance has not been fully appreciated. We found that these patients frequently had a mild systemic illness marked by musculoskeletal complaints and serologic abnormalities. Forty-eight percent had systemic LE by American Rheumatism Association criteria; however, none had serious CNS or renal disease. Thus, those with SCLE are a subset of patients with LE who generally have an illness intermediate in severity between discoid LE and severe systemic LE. (Arch Dermatol 115:1409-1415, 1979) References 1. Kiel H: Conception of lupus erythematosus and its morphologic variants. With particular references to "systemic" lupus erythematosus . Arch Dermatol 36:729-757, 1937. 2. Gilliam JN: The cutaneous signs of lupus erythematosus . Continuing Educ 6:34-40, 1977. 3. Cohen AS, Reynolds WE, Franklin EC, et al: Preliminary criteria for the classification of systemic lupus erythematosus . Bull Rheum Dis 21:643-648, 1971. 4. Prystowsky SD, Gilliam JN: Antinuclear antibody studies in chronic cutaneous discoid lupus erythematosus . Arch Dermatol 113:183-186, 1977.Crossref 5. Sontheimer RD, Gilliam JN: An immunofluorescence assay for double-stranded DNA antibodies using the Crithidia luciliae kinetoplast as a native DNA substrate . J Lab Clin Med 91:550-558, 1978. 6. Nelson RA, Jensen S, Gigli I, et al: Methods for the separation, purification and measurement of nine components of hemolytic complement in guinea pig serum . Immunochemistry 3:111-135, 1966.Crossref 7. Gilliam JN, Cheatum DE, Hurd ER, et al: Immunoglobulin in clinically uninvolved skin in systemic lupus erythematosus: Association with renal disease . J Clin Invest 53:1434-1440, 1974.Crossref 8. Gilliam JN, Stastny P: Subacute cutaneous lupus erythematosus, a form of lupus erythematosus associated with HLA-B8 and DRw3 , abstracted. Arthritis Rheum 22:612, 1979. 9. O'Loughlin S, Schroeter AL, Jordan RE: A study of lupus erythematosus with particular reference to generalized discoid lupus . Br J Dermatol 99:1-11, 1978.Crossref 10. Dubois EL, Tuffanelli DL: Clinical manifestations of systemic lupus erythematosus . JAMA 190:104-111, 1964.Crossref 11. Prystowsky SD, Herndon JH, Gilliam JN: Chronic cutaneous lupus erythematosus (DLE) . Medicine 55:183-191, 1975.Crossref 12. Gladman DD, Chalmers A, Urowitz MB: Systemic lupus erythematosus with negative LE cells and antinuclear factor . J Rheumatol 5:142-147, 1978. 13. Fessel WJ: ANA-negative systemic lupus erythematosus . Am J Med 64:80-86, 1978.Crossref 14. Provost TT, Ahmed AR, Maddison PJ, et al: Antibodies to cytoplasmic antigens in lupus erythematosus: Serologic marker for systemic disease . Arthritis Rheum 20:1457-1463, 1977.Crossref 15. Agnello V: Complement deficiency states . Medicine 57:1-23, 1978.Crossref 16. Baart de la Faille-Kuyper EH, Cormane RH: The occurrence of certain serum factors in the dermal-epidermal junction and vessel walls of the skin in lupus erythematosus and other (skin) diseases . Acta Derm Venereol 48:578-588, 1968. 17. Kay DM, Tuffanelli DL: Immunofluorescent techniques in clinical diagnosis of cutaneous disease . Ann Intern Med 71:753-762, 1969.Crossref 18. Cripps DJ, Rankin J: Action spectra of lupus erythematosus and experimental immunofluorescence . Arch Dermatol 107:563-567, 1973.Crossref 19. Kozin F, Mackel S, Rapoport R, et al: Immunoglobulin and complement deposits in blood vessels in rheumatoid arthritis: Clinical correlations , abstracted. Clin Res 26:381A, 1978. 20. Stastny P, Stembridge VA, Ziff M: Homologous disease in the adult rat, a model for autoimmune disease . J Exp Med 118:635-648, 1963.Crossref 21. Lerner KG, Kao GF, Storb R, et al: Histopathology of graft-versus-host reaction (GVHR) in human recipients of marrow from HLA-matched sibling donors . Transplant Proc 6:367-371, 1974. 22. Hood AF, Soter NA, Rappeport J, et al: Graft-versus-host reaction: Cutaneous manifestations following bone marrow transplantation . Arch Dermatol 113:1087-1091, 1977.Crossref 23. Gratwhol AA, Moutsopoulos HM, Chused TM, et al: Sjogren-type syndrome after allogeneic bone marrow transplantation . Ann Intern Med 87:703-706, 1977.Crossref 24. McCreight WG, Montgomery H: Cutaneous changes in lupus erythematosus: Histologic aspects, with special reference to vascular changes . Arch Dermatol Syphilol 61:1-11, 1950.Crossref 25. Wong KO: Systemic lupus erythematosus: A report of 45 cases with unusual clinical and immunological features . Br J Dermatol 81:186-190, 1969.Crossref 26. Sehgal VN, Rege VL, Vadiraj SN: An unusual cutaneous manifestation of systemic lupus erythematosus . Arch Dermatol 103:463-464, 1971.Crossref 27. Rekant SI, Becker LE: Auto-immune annular erythema: A variant of lupus erythematosus? Arch Dermatol 107:424-426, 1973.Crossref 28. Feely RH: Skin manifestations in systemic lupus erythematosus . Ir J Med Sci 145:253-259, 1976.Crossref 29. O'Leary PA: Disseminated lupus erythematosus . Minn Med 17:637-644, 1934.

Okun, Milton R.

1979 Archives of Dermatology

doi: 10.1001/archderm.1979.04010120014007

Abstract Three cases of malignant melanoma resembling spindle and epithelioid cell nevus histologically are presented. Lesions having histologic features of spindle and epithelioid cell nevus (Spitz nevus or juvenile melanoma) at or after puberty should be regarded with caution, particularly when they are heavily melanized. Such lesions are in a histologic "gray zone" and may be malignant. (Arch Dermatol 115:1416-1420, 1979) References 1. Spitz S: Spindle and epithelioid cell nevi in the adult . Am J Pathol 25:591-609, 1948. 2. Echevarria R, Ackerman LV: Spindle and epithelioid cell nevi in the adult . Cancer 20:175-189, 1967.Crossref 3. Kernen JA, Ackerman LV: Spindle cell nevi and epithelioid cell nevi (so-called juvenile melanomas) in children and adults: A clinicopathological study of 27 cases . Cancer 13:612-625, 1960.Crossref 4. Helwig B: Malignant melanoma in children , in Freitag SB, Culhane DL, Demec JC (eds): Neoplasms of the Skin and Malignant Melanoma . Chicago, Year Book Medical Publishers Inc, 1976, p 19. 5. Paniago-Pereira C, Maize JC, Ackerman AB: Nevus of large spindle and/or epithelioid cells (Spitz's nevus) . Arch Dermatol 114:1811-1823, 1978.Crossref 6. Lever WF, Schaumburg-Lever G: Histopathology of the Skin . Philadelphia, JB Lippincott Co, 1975, p 671. 7. Okun M, Edelstein L: Gross and Microscopic Pathology of the Skin . Boston, Dermatopathology Foundation Press, 1976, vol 2, pp 958, 985. 8. McGovern V: Malignant Melanoma: Clinical and Histologic Diagnosis . New York, John Wiley & Sons Inc, 1976, p 149.

Eaglstein, William H.;Ginsberg, Lawrence D.;Mertz, Patricia M.

1979 Archives of Dermatology

doi: 10.1001/archderm.1979.04010120019008

Abstract The effect of combined topical applications of a steroid and nonsteroid antiinflammatory agent on erythema induced by ultraviolet-B irradiation (UV-B) was evaluated. In human volunteers, the combination more effectively suppressed UV-B-induced erythema than either agent alone. When applied singly, the nonsteroid agent was far more effective than the steroid. The combination, or either agent alone, was most effective when applied immediately after irradiation. This study demonstrates that for the treatment of UV-B-induced erythema, the anti-inflammation effects of these two classes of anti-inflammatory agents are greater when used in combination than when either agent is used alone. However, the effect of the combination in this study is not sufficiently long-lasting to be therapeutically useful. (Arch Dermatol 115:1421-1423, 1979) References 1. Snyder DS, Eaglstein WH: Intradermal anti-prostaglandin agents and sunburn . J Invest Dermatol 62:47-50, 1974.Crossref 2. Vane JR: Inhibition of prostaglandin synthesis as mechanism of action for aspirin-like drugs . Nature N Biol 231:232-235, 1971.Crossref 3. Greenberg RA, Eaglstein WH, Turnier H, et al: Orally given indomethacin and blood flow response to UVL . Arch Dermatol 111:328-330, 1975.Crossref 4. Snyder DS, Eaglstein WH: Topical indomethacin and sunburn . Br J Dermatol 90:91-93, 1974.Crossref 5. Eaglstein WH: Indomethacin: Treatment for sunburn or investigative tool in ultraviolet light inflammation? Int J Dermatol 14:501-502, 1975.Crossref 6. Snyder DS: Cutaneous effects of topical indomethacin, an inhibitor of prostaglandin synthesis, on UV-damaged skin . J Invest Dermatol 64:322-325, 1975.Crossref 7. Hong SL, Levine L: Inhibition of arachidonic acid release from cells as the biochemical action of anti-inflammatory corticosteroids . Proc Nati Acad Sci USA 73:1730-1734, 1976.Crossref 8. Snyder DS: Effect of topical indomethacin on UVR-induced redness and prostaglandin E levels in sunburned guinea pig skin . Prostaglandins 11:631-643, 1976.Crossref 9. Eaglstein WH, Sakai M, Mizuno N: Leukocyte role in inflammation induced by ultraviolet radiation . J Invest Dermatol 72:59-63, 1979.Crossref 10. Athens JW, Haab OP, Raab SO, et al: Leukokinetic studies: IV. The total blood, circulating and marginal granulocyte pools and the granulocyte turnover rate in normal subjects . J Clin Invest 40:989-995, 1961.Crossref 11. Moore-Robinson M, Christie GA: Vasoconstrictor activity of topical corticosteroids—methodology and results . Br J Dermatol 82( (suppl 6) ):93-98, 1970.Crossref

1979 Archives of Dermatology

doi: 10.1001/archderm.1979.04010120021009

This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables. Abstract In the article titled "Comparison of Crude Coal Tar and Topical Methoxsalen in Treatment of Psoriasis," published in the September Archives (115:1061-1063,1979), in line 6 under the heading "Treatment" (p 1061), the word "after" should have been "before." The sentence should read, "Both agents were applied to localized symmetrical plaques or to body areas two hours before irradiation."

Elliott, Susan T.;Hanifin, Jon M.

1979 Archives of Dermatology

doi: 10.1001/archderm.1979.04010120022010

Abstract Studies of patients with atopic dermatitis (AD) have demonstrated several clinical and laboratory indications of immunity defects, but with frequently contradictory results. We have recently shown that many patients with negative cutaneous delayed type hypersensitivity to candidin and streptokinase-streptodornase may have normal in vitro lymphocyte transformation to the same antigens. We hypothesized that this represents recovery of immunocompetent cells when they are isolated in vitro. This report describes phytohemagglutinin-induced transformation of lymphocytes immediately after isolation and after four days in culture (precultured). Responses of lymphocytes from patients with AD were initially subnormal, but increased to normal levels after the preculture period. Our results suggest that defective immune function in AD is not due to a permanent intrinsic lymphocyte defect, but is more likely due to factors associated with disease activity and severity. (Arch Dermatol 115:1424-1426, 1979) References 1. Rajka G: Atopic Dermatitis . Major Problems in Dermatology. Philadelphia, WB Saunders Co, 1975, vol 3, pp 19-21. 2. Pauly CR, Artis WM, Jones HE: Atopic dermatitis, impaired cellular immunity, and molluscum contagiosum . Arch Dermatol 114:391-393, 1978.Crossref 3. Forsbeck A, Hovmark A, Skog E: Patch testing, tuberculin testing and sensitization with DNCB and NDMA of patients with atopic dermatitis . Acta Derm Venereol 56:135-138, 1976. 4. Jones HE, Lewis CW, McMarlin SL: Allergic contact sensitivity in atopic dermatitis . Arch Dermatol 107:217-222, 1973.Crossref 5. Rajka G: Delayed dermal and epidermal reactivity in atopic dermatitis (prurigo Besnier) . Acta Derm Venereol 48:186-191, 1968. 6. McGeady SJ, Buckley RH: Depression of cell-mediated immunity in atopic eczema . J Allergy Clin Immunol 56:393-406, 1975.Crossref 7. Uehara M: Atopic dermatitis and tuberculin reactivity . Arch Dermatol 113:1226-1228, 1977.Crossref 8. Hovmark A: An in vitro study of depressed cell-mediated immunity and of T and B lymphocytes in atopic dermatitis . Acta Derm Venereol 57:237-242, 1977. 9. Thestrup-Pedersen K, Ellegaard J, Thulin H, et al: PPD and mitogen responsiveness of lymphocytes from patients with atopic dermatitis . Clin Exp Immunol 27:118-127, 1977. 10. Lobitz WC, Honeyman JF, Winkler NW: Suppressed cell-mediated immunity in two adults with atopic dermatitis . Br J Dermatol 86:317-328, 1972.Crossref 11. Rachelefsky GS, Opelz G, Mickey MR, et al: Defective T cell function in atopic dermatitis . J Allergy Clin Immunol 57:569-576, 1976.Crossref 12. Grove DI, Reid JG, Forbes IJ: Humoral and cellular immunity in atopic eczema . Br J Dermatol 92:611-618, 1975.Crossref 13. Schoepf E, Boehringer D: IgE and cell-mediated immunity in atopic dermatitis . J Dermatol 1:133-144, 1974. 14. Elliott ST, Hanifin JM: Delayed cutaneous hypersensitivity and lymphocyte transformation in atopic dermatitis: Dissociation in atopic dermatitis . Arch Dermatol 115:36-39, 1979.Crossref 15. Hanifin JM, Lobitz WC Jr: Newer concepts of atopic dermatitis . Arch Dermatol 113:663-670, 1977.Crossref 16. Boyum A: Isolation of mononuclear cells and granulocytes from human blood . Scand J Clin Lab Invest 21( (suppl 97) ):77-89, 1968.Crossref 17. Hanifin JM, Bauman R, Rogge JL: Chemotaxis inhibition by plasma from patients with atopic dermatitis , abstracted. Clin Res 25:198, 1977. 18. Snyderman R, Rogers E, Buckley RH: Abnormalities of leukotaxis in atopic dermatitis . J Allergy Clin Immunol 60:121-126, 1977.Crossref 19. Strannegard IL, Strannegard O: Increased sensitivity of lymphocytes from atopic individuals to histamine-induced suppression . Scand J Immunol 6:1225-1231, 1977.Crossref 20. Stobo J, Paul S, Van Scoy RE: Suppressor thymus-derived lymphocytes in fungal infection . J Clin Invest 57:319-328, 1976.Crossref 21. Goodwin JS, Messner RP, Bankhurst AD, et al: Prostaglandin-producing suppressor cells in Hodgkin's disease . N Engl J Med 297:963-968, 1977.Crossref 22. Roth HL, Kierland RR: The natural history of atopic dermatitis: A 20-year follow-up study . Arch Dermatol 89:209-214, 1964.Crossref 23. Musgrove K, Morgan JK: Infantile eczema . Br J Dermatol 95:365-372, 1976.Crossref

Penneys, Neal S.;Wiley, Henry E.

1979 Archives of Dermatology

doi: 10.1001/archderm.1979.04010120025011

Abstract Four patients with systemic lupus erythematosus (SLE) had a vesicobullous eruption that histologically resembled dermatitis herpetiformis. Immunofluorescence microscopy patterns in the skin studied in three patients, however, were characteristic of SLE. Treatment of the underlying collagen-vascular disease improved the eruption, while recurrence coincided with exacerbation of the systemic disease. This distinctive lesion is an important parameter of SLE activity. (Arch Dermatol 115:1427-1428, 1979) References 1. Estes D, Christian DL: The natural history of systemic lupus erythematosus by prospective analysis . Medicine 50:85-95, 1971.Crossref 2. Uses for immunofluorescence tests of skin and sera: Utilization of immunofluorescence in the diagnosis of bullous diseases, lupus erythematosus, and certain other dermatoses . Arch Dermatol 111:371-381, 1975.Crossref 3. Grossman J, Callerame ML, Condemi JJ: Skin immunofluorescence studies on lupus erythematosus and other antinuclear-antibody-positive diseases . Ann Intern Med 80:496-500, 1974.Crossref 4. Katz SI, Strober W: The pathogenesis of dermatitis herpetiformis . J Invest Dermatol 70:63-75, 1978.Crossref 5. Gibson TP, Dibone GF: Use of the American Rheumatism Association's preliminary criteria for the classification of systemic lupus erythematosus . Ann Intern Med 77:754-756, 1972.Crossref 6. Katz SI: Dermatitis herpetiformis: Clinical, histologic, therapeutic and laboratory clues . Int J Dermatol 17:529-535, 1978.Crossref 7. Seah PP, Fry L: Immunoglobulins in the skin in dermatitis herpetiformis and their relevance in diagnosis . Br J Dermatol 92:157-166, 1975.Crossref 8. MacVicar DN, Graham JH, Burgoon CF Jr: Dermatitis herpetiformis, erythema multiforme and bullous pemphigoid: A comparative histopathological and histochemical study . J Invest Dermatol 41:289-300, 1963.Crossref 9. Moncada B: Dermatitis herpetiformis: In association with systemic lupus erythematosus . Arch Dermatol 109:723-725, 1974.Crossref 10. Vandersteen PR, Jordan RE: Dermatitis herpetiformis with discoid lupus erythematosus: Occurrence of sulfone-induced discoid lupus erythematosus . Arch Dermatol 110:95-98, 1974.Crossref 11. Jordan RE, Muller SA, Hale WL, et al: Bullous pemphigoid associated with systemic lupus erythematosus . Arch Dermatol 99:17-25, 1969.Crossref 12. Kumar V, Binder WL, Schotland E, et al: Co-existence of bullous pemphigoid and systemic lupus erythematosus . Arch Dermatol 114:1187-1190, 1978.Crossref

Goodenberger, Daniel M.;Lawley, Thomas J.;Strober, Warren;Wyatt, Larry;Sangree, M. Huyett;Sherwin, Robert;Rosenbaum, Haskell;Braverman, Irwin;Katz, Stephen I.

1979 Archives of Dermatology

doi: 10.1001/archderm.1979.04010120027012

Abstract Two patients with clinical and histologic findings consistent with necrolytic migratory erythema are presented. Unlike previously described patients with this disorder, neither patient had substantially elevated glucagon levels nor an associated pancreatic islet cell tumor. The cause of the skin disease in these patients remains unknown but may be related to the underlying small-bowel disorder present in both. (Arch Dermatol 115:1429-1432, 1979) References 1. Becker SW, Kahn D, Rothman S: Cutaneous manifestations of internal malignant tumors . Arch Dermatol Syphilol 45:1069-1080, 1942.Crossref 2. Wilkinson DS: Necrolytic migratory erythema with carcinoma of the pancreas . Trans St Johns Hosp Dermatol Soc 59:244-250, 1973. 3. Fisher M, Sherwin RS, Hendler R, et al: Kinetics of glucagon in man: Effects of starvation . Proc Natl Acad Sci USA 73:1735-1739, 1976.Crossref 4. Mallinson CN, Bloom SR, Warin AP, et al: A glucagonoma syndrome . Lancet 2:15, 1974. 5. Kahan RS, Perez-Figaredo RA, Neimanis A: Necrolytic migratory erythema: Distinctive dermatosis of the glucagonoma syndrome . Arch Dermatol 113:792-797, 1977.Crossref 6. Binnick AN, Spencer SK, Dennison WL, et al: Glucagonoma syndrome: Report of two cases and literature review Arch Dermatol 113:749-754, 1977.Crossref 7. Scully RE (ed): Case records of the Massachusetts General Hospital . N Engl J Med 292:1117-1123, 1975.Crossref 8. Sweet RD: A dermatosis specifically associated with a tumor of pancreatic alpha cells . Br J Dermatol 90:301-308, 1974.Crossref

Greer, Kenneth E.;Gross, Gary P.;Cooper, Philip H.;Harding, Sally A.

1979 Archives of Dermatology

doi: 10.1001/archderm.1979.04010120031013

Abstract Chromomycosis is a chronic, slowly progressive disease of the skin and subcutaneous tissue produced by several species of dematiaceous or pigmented fungi, especially Phialophora gougeroti. Verrucous nodules and flattened annular plaques are the most frequently reported skin lesions in chromomycosis, but deep abscesses and cystic lesions have also been reported. We describe herein a case of cystic chromomycosis due to Wangiella dermatitidis that developed following a nonpenetrating injury to the thumb. (Arch Dermatol 115:1433-1434, 1979) References 1. Vollum DI: Chromomycosis: A review . Br J Dermatol 96:454-458, 1977.Crossref 2. Carrión AL: Chromoblastomycosis and related infections: New concepts, differential diagnosis, and nomenclatorial implications . Int J Dermatol 14:27-32, 1975.Crossref 3. Padhye AA, McGinnis MR, Ajello L: Thermotolerance of Wangiella dermatitidis . J Clin Microbiol 8:424-426, 1978. 4. Bayles MAH: Chromomycosis: Treatment with thiabendazole . Arch Dermatol 104:476-485, 1971.Crossref 5. Tsai CY, Lü YC, Wang LT, et al: Systemic chromoblastomycosis due to Hormodendrum dermatitidis (Kano) Conant: Report of the first case in Taiwan . Am J Clin Pathol 46:103-114, 1966. 6. Ulrich E: Sporotrichosis produced by Sporotrichum gougeroti: Report of a case and review of the literature . Arch Dermatol Syphilol 67:44-52, 1953.Crossref 7. Jotisankasa V, Nielsen HS, Conant NF: Phialophora dermatitidis: Its morphology and biology . Sabouradia 8:98-107, 1970.Crossref 8. Rippon JW: Medical Mycology . Philadelphia, WB Saunders Co, 1974, p 244. 9. Mauceri AA, Cullen SI, Vandevelde AG, et al: Flucytosine: An effective oral treatment for chromomycosis . Arch Dermatol 109:873-876, 1974.Crossref

Schlossberg, David;Kandra, Joseph;Kreiser, Joseph

1979 Archives of Dermatology

doi: 10.1001/archderm.1979.04010120033014

Abstract We describe a 20-year-old woman in whom an illness developed that was consistent with Kawasaki disease. Kawasaki disease may not be confined exclusively to the pediatric age group. (Arch Dermatol 115:1435-1436, 1979) References 1. Hussey HH: Mucocutaneous lymph node syndrome . JAMA 236:292, 1976.Crossref 2. Reilly HD Jr: Mucocutaneous lymph node syndrome (Kawasaki disease) . Infect Dis 134:302-305, 1976.Crossref 3. Darby CP, Kyong CU: Mucocutaneous lymph node syndrome . JAMA 236:2295-2299, 1976.Crossref 4. Mornes DM, O'Brien RJ: From the Center for Disease Control: Kawasaki disease in the United States . J Infect Dis 137:91-93, 1978.Crossref 5. Melish EM, Hicks RM, Larson EJ: Mucocutaneous lymph node syndrome in the United States . Am J Dis Child 130:599-607, 1976. 6. Lee TJ, Vaughan D: Mucocutaneous lymph node syndrome in a young adult . Arch Intern Med 139:104-105, 1979.Crossref 7. Prestia AE, Lynfield YL: Scarlatiniform eruption in viral hepatitis . Arch Dermatol 101:352-355, 1970.Crossref 8. Margileth AM: Scalded skin syndrome . South Med J 68:447-454, 1975.Crossref 9. Melish MD, Glasgow LA: Staphylococcal scalded syndrome . J Pediatr 78:958-967, 1971.Crossref 10. Schlievert PM, Schoettle DJ, Watson DW: Purification and physicochemical and biologic characterization of a staphylococcal pyrogenic exotoxin . Infect Immun 23:609-617, 1979.

Mills, Stacey E.;Cooper, Philip H.;Beacham, Bruce E.;Greer, Kenneth E.

1979 Archives of Dermatology

doi: 10.1001/archderm.1979.04010120035015

Abstract We describe two brothers with dyskeratosis congenita and intracranial calcifications. The calcifications were massive, approximately symmetric, and showed a predilection for the basal ganglia and dentate nuclei. No underlying causes for this finding were identified. Idiopathic familial intracranial calcification of this type has been described, but an association with dyskeratosis congenita has not previously been observed. (Arch Dermatol 115:1437-1439, 1979) References 1. Sirinavin C, Trowbridge AA: Dyskeratosis congenita: clinical features and genetic aspects: Report of a family and review of the literature . J Med Genet 12:339-354, 1975.Crossref 2. Inoue S, Mekanik G, Mahallati M, et al: Dyskeratosis congenita with pancytopenia: Another constitutional anemia . Am J Dis Child 126:389-396, 1973.Crossref 3. Steier W, Van Voolen GA, Selmanowitz VJ: Dyskeratosis congenita: Relationship to Fanconi's anemia . Blood 39:510-521, 1972. 4. Sorrow JM Jr, Hitch JM: Dyskeratosis congenita: First report of its occurrence in a female and a review of the literature . Arch Dermatol 88:340-347, 1963.Crossref 5. Bodalski J, Defecinska E, Judkiewicz L, et al: Fanconi's anemia and dyskeratosis congenita as a syndrome . Dermatologica 127:330-342, 1963.Crossref 6. Cole HN, Cole HN Jr, Lascheid WP: Dyskeratosis congenita: Relationship to poikiloderma atrophicans vasculare and to aplastic anemia of Fanconi . Arch Dermatol 76:712-718, 1957.Crossref 7. Bryan HG, Nixon RK: Dyskeratosis congenita and familial pancytopenia . JAMA 192:203-208, 1965.Crossref 8. Gutman A, Frumkin A, Adam A, et al: X-linked dyskeratosis congenita with pancytopenia . Arch Dermatol 114:1667-1671, 1978.Crossref 9. Ortega JA, Swanson VL, Landing BH, et al: Congenital dyskeratosis: Zinsser-Engman-Cole syndrome with thymic dysplasia and aplastic anemia . Am J Dis Child 124:701-704, 1972.Crossref 10. Löwenthal A, Bruyn GW: Calcification of the striopallidodentate system , in Vinken PJ, Bruyn GW (eds): Handbook of Clinical Neurology . New York, John Wiley & Sons Inc, 1968, vol 6, pp 703-725. 11. Neill CA, Dingwall MM: A syndrome resembling progeria and a review of two cases . Arch Dis Child 25:213-223, 1950.Crossref

Blank, Harvey

1979 Archives of Dermatology

doi: 10.1001/archderm.1979.04010120038016

Abstract Herpetism, an abnormal constitutional condition predisposing to herpes (Webster's New International Dictionary, ed 2, Springfield, Mass, G & C Merriam Co, 1923, p 1010; French: herpétisme), as manifest by recurrent lesions, is an increasingly common and distressing problem. It results from an infection with either the orofacial (type 1) or the genital (type 2) herpes simplex virus. After primary infection of skin or mucosa the virus makes its way to the nuclei of the cells of the regional nerve ganglia. Incorporation of the viral DNA into the host DNA1 provides an impregnable intracellular site for a lifelong infection beyond the reach of antibody, cell-mediated immune responses, or chemotherapy. As a result of cell mechanisms not yet understood but often triggered by fever, sunburn, emotions, or unknown factors, the latent infection becomes manifest as a recurrent endogenous infection in the cutaneous, ocular, or genital epithelium. Exogenous reinfection is also possible, References 1. Kit S, Kurchak M, Wray W, et al: Binding to chromosomes of herpes simplex-related antigens in biochemically transformed cells . Proc Natl Acad Sci USA 75:3288-3291, 1978.Crossref 2. Hartman MD, Ziegler RJ: The relative ability of immunological defense mechanism to inhibit herpes simplex virus replication in rat dorsal root ganglia cultures , in Abstracts of the Annual Meeting of the American Society for Microbiology—1978 . Washington, DC, American Society for Microbiology, 1978, p 252. 3. Pazin GJ, Monto H, Jannetta PJ: Reactivation of herpes simplex virus after decompression of the trigeminal nerve root . J Infect Dis 138:405, 1978.Crossref 4. Naraqi S, Jackson GG, Jonasson O, et al: Prospective study of prevalence, incidence and source of herpes-virus infections in patients with renal allografts . J Infect Dis 136:531-540, 1977.Crossref 5. Rand KH, Rasmussen LE, Pollard RB, et al: Cellular immunity and herpesvirus infections in cardiac-transplant patients . N Engl J Med 296:1372-1377, 1977.Crossref 6. Romano TJ, Shore SL: Lysis of virus infected target cells by antibody dependent cellular cytotoxicity . Cell Immunol 30:66-81, 1977.Crossref 7. Shillitoe EJ, Wilton JMA, Lehner T: Sequential changes in cell mediated immune responses to herpes simplex virus after recurrent herpetic infection in humans . Infect Immun 18:130-137, 1977. 8. Rasmussen L, Merigan TC: Role of T lymphocytes in cellular immune responses during herpes simplex virus infection in humans . Proc Natl Acad Sci USA 75:3957-3961, 1978.Crossref 9. Reichman RC, Dolin R, Vincent MM, et al: Cell-mediated cytotoxicity in recurrent herpes simplex virus infections in man . Proc Soc Exp Biol Med 155:571-576, 1977.Crossref 10. Costa J, Rabson AS, Yee C, et al: Immunoglobulin binding to herpes virus-induced Fc receptors inhibits virus growth . Nature 269:251-252, 1977.Crossref 11. Adler R, Glorioso JP, Cossman J, et al: Possible role of Fc receptors on cells infected and transformed by herpesvirus: Escape from immune cytolysis . Infect Immun 21:442-447, 1978. 12. Daniels CA, LeGoff SG, Notkins AL: Shedding of infectious virus/antibody complexes from vesicular lesions of patients with recurrent herpes labialis . Lancet 2:524-528, 1975.Crossref 13. Kazmierowski JA, Wuepper KD: Erythema multiforme: Immune complex vasculitis of the superficial cutaneous microvasculature . J Invest Dermatol 71:366, 1978.Crossref 14. Kalimo K: Rheumatoid factor in sera of dermatitis herpetiformis patients . Br J Dermatol 98:79-83, 1978.Crossref 15. Strnad BC, Aurelian L: Proteins of herpesvirus type 2 . Virology 87:401-415, 1978.Crossref 16. Kitces EN, Morahan PS, Tew TG, et al: Protection from oral herpes simplex virus infection by a nucleic acid-free vaccine . Infect Immun 16:955-960, 1977. 17. Cohen GH, Katze M, Hydrean-Stern C, et al: Type-common of CP-1 antigen of herpes simplex virus is associated with a 59,000-molecular-weight envelope glycoprotein . J Virol 27:172-181, 1978. 18. Wise TG, Pavan PR, Ennis FA: Herpes simplex virus vaccines . J Infect Dis 136:706-711, 1977.Crossref 19. Russell AS, Brisson E, Grace M: A double blind, controlled trial of levamisole in the treatment of recurrent herpes labialis . J Infect Dis 137:597-600, 1978.Crossref 20. Whitley RJ, Soong SJ, Dolin R, et al: Adenine arabinoside therapy of biopsy-proved herpes simplex encephalitis . N Engl J Med 297:289-294, 1977.Crossref 21. Spruance SL, Crumpacker CS, Haines H, et al: Ineffectiveness of topical adenine arabinoside 5′-monophosphate in recurrent herpes labialis . N Engl J Med 300:1180-1184, 1979.Crossref

WALTER, JOSEPH F.

1979 Archives of Dermatology

doi: 10.1001/archderm.1979.04010120040017

Abstract PATHOLOGIC QUIZ CASE 1 Leslie A. Mark, MD, San DiegoSince birth, a 24-year-old woman has had linear whorled hypopigmentation of the skin of her trunk and extremities (Fig 1 and 2). She was also noted to have grouped baggy herniations of fat covered by a thin layer of hypopigmented and hyperpigmented skin on the right part of her thorax and the posterior part of her right thigh. Other congenital lesions consist of microcephaly, depressed nasal bridge, with hypoplasia of the right part of the clavicle, four hypoplastic ribs, pectus excavatum, and radialulnar synostosis. Severe bilateral hand defects include supernumerary digits, syndactylism of the third and fourth fingers, single palmar crease, a broad bifid left thumb, rudimentary fifth finger, and camptodactyly of the right forefinger. During the first decade of life, patchy alopecia of the scalp, scoliosis, and angiofibromatous nodules of the lip and ocular canthi developed. She is now References 1. Goltz RW, Peterson WC, Gorlin RJ, et al: Focal dermal hypoplasia . Arch Dermatol 86:708-717, 1962.Crossref 2. Holden JD, Akers WA: Goltz's syndrome: Focal dermal hypoplasia . Am J Dis Child 114:292-300, 1967.Crossref 3. Smith DW: Recognizable Patterns of Human Malformation: Genetic, Embryologic, and Clinical Aspects . Philadelphia, WB Saunders Co, 1976, pp 170-171. 4. Lever WF, Schaumburg-Lever G: Histopathology of the Skin , ed 5. Philadelphia, JB Lippincott Co, 1975, pp 639-642. 5. Strong EW, McDivitt RW, Brasfield RD: Granular cell myoblastoma . Cancer 25:415-422, 1970.Crossref 6. Fisher ER, Wechsler H: Granular cell myoblastoma—a misnomer: Electron microscopic and histochemical evidence concerning its Schwann cell derivation and nature (granular cell schwannoma) . Cancer 15:936-954, 1962.Crossref

Baran, Robert

1979 Archives of Dermatology

doi: 10.1001/archderm.1979.04010120044018

Abstract In 1970, Laugier and Hunziker1 reported five cases of essential melanotic pigmentation of the mouth and the lips. Two of these patients also displayed pigmentary changes in the nails. Sartoris et al2 reported two cases with a nail anomaly in one, and in 1977, Laugier et al3 also described another patient with pigmented nails. We have encountered Laugier-Hunziker syndrome in nine patients, five of whom had nail involvement. Nine patients (six women and three men) between 30 and 55 years of age consulted me for the presence of pigmented spots on the mucous membranes of the lower lip of up to five years' duration (Fig 1). In four patients, examination of the oral cavity revealed involvement of the buccal mucosa as well. In four patients, further examination of the nails revealed pigmentation of the fingernails, involving one finger only in one patient and three to six in the References 1. Laugier P, Hunziker N: Pigmentation mélanique lenticulaire, essentielle, de la muqueuse jugale et des lèvres . Arch Belg Dermatol Syphiligr 26:391-399, 1970. 2. Sartoris S, Pippione M, De Paoli MA, et al: Pigmentatione melanica idiopatica . G Ital Dermatol 110:382-385, 1975. 3. Laugier P, Hunziker N, Olmos L: Pigmentation mélanique lenticulaire essentielle de la muqueuse jugale et des lèvres . Ann Dermatol Venereol 104:181-184, 1977. 4. Becker SW: Melanin pigmentation: A systematic study of the pigment of the human skin and upper mucous membranes, with special consideration of pigmented dendritic cells . Arch Dermatatol Syphilol 16:259-290, 1927. 5. Fry L, Almeyda JR: The incidence of buccal pigmentation in caucasoids and negroids in Britain . Br J Dermatol 80:244-247, 1968.Crossref 6. Weathers DR, Corio RL, Crawford BE, et al: The labial melanotic macule . Oral Surg 42:196-205, 1976.Crossref 7. Page LR, Corio RL, Crawford BE, et al: The oral melanotic macule . Oral Surg 44:219-226, 1977.Crossref

Neils, Richard E.;Dailey, Michael P.;Ginsberg, Robert A.;Russell, Thomas J.

1979 Archives of Dermatology

doi: 10.1001/archderm.1979.04010120045019

Abstract A chronic erosive form of herpes A simplex virus (HSV) infection has been reported in immunosuppressed patients.1,2 Topical idoxuridine appears to have helped several patients,2 and a reduction in the quantity of immunosuppressive agents has been of benefit.1 Some patients have exhibited protracted or recurrent courses of HSV infections.2 Vidarabine (adenine arabinoside, ara-A), an effective agent for herpetic keratitis, has been used parenterally with partial success and minimal toxicity in varicellazoster infection.3,4 It has now been authorized for use in HSV encephalitis. Report of a Case A 65-year-old man was referred to our clinic on July 24, 1978, with a four-month history of a progressive, pruritic, and extremely painful eruption of his face. This eventually ulcerated and coalesced to involve much of the bearded area. He noted no preceding "cold sore." Chronic lymphocytic leukemia had been diagnosed in 1974. Since mid-1976, the patient had been References 1. Stone WJ, Scowden EB, Spannuth CL, et al: Atypical herpesvirus hominis type 2 infection in uremic patients receiving immunosuppressive therapy . Am J Med 63:511-516, 1977.Crossref 2. Shneidman DW, Barr RJ, Graham JH: Chronic cutaneous herpes simplex . JAMA 241:592-594, 1979.Crossref 3. Whitley RJ: Antiviral chemotherapy , in Dolin R, Reichman RC, Mazur MH, et al: Herpes zoster-varicella infections in immunosuppressed patients. Ann Intern Med 89:375-388, 1978.Crossref 4. Aronson MD, Phillips CF, Gump DW, et al: Vidarabine therapy for severe herpesvirus infections . JAMA 235:1339-1342, 1976.Crossref 5. Whitley RJ, Soong S, Dolin R, et al: Adenine arabinoside therapy of biopsy-proved herpes simplex encephalitis: National Institute of Allergy and Infectious Diseases collaborative antiviral study . N Engl J Med 297:289-294, 1977.Crossref 6. Ross AH, Julia, A, Balakrishnan C: Toxicity of adenine arabinoside in humans . J Infect Dis 133( (suppl) ):A192-A198, 1976.Crossref

Fisher, Alexander A.;Brancaccio, Ronald R.

1979 Archives of Dermatology

doi: 10.1001/archderm.1979.04010120047020

Abstract A particular sterile lubricant (K-Y Lubricating Jelly) has been widely used for medical examinations and instrumentations. To our knowledge, there are no previous reports in the literature of allergic reactions to this lubricant. This report cites three patients who acquired allergic contact reactions from three different types of exposure to this product. Report of Cases Case 1.— References 1. Hannuksela M, Pirila V, Salo OP: Skin reactions to propylene glycol . Contact Dermatitis 1:112-116, 1975.Crossref 2. Fisher AA: Propylene glycol dermatitis . Cutis 21:166, 170, 174-178, 1978. 3. Goldsmith LA: Propylene glycol . Int J Dermatol 11:703-705, 1978. 4. Hannuksela M, Förström L: Reactions to peroral propylene glycol . Contact Dermatitis 4:41-45, 1978.Crossref

Kaplan, Lee A.;Walter, Joseph F.;Macknet, Kenneth D.

1979 Archives of Dermatology

doi: 10.1001/archderm.1979.04010120048021

Abstract Scarring is an uncommon accompaniment to fluorouracil therapy of superficial erythematous basal cell carcinoma,1 When scarring occurs, it typically appears as mild atrophy.2 We could find no previous reports of hypertrophic scarring complicating fluorouracil therapy of superficial erythematous basal cell carcinoma, and present the following case. Report of a Case A 42-year-old man initially came to the Dermatology Clinic, University of California Medical Center, San Diego, in June 1978 with an 18-month history of a skin lesion on the left side of the upper part of the back. There was no history of previous trauma, skin cancer, or arsenic or x-ray exposure. The patient had sporadically treated the lesion with tolnaftate cream without response.Physical examination revealed a 2.5 × 2.0-cm erythematous, slightly raised plaque with fine scaling in the above site (Fig 1). An examination for fungi using potassium hydroxide was negative.A tentative diagnosis of nummular References 1. Klein E, Stoll HL, Milgrom H, et al: Tumors of the skin: XII. Topical 5-fluorouracil for epidermal neoplasms . J Surg Oncol 3:331-349, 1971.Crossref 2. Klein E, Stoll HL, Milgrom H, et al: Tumors of the skin: V. Local administration of anti-tumor agents to multiple superficial basal cell carcinomas . J Invest Dermatol 45:489-497, 1965.Crossref 3. Dillaha CJ, Jansen GT, Honeycutt WM, et al: Selective cytotoxic effect of topical 5-fluorouracil . Arch Dermatol 88:247-256, 1963.Crossref 4. Goette DK, Odom RB, Owens R: Allergic contact dermatitis from topical fluorouracil . Arch Dermatol 113:196-198, 1977.Crossref 5. Burnett JW: Two unusual complications of topical fluorouracil therapy . Arch Dermatol 111:398, 1975.Crossref 6. Bart BJ, Bean SF: Bullous pemphigoid following the topical use of fluorouracil . Arch Dermatol 102:457-460, 1970.Crossref 7. Dillaha CJ, Jansen GT, Honeycutt WM, et al: Further studies with topical 5-fluorouracil . Arch Dermatol 92:410-416, 1965.Crossref

Morman, Manuel R.;Lin, Ruey-Yen;Petrozzi, John W.

1979 Archives of Dermatology

doi: 10.1001/archderm.1979.04010120049022

Abstract Benign dermatologic conditions, including sarcoidosis, erythema multiforme, urticaria, erythema nodosum, and others, have developed at the sites of vaccination.1 Scars from burns, x-rays, lupus vulgaris, lupus erythematosus, and chronic osteomyelitis are susceptible to cancerous change.2 The development of malignancy in vaccination scars is also a well-recognized event, with at least five different tumors having been described in vaccination sites: basal cell carcinoma, malignant melanoma, squamous cell carcinoma, fibrosarcoma, and dermatofibrosarcoma protuberans. We describe a patient in whom dermatofibrosarcoma protuberans developed at the site of multiple immunizations. Report of a Case A 33-year-old man had a rapidly growing mass in the deltoid region of his left arm. He had had multiple immunizations for plague, yellow fever, and tetanus at that site in 1965 at the time of his armed forces induction physical examination. His records were lost and he was subjected to the same injections into the same area References 1. White CS, Ray PR, Waechter CJ, et al: Repeated immunization: Possible adverse effects: Reevaluation of human subjects at 25 years . Ann Intern Med 81:594-560, 1974.Crossref 2. Bowers RF, Young JM: Carcinoma arising in scars, osteomyelitis, and fistulae . Arch Surg 80:564-569, 1964.Crossref 3. Hashimoto K, Brownstein MH, Jacobiec FA, et al: Dermatofibrosarcoma protuberans: A tumor with perineural and endoneural cell features . Arch Dermatol 110:874-885, 1974.Crossref 4. Taylor HB, Helwig EB: Dermatofibrosarcoma protuberans: A study of 115 cases . Cancer 15:717-725, 1962.Crossref 5. Woolridge WE: Dermatofibrosarcoma protuberans: Tumor too lightly considered . Arch Dermatol 75:132-134, 1957.Crossref