doi: 10.1001/archderm.1985.01660010017001
This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables.
DiGiovanna, John J.;Blank, Harvey
doi: 10.1001/archderm.1985.01660010025003
Abstract In Reply.— As Dr Kagan has carefully noted, we failed to indicate the isometric form of lysine. The pure L-isomer of lysine hydrochloride was used in our study and we should have stated that in the original article.Kagan states that the lysine dosage used in our study was "low." We chose this dosage because of Kagan's study, in which this was the highest dosage administered ("312-1,200 mg of lysine daily").1 With doses of this magnitude or less, the results reported from the article were described as follows. The pain disappeared abruptly overnight in virtually every instance, new vesicles failed to appear, and resolution in the majority was considered to be more rapid than in their past experience. The most encouraging finding... was the reduction in frequency of recurrences. Taking therapeutic doses of 500-1,000 mg or increasing the maintenance dose would invariably abort recurrence.Since our dose (1,200 mg) References 1. Griffith RS, Norins AL, Kagan C: A multicentered study of lysine therapy in herpes simplex infection . Dermatologica 1978;156:257-267.Crossref
doi: 10.1001/archderm.1985.01660010025002
Abstract To the Editor.— In the January Archives, DiGiovanna and Blank1 reported failure of lysine in frequently recurrent herpes simplex infection. Caution is urged in the interpretation of their results. The L-isomer allosterically inhibits herpes in vitro,2,3 while the D-isomer is biologically inactive. It is not stated whether the lysine used was pure L-isomer. Assuming it was, the small number of patients (ten control, ten treated), the severity of the cases (patients had lesions present more than 40% of the time), and the low dosage (1,200 mg/day) all raise questions. In severe cases, high doses (3 g/day) are often required. In addition, there was no true control group, since all the patients were arginine restricted, an integral part of the therapy. This may explain why "most of our patients did indeed think that they were receiving the active medication and that it was having a beneficial effect." Thus the References 1. DiGiovanna JJ, Blank H: Failure of lysine in frequently recurrent herpes simplex infection . Arch Dermatol 1984;120:48-51.Crossref 2. Tankersley RW Jr: Amino acid requirements of herpes virus in human cells . J Bacteriol 1964;87:609-613. 3. Griffith RS, Delong D, Nelson J: Relation of arginine-lysine antagonism to herpes simplex growth in tissue culture . Chemotherapy 1981;27:209-213.Crossref 4. Griffith RS, Norins AL, Kagan C: A multicentered study of lysine in herpes simplex infection . Dermatologica 1978;156:257-267.Crossref 5. Walsh DE, Griffith RS, Behforooz A: Subjective response to lysine in the therapy of herpes simplex . J Antimicrob Ther 1983;12:489-496.Crossref 6. Peng Y, Gubin J, Harper AE, et al: Food intake regulation: Amino acid toxicity and changes in rat brain and plasma amino acids . J Nutr 1973;103:608-617.
doi: 10.1001/archderm.1985.01660010025004
Abstract To the Editor.— In the May Archives, Kumari1 described 75 patients with vitiligo treated with clobetasol propionate. Twenty-five patients with facial involvement, including the eyelids, were treated with a 0.05% ointment, applied twice daily for a period of eight weeks. The maximum amount was 25 g (12.5 mg clobetasol propionate) per course. The amounts applied to the eyelids are not stated. When needed, a second course was given after an interval of four months without treatment. The report stated that these patients were carefully observed for ocular side effects and that none were noted. It is presumed, but not specifically stated, that intraocular pressure was measured in these patients.Howell2 recommended that patients receiving topical steroid treatment to eyelids for longer than one to two weeks should be monitored for IOP by an ophthalmologist. If indeed there were no measurable (even though transient) increases in IOP in Kumari's References 1. Kumari J: Vitiligo treated with topical clobetasol propionate . Arch Dermatol 1984;120:631-635.Crossref 2. Howell JB: Eye diseases induced by topically applied steroids . Arch Dermatol 1976;112:1529-1530.Crossref
Christensen, Patricia;Barr, Ronald J.
doi: 10.1001/archderm.1985.01660010026006
Abstract To the Editor.— A wattle is a rare congenital anomaly occurring much less frequently than branchial cysts or sinuses. Wattles are found on satyrs and fauns of Greek and Roman mythology. Statues of these creatures are probably the earliest shown cases. The term is usually applied to the dewlap of birds such as turkeys. In mammals, a wattle is a fleshy appendage beneath the throat consisting of skin, subcutaneous fat, striated muscle, and a strip of cartilage. Report of a Case.— A 12-year-old boy was seen with a congenital tumor on the neck. On physical examination, a 15 × 6-mm soft, flesh-colored, elongated tumor hung from the patient's anterior neck (Fig 1). The lesion was completely excised, and there was no evidence of recurrence on follow-up examination.The microscopic sections exhibited a pedunculated lesion with an essentially normal epidermis, with the exception of mild hyperkeratosis. Numerous hair follicles were present References 1. Hogan D, Wilkinson RD, Williams A: Congenital anomalies of the head and neck . Int J Dermatol 1980;19:479-486.Crossref 2. Albers GD: Branchial anomalies . JAMA 1963;183:103-113.Crossref 3. Clarke JA: Are wattles auricular or branchial origin? Br J Plast Surg 1976;29:238-244.Crossref
doi: 10.1001/archderm.1985.01660010025005
This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables. Abstract In Reply.— The average amount of 0.05% clobetasol propionate in paraffin base was 2.5 g every four weeks, when applied to whole of the skin of upper and lower eyelids of one eye. The amount was correspondingly lower when applied to smaller areas of the eyelids. Patients were instructed to apply the ointment sparingly and to avoid seepage of ointment in the eye. No routine IOP studies were undertaken, as our ophthalmologist did not think it necessary because of the small amount of ointment used.
Serrano, Gabriel;Aliaga, Adolfo;Febrer, Isabel;Bonillo, Juan;Pelufo, Cristina;Otero, Dolores
doi: 10.1001/archderm.1985.01660010027007
Abstract To the Editor.— Neonatal gangrene of the buttock is a rare condition mainly due to iatrogenic causes. Most cases occur after umbilical artery catheterization,1,2 exchange transfusions,3 and cord injections by means of syringes.4 Exceptional causes of gangene during the neonatal period include infections and hypernatraemic dehydration of infancy.5 The following case supports that perinatal gangrene of the buttock may also arise as a spontaneous condition. Report of a Case.— A 2-day-old male was delivered spontaneously at term with vertex presentation. His birth weight was 3,100 g. The mother, a 23-year-old woman (gravida 1), had no known medical problems prior to the delivery. Approximately 30 minutes after birth, a nurse noted a red patch on the left buttock and perineal region of the infant. During the next hours, the lesion became swollen, and a purple discoloration appeared and extended to the scrotum (Fig 1). Examination revealed a References 1. Rudolph N, Wang HH, Dragutsky D: Gangrene of the buttock: Complication of umbilical artery catheterization . Pediatrics 1974;53:106-109. 2. Book LS, Herbs JJ, Stewart D: Hazards of calcium gluconate therapy in the newborn infant: Intra-arterial injection producing intestinal necrosis in rabbit ileum . J Pediatr 1978;92:793-797.Crossref 3. Origel AV, Guzman LM, Gutierrez LJ: Necrosis glutea: Complicación rara de la exanguinotransfusión . Rev Med del IMSS 1979;18:127-130. 4. Bonifazi E, Meneghini C: Perinatal gangrene of the buttock: An iatrogenic or spontaneous condition? J Am Acad Dermatol 1980;3:596-598.Crossref 5. Comay SC, Karabus CD: Peripheral gangrene in hypernatraemic dehydration of infancy . Arch Dis Child 1975;50:616-619.Crossref
Clement, Michele;Guy, R.;Pembroke, A. C.
doi: 10.1001/archderm.1985.01660010028008
Abstract To the Editor.— Although the development of squamous cell carcinoma at sites of chronic skin damage is a well-recognized phenomenon, to our knowledge there is only one previous report in the literature of its appearing in an area of necrobiosis lipoidica. We would like to report another case. Report of a Case.— A 59-year-old woman had suffered from insulin-dependent diabetes mellitus since 1932. In 1944, extensive necrobiosis lipoidica of the legs and feet developed, and, in 1947, granuloma annulare of the hands. The granuloma annulare cleared but the necrobiosis lipoidica persisted and extended. Ulceration of the lesions first occurred in 1975 but healed in a few months. In 1977, an ulcer developed above the right lateral malleolus in an area of necrobiosis lipoidica that had been noted by a dermatologist in 1944 and recorded on several occasions since. This ulcer persisted and continued to enlarge despite four months' inpatient treatment References 1. Byrd BF Jr, Munoz AJ, Ferguson H: Carcinoma of the skin following acute and chronic trauma . South Med J 1961;54:1262-1267.Crossref 2. Giblin T, Pickrell K, Pitts W, et al: Malignant degeneration in burn scars: Marjolin's ulcer . Ann Surg 1965;162:291-297.Crossref 3. Rossis CG, Yiacoumettis AM, Elemenoglou J: Squamous cell carcinoma of the heel developing at site of previous frostbite . J R Soc Med 1982;75:715-719. 4. Hejna WF: Squamous cell carcinoma developing in the chronic draining sinuses of osteomyelitis . Cancer 1965;18:128-132.Crossref 5. Muller SA, Winkelmann RK: Necrobiosis lipoidica diabeticorum: A clinical and pathological investigation of 171 cases . Arch Dermatol 1966;93:272-281.Crossref
doi: 10.1001/archderm.1985.01660010029010
Abstract To the Editor.— Dr Bargman1 was unable to find a previous reference to trichomycosis of the scrotal hair: perhaps we can help him. In our study of the bacterial flora of trichomycosis axillaris2 we examined 874 patients in an institute for the mentally retarded. We recorded that 14 (5%) of the 265 women, and 216 (35%) of the 609 men, had trichomycosis of the armpits. Sixteen (2.6%) of the men had trichomycosis of the scrotal hair, and three of these had no associated trichomycosis of the armpits. There is little new under the sun, or even below the belt. References 1. Bargman H: Trichomycosis of the scrotal hair . Arch Dermatol 1984;120:299-300.Crossref 2. Savin JA, Somerville DA, Noble WC: The bacterial flora of trichomycosis axillaris . J Med Microbiol 1970;3:352-356.Crossref
Rosove, Michael H.;Harwig, Sylvia S. L.;Ahmed, Razzaque A.
doi: 10.1001/archderm.1985.01660010029009
Abstract To the Editor.— Dapsone (4,4′-diaminodiphenylsulfone) causes dose-limiting hemolysis and methemoglobinemia, with formation of Heinz bodies (denatured hemoglobin particles) and characteristic poikilocytes.1 It has been proposed that Heinz body testing during dapsone treatment might be useful2; we have found it to be of restricted value.Twelve clinically stable, nonsplenectomized patients with normal erythrocyte glucose-6-phosphate dehydrogenase levels3 had been treated with constant dosage of dapsone for various skin disorders for at least one month. Mean (±SD) daily drug dosage was 122 (±69) mg. Complete blood cell counts, methemoglobin levels,4 reticulocyte counts,5 and Heinz body quantifications6 were performed two to four times (mean interval [±SD], 6.9 ± 5.7 weeks, minimum interval, one week, 35 studies).Normal values used for hemoglobin levels, reticulocyte count, methemoglobin levels, and Heinz body counts are 13 to 17 g/dL, 25,000 to 75,000/cu mm, less than 1.0%, and none detected, respectively. Respective mean References 1. DeGowin RL: A review of therapeutic and hemolytic effects of dapsone . Arch Intern Med 1967;120:242-248.Crossref 2. Smith RS, Alexander S: Heinz-body anaemia due to dapsone . Br Med J 1959;1:625-627.Crossref 3. Beutler E: Erythrocyte enzyme assays , in Williams WJ, Beutler E, Erslev AJ, et al (eds): Hematology , ed 3. New York, McGraw-Hill Book Co, 1983, pp 1623-1626. 4. Beutler E: Carboxyhemoglobin, methemoglobin, and sulfhemoglobin determinations , in Williams WJ, Beutler E, Erslev AJ, et al (eds): Hematology , ed 3. New York, McGraw-Hill Book Co, 1983, pp 1632-1634. 5. Erslev AJ, Atwater J: Reticulocyte staining , in Williams WJ, Beutler E, Erslev AJ, et al (eds): Hematology , ed 3. New York, McGraw-Hill Book Co, 1983, pp 1604-1605. 6. Schwab MLL, Lewis AE: An improved stain for Heinz bodies . Am J Clin Pathol 1969;39:93-95.
doi: 10.1001/archderm.1985.01660010029011
Abstract To the Editor.— I was interested to read of the effect of 5-fluorouracil cream in the treatment of vitiligo as reported from Japan by Tsuji and Hamada.1 They found that while fluorouracil alone had no effect, its use following epidermal abrasion resulted in repigmentation in the majority of patients.I wish to report the results of a pilot study of fluorouracil in dimethyl sulfoxide in vitiligo.2 Dimethyl sulfoxide is known to enhance the penetration of many substances through the intact epidermis. Pretreatment with dimethyl sulfoxide has been reported to enhance the effect of fluorouracil in the treatment of solar keratoses. Thus, theoretically, dimethyl sulfoxide might allow the fluorouracil to induce repigmentation in vitiligo without epidermal abrasion.Eight adult patients with vitiligo for at least one year were recruited to the study with their informed consent. Three patients were white, and five Indian. The subjects applied 2.5% fluorouracil in References 1. Tsuji T, Hamada T: Topically administered fluorouracil in vitiligo . Arch Dermatol 1983;119:722-727.Crossref 2. Garcia-Perez A, Aparicio M, Carapeto FJ: Comparison of the clinical and histological effects of 5-fluorouracil (5-FU) alone and of 5-FU preceded by dimethyl-sulfoxide (DMSO) on senile keratosis . Dermatologica 1970;140( (suppl 1) ):119-126.Crossref 3. Pegum JS: Dissociated depigmentation in vitiligo . Br J Dermatol 1955; 67:348-350.Crossref 4. Sweet RD: Vitiligo as a Köbner phenomenon . Br J Dermatol 1978;99: 223-224.Crossref
doi: 10.1001/archderm.1985.01660010030014
Abstract To the Editor.— Systemic lupus erythematosus (SLE) is a collagen vascular disease with multisystem involvement, including often the integument. Pemphigus is a group of bullous diseases affecting the skin and mucous membranes.1 Although both conditions are generally believed to be part of the autoimmune spectrum, each have distinctive clinical and immunopathologic characteristics. Pemphigus is also an organ-specific autoimmune disease with antibodies targeted only on the skin and mucous membranes with stratified epithelia, whereas SLE is non-organ specific autoimmune disease with several types of antinuclear antibodies (ANA) affecting many organs. We describe herein a patient with definite evidence of SLE in whom typical features of pemphigus vulgaris developed four months later, while the patient was receiving corticosteroid therapy. Report of a Case.— A 59-year-old Chinese woman was seen at the Singapore General Hospital in July 1982, because of a sixmonth history of polyarthritis involving the knees, elbows, wrists, and fingers. References 1. Ahmed AR, Graham J, Jordon RE, et al: Pemphigus: Current concepts . Ann Intern Med 1980;92:396-405.Crossref 2. Tan EM, Cohen AS, Fries JF, et al: The 1983 revised criteria for the classification of systemic lupus erythematosus . Arthritis Rheum 198225:1271-1277.Crossref 3. Senear FE, Usher B: An unusual type of pemphigus combining features of lupus erythematosus . Arch Dermatol 1926;13:761-781. 4. Chorzelski T, Jablonska S, Blaszczyk M: Immunopathological investigations in the Senear-Usher syndrome (coexistence of pemphigus and lupus erythematosus) . Br J Dermatol 1968;80:211-217.Crossref 5. Jordon JE: Pemphigus erythematosus: A unique member of the pemphigus group . Arch Dermatol 1982;118:742.Crossref 6. Somorin AO, Agbakwu SN, Nwaefuna A: Systemic lupus erythematosus and pemphigus vulgaris preceded by depressive psychosis . Cent Afr J Med 1981;27:12-14.
doi: 10.1001/archderm.1985.01660010030012
Abstract To the Editor.— Despite its dramatic effectiveness in the treatment of cystic acne, relapses have occurred after treatment with oral isotretinoin.1 I recently saw a patient who had a beneficial response to a four-month course of oral isotretinoin, but who had a "recurrence" of acne five months after drug therapy had been discontinued. Her new eruption was not a recurrence but was, instead, new-onset acne cosmetica.2 Report of a Case.— A 19-year-old woman had cystic acne involving the face, chest, and back that was unresponsive to previous conventional treatment. In August 1983, she was started on an 80 mg/day regimen of oral isotretinoin. Within two months her condition had clearly improved; by the end of four months the appearance of new lesions had virtually ceased, and the isotretinoin therapy was discontinued.The patient was seen again in June 1984, complaining of a "new rash" on her face. She References 1. Strauss JS, Rapini RP, Shalita AR, et al: Isotretinoin therapy for acne: Results of a multicenter dose-response study . J Am Acad Dermatol , 1984;10:490-496.Crossref 2. Kligman AM, Mills OH: Acne cosmetica . Arch Dermatol 1972;106:843-850.Crossref
doi: 10.1001/archderm.1985.01660010030013
Abstract To the Editor.— In the June Archives, McCormack et al1 reported a case of linear hypopigmentation following an intra-articular corticosteroid injection of a metatarsophalangeal joint and reviewed other instances of similar occurrences. I report herein a case of hypopigmentation following the injection of a ganglion. Report of a Case.— On Nov 29, 1983, a 26-year-old woman had been seen by a surgeon for what apparently was a 1 cm ganglion of her left hand. With the patient under local infiltrative anesthesia, the lesion was "aspirated and then punctured cyst with pressure." Following this, one-half mL of prednisolone tebutate (10 mg) was injected into the area and an elastic wrap was applied. Two or three weeks later, the patient noted "white spots" over the areaExtended area of hypopigmentation from hand to forearm. where the ganglion had been. These depigmented areas began to spread, first involving the surrounding skin and References 1. McCormack PC, Ledesma GN, Vaillant JG: Linear hypopigmentation after intra-articular corticosteroid injection . Arch Dermatol 1984;120:708-709.Crossref
doi: 10.1001/archderm.1985.01660010038015
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 New Name. Same Power. Lidex (fluocinonid) × 0.05% y Brief Summary of Prescribing Information LIDEX® (fluocinonide) Gel 0.05% Description: LIDEX gel 0.05% is intended for topical administration. The active component is the corticosteroid fluocinonide, which is the 21-acetate ester of fluocinolone acetonide and has the chemical name pregna-1,4-diene-3,20-dione,21-(acetyloxy)-6,9-difluoro-11 -hydroxy-16,17-[(1-methylethylidene)bis(oxy)]-, (6α,11β,16α)LIDEX gel contains fluocinonide 0.5 mg/g in a specially formulated gel base consisting of propylene glycol, propyl gallate, edetate disodium, and carbomer 940, with NaOH and/or HCl added to adjust the pH. This clear, colorless thixotropic vehicle is greaseless, non-staining and completely water miscible In this formulation, the active ingredient is totally in solution. Indications: Relief of inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses Contraindications: Hypersensitivity to any ingredient. Precautions General Periodically evaluate patients given a large dose of a potent topical steroid applied to a large area or under occlusive dressing for HPA suppression by using urinary free cortisol and
doi: 10.1001/archderm.1985.01660010053016
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 With this issue, the Archives of Dermatology enters the second year of publication under the guidance of the current Editor and Editorial Board. I would like to take this opportunity to share with the readers some of the highlights of 1984 for the Archives and to sketch our plans for the future. THE EDITORIAL BOARD Of the 18 board members, 11 accepted the invitation to join with me and others already on the board in shaping the content and format of the Archives. The following photographs and short autobiographic legends introduce those responsible for the philosophic and practical management of the Archives. I am fortunate to have the assistance of this talented group of clinicians and scientists from centers in virtually all geographic areas of the United States. They have varied backgrounds, interests, and areas of clinical and laboratory expertise, contributing to the journal a wealth of knowledge and experience
doi: 10.1001/archderm.1985.01660010055017
This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables.
doi: 10.1001/archderm.1985.01660010059018
Abstract The interaction between androgenic hormones and the skin has been a fascinating area of research that has tantalized dermatologists for several decades. Hirsutism, balding, and acne are all androgen-related disorders. Elevated levels of circulating androgens have recently been discovered in at least 80% of women suffering from hirsutism1 and, to a lesser extent, in women with female-pattern hair loss and acne.2 However, some obvious questions persist: Why does androgen cause hair to grow in some areas, such as the face, but cause it to regress to vellus hairs in other areas, such as the scalp? Why, with similar degrees of hyperandrogenemia, does severe acne develop in one woman and hirsutism in another? Answers to these questions seem to lie within the skin itself. An understanding of the response of the skin and its appendages to circulating hormones requires innovative research. We would all like to see a topical References 1. Hatch R, Rosenfield RL, Kim MH, et al: Hirsutism: Implications, etiology, and management . Am J Obstet Gynecol 1981; 140:815-830. 2. Lucky AW, McGuire JS, Rosenfield RL, et al: Plasma androgens in women with acne vulgaris . J Invest Dermatol 1983;81:70-74.Crossref 3. Stewart ME, Pochi PE: Antiandrogens and the skin . Int J Dermatol 1978;17:167-179.Crossref 4. Hamilton JB, Montagna W: The sebaceous glands of the hamster: I. Morphological effects of androgens on integumentary structures . Am J Anat 1950;86:191-233.Crossref 5. Vermorken AJM, Goos CMAA, Wirtz P: Evaluation of the hamster flank organ test for the screening of anti-androgens . Br J Dermatol 1982;106:99-101.Crossref 6. Weissmann A, Bowden J, Frank BL, et al: Antiandrogenic effects of topically spironolactone on the hamster flank organ . Arch Dermatol 1985;121:57-62.Crossref 7. Luderschmidt C, Bidlingmaier F, Plewig G: Inhibition of sebaceous gland activity by spironolactone in Syrian hamster . J Invest Dermatol 1982;78:253-255.Crossref 8. Shapiro G, Evron S: A novel use of spironolactone: Treatment of hirsutism . J Clin Endocrinol Metabol 1980;51:429-432.Crossref 9. Cumming DC, Yang JC, Rebar RW, et al: Treatment of hirsutism with spironolactone . JAMA 1982;247:1295-1298.Crossref 10. Kaszynski E: The stimulation of hair growth in the flank organs of female hamsters by subcutaneous testosterone propionate and its inhibition by topical cyproterone acetate: Doseresponse studies . Br J Dermatol 1983;109:565-569.Crossref 11. Vermorken AJM, Goos CMAA, Roelofs HMJ: The antiandrogenic effect of progesterone on the hamster flank organ . Br J Dermatol 1980;102:455-460.Crossref 12. Vermorken AJM, Goos CMAA, Roelofs HMJ: A method for the evaluation of the local antiandrogenic action of 5alphareductase inhibitors on human skin . Br J Dermatol 1980;102:695-701.Crossref
Weissmann, Arthur;Bowden, Jeffrey;Frank, Beryn L.;Horwitz, Stephen N.;Frost, Phillip
doi: 10.1001/archderm.1985.01660010061019
Abstract • The effects of topically applied spironolactone on the sebaceous glands of flank organs in adult male golden hamsters were investigated. Daily treatment with spironolactone (0.3 mg and 3 mg) on one side only significantly reduced the size of the treated flank organs, while the contralateral flank organs remained unchanged. Lower doses of spironolactone and the vehicle had no effect. Cyproterone acetate therapy resulted in the bilateral reduction of flank organ sizes. In vivo measurement of the palpable bulk of the flank organs correlated with flank organ volumes as determined by computer-assisted planimetry of serial histologic sections. Dry weights of seminal vesicles in animals treated with spironolactone did not differ significantly from those of the control group, while topically applied cyproterone acetate significantly reduced seminal vesicle weight. Topically administered spironolactone appears to have only local antiandrogenic effects, as indicated by the lack of changes in the untreated contralateral flank organs and in the weights of seminal vesicles. (Arch Dermatol 1985;121:57-62) References 1. Mann NM: Gynecomastia during therapy with spironolactone . JAMA 1963;190:160-162. 2. Rose LI, Underwood RH, Newmark SR, et al: Pathophysiology of spironolactone-induced gynecomastia . Ann Intern Med 1977; 87:398-403.Crossref 3. Menard RH, Stripp B, Gillette JR: Spironolactone and testicular cytochrome P-450: Decreased testosterone formation in several species and changes in hepatic drug metabolism . Endocrinology 1974;94:1628-1636.Crossref 4. Menard RH, Martin HF, Stripp B, et al: Spironolactone and cytochrome P-450: Impairment of steroid hydroxylation in the adrenal cortex . Life Sci 1975;15:1639-1648.Crossref 5. Corvol P, Michaued A, Menard J, et al: Antiandrogenic effect of spironolactones: Mechanism of action . Endocrinology 1975; 97:52.Crossref 6. Pita JC Jr, Lippman ME, Thompson EB, et al: Interaction of spironolactone and digitalis with the 5-α-dihydrotestosterone (DHT) receptor of rat ventral prostate . Endocrinology 1975; 97:1521-1527.Crossref 7. Rifka SM, Pita JC, Vigersky RA, et al: Interaction of digitalis and spironolactone with the human sex steroid receptors . J Clin Endocrinol Metabol 1977;46:338-344.Crossref 8. Boiselle A, Tremblay RR: Clinical usefulness of spironolactone in the treatment of acne and hirsutism , abstracted. Clin Res 1978;26:840A. 9. Boiselle A, Tremblay RR: New therapeutic approach to the hirsute patient . Fertil Steril 1979;32:276-279. 10. Shapiro G, Euron S: A novel use of spironolactone: Treatment of hirsutism . J Clin Endocrinol Metabol 1980;51:429-432.Crossref 11. Nielsen PG: Treatment of idiopathic hirsutism with spironolactone . Dermatologica 1982;165:194-196.Crossref 12. Cumming DC, Yang JC, Rebar RW, et al: Treatment of hirsutism with spironolactone . JAMA 1982;247:1295-1298.Crossref 13. Luderschmidt C, Bidlingmaier F, Plewig G: Inhibition of sebaceous gland activity by spironolactone in Syrian hamster . J Invest Dermatol 1982;78:253-255.Crossref 14. Frost P, Gomez E: Inhibitors of sex hormones: Development of experimental models , in Montagna W, Stoughton RB, Van Scott EJ (eds): Pharmacology and the Skin . New York, Appleton-Century-Crofts, 1972, pp 403-420. 15. Frost P, Giegel JL, Weinstein GD, et al: Biodynamic studies of the hamster flank organ growth: Hormonal influences . J Invest Dermatol 1973;61:159-167.Crossref 16. Voigt W, Hsia SL: The antiandrogenic action of 4-androsten-3-one-17 β-carboxylic acid and its methyl ester on hamster flank organ . Endocrinology 1973;92:1216-1222.Crossref 17. Weissmann A, Bowden J, Frank B, et al: Morphometric studies of the hamster flank organs: An improved model for pharmacological influences on sebaceous glands . J Invest Dermatol 1984;82:522-525.Crossref 18. Blum I, Kaufman H, Marilus R, et al: Successful treatment of polycystic ovary syndrome with spironolactone or bromocryptine . Obstet Gynecol 1981;57:661-665. 19. Kasick JM, Bergfeld WF, Steck WD, et al: Adrenal androgenic female pattern alopecia-1: Sex hormones and the balding woman . Cleve Clin Q 1983;50:111-122.Crossref 20. Wendt H, Hansan SH, Heinze I, et al: Systemic effects of local antiandrogen therapy . Arch Dermatol Res 1982;273:171. 21. Neumann F: Antiandrogene-Grundlagen und experimentelle Befunde an der Haut , in Orfanos CE: Haar und Haarkrankheiten . Stuttgart, Gustav Fischer Verlag, 1979. 22. Hammerstein J, Meckies J, Leo-Rossberg J, et al: Use of cyproterone acetate (CPA) in the treatment of acne, hirsutism and virilism . J Steroid Biochem 1975;6:827-831.Crossref 23. Hammerstein J: Antiandrogens: Basic concepts for treatment , in Orfanos CE, Montagna W, Stuttgen CT (eds): Hair Research: Status and Future Aspects . New York, Springer-Verlag Inc, 1981. 24. Sansone G, Reisner RM: Differential rates of conversion of testosterone to dihydrotestosterone in acne and in normal skin: A possible pathogenic factor in acne . J Invest Dermatol 1971;56:366-372.Crossref 25. Takayasu S, Adachi K: The conversions of testosterone to 17-β-hydroxy-5α-androstan-3-one (dihydrotestosterone) by human hair follicles . J Clin Endocrinol Metabol 1972;34:1098-1101.Crossref 26. Price VH: Testosterone metabolism in the skin: A review of its function in androgenetic alopecia, acne vulgaris, and idiopathic hirsutism including recent studies with antiandrogens . Arch Dermatol 1975;111:1496-1502.Crossref 27. Thomas JP, Oake RJ: Androgen metabolism in the skin of hirsute women . J Clin Endocrinol Metabol 1974;38:19-22.Crossref 28. Schweikert HU, Wilson JD: Regulation of human hair growth by steroid hormones: I. Testosterone metabolism in isolated hairs . J Clin Endocrinol Metabol 1974;38:811-819.Crossref 29. Takayasu S, Wakimoto H, Itami S, et al: Activity of testosterone 5-α-reductase in various tissues of human skin . J Invest Dermatol 1980;74:187-191.Crossref 30. Gomez EC, Llewellyn A, Frost P: Metabolism of testosterone-4-14C by hamster skin and flank organ . J Invest Dermatol 1974;63:383-387.Crossref 31. Mowszowicz I, Riahi M, Wright F, et al: Androgen receptor in human skin cytosol . J Clin Endocrinol Metabol 1981;52:338-344.Crossref 32. Svensson J, Snochowski M: Androgen receptor levels in preputial skin from boys with hypospadias . J Clin Endocrinol Metabol 1979;49:340-345.Crossref 33. Adachi K, Kano M: The role of receptor proteins in controlling androgen actions in the sebaceous glands of hamsters . Steroids 1972;19:567-574.Crossref 34. Adachi K: Receptor proteins for androgen in hamster sebaceous glands . J Invest Dermatol 1974;62:217-223.Crossref 35. Fichman LF, Nyberg LM, Bujnovszky P, et al: The ontogeny of the androgen receptor in human foreskin . J Clin Endocrinol Metabol 1981;52:919-923.Crossref 36. Szalay R, Krieg, M, Schmidt H, et al: Metabolism and mode of action of androgens in target tissues of male rats: V. Uptake and metabolism of cyproterone acetate and its influence on the uptake and metabolism of testosterone and 5α-dihydrotestosterone in target organs and peripheral tissues . Acta Endocrinol 1975;80:592-595. 37. Stripp B, Taylor AA, Bartter FC, et al: Effect of spironolactone on sex hormones in man . J Clin Endocrinol Metabol 1975;41:777-781.Crossref 38. Baba S, Murai M, Jitsukawa S, et al: Antiandrogenic effects of spironolactone: Hormonal and ultrastructural studies in dogs and men . J Urol 1978;119:375-380. 39. Karim A: Spironolactone: Disposition, metabolism, pharmacodynamics and bioavailability . Drug Metabol Rev 1978;8:151-188.Crossref 40. Karim A, Hribar J, Doherty M, et al: Spironolactone: Diversity in metabolic pathways . Xenobiotica 1977;7:585-600.Crossref 41. Sherry JH, O'Donnell JP, Colby HD: Conversion of spironolactone to an active metabolite in target tissues: Formation of 7α-thiospironolactone by microsomal preparations from guinea pig liver adrenals, kidneys, and testes . Life Sci 1981;29:2727-2736.Crossref 42. Ramsay L, Shelton J, Harrison I, et al: Spironolactone and potassium canrenoate in normal man . Clin Pharmacol Ther 1976;20:157-177. 43. Abshagen U, Besenfelder R, Endele R, et al: Kinetics of canrenone after single and multiple doses of spironolactone . Eur J Clin Pharmacol 1979;16:255-262.Crossref 44. Ramsay L, Asbury N, Shelton J, et al: Spironolactone and canrenoate-K: Relative potency at steady state . Clin Pharmacol Ther 1977;21:602-609. 45. Greiner JW, Rumbaugh RC, Kramer RE, et al: Relation of canrenone to the actions of spironolactone on adrenal cytochrome P-450-dependent enzymes . Endocrinology 1978;103:1313-1320.Crossref 46. Albring M, Schumann P, Okon C, et al: SH-434: A topically active inhibitor of sebum production . Arch Dermatol Res 1982; 273:170-171.
Cornell, Roger C.;Stoughton, Richard B.
doi: 10.1001/archderm.1985.01660010067020
Abstract • A large group of glucocorticosteroid formulations were assayed by the vasoconstriction test in normal skin sites and paired comparison studies in patients with psoriasis. Excellent correlation between the vasoconstriction assay and selected paired comparison studies occurred in 20 of 23 instances. In three instances, involving two glucocorticosteroid formulations tested, correlation was absent. The vasoconstrictor assay is an inexpensive and reliable method for screening glucocorticosteroid formulations for clinical activity in psoriasis. (Arch Dermatol 1985;121:63-67) References 1. McKenzie AW, Stoughton RB: Method for comparing percutaneous absorption of steroids . Arch Dermatol 1962;86:608-610.Crossref 2. Stoughton RB: Bioassay system for formulations of topically applied glucocorticosteroids . Arch Dermatol 1972;106:825-827.Crossref 3. Burdick KH: Various vagaries of vasoconstriction . Arch Dermatol 1974;110:238-242.Crossref 4. Greeson TP, Levan NE, Freedman RI, et al: Corticosteroid-induced vasoconstriction studied by xenon 133 clearance . J Invest Dermatol 1973;61:242-244.Crossref 5. Barry BS, Woodford R: Activity and bioavailability of topical steroids: In vivo/in vitro correlations for the vasoconstriction test . J Clin Pharmacol 1978;3:43-65. 6. Clanachan I, Devitt H, Foreman M, et al: The human vasoconstrictor assay for topical steroids . J Pharmacol Methods 1980;4:209-220.Crossref 7. Rampini E, Rastelli A, Cardo P, et al: Comparative study of the vasoconstrictor activity of halopredone acetate in a modified McKenzie test . Eur J Clin Pharmacol 1978;14:325-329.Crossref 8. Stoughton RB: Vasoconstrictor activity and percutaneous absorption of glucocorticosteroids . Arch Dermatol 1969;99:753-756.Crossref 9. Poulsen BJ, Burdick K, Bessler S: Paired comparison vasoconstrictor assays . Arch Dermatol 1974;109:367-371.Crossref 10. Place V, Giner-Velazquez J, Burdick K: Precise evaluation of topically applied corticosteroid potency . Arch Dermatol 1970;101:531-537.Crossref 11. Stoughton RB: Bioassay of formulation . Arch Dermatol 1970;101:161-166.Crossref 12. Stoughton RB: A perspective of topical corticosteroid therapy , in Farber E, Cox A (eds): Psoriasis . New York, Yorke Medical Books, 1976, pp 219-225. 13. Wells GC: The effect of hydrocortisone on standard skin surface trauma . Br J Dermatol 1957;69:11.Crossref
doi: 10.1001/archderm.1985.01660010072021
Abstract • While the prior application of triamcinolone acetonide to skin does not strongly influence patch test reactions, the presence of triamcinolone in the materials used for patch testing has a profound effect. Both irritant and allergic reactions to thimerosal are consistently negated when triamcinolone acetonide is present in concentrations of 0.1% and 0.025%. (Arch Dermatol 1985;121:68-69) References 1. Clark RA, Rietschel RL: 0.1% Triamcinolone acetonide ointment and patch test responses . Arch Dermatol 1982;118:163-165.Crossref 2. Dahl MV, Jordan WP Jr: Topical steroids and patch tests . Arch Dermatol 1983;119:3-4.Crossref 3. Provost TT, Jillson OF: Ethylenediamine contact dermatitis . Arch Dermatol 1967;96:231-234.Crossref 4. Fisher AA: Topical adrenal steroids and patch tests . Arch Dermatol 1983;119:956.Crossref 5. Epstein E, Maibach HI: Ethylenediamine . Arch Dermatol 1968;98:476-477.Crossref 6. Kaidbey KH, Kligman AM: Assay of topical corticosteroids . Arch Dermatol 1976;112:808-813.Crossref 7. Feldman RJ, Maibach HI: Penetration of 14C hydrocortisone through normal skin: The effect of stripping and occlusion . Arch Dermatol 1965;91:661-665.Crossref 8. Vickers CFH: Dam, reservoir, or filter . Trans St John's Hosp Dermatol Soc 1973;59:10-29.
Dahl, Mark V.;Falk, Ronald J.;Carpenter, Randall;Michael, Alfred F.
doi: 10.1001/archderm.1985.01660010074022
Abstract • The assembly of membrane attack complex (MAC) of complement implies activation of complement to the attachment of C9 and the presence of MAC on tissue suggests a possible pathogenic role for complement in disease since MAC is able to damage membranes. We examined normal skin of five patients with dermatitis herpetiformis for the presence of MAC using a monoclonal antibody (poly C9-MA) that recognizes a neoantigen of C9 that is not present on monomeric C9 but is common to both isolated MAC and to polymerized C9. Granular deposits of polymerized C9 were found at the sites of IgA deposition in the dermal papillae of normal skin from all patients. The pathologic importance of this finding is uncertain. (Arch Dermatol 1985;121:70-72) References 1. Katz SI, Strober W: The pathogenesis of dermatitis herpetiformis . J Invest Dermatol 1978;10:63-75.Crossref 2. Michel B, Milner Y, David K: Preservation of tissue-fixed immunoglobulins in skin biopsies of patients with lupus erythematosus and bullous diseases: Preliminary report . J Invest Dermatol 1973;59:449-452.Crossref 3. Dahl MV, Falk RJ, Carpenter R, et al: Deposition of the membrane attack complex of complement in bullous pemphigoid . J Invest Dermatol 1984;82:132-135.Crossref 4. Falk RJ, Dalmasso AP, Kim Y, et al: Neoantigen of the polymerized ninth component of complement: Characterization of a monoclonal antibody and immunohistochemical localization in renal disease . J Clin Invest 1983;72:560-573.Crossref 5. Van der Meer JB: Granular deposits of immunoglobulins in the skin of patients with dermatitis herpetiformis: An immunofluorescent study . Br J Dermatol 1969;81:493-503.Crossref 6. Holubar K, Doralt M, Eggerth G: Immunofluorescence patterns in dermatitis herpetiformis . Br J Dermatol 1971;85:505-510.Crossref 7. Mohammad I, Holborow EJ, Fry L, et al: Multiple immune complexes and hypocomplementaemia in dermatitis herpetiformis and coeliac disease . Lancet 1976;2:487-490.Crossref 8. Fraser NG, Beck JS, Albert-Recht F: Serum complement (C3) and immunoglobulin levels in dermatitis herpetiformis . Br J Dermatol 1971;85:314-319.Crossref 9. Provost TT, Tomasi TB Jr: Evidence for activation of complement via the alternative pathway in skin diseases: II. Dermatitis herpetiformis . Clin Immunol Immunopathol 1974;3:178-186.Crossref 10. Seah PP, Fry L, Mazaheri MR, et al: Alternate pathway complement fixation by IgA in the skin in dermatitis herpetiformis . Lancet 1973;2:175-177.Crossref 11. Katz SI, Hertz KC, Crawford PS, et al: Effect of dapsone on complement deposition in dermatitis herpetiformis and on complement-mediated guinea pig reactions . J Invest Dermatol 1976; 67:688-690.Crossref 12. Haffenden G, Wojnarowska F, Fry L: Comparison of immunoglobulin and complement deposition in multiple biopsies from the uninvolved skin in dermatitis herpetiformis . Br J Dermatol 1979;101:39-45.Crossref 13. Seah PP, Mazaheri MR, Fry L: Complement in the skin of dermatitis herpetiformis . Br J Dermatol 1973;89( (suppl) ):12. 14. Yaoita H, Katz SI: Immunoelectron microscopic localization of IgA in skin of patients with dermatitis herpetiformis . J Invest Dermatol 1976;67:502-506.Crossref 15. Stingl G, Honigsmann H, Holubar K, et al: Ultrastructural localization of immunoglobulins in dermatitis herpetiformis . J Invest Dermatol 1976;67:507-512.Crossref
Niwa, Yukie;Sakane, Tsuyoshi;Shingu, Masao;Yanagida, Ichiro;Komura, Jinro;Miyachi, Yoshiki
doi: 10.1001/archderm.1985.01660010077023
Abstract • To examine the possible correlation between tissue injury and neutrophil-produced active oxygens (AOs) in patients with linear IgA bullous dermatosis (BD), we studied the capacity of neutrophils from six patients with BD to generate AOs. Cultured endothelial cells from human umbilical-cord vein were also incubated with the patients' neutrophils to assess AO-induced tissue injury. The AO production by patients' neutrophils was significantly elevated. The patients' neutrophils, as well as those from healthy controls preincubated with patients' serum, produced significantly increased levels of cytotoxic response on coincubation with chromium 51-labeled human endothelial cells. These results suggest that the tissue damage observed in BD may be partially due to both excessive production of AOs by neutrophils and a serum factor present in the patients, and further postulate the similar pathogenic process in dermatitis herpetiformis. (Arch Dermatol 1985;121:73-78) References 1. Fridovich I: Oxygen radicals, hydrogen peroxide and oxygen toxicity , in Pryor WA (ed): Free Radicals in Biology . New York, Academic Press Inc, 1976, pp 239-251. 2. Salin ML, McCord JM: Free radicals and inflammation: Protection of phagocytosing leukocytes by superoxide dismutase . J Clin Invest 1975;56:1319-1323.Crossref 3. McCord JM, Fridovich I: The biology and pathology of oxygen radicals . Ann Intern Med 1978;89:122-127.Crossref 4. Niwa Y, Miyake S, Sakane T, et al: Autooxidative damage in Behçet's disease: Endothelial cell damage following the elevated oxygen radicals generated by stimulated neutrophils . Clin Exp Immunol 1982;49:247-255. 5. Niwa Y, Sakane T, Shingu M, et al: Effect of stimulated neutrophils from the synovial fluid of patients with rheumatoid arthritis on lymphocytes: A possible role of increased oxygen radicals generated by the neutrophils . J Clin Immunol 1983;3:228-240.Crossref 6. Sacks T, Moldow CF, Craddock PR, et al: Oxygen radicals mediate endothelial cell damage by complement-stimulated granulocytes . J Clin Invest 1978;62:1161-1167.Crossref 7. Klebanoff SJ: Antimicrobial mechanisms in neutrophilic polymorphonuclear leukocytes . Semin Hematol 1975;12:117-142. 8. Niwa Y, Sohmiya K: Enhanced neutrophilic functions in mucocutaneous lymph node syndrome (MCLS): With special reference to the possible role of increased oxygen intermediate generation in the pathogenesis of coronary thromboarteritis . J Pediatr 1984;104:56-60.Crossref 9. Boxer LA, Oliver JM, Spielberg SP, et al: Protection of granulocytes by vitamin E in glutathione synthetase deficiency . N Engl J Med 1979;301:901-905.Crossref 10. Spielberg SP, Boxer LA, Corash LM: Improved erythrocyte survival with high-dose vitamin E chronic hemolyzing G6PD and glutathione synthetase deficiencies . Ann Intern Med 1979;90:53-54.Crossref 11. Necheles TF, Maldonado N, Barquet-Chediak H: Homozygous erythrocyte glutathione-peroxidase deficiency: Clinical and biochemical studies . Blood 1969;33:164-169. 12. Skosey JL, Chow DC, Musinow S, et al: Effect of oxygen tension on human peripheral blood leukocytes . J Cell Biol 1981;88:358-363.Crossref 13. Metzger Z, Hoffeld JT, Oppenheim JJ: Macrophage-mediated suppression . J Immunol 1980;124:983-988. 14. Nishida H, Tanimoto K, Akaoka H: Effect of free radicals on the lymphocytes . Clin Immunol Immunopathol 1981;19:319-324.Crossref 15. Murray HW, Cohn ZA: Macrophage oxygen-department antimicrobial activity: I. Susceptibility of toxoplasma gondii to oxygen intermediates . J Exp Med 1979;150:938-949.Crossref 16. Murray HW, Juangbhnich CW, Nathan CF, et al: Macrophage oxygen-department antimicrobial activity: II. The role of oxygen intermediates . J Exp Med 1979;150:950-964.Crossref 17. Babior MB: Oxygen-dependent microbial killing by phagocytes . N Engl J Med 1978;298:659-668.Crossref 18. Takayama K, Noguchi T, Nakano M, et al: Reactivities of diphenylfuran (a singlet oxygen trap) with singlet oxygen and hydroxyl radical in aqueous systems . Biochem Biophys 1977;75:1052-1058.Crossref 19. Heikkila RE, Cabbat FS: Chemiluminescence from autooxidizing 6-hydroxydopamine: The involvement of activated forms of oxygen . Photochem Photobiol 1978;28:677-680.Crossref 20. Ushijima Y, Nakano M: No or little production of singlet molecular oxygen in HOCl or HOCl/H2O2. A model system for myeloperoxidase/H2O2/Cl- . Biochem Biophys 1980;93:1232-1237.Crossref 21. Chorzelski TP, Jablonska S, Beutner EH: Linear IgA bullous dermatosis , in Beutner EH, Chorzelski TP, Bean SF (eds): Immunopathology of the Skin , ed 2. New York, John Wiley & Sons Inc, 1979, pp 315-323. 22. Stendahl O, Molin L, Dahlgren C: The inhibition of polymorphonuclear leukocyte cytotoxicity by dapsone . J Clin Invest 1978;62:214-220.Crossref 23. Cornbleet T: Sulfoxone (diasone) sodium for dermatitis herpetiformis . Arch Dermatol 1951;64:684-687.Crossref 24. Sheddon IB, Wilkinson DS: Subcorneal pustular dermatosis . Br J Dermatol 1956;68:385-394.Crossref 25. MacMillan AL, Champion RH: Generalized pustular psoriasis treated with dapsone . Br J Dermatol 1973;88:183-185.Crossref 26. Winkelmann RK, Ditto WB: Cutaneous and visceral symptoms of necrotizing or `allergic' angiitis: A study of 38 cases . Medicine 1964;43:59-89.Crossref 27. Williams K, Capstick RB, Lewis DA, et al: Anti-inflammatory actions of dapsone and its related biochemistry . J Pharm Pharmacol 1976;28:555-558.Crossref 28. Ward M, McManns JPA: Dapsone in Crohn's disease . Lancet 1975;1:1236-1237.Crossref 29. Niwa Y, Sakane T, Miyachi Y: Dissociation of the inhibitory effect of dapsone on the generation of oxygen intermediates: In comparison with that of colchicine and various scavengers . Biochem Pharmacol 1984;35:2355-2360.Crossref 30. Miyachi Y, Niwa Y: Effect of potassium iodide, colchicine and dapsone on the generation of polymorphonuclear leukocytederived oxygen intermediates . Br J Dermatol 1982;107:209-214.Crossref 31. Ikai M, Imamura S: Pemphygus-like antibodies in dermatitis herpetiformis . Dermatologica 1976;152:302-308.Crossref 32. Miller DR, Kaplan HG: Decreased nitroblue tetrazolium dye reduction in the phagocytes of patients receiving prednisone . Pediatrics 1970;45:861-865. 33. Oyanagui Y: Inhibition of superoxide anion production in macrophages by anti-inflammatory drugs . Biochem Pharmacol 1976;25:1473-1480.Crossref 34. Skosey JL, Chow DC, Damgaard E, et al: Effect of cytochalasin B on the response of human polymorphonuclear leukocytes to zymosan . J Cell Biol 1973;57:237-240.Crossref 35. Skosey JL, Damgaard E, Chow DC, et al: Modification of zymosan-induced release of lysosomal enzymes from human polymorphonuclear leukocytes by cytochalasin B . J Cell Biol 1974;62:625-634.Crossref 36. Cohen PP: Suspending media for normal tissues , in Umbreit WW (ed): Monometric Techniques and Tissues Metabolism . Minneapolis, Burgess Publishing Co, 1957, pp 149-150. 37. Jaffe EA, Nachman RL, Becker CG, et al: Culture of human endothelial cells derived from umbilical veins . J Clin Invest 1973;52:2745-2756.Crossref 38. Maciag T, Hoover GA, Stemerman MB, et al: Serial propagation of human endothelial cells in vitro . J Cell Biol 1981;91:420-426.Crossref 39. Johnson AR, Erdos G: Metabolism of vasoactive peptides by human endothelial cells in culture . J Clin Invest 1977;59:684-695.Crossref 40. Hoyer LW, Santos RP, Hoyer JR: Antihemophilic factor antigen: Localization in endothelial cells by immunofluorescence microscopy . J Clin Invest 1976;52:2737-2744.Crossref 41. Jaffe EA: Endothelial cells and biology of the factor 8 . N Engl J Med 1976;296:377-383. 42. Cochrane CG: Mechanisms involved in the deposition of immune complexes in tissues . J Exp Med 1971;134( (suppl) ):75s-89s.Crossref 43. Kniker WT, Cochrane CG: The localization of immune complexes in experimental serum sickness: The role of vasoactive amines and hydrodynamic forces . J Exp Med 1968;127:119-136.Crossref 44. Weissman G, Znrier RB, Spieler PJ, et al: Mechanisms of lysosomal enzyme release from leukocytes exposed to immune complexes and other particles . J Exp Med 1971;134( (suppl) ):149s-165s. 45. Michelson AM: Oxygen radicals , in Parnham MJ, Winkelmann J (eds): Agents and Actions . Basel, Switzerland, Birkhäuser Verlag, 1982, vol 11 ( (suppl) ), pp 179-201. 46. Emerit I, Michelson AM: Mechanism of photosensitivity in systemic lupus erythematosus patients . Proc Natl Acad Sci USA 1981;78:2537-2540.Crossref 47. Cochrane CG: Immunologic tissue injury mediated by neutrophilic leukocytes . Adv Immunol 1968;9:97-162. 48. Weissman G: Lysosomal mechanisms of tissue injury in arthritis . N Engl J Med 1972;286:141-147.Crossref 49. Janoff A: At least three human neutrophil lysosomal proteases are capable of degrading joint connective tissues . Ann NY Acad Sci 1975;256:402-408.Crossref 50. Cochrane CG, Unanue ER, Dixon FJ: A role of polymorphonuclear leukocytes and complement in nephrotoxic nephritis . J Exp Med 1965;122:99-116.Crossref 51. Katz SI, Strober W: The pathogenesis of dermatitis herpetiformis . J Invest Dermatol 1978;70:63-75.Crossref
Moy, Larry S.;Tan, Elaine M. L.;Holness, Ronald;Uitto, Jouni
doi: 10.1001/archderm.1985.01660010083024
Abstract • Phenytoin has been proposed for the treatment of certain dermatologic conditions involving connective tissue abnormalities. To understand the biochemical basis of connective tissue changes, we incubated human skin fibroblasts in culture with varying concentrations of phenytoin. The results indicated that fibroblast proliferation, detected by tritiated thymidine incorporation into cells, was slightly stimulated when short incubation periods and low concentrations of phenytoin were employed. However, with longer incubation times and higher phenytoin concentrations, a significant reduction in fibroblast proliferation was observed. Further studies demonstrated that incubation of cells with phenytoin did not affect the production of procollagen, measured as synthesis of radioactive hydroxyproline in the cultures. However, assay of prolyl hydroxylase, an enzyme participating in the post-translational synthesis of hydroxyproline during collagen biosynthesis, was significantly reduced in the fibroblast cultures. The activity of collagenase, an enzyme participating in degradation of collagen, was markedly decreased in cultures treated with phenytoin. Thus, phenytoin may modulate collagen metabolism primarily by affecting the degradation of collagen. The results support previous suggestions that phenytoin may be useful for treatment of patients with increased levels of collagenase, such as in recessive dystrophic epidermolysis bullosa. (Arch Dermatol 1985;121:79-83) References 1. Klar L: Gingival hyperplasia during Dilantin therapy: A survey of 321 patients . J Public Health Dent 1973;33:180-185.Crossref 2. Ziskin DE, Stowe LR, Zegarelli EV: Dilantin hyperplastic gingivitis: Its cause and treatment: Differential appraisal . Am J Orthod 1941;27:350-363. 3. Hassell TM, Page RC, Lindhe J: Histologic evidence for impaired growth control in diphenylhydantoin gingival overgrowth in man . Arch Oral Biol 1978;23:381-384.Crossref 4. Eisenberg M, Stekeus LH, Schofield PJ: Epidermolysis bullosa: New therapeutic approaches . Australas J Dermatol 1978;19: 1-8.Crossref 5. Bauer EA, Cooper TW, Tucker DR, et al: Phenytoin effects on recessive dystrophic epidermolysis bullosa . N Engl J Med 1980;303:776-781.Crossref 6. Bauer EA, Gedde-Dahl T, Eisen AZ: The role of human skin collagenase in epidermolysis bullosa . J Invest Dermatol 1977; 68:119-124.Crossref 7. Bauer EA, Eisen AZ: Recessive dystrophic epidermolysis bullosa: Evidence for increased collagenase as a genetic characteristic in cell culture . J Exp Med 1978;148:1378-1387.Crossref 8. Morgan RJ: Scleroderma: Treatment with diphenylhydantoin . Cutis 1971;8:278-282. 9. Neldner KH: Treatment of localized linear scleroderma with phenytoin . Cutis 1978;22:569-572. 10. Moy LS, Tan EML, Holness R, et al: Effects of phenytoin on collagen metabolism and growth of skin fibroblasts in culture . Clin Res 1983;31:22A. 11. Benveniste K, Bitar M: Effects of phenytoin on cultured human gingival fibroblasts , in Hassell TM, Johnston MC, Dudley KH (eds): Phenytoin-Induced Teratology and Gingival Pathology . New York, Raven Press, 1980, pp 199-213. 12. Booth BA, Polak KL, Uitto J: Collagen biosynthesis by human skin fibroblasts: I. Optimization of the culture conditions for synthesis of type I and type III procollagens . Biochim Biophys Acta 1980;607:145-160.Crossref 13. Juva K, Prockop DJ: Modified procedure for the assay of H3or C14-labeled hydroxyproline . Anal Biochem 1966;15:77-83.Crossref 14. Booth BA, Uitto J: Collagen biosynthesis by human skin fibroblasts: III. The effects of ascorbic acid on procollagen production and prolyl hydroxylase activity . Biochim Biophys Acta 1981;675:117-122.Crossref 15. Bauer EA, Stricklin GP, Jeffrey JJ, et al: Collagenase production by human skin fibroblasts . Biochem Biophys Res Commun 1975;64:232-240.Crossref 16. Ryhänen L, Rantala-Ryhänen S, Tan EML, et al: Assay of collagenase activity by a rapid, sensitive, and specific method . Coll Relat Res 1982;2:117-130.Crossref 17. Bieth J, Spiess B, Wermuth CG: The synthesis and analytical use of a highly sensitive and convenient substrate of elastase . Biochem Med 1974;11:350-357.Crossref 18. Bourdillon MC, Brechemier D, Blaes M, et al: Elastase-like enzymes in skin fibroblasts and rat aorta smooth muscle cells . Cell Biol Int Rep 1980;4:313-320.Crossref 19. Oikarinen AI, Palatsi R, Adomian GE, et al: Anetoderma: Biochemical and ultrastructural demonstration of an elastin defect in the skin of three patients . J Am Acad Dermatol 1984;11:64-72.Crossref 20. Giro MG, Oikarinen AI, Oikarinen H, et al: Demonstration of elastin gene expression in human skin fibroblast cultures and reduced tropoelastin production by cells from a patient with atrophoderma . J Clin Invest , in press. 21. Burton K: A study of the conditions and mechanisms of diphenylamine reaction for the colorimetric estimation of deoxyribonucleic acid . Biochem J 1956;62:315-323. 22. Lowry OH, Rosebrough NJ, Farr AL, et al: Protein measurement with the Folin phenol reagent . J Biol Chem 1951;193:265-275. 23. Kantor ML, Hassell TM: Increased accumulation of sulfated glycosaminoglycans in cultures of human fibroblasts from phenytoin-induced gingival overgrowth . J Dent Res 1983;62:383-387.Crossref 24. Bergenholtz A, Hänström L: The effect of diphenylhydantoin upon the biosynthesis and degradation of collagen in cat palatal mucosa in organ culture . Biochem Pharmacol 1979;28:2653-2659.Crossref 25. Goultschin J, Shoshan S: Inhibition of collagen breakdown by diphenylhydantoin . Biochim Biophys Acta 1980;631:188-191.Crossref 26. Prockop DJ, Berg RA, Kivirikko KI, et al: Intracellular steps in the biosynthesis of collagen , in Ramachandran GN, Reddi AH (eds): Biochemistry of Collagen . New York, Plenum Publishing Corp, 1976, pp 163-273. 27. Murad S, Sivarajah A, Pinnell SR: Regulation of prolyl and lysyl hydroxylase activities in cultured human skin fibroblasts by ascorbic acid . Biochem Biophys Res Commun 1981;101:868-875.Crossref 28. Liu TZ, Bhatnagar RS: Inhibition of protocollagen proline hydroxylase by dilantin . Proc Soc Exp Biol Med 1973;142:253-255.Crossref 29. Prockop DJ, Juva K: Synthesis of hydroxyproline in vitro by the hydroxylation of proline in a precursor of collagen . Proc Natl Acad Sci USA 1965;53:661-668.Crossref 30. Hassell TM, Page RC, Narayanan AS, et al: Diphenylhydantoin (Dilantin) gingival hyperplasia: Drug-induced abnormality of connective tissue . Proc Natl Acad Sci USA 1976;73:2909-2912.Crossref 31. Hassell TM: Epilepsy and the Oral Manifestations of Phenytoin Therapy . Basel, Switzerland, S Kanger AG, 1981. 32. Kasai S, Hachimine K: Effect of 5,5-diphenylhydantoin sodium on the synthesis of collagen by some fibroblastic cell lines including gingiva derived cells . Bull Tokyo Dent Coll 1974;15:53-62. 33. Blumenkrantz N, Asboe-Hansen G: Effect of diphenylhydantoin on connective tissue . Acta Neurol Scand 1974;50:302-306.Crossref
Kamiński, Marek;Pawińska, Maria;Jablonska, Stefania;Szmurło, Andrzej;Majewski, Sławomir;Orth, Gerard
doi: 10.1001/archderm.1985.01660010088025pmid: 2981519
Abstract • Six patients with epidermodysplasia verruciformis (EV) were studied for natural killer cell (NKC) cytotoxic response of their peripheral blood mononuclear cells against K-562 target cells in an 18-hour chromium 51-release assay. Four patients displayed higher cytotoxic responses than controls did, whereas two others did not differ from controls. Patients with EV who had increased NKC activity were found to be infected with potentially oncogenic human papillomaviruses (types 5, 8, 9, 14, 17, 19, 22, 24, and others), and they have had multiple skin carcinomas and/or Bowen's precancerous dermatosis. Two patients with EV who had normal cytotoxic response were free of skin malignancies. (Arch Dermatol 1985;121:84-86) References 1. Orth G, Jabłońska S, Favre M, et al: Characterization of two types of human papillomaviruses in lesions of epidermodysplasia verruciformis . Proc Natl Acad Sci USA 1978;75:1537-1541.Crossref 2. Orth G, Favre M, Breitburd F, et al: Epidermodysplasia verruciformis: A model for the role of papillomaviruses in human cancer , in Essex M, Todaro M, zur Hausen H (eds): Virus in Naturally Occurring Cancers . Cold Spring Harbor, NY, Cold Spring Harbor Laboratory, 1980, vol A, pp 259-282. 3. Jablonska S, Da̧browski J, Jakubowicz K: Epidermodysplasia verruciformis as a model in studies on the role of papovaviruses in oncogenesis . Cancer Res 1972;32:583-589. 4. Glinski W, Jablonska S, Langner A, et al: Cell mediated immunity in epidermodysplasia verruciformis . Dermatologica 1976;153:218-227.Crossref 5. Gliński W, Obalek S, Jabłońska S, et al: T-cell defect in patients with epidermodysplasia verruciformis due to human papillomavirus type 3 and 5 . Dermatologica 1981;162:141-147.Crossref 6. Prawer SE, Pass F, Vance J, et al: Depressed immune function in epidermodysplasia verruciformis . Arch Dermatol 1977;113:495-499.Crossref 7. Claudy AL, Touraine JL, Mitanne A: Epidermodysplasia verruciformis induced by a new human papillomavirus (HPV-8) . Arch Dermatol Res 1982;274:213-219.Crossref 8. Jabłońska S, Orth G, Lutzner MA: Immunopathology of papillomavirus-induced tumors in different tissues . Semin Immunopathol 1982;5:33-62. 9. Roder JC, Pross HF: The biology of the human natural killer cell . J Clin Immunol 1982;2:249-263.Crossref 10. Goldfarb RH, Herberman RB: Characteristics of natural killer cells as possible mechanisms for their cytotoxic activity , in: Weissman G (ed): Advances in Inflammation Research . New York, Raven Press, 1982, vol 4, pp 45-72. 11. Tilden AB, Abo T, Balck CM: Suppressor cell function of human granular lymphocytes identified by the HNK-1 (Leu 7) monoclonal antibody . J Immunol 1983;130:1171-1175. 12. Bloom N, Minato N, Neighbour A, et al: Interferon and NK cells in resistance of persistently virus-infected cells and tumors , in Herberman RB (ed): Natural Cell-Mediated Immunity Against Tumors . New York, Academic Press Inc, 1980, pp 505-524. 13. Flad HD, Betzler M, Scholz W, et al: Modulation of NK cell activity in patients with solid malignancies by surgical tumor reduction and fibroblast interferon . Human Cancer Immunol 1982;4:115-204. 14. Orth G, Jablonska S, Obałek S, et al: Epidermodysplasia verruciformis (EV): A rare and puzzling disease . Read before the European Molecular Biology Organization Workshop on Papillomaviruses, Örenas, Sweden, July 27-30, 1983 . 15. Kremsdorf D, Jablonska S, Favre M, et al: Biochemical characterization of two types of human papillomaviruses associated with epidermodysplasia verruciformis . J Virol 1982;43:436-447. 16. Kremsdorf D, Jablonska S, Favre M, et al: Human papillomaviruses associated with epidermodysplasia verruciformis: II. Molecular cloning and biochemical characterization of HPV-3a, HPV-8, and HPV-12 genomes . J Virol 1983. 17. Jablonska S, Orth G, Jarza̧bek-Chorzelska M, et al: Epidermodysplasia verruciformis versus disseminated verrucae planae: Is epidermodysplasia verruciformis a generalized infection with wart virus? J Invest Dermatol 1979;72:114-119.Crossref 18. Tsokos GC, Rook AH, Djeu JY, et al: Natural killer cells and interferon response in patients with systemic lupus erythematosus . Clin Exp Immunol 1982;50:239-245. 19. Katz P, Zaytoun AM, Lee JH Jr, et al: Abnormal natural killer cell activity in systemic lupus erythematosus: An intrinsic defect in the lytic event . J Immunol 1982;129:1966-1971. 20. Kamiński MJ, Nowaczyk M, Skopińska-Różewska E, et al: Human peripheral blood lymphocyte subpopulations isolated on the basis of their affinity for SRBC differ in angiogenesis-inducing capability . Clin Exp Immunol 1981;46:237-331. 21. Kozlowski S, Hirsen DJ, Jackson EJ: Comparison of natural killing with antibody dependent cell mediated cytotoxicity in patients with systemic lupus erythematosus . J Rheumatol 1982; 9:59-62. 22. Huddlestone JR, Meringan TC, Oldstone MBA: Induction and kinetics of natural killer cells in humans . Nature 1979;282:417.Crossref 23. Einhorn S: Enhancement of human NK activity by interferon: In vivo and in vitro studies , in Herberman RB (ed): Natural Cell-Mediated Immunity Against Tumors . New York, Academic Press Inc, 1980, p 529. 24. Orth G, Jablonska S, Jarzabek-Chorzelska M, et al: Characteristics of the lesions and risk of malignant conversion associated with the type of human papillomavirus involvement in epidermodysplasia verruciformis . Cancer Res 1979;39:1074-1082. 25. Herberman RB (ed): Natural Cell-Mediated Immunity Against Tumors . New York, Academic Press Inc, 1980.
Connelly, Marcus G.;Winkelmann, R. K.
doi: 10.1001/archderm.1985.01660010091026
Abstract • Persistent solid edema of the face in four healthy young adults seemed to be secondary to preexisting acne vulgaris. Elastic compression and intensive acne therapy were of minimal benefit in resolving the edema. Facial inflammation accompanying acne should be recognized as a rare complication of the acne process. (Arch Dermatol 1985;121:87-90) References 1. Plewig G, Klingman AM: Acne: Morphogenesis and Treatment . New York, Springer-Verlag Inc, 1975. 2. Frank SB: Acne: Update for the Practitioner . New York, Yorke Medical Books, 1979. 3. Hornstein OP: Differentialdiagnose dermatogener Wangenschwellungen . HNO 1979;27:129-137. 4. Gorlin RJ, Pindborg JJ, Cohen MM Jr: Syndromes of the Head and Neck , ed 2. New York, McGraw-Hill Book Co, 1976. 5. Merklen FP, Cottenot F, Pennec J, et al: Infiltration massive persistante du front avec fort oedème palpébral . Bull Soc Fr Dermatol Syphiligr 1972;79:221-222. 6. O'Leary PA: Localized solid edema of the extremities in association with exophthalmic goiter . Arch Dermatol Syphilol 1930;21:57-70.Crossref 7. Hornstein OP: Melkersson-Rosenthal syndrome: A neuromuco-cutaneous disease of complex origin . Curr Probl Dermatol 1973;5:117-156. 8. Strauss JS: Sebaceous glands , in Fitzpatrick TB, Eisen AZ, Wolff K, et al (eds): Dermatology in General Medicine , ed 2. New York, McGraw-Hill Book Co, 1979, pp 437-458. 9. Juergens JL, Lofgren KA: Chronic venous insufficiency (postphlebitic syndrome, chronic venous stasis) , in Juergens JL, Spittell JA Jr, Fairbairn JF II (eds): Allen-Barker-Hines Peripheral Vascular Diseases , ed 5. Philadelphia, WB Saunders Co, 1980, pp 809-821.
doi: 10.1001/archderm.1985.01660010094027
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 entitled "Progressive Cutaneous Herpes Simplex Infection in Acute Myeloblastic Leukemia," published in the July Archives (1984;120:922-926), Amichai Schattner, MD, should be included in the by-line.
McAuley, Diane;Miller, Robert A.
doi: 10.1001/archderm.1985.01660010095028
Abstract • Several reports of acne fulminans (acute febrile ulcerative acne) have described associated musculoskeletal manifestations. We report herein a case of this rare disorder that occurred simultaneously with the onset of Crohn's disease. (Arch Dermatol 1985;121:91-93) References 1. Burns RE, Colville JM: Acne conglobata with septicemia . Arch Dermatol 1959;79:361-363.Crossref 2. Goldschmidt H, Leyden J, Stein KH: Acne fulminans . Arch Dermatol 1977;113:444-449.Crossref 3. Kelly AP, Burns RE: Acute febrile ulcerative conglobata acne with polyarthralgia . Arch Dermatol 1971;104:182-187.Crossref 4. Kirsner JB: The idiopathic inflammatory bowel disease . Arch Dermatol 1982;118:280-282.Crossref 5. Levine N, Bangert J: Cutaneous granulomatosis in Crohn's disease . Arch Dermatol 1982;1006-1009.
VanHale, Harriet M.;Rogers, Roy S.;Zone, John J.;Greipp, Philip R.
doi: 10.1001/archderm.1985.01660010098029
Abstract • Pyostomatitis vegetans is a rarely occurring disorder of the oral mucosa, which has a dramatic clinical picture and a striking histopathologic pattern. Moreover, the condition is a highly specific oral mucosal marker for inflammatory bowel disease, particularly ulcerative colitis. Our findings in two cases and a review of the literature emphasize the relationship of pyostomatitis vegetans to inflammatory bowel disease and the vegetating dermatoses. (Arch Dermatol 1985;121:94-98) References 1. Hallopeau H: `Pyodermite végétante," ihre Beziehungen zur Dermatitis herpetiformis und dem Pemphigus vegetans . Arch Dermatol Syph 1898;43:289-306.Crossref 2. Wallhauser HJF: Dermatitis vegetans: Report of two cases of the Hallopeau type . Arch Dermatol 1929;19:77-88. 3. Goldsmith WN: A case of pyodermite végétante (Hallopeau) . Br J Dermatol 1941;53:299-318.Crossref 4. McCarthy FP: Pyostomatitis vegetans: Report of three cases . Arch Dermatol 1949;60:750-764. 5. Hays MA: Pyostomatitis vegetans: Report of a case . Oral Surg 1961;14:1053-1056.Crossref 6. Margoles JS, Wenger J: Stomal ulceration associated with pyoderma gangrenosum and chronic ulcerative colitis . Gastroenterology 1961;41:594-598. 7. Zegarelli EV, Kutscher AH: Oral `pyoderma': Report of two cases . Dig Dis Sci 1962;7:281-288.Crossref 8. Marks JM: Ulcerative colitis with pyodermite végétante . Proc R Soc Med 1962;55:1072-1073. 9. McCarthy P, Shklar G: A syndrome of pyostomatitis vegetans and ulcerative colitis . Arch Dermatol 1963;88:913-919.Crossref 10. Forman L: Two cases of pyodermite végétante (Hallopeau): An eosinophilic pustular and vegetating dermatitis with conjunctival, oral and colonic involvement . Proc R Soc Med 1965;58:244-249. 11. Naish JM, Batchvarov BD, Lawoyin VL: A case of ulcerative colitis and pyostomatitis vegetans in an African . Gut 1970;11:38-40.Crossref 12. Hornstein O: Zur Kenntnis der pyo-(rhino-) stomatitis vegetans . Arch Klin Exp Dermatol 1957;205:357-372.Crossref 13. Cataldo E, Covino MC, Tesone PE: Pyostomatitis vegetans . Oral Surg 1981;52:172-177.Crossref 14. Kelley ML Jr: Skin lesions associated with chronic ulcerative colitis . Dig Dis Sci 1962;7:255-272.Crossref 15. Lever WF, Schaumberg-Lever G: Histopathology of the Skin , ed 6. Philadelphia, JB Lippincott Publishers, 1983, pp 109-110, 294. 16. Su WP, Duncan SC, Perry HO: Blastomycosis-like pyoderma . Arch Dermatol 1979;115:170-173.Crossref 17. Ledermann R: Ein Fall von Pyodermite végétante . Berl Klin Wochenschr 1905;42:146-150. 18. Leydhecker W, Lund O-E: Augenbeteiligung bei Pyostomatitis vegetans . Klin Monatsbl Augenheilkd 1962;141:595-602.
Marshall, M. Ernest;Hatfield, Stephanie T.;Hatfield, Danny R.
doi: 10.1001/archderm.1985.01660010103030
Abstract • A patient whose condition was initially misdiagnosed as Kaposi's sarcoma involving the left foot received radiation therapy for that disorder. Subsequent examination yielded a correct diagnosis of arteriovenous (AV) malformation. Such cases of AV malformations with skin changes resembling Kaposi's sarcoma have been called pseudo-Kaposi's sarcoma. The clinicopathologic distinctions between Kaposi's sarcoma and pseudo-Kaposi's lesions are discussed. All patients suspected of having Kaposi's sarcoma, especially those younger than 30 years of age, should have careful evaluation for an unsuspected AV malformation. (Arch Dermatol 1985;121:99-101) References 1. Coursley G, Ivins JC, Barker NW: Congenital arteriovenous fistulas in the extremities: An analysis of 69 cases . Angiology 1956;7:201-217.Crossref 2. Waterson KW Jr, Shapiro L, Dannenberg M: Developmental arteriovenous malformation with secondary angiodermatitis . Arch Dermatol 1969;100:297-302.Crossref 3. Bluefarb SM, Adams LA: Arteriovenous malformation with angiodermatitis: Stasis dermatitis simulating Kaposi's disease . Arch Dermatol 1967;96:176-181.Crossref 4. Mali JWH, Kuiper JP, Hamers AA: Acroangiodermatitis of the foot . Arch Dermatol 1965;92:515-518.Crossref 5. Earhart RN, Aeling JA, Nuss DD, et al: Pseudo-Kaposi sarcoma: A patient with arteriovenous malformation and skin lesions simulating Kaposi's sarcoma . Arch Dermatol 1974;110:907-910.Crossref 6. Brenner S, Ophir J, Krakowski A, et al: Kaposi-like arteriovenous malformation and angiodermatitis (pseudo-Kaposi) . Cutis 1982;30:240-256. 7. Delaney JP: Congenital arteriovenous fistulae of the extremities . Minn Med 1961;44:160-166. 8. Lawton RL, Tidrick RT, Brintnall ES: A clinicopathologic study of multiple congenital arteriovenous fistulae of the lower extremities . Angiology 1957;8:161-169.Crossref
Levine, Lawrence E.;Medenica, Maria M.;Lorincz, Allan L.;Soltani, Keyoumars;Raab, Benjamin;Ma, Alice
doi: 10.1001/archderm.1985.01660010106031
Abstract • A distinctive acral erythema developed in four patients with myelogenous leukemia, subsequent to blood transfusions and intensive chemotherapy with cytarabine. The clinical and histopathologic features of the eruption were suggestive of a drug-induced toxic eruption. To our knowledge, only one previous similar case has been reported in the literature. For patients in whom this self-limited condition develops, reassurance should serve as the mainstay of therapy. (Arch Dermatol 1985;121:102-104) References 1. Burgdorf WHC, Gilmore WA, Ganick RG: Peculiar acral erythema secondary to high-dose chemotherapy for acute myelogenous leukemia . Ann Intern Med 1982;97:61-62.Crossref
Hoshaw, Richard A.;Zimmerman, Kent G.;Menter, Alan
doi: 10.1001/archderm.1985.01660010109032
Abstract • Two patients had pitch-black pigmentation and colloid milium formation following the use of 2% hydroquinone-containing bleaching creams. These are among the first known cases in American blacks, although this phenomenon has been recognized previously in African blacks. Ultrastructural studies indicated that the pigment was due to the formation of elastotic fibers. These fibers attained an enormous size and disintegrated, leaving irregular fibers and fragments dispersed in the dermis. It is important that this clinical picture be recognized, since the use of these bleaching creams is widespread. (Arch Dermatol 1985;121:105-108) References 1. Virchow R: Ein fall von allgemeiner Ochronoses der Knorpel und knorphelähnlichen Theile . Arch Path Anat 1866;37:212. 2. Zannoni VG, et al: Studies on ochronosis: II. Studies on benzoquinoneacetic acid, a probable intermediate in the connective tissue pigmentation of alcaptonuria . Arthritis Rheum 1962; 5:547-556. 3. Pick L: Über die Ochronose . Klin Wochenschr 1906;43:478. 4. Thomas AE, Gisburn MA: Exogenous ochronosis and myxoedema from resorcinol . Br J Dermatol 1961;73:378-381. 5. Woolley PB: Exogenous ochronosis . Br Med J 1952;2:760-761. 6. Findlay GH, Morrison JGL, Simson IW: Exogenous ochronosis and pigmented colloid milium from hydroquinone bleaching creams . Br J Dermatol 1975;93:613-622. 7. Cullison D, Abele DC, O'Quinn JL: Localized exogenous ochronosis . J Am Acad Dermatol 1983;6:882-889. 8. McDowell EM: Fixation and processing , in Trump BF, Jones RT (eds): Diagnostic Electron Microscopy . New York, John Wiley & Sons Inc, 1978, vol 1, p 118. 9. Spurr AR: A low viscosity epoxy resin embedding medium for electron microscopy . J Ultrastruct Res 1969;26:31-43. 10. Findlay GH, DeBeer HA: Chronic hydroquinone poisoning of the skin from skin-lightening cosmetics . S Afr Med J 1980; 57:187-190. 11. Bazex A, Dupré A: L'ochronose est-elle une maladie du tissu conjuctif? Ann Dermatol Syph 1962;89:723. 12. Friderich H, Nikolowski W: Endogene ochronose . Arch Dermatol Syph 1951;192:273. 13. Teller H, Winkler K: Zur Klinik und Histopathologie der endogenen Ochronose . Hautarzt 1973;24:537-545. 14. Tsuji T, Hamada T: Elastotic material and elastic fibers in aged skin: An ultrastructural study with conventional and tannic acid stain . Acta Derm Venereol 1981;61:93-100. 15. Mitchell RE: Chronic solar dermatosis: A light and electron microscopic study of the dermis . J Invest Dermatol 1967;48:203-220. 16. Nürnberger F, et al: Actinic elastosis in black skin: A light and electron microscopic study . Arch Dermatol Res 1978;262:7-14. 17. Lichtenstein L, Kaplan L: Hereditary ochronosis . Am J Pathol 1954;30:99-125. 18. Kutty MK, Igbal QM, Teh EC: Ochronotic arthropathy . Arch Pathol 1974;98:55-57. 19. Findlay GH: Ochronosis following skin bleaching with hydroquinone . J Am Acad Dermatol 1982;6:1092-1093. 20. O'Donoghue MN, Lynfield YL, Derbes V: Ochronosis due to hydroquinone . J Am Acad Dermatol 1983;1:123.
doi: 10.1001/archderm.1985.01660010113033
Abstract • Brown-black reticular pigmentation developed on the face and neck of a man. This was associated with severe seborrhea and the formation of multiple epithelial cysts on the trunk. We propose the term pigmentatio reticularis faciei et colli with multiple epithelial cysts as a suitable title for this disorder, and we hypothesize that these skin changes in this disorder are of nevoid origin. One similar case has been reported as "lentiginosis senilis" in the Japanese literature. (Arch Dermatol 1985;121:109-111) References 1. Hasegawa S, Mukai H, Katsuoka N, et al: Lentiginosis senilis . Hifubyoh-Shinryoh 1980;2:499-502. 2. Arai H: Nevoid basal cell epithelioma syndrome . Jpn J Clin Dermatol 1976;30:131-139. 3. Kitamura K, Akamatsu S, Hirokawa K: Eine besondere Form der Akropigmentation: `Acropigmentatio reticularis.' Hautarzt 1953;4:152-156. 4. Shono S, Toda K: The effect of fatty acids on tyrosinase activity , in Seiji M (ed): Pigment Cell: Phenotypic Expression in Pigment Cells . Tokyo, University of Tokyo Press, 1981, pp 263-268. 5. Mishima Y, Rudner E: Erythromelanosis follicularis faciei et colli . Dermatologica 1966;132:269-287.Crossref 6. Jung EG: `Das pigmentierte Xerodermoid': Ein Defect der Rekombinations-Erholung von UV-Schäden . Arch Dermatol Res 1971;241:33-43.Crossref
Hebert, Adelaide A.;Jorizzo, Joseph L.;Schoen, Irwin;Graham, Gary;Weiss, Gary
doi: 10.1001/archderm.1985.01660010116034
Abstract • A 42-year-old man had idiopathic lipemic tears and massive seborrhea. Recent investigations have shown that cholesterol and other lipids occasionally found in tears are produced by meibomian rather than lacrimal glands. The finding in this patient of hypersecretion by both sebaceous glands and meibomian glands, a sebaceous gland variant, suggests that a common mechanism may regulate secretory control of both of these glands. (Arch Dermatol 1985;121:112-114) References 1. Van Haeringen NJ, Glasius E: Cholesterol in human tear fluid . Exp Eye Res 1975;20:271-274.Crossref 2. Montagna W, Ford DM: Histology and cytochemistry of human skin: XXXIII. The eyelid . Arch Dermatol 1969;100:328-335.Crossref 3. Landthaler M, Kummermehr J, Wagner A, et al: Inhibitory effects of 13-cis retinoic acid on human sebaceous glands . Arch Dermatol Res 1980;269:279-309. 4. Russell WG, Page DL, Hough AJ, et al: Sebaceous carcinoma of meibomian gland origin: The diagnostic importance of pagetoid spread of neoplastic cells . Am J Clin Pathol 1980;73:504-511. 5. Perry HD, Seiniuk RA: Conservative treatment of chalazia . Ophthalmology 1980;87:218-221.Crossref 6. Henriquez AS, Korb DR: Meibomian glands and contact lens wear . Br J Ophthalmol 1981;65:108-111.Crossref 7. Lempert SL, Jenkins MS, Brown SI: Chalazia and rosacea . Arch Ophthalmol 1979;97:1652-1653.Crossref 8. Nicolaides N, Kaitaranta JK, Rawdah TN, et al: Meibomian gland studies: Comparison of steer and human lipids . Invest Ophthalmol Vis Sci 1981;20:522-536. 9. Jester JV, Nicholaides N, Smith RE: Meibomian gland studies: Histologic and ultrastructural investigations . Invest Ophthalmol Vis Sci 1981;20:537-547. 10. Doughman D: Corneal physiology , in Peyman GA (ed): Principles and Practice of Ophthalmology . Philadelphia, WB Saunders Co, 1980, pp 356-390. 11. Pochi PE, Strauss JS: Endocrinologic control of the development and activity of the human sebaceous gland . J Invest Dermatol 1974;62:191-201.Crossref 12. Cunliffe WJ: Acne vulgaris: Pathogenesis and treatment . Br Med J 1980;280:1394-1396.Crossref
Fenske, Neil A.;Lober, Clifford W.;Pautler, Scott E.
doi: 10.1001/archderm.1985.01660010119035
Abstract † The successful treatment of congenital bullous urticaria pigmentosa was accomplished by the concomitant use of H1- and H2-receptor antagonists. (Arch Dermatol 1985;121:115-118) References 1. Robinson HM, Kile RL, Hitch JM, et al: Bullous urticaria pigmentosa . Arch Dermatol 1962;85:86-94.Crossref 2. Klaus SN, Winkelmann RK: Course of urticaria pigmentosa in children . Arch Dermatol 1962;86:116-119.Crossref 3. Allison J: Skin mastocytosis presenting as a neonatal bullous eruption . Aust J Dermatol 1967;9:83-85.Crossref 4. Davis RJ, Waisman M: Urticaria pigmentosa: Report of a case with autopsy examination . Arch Dermatol 1959;79:649-650.Crossref 5. Lipschutz A, Shaffer B: Urticaria pigmentosa . J Pediatr 1951;39:745-749.Crossref 6. Little EG: A contribution to the study of urticaria pigmentosa . Br J Dermatol 1905;17:355-373. 7. Baart de la Faille H, Uitterdijk D: Cutaneous mastocytosis . Br J Dermatol 1979;101:223-224. 8. Nettleship E: Rare forms of urticaria . Br Med J 1869;2:323-324.Crossref 9. Dewar WA, Milne JA: Bullous urticaria pigmentosa: Summary of literature and report of two cases . Arch Dermatol 1955;71:717-721.Crossref 10. Bloom G, Duner H, Pernow B, et al: Spontaneous histamine shocks in urticaria pigmentosa . Acta Pediatr 1958;47:152-162.Crossref 11. Herxheimer A: Urticaria pigmentosa with attacks of flushing . Br J Dermatol 1958;70:427. 12. Black JW, Duncan WAM, Durant CJ, et al: Definition and antagonism of histamine H2 receptors . Nature 1972;236:385-390.Crossref 13. Greaves MW, Marks R, Robertson I: Subclasses of histamine receptors on human skin blood vessels and their possible clinical significance . Br J Clin Pharmacol 1977;4:657.Crossref 14. Lichtenstein LM, Gillespie E: The effects of the H1 and H2 antihistamines on `allergic' histamine release and its inhibition by histamine . J Pharmacol Exp Ther 1975;192:441-450. 15. Greaves MW: H2 receptor antagonists and delayed hypersensitivity . Lancet 1978;1:880-881.Crossref 16. Francis D, Greaves MW, Yamamota S: Enzymatic histamine degradation by human skin . Br J Pharmacol 1977;60:583-587.Crossref 17. Matthews CNA, Boss JM, Warin RP, et al: The effect of H1 and H2 histamine antagonists on symptomatic dermographism . Br J Dermatol 1979;101:57-61.Crossref 18. Bredefeldt JE, O'Laughlin JC, Durham JB, et al: Malabsorption and gastric hyperacidity in systemic mastocytosis . Am J Gastroenterol 1980;74:133-137. 19. Johnson GJ, Silvis SE, Roitman B, et al: Long-term treatment of systemic mastocytosis with histamine H2 receptor antagonists . Am J Gastroenterol 1980;74:485-489. 20. Hirschowitz BI, Groarke JF: Effect of cimetidine on gastric hypersecretion and diarrhea in systemic mastocytosis . Ann Intern Med 1979;90:769-771.Crossref 21. Gerrard JW, Ko C: Urticaria pigmentosa: Treatment with cimetidine and chlorpheniramine . J Pediatr 1979;94:843-844.Crossref 22. Riley JF: Mast cells and anaphylaxis . Lancet 1964;1:1155-1157.Crossref 23. Demis DJ, Walton MD, Wooley D, et al: Further studies of histidine and histamine metabolism in urticaria pigmentosa . J Invest Dermatol 1961;37:513-521.Crossref 24. Hagen P, Lee FL: Amino acid decarboxylases of mouse mast cells . J Physiol 1958;143:7. 25. Birt AR, Nickerson M: Generalized flushing of skin with urticaria pigmentosa . Arch Dermatol 1959;80:311-317.Crossref 26. Szweda JA, Abraham JP, Fine G, et al: Systemic mast cell disease . Am J Med 1962;32:227-239.Crossref 27. McKee WD, Cochrane CG, Farr RS: A clinical study of an unusual case of asthma associated with urticaria pigmentosa . J Allergy 1966;37:38-47.Crossref 28. Demis DJ: The mastocytosis syndrome: Clinical and biological studies . Ann Intern Med 1963;59:194-206.Crossref 29. Gonnella JS: Mast cell disease . Prog Clin Cancer 1967;3:281-293.
Montes, Leopoldo F.;Wilborn, Walter H.
doi: 10.1001/archderm.1985.01660010123036
Abstract † Candidiasis and its causative agent, Candida albicans, have been under continuous study in our clinics and laboratories for the past 20 years. Cultured cells of C albicans and tissues from natural and experimental infections were used for observations by light microscopy, transmission electron microscopy, scanning electron microscopy and freeze fracture techniques. In cultures, the cells of C albicans revealed a more complex cell wall, plasma membrane, intracellular organelles, and biochemical organization than those described in classic textbooks on mycology. In infected tissues, noteworthy characteristics of C albicans were prominent vacuoles and invasion of host cells with subsequent intracellular localization and lysis of tissues surrounding the fungus. These findings are discussed in relation to their importance in the pathogenesis and management of candidiasis and to the mechanism of action of anticandida agents. (Arch Dermatol 1985;121:119-124) References 1. Montes LF, Patrick TA, Martin S, et al: Ultrastructure of blastospores of Candida albicans after permanganate fixation . J Invest Dermatol 1965;45:227-232.Crossref 2. Montes LF, Wilborn WH: Ultrastructural features of hostparasite relationship in oral candidiasis . J Bacteriol 1968;96:1349-1356. 3. Mizuno N, Montes LF: Oxidative enzymes in Candida albicans . Sabouraudia 1966;5:46-51.Crossref 4. Montes LF, Wilborn WH: Acid phosphatase activity during phases of growth in Candida albicans . Int J Dermatol 1970;9:220-225.Crossref 5. Montes LF, Constantine VS: Cytochemical demonstration of aminopeptidase in Candida albicans . J Invest Dermatol 1968; 51:1-3.Crossref 6. Montes LF: Fungi and fungal infection , in Zelickson AS (ed): Ultrastructure of Normal and Abnormal Skin . Philadelphia, Lea & Febiger, 1967, pp 347-364. 7. Wilborn WH, Montes LF, Lyons RE, et al: Ultrastructural basis for the assay of topical acne treatments: Transmission and scanning electron microscopy of untreated comedones . J Cutaneous Pathol 1978;5:165-183.Crossref 8. Wilborn WH, Montes LF: Ultrastructure of fungal-host relationship in kidneys of experimental candidiasis , in Symposium on Fungal Infections . Springfield, Ill, Charles C Thomas Publisher, 1974. 9. Conant NF, Smith DT, Baker RD, et al: Manual of Clinical Mycology . Philadelphia, WB Saunders Co, 1971. 10. Baker BL, Montes LF: Histochemical changes in the skin following local application of cortisol and prednisolone . Anat Rec 1961;139:133-143.Crossref 11. Biempica L, Montes LF: Secretory epithelium of the large axillary sweat glands: A cytochemical and electron microscopic study . Am J Anat 1965;117:47-72.Crossref 12. Chattaway FW, Odds FC, Barlow AJE: An examination of the production of hydrolytic enzymes and toxins by pathogenic strains of Candida albicans . J Gen Microbiol 1971;67:255-263.Crossref 13. Braun PC, Calderone RA: Chitin synthesis in Candida albicans: Comparison of yeast and hyphal forms . J Bacteriol 1978;133:1472-1477. 14. Braun PC, Calderone RA: Regulation and solubilization of Candida albicans synthetase . J Bacteriol 1979;140:666-670. 15. Orlean AB: (1,3)-β-D-glucan synthase from budding and filamentous cultures of the dimorphic fungus Candida albicans . Eur J Biochem 1982;127:397-403.Crossref 16. Matile PH, Moor H, Robinow CF: Yeast cytology , in The Yeasts . New York, Academic Press, 1969. 17. Scherwitz C, Martin R, Weberberg H: Ultrastructural investigations of the formation of Candida albicans germ tubes and septa . Sabouraudia 1978;16:115-124.Crossref 18. Djaczenko W, Cassone A: Visualization of new ultrastructural components in the cell wall of Candida albicans with fixatives containing TAPO . J Cell Biol 1971;52:186-190.Crossref 19. Müller J, Takamiya H, Jaeger R: Elektronenmikroskopische Darstellung von Immunreaktionen and Candida-Zellen: Asteroid Bodies bei Candida albicans im Urin von Nephritis-Patienten . Sabouraudia 1977;15:87-93.Crossref 20. Müller J, Douchet C, Sakuma S: Electronmicroscopic studies on the host-parasite relations of the experimental Candida albicans infection of the mouse: The Candida granuloma in the kidney . Proceedings of the Second International Special Symposium on Yeasts , Tokyo, 1978. 21. Howlett JA, Squier CA: Candida albicans ultrastructure: Colonization and invasion of oral epithelium . Infect Immun 1980;29:253-260. 22. Müller J, Douchet C, Sakuma S: Elektronenmikroskopische Untersuchungen zur Wirt-Parasit-Auseinandersetzung bei der experimentellen Candida-Infekter Maus: Ion Singulare Candida-Zellen im Nierengewebe . Dermatol Monatsschr 1973;159:327-330. 23. Müller J: Immunobiological aspects of Candida mycoses: A review of electron microscopic studies . Mykosen 1978;21:289-297. 24. Montes LF, Pittillo RF, Hunt D, et al: Microbial flora of infant's skin: Comparison of types of microorganisms between normal skin and diaper dermatitis . Arch Dermatol 1971;103:400-406.Crossref 25. Wilborn WH, Montes LF: Scanning electron microscopy of oral lesions in chronic mucocutaneous candidiasis . JAMA 1980; 144:2294-2297.Crossref 26. Kaufman L: Laboratory diagnosis of candidiasis . Microbiology , 1981, pp 205-209.
Levin, L. Stefan;Witbeck, Ernest
doi: 10.1001/archderm.1985.01660010129037
Abstract REPORT OF A CASE A 55-year-old man, on routine oral examination, had a blue, raised, soft-tissue lesion on the crest of the right anterior mandibular alveolar ridge (Fig 1). The region was edentulous; the teeth had been extracted previously for unknown reasons. When the patient closed his mouth, the right maxillary lateral incisor traumatized the lesion. The patient had a history of maturity-onset diabetes mellitus and congestive heart failure. His diabetes was complicated by retinopathy, peripheral neuropathy, and gangrene of his toes, which required a below-the-knee leg amputation. The oral lesion was excised with the patient under local anesthesia, and it was submitted for microscopic examination. At the same time, the remaining teeth were removed because of periodontal disease.On microscopic examination, the specimen was covered with nonulcerated stratified squamous epithelium (Figs 2 and 3). In the center of the specimen, separated from the epithelium by a zone of dense References 1. Eversole LR, Rovin S: Reactive lesions of the gingiva . J Oral Pat Pathol 1972;1:30-38.Crossref 2. Bhaskar SN, Jacoway JR: Pyogenic granuloma—Clinical features, incidence, histology, and result of treatment: Report of 242 cases . Oral Surg 1966;24:391-398. 3. Phillips RL, Shafer WG: An evaluation of the peripheral giant cell tumor . J Periodontol 1955;26:216-222. 4. Giansanti JS, Waldron CA: Peripheral giant cell granuloma: Review of 720 cases . Oral Surg 1969;27:787-791. 5. Shafer WG, Hine MK, Levy BM: A Textbook of Oral Pathology , ed 3. Philadelphia, WB Saunders Co, 1983. 6. Sapp JP: Ultrastructure and histogenesis of peripheral giant cell reparative granuloma of the jaws . Cancer 1972;30:1119-1129.Crossref 7. Waldron CA, Shafer WG: The central giant cell reparative granuloma of the jaws: An analysis of 38 cases . Amer J Clin Pathol 1966;45:437-447. 8. Rosenberg EH, Guralnick WC: Hyperparathyroidism: A review of 220 proved cases, with special emphasis on findings in the jaws . Oral Surg 1962;15( (suppl 2) ):84-94.
doi: 10.1001/archderm.1985.01660010131038
Abstract REPORT OF A CASE A 33-year-old man was admitted to the hospital for evaluation of a seizure disorder, when he was noted to have multiple lesions on his face. A lesion had first developed on the left side of his nose when he was six years old. Since that time, many similar asymptomatic lesions had gradually appeared on his face. There was no family history of skin disorders.Physical examination revealed numerous individual and confluent, round, flesh-colored, papules and nodules distributed symmetrically over the forehead, nose, nasolabial folds, chin, and external ears (Figs 1 through 3). Telangiectases were present on the surface of some of the lesions, but none was ulcerated. Additional findings of the cutaneous examination were normal. A biopsy of one of the facial lesions was performed, and representative histologic sections are shown in Figs 4 and 5.What is your diagnosis? QUESTIONS For each of the following multiple-choice questions References 1. Brooke HG: Epithelioma adenoides cysticum . Br J Dermatol 1892;4:269-286. 2. Fordyce JA: Multiple benign cystic epithelioma of the skin . J Cutan Dis 1892;10:459-473. 3. Zeligman I: Solitary trichoepithelioma . Arch Dermatol 1960; 82:35-40.Crossref 4. Anderson DE, Howell JB: Epithelioma adenoides cysticum: Genetic update . Br J Dermatol 1976;95:225-232.Crossref 5. Gray HR, Helwig EB: Epithelioma adenoides cysticum and solitary trichoepithelioma . Arch Dermatol 1963;87:102-114.Crossref
doi: 10.1001/archderm.1985.01660010133039
Abstract REPORT OF A CASE A 38-year-old woman was seen with a 12-year history of sudden and recurrent swelling of the lips and perioral skin. The edema lasted from days to weeks, generally worsening during the course of the day and sometimes impeding speech.The patient was unaware of any allergies or provoking agents. She was otherwise healthy and was taking no medications. No family member had a similar condition.Physical examination revealed indurated erythematous edema of the lips and face (Fig 1). The tongue was fissured. Results of a neurologic examination and an examination of the gums, teeth, and mucous membranes were normal.The chest roentgenogram was normal, as were the results of laboratory studies, including the complete blood cell count, ESR, liver function tests, and serum electrolytes.A labial biopsy specimen showed a patchy perivascular lymphohistiocytic and plasma cell infiltrate throughout the submucosa (Fig 2) and an occasional epithelioid References 1. Miescher G: Cheilitis et Pareitis granulomatosa ohne Facialisparese bei Vorhandensein einer Lingua scrotalis . Dermatologica 1956;112:536-541. 2. Alexander RW, James RB: Melkersson-Rosenthal syndrome: Review of literature and report of case . Oral Surg 1972;30:599-604. 3. Worsaae N, Christensen KC, Schiodt M, et al: Melkersson-Rosenthal syndrome and cheilitis granulomatosa . Oral Surg 1982; 54:404-413.Crossref 4. Carr RD: Is the Melkersson-Rosenthal syndrome hereditary? Arch Dermatol 1966;93:426-427.Crossref 5. Roseman B, Mulvihill JJ: Melkersson-Rosenthal syndrome in a 7-year-old girl . Pediatrics 1978;61:490-491.Crossref 6. Worsaae N, Pindborg JJ: Granulomatous gingival manifestations of Melkersson-Rosenthal syndrome . Oral Surg 1980;49:131-138.Crossref 7. Hornstein OP: Melkersson-Rosenthal syndrome: A neuromucocutaneous disease of complex origin . Curr Probl Dermatol 1973;5:117-156. 8. Mulvihill JJ, Eckman WW, Fraumeni JF Jr, et al: Melkersson-Rosenthal syndrome, Hodgkin disease, and corneal keratopathy . Arch Intern Med 1973;132:116-117.Crossref 9. Worsaae N, Christensen KC, Bondeson S, et al: Melkersson-Rosenthal syndrome and Crohn's disease . Oral Surg 1980;18:254-258.Crossref 10. Scott GA: Observations on Melkersson's syndrome . Postgrad Med 1968;44:447.Crossref 11. Madanes AE, Farber M: Danazol . Ann Intern Med 1982;96:625-630.Crossref
doi: 10.1001/archderm.1985.01660010137041
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 The fourth edition of Lehrbuch der Hautkrankheiten und venerischen Infektionen (Textbook on Skin Diseases and Venereal Infections) by Professor Theodor Nasemann was published in 1981. Fundamentals of Dermatology is an American revised translation by Walter C. H. Burgdorf, MD, of the University of Oklahoma, Oklahoma City. Burgdorf believed that both students and nondermatologic physicians in the United States would find it a useful primer for the study of cutaneous diseases. The six months he spent as a guest physician at a skin clinic in Frankfurt, Germany, directed by Nasemann optimally qualifies him for this task. To the original text, Burgdorf has added chapters on tropical dermatology and cutaneous surgery, the latter is authored by Roland G. Wheeland, MD, also of the University of Oklahoma. Throughout the book, dermatologic therapy is adapted to American practice. To enlarge the scope of treatment for the various skin conditions, Burgdorf composed an appendix called
doi: 10.1001/archderm.1985.01660010137040
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 soft-cover book was written in response to the frustration felt by residents when they are first exposed to the bewildering field of dermatopathology. Unlike most textbooks, Primer of Dermatopathology is organized by anatomic location and pattern of pathologic change, so that changes observed via microscopy can be easily matched with the proper chapter. To use this book, the reader first examines a microscopic slide, using a low power objective, to identify the site of major pathologic change. Using this information, the findings are matched with one of five sections organized by location of pathologic change: epidermis, basement membrane, dermis, appendages, and panniculus. After examining the slide more carefully to detect additional changes, such as the composition of the cellular infiltrate, the correct diagnosis is further narrowed to one of the 25 chapters. Each chapter is in outline form, with the information organized into three vertical columns. The first column
doi: 10.1001/archderm.1985.01660010146042
This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables.