doi: 10.1001/archderm.1995.01690180004001
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.1995.01690180019002
Abstract IN THE United States, gonorrhea is an important cause of urethritis in men and cervicitis in women; reproductive complications include infertility and ectopic pregnancy. During 1981-1993, the annual incidence rate of gonorrhea in Minnesota declined; the average annual change in the rate of infection was -8.5%. However, in 1994, the incidence rate increased 32% (from 56 cases per 100,000 persons in 1993 to 74 cases per 100,000 in 1994). No corresponding increases occurred in rates of other reportable sexually transmitted diseases (STDs), including chlamydial infection and early syphilis. To elucidate possible explanations for the increased rate of gonorrhea in Minnesota in 1994, the Minnesota Department of Health (MDH) analyzed surveillance data for 1994 and compared it with data for 1993. This report presents the findings of the analysis. In 1994, a total of 3346 gonorrhea cases* were reported to MDH, compared with 2543 cases in 1993. From 1993 to 1994, References 1. CDC. 1993 Sexually transmitted diseases treatment guidelines . MMWR 1993;42(no. (RR-14) ). 2. Laga M, Manoka A, Kivuvu M, et al. Nonulcerative sexually transmitted diseases as risk factors for HIV-1 transmission in women: results from a cohort study . AIDS 1993;7:95-102.Crossref 3. Wasserheit JN. Epidemiological synergy: interrelationships between human immunodeficiency virus infection and other sexually transmitted diseases . Sex Transm Dis 1992;19:61-77.Crossref 4. CDC. Sexually transmitted disease surveillance, 1993 . Atlanta: US Department of Health and Human Services, Public Health Service, CDC, (December) 1994. 5. Piot P, Islam MQ. Sexually transmitted diseases in the 1990s: global epidemiology and challenges for control . Sex Transm Dis 1994;21 ( (suppl 2) ):S7-S13. 6. CDC. Premarital sexual experience among adolescent women-United States, 1970-1988 . MMWR 1991;39:929-32. 7. CDC. Decreased susceptibility of Neisseria gonorrhoeae to fluoroquinolones—Ohio and Hawaii, 1992-1994 . MMWR 1994;43:325-7.
Hoss, Diane M.;Feder, Henry M.
doi: 10.1001/archderm.1995.01690180021003
Abstract REPORT OF A CASE A 33-year-old man presented to the University of Connecticut Health Center, Farmington, because of recurrent ''boils'' on his face. During the prior 5 years, Staphylococcus aureus, susceptible to cloxacillin and cephalexin, was recovered from the boils. He received multiple courses of oral antibiotics, but facial ''boils'' continued to develop, both while receiving and not receiving therapy. When first seen, the patient had two facial furuncles. Treatment with cloxacillin (250 mg four times daily), topical chlorhexidine washes, and nightly applications of intranasal mupirocin ointment was effective initially, but the lesions recurred while he was still receiving this therapy. The oral antibiotic was changed to cephalexin (500 mg twice daily). Despite this therapy, new facial furuncles developed over the next several months. THERAPEUTIC CHALLENGE Treatment of persistent or recurrent furunculosis caused by S aureus. SOLUTION Cephalexin therapy (500 mg twice daily) was continued, and rifampin therapy (300 mg References 1. Tulloch LG, Alder VG, Gillespie WA. Treatment of chronic furunculosis . BMJ. 1960;2:354-356.Crossref 2. Copeman PWM. Treatment of recurrent styes . Lancet. 1958;2:728-729.Crossref 3. Hobbs BC, Carruthers HL, Gough J. Sycosis barbae . Lancet. 1947;2:572-574.Crossref 4. Wheat LJ, Kohler RB, White A. Treatment of nasal carriers of coagulasepositive staphylococci . In: Maibach H, Aly R, eds. Skin Microbiology: Relevance to Clinical Infection . New York, NY: Springer-Verlag NY Inc; 1981:50-58. 5. Wheat LJ, Kohler RB, White A. Prevention of infections of skin and skin structures . Am J Med. 1984;76:187-190.Crossref 6. Doebbeling BN, Breneman DL, Neu HC, et al. Elimination of Staphylococcus aureus nasal carriage in health care workers: analysis of six clinical trials with calcium mupirocin ointment . Clin Infect Dis. 1993;17:466-474.Crossref 7. Wheat LJ, Kohler RB, Luft FC, White A. Long-term studies of the effect of rifampin on nasal carriage of coagulase-positive staphylococci . Rev Infect Dis. 1983;5( (suppl) ):s459-s462.Crossref 8. Tsankov NK, Kamarasher JA. Rifampin in dermatology . Int J Dermatol. 1993; 32:401-406.Crossref 9. Kapusnik JE, Parenti F, Sande MA. The use of rifampicin in staphylococcal infections: a review . J Antimicrob Chemother. 1984;13( (suppl C) ):61-66.Crossref 10. Traczewski MM, Goldman DA, Murphy P. In vitro activity of rifampin in combination with oxacillin against Staphylococcus aureus . Antimicrob Agents Chemother. 1983;23:571-576.Crossref 11. Hoeprich PD. Prediction of antimeningococcic chemo-prophylactic efficacy . J Infect Dis. 1971;123:125-133.Crossref 12. Farr B, Mandell GL. Rifampin . Med Clin North Am. 1982;66:157-165. 13. Grosset J, Leventis S. Adverse effects of rifampin . Rev Infect Dis 1983;5( (suppl) ): 440-444.Crossref
doi: 10.1001/archderm.1995.01690180025004
Abstract To be held in London, August 4th to 8th, inclusive, 1896. REGULATIONS. All duly qualified medical men, British or foreign, or others interested in science invited by the council, who shall have paid the fee of one pound sterling,* and who shall have enrolled themselves, shall be members of the congress and entitled to the volume of Transactions.J Cutan Genito-Urin Dis.June 1895;13:266-267.First, the good news: In 1895 £1 sterling equaled $5; in 1995 it takes only $1.50 to buy £1 British.Next, the not-so-good news: Although 100 years ago $1 was worth 4 German marks, in 1995 $1 is only worth 1.5 deutsche marks. Still, in 1895 $1 was worth only 5 Italian lire, and nowadays $1 will get you more than 1600 lire!Now, the bad news: $1 in 1895 would be worth 18 cents today.
doi: 10.1001/archderm.1995.01690180034005
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 ''IgE-Mediated Hypersensitivity and Contact Sensitivity to Multiple Environmental Allergens in Atopic Dermatitis'' that appeared in the November 1994 issue of the Archives (1994;130:1393-1401), there were errors in Figure 3, on page 1396, and Figures 4 and 5, on page 1399. In Figure 3, the x-axis should have read ''Patch Test.'' In Figure 4, the key in the figure should have appeared as follows: the dark gray box should have keyed ''AD + ARD [atopic dermatitis with allergic respiratory disease],'' and the light gray box should have keyed ''Pure AD [pure atopic dermatitis].'' In Figure 5, the key in the figure should have appeared as follows: the dark gray box should have keyed ''AD [atopic dermatitis],'' and the light gray box should have keyed ''HC [healthy age-matched control subjects].''
Zelickson, Brian;Matsumura, Kunie;Kist, David;Epstein, Ervin H.;Bart, Bruce J.
doi: 10.1001/archderm.1995.01690180037006
Abstract Background and Design: Bart's syndrome, originally described in a large family in 1966, consists of congenital localized absence of skin, blistering, and associated nail abnormalities. Since then, several descriptions of patients with similar clinical findings have suggested that this syndrome may represent any of the three subtypes of epidermolysis bullosa: epidermal, junctional, or dermal. Because no histologic or ultrastructural studies were done in Bart's kindred, and neither immunohistologic nor genetic linkage technology was available at that time, classification of the syndrome has been unclear. We report the findings of clinical, ultrastructural, immunohistologic, and genetic linkage studies of the original kindred and their descendants. We contacted original family members and their descendants by telephone and questionnaire. Skin biopsy specimens adjacent to blisters were obtained for ultrastructural and immunochemical analysis. Blood samples were drawn from affected members and their spouses and children for genetic linkage studies. Results: The clinical findings seen in the descendants of the original family with Bart's syndrome were similar to those described in 1966. We did, however, detect persistence of blistering into adult life and mild atrophic scarring and milia formation at sites of blistering in some family members, a finding not noted in the original study. Hypertrophic scarring and albopapuloid lesions were not detected. Ultrastructural analysis of skin from affected family members showed poorly formed anchoring fibrils and cleavage below the lamina densa. Immunohistochemical staining localized type IV collagen at the roof of blistered skin. Staining for type VII collagen was found to have a normal distribution in nonblistered skin. Genetic linkage studies mapped the gene for the disease in this family to chromosome 3p at or near the site of the gene encoding type VII collagen. Conclusion: Bart's syndrome is a subtype of dominantly inherited dystrophic epidermolysis bullosa.(Arch Dermatol. 1995;131:663-668) References 1. Bart BJ, Gorlin RJ, Anderson VE, Lynch FW. Congenital localized absence of skin and associated abnormalities resembling epidermolysis bullosa: a new syndrome . Arch Dermatol. 1966;93:296-304.Crossref 2. Bonifas JM, Rothman AL, Epstein EH Jr. Epidermolysis bullosa simplex: evidence in two families for keratin gene abnormalities . Science. 1991;254:1202-1205.Crossref 3. Hall JM, Friedman L, Guenther C, et al. Closing in on a breast cancer gene on chromosome 17q . Am J Hum Genet. 1992;50:1235-1242. 4. Christiano AM, Chung-Honet LC, Hovnanian A, Uitto J. PCR-based detection of two exonic polymorphisms in the human type VII collagen gene (COL7A1) at 3p21.1 . Genomics. 1992;14:827-828.Crossref 5. Ott J. Analysis of Human Genetic Linkage . rev ed. Baltimore, Md: Johns Hopkins University Press; 1992. 6. Olaisen B, Gedde-Dahl T Jr. GPT-epidermolysis bullosa simplex (EBS Ogna) linkage in man . Hum Hered. 1973;23:189-196.Crossref 7. Weissenbach J, Gyapay G, Dib C, et al. A second-generation linkage map of the human genome . Nature. 1992;359:794-801.Crossref 8. Frieden IJ. Aplasia cutis congenita . J Am Acad Dermatol. 1986;14:646-660.Crossref 9. Fine JD, Bauer EA, Briggaman RA, et al. Revised clinical and laboratory criteria for subtypes of inherited epidermolysis bullosa . J Am Acad Dermatol. 1991; 24:119-135.Crossref 10. Epstein EH Jr. Molecular genetics of epidermolysis bullosa . Science. 1992; 256:799-803.Crossref 11. Marinkovich MP. The molecular genetics of basement membrane diseases . Arch Dermatol. 1993;129:1557-1565.Crossref 12. Hovnanian A. The molecular genetics of dystrophic epidermolysis bullosa . Arch Dermatol. 1993;129:1566-1570.Crossref 13. Leigh IM, Lane EB. Mutations in the genes for epidermal keratins in epidermolysis bullosa and epidermolytic hyperkeratosis . Arch Dermatol. 1993;129: 1571-1577.Crossref 14. Smith LT. Ultrastructural findings in epidermolysis bullosa . Arch Dermatol. 1993; 129:1578-1584.Crossref 15. Bart BJ. Epidermolysis bullosa and congenital localized absence of skin . Arch Dermatol. 1970;101:78-81.Crossref 16. Smith SZ, Cram DL. A mechanobullous disease of the newborn: Bart's syndrome . Arch Dermatol. 1978;114:81-84.Crossref 17. Kanzler MH, Smoller B, Woodley DT. Congenital localized absence of the skin as a manifestation of epidermolysis bullosa . Arch Dermatol. 1992;128:1087-1090.Crossref 18. Skoven I, Drzewiecki KT. Congenital localized skin defect and epidermolysis bullosa hereditaria letalis . Acta Derm Venereol (Stockh) . 1979;59:533-537. 19. Wojnarowska FT, Eady RAJ, Wells RS. Dystrophic epidermolysis bullosa presenting with congenital localized absence of skin: report of four cases . Br J Dermatol. 1983; 108:477-483.Crossref 20. Bouwes Bavinck JN, Van Haeringen A, Ruiter D, Van der Schroeff JG. Autosomal dominant epidermolysis bullosa dystrophica . Clin Genet. 1987;31:416-424.Crossref 21. Joensen HD. Epidermolysis bullosa dystrophica dominans in two families in the Faroe Islands . Acta Derm Venereol (Stockh) . 1973;53:53-60. 22. Butler DF, Berger TG, James WD, Smith TL, Stanley JR, Rodman OG. Bart's syndrome: microscopic, ultrastructural and immunofluorescent mapping features . Pediatr Dermatol. 1986;3:113-118.Crossref 23. Gruis NA, Bouwes Bavinck JN, Steijlen PM, et al. Genetic linkage between the collagen VII (COL7A1) gene and the autosomal dominant form of dystrophic epidermolysis bullosa in two Dutch kindreds . J Invest Dermatol. 1992;99:528-530.Crossref
Guibal, Fabien;Bastuji-Garin, Sylvie;Chosidow, Olivier;Saiag, Philippe;Revuz, Jean;Roujeau, Jean-Claude
doi: 10.1001/archderm.1995.01690180043007
Abstract Background and Design: The usefulness of steroid therapy in toxic epidermal necrolysis (TEN) remains controversial. Up to 5% of the TEN cases occur in patients who undergo long-term steroid therapy. We, thus, looked for the potential effect of long-term glucocorticosteroid therapy before the onset of TEN on altering the progression of the disease. The records of 179 patients were reviewed. The characteristics of the 13 patients who were undergoing long-term glucocorticosteroid therapy were compared with those of 166 other patients with TEN. The following parameters were studied: age, mortality, delay between the introduction of the suspect drug and the onset of TEN, length of hospital stay, body surface area involved, time elapsed between the first symptom of TEN and hospital admission, number of medications taken by the patients before the onset of TEN, lymphocyte count, granulocyte count, platelet count, glycemia, serum aspartate aminotransferase level, and total disease duration. Results: Patients who were undergoing long-term glucocorticosteroid therapy differed from other patients with TEN in the administration of more drugs, longer delay between the introduction of the suspect drug and the onset of TEN, and a longer time elapsed between the first symptom of TEN and hospital admission. We observed no differences for the other parameters that were studied. Conclusion: Our study shows that long-term steroid therapy may delay the onset of TEN, but it does not hall its progression.(Arch Dermatol. 1995;131:669-672) References 1. Roujeau JC, Chosidow O, Saiag P, et al. Toxic epidermal necrolysis (Lyell syndrome) . J Am Acad Dermatol. 1990;23:1039-1058.Crossref 2. Revuz J, Penso D, Roujeau JC. Toxic epidermal necrolysis: clinical findings and prognosis factors in 87 patients . Arch Dermatol. 1987;123:1160-1165.Crossref 3. Avakian R, Flowers FP, Araujo OE, et al. Toxic epidermal necrolysis: a review . J Am Acad Dermatol. 1991;25:69-79.Crossref 4. Parsons JM. Toxic epidermal necrolysis . Int J Dermatol. 1992;31:749-768.Crossref 5. Rzany B, Schmitt H, Schöpf E. Toxic epidermal necrolysis in patients receiving glucocorticosteroids . Acta Derm Venereol (Stockh). 1991;71:171-172. 6. Jones WG, Halebian P, Madden M, et al. Drug-induced toxic epidermal necrolysis in children . J Pediatr Surg. 1989;24:167-170.Crossref 7. Heimbach DM. Engrav LH, Marvin JA, et al. Toxic epidermal necrolysis: a step forward in treatment . JAMA. 1987;257:2171-2175.Crossref 8. Okano M, Kitano Y, lgarashi T. Toxic epidermal necrolysis due to rifampicin . J Am Acad Dermatol. 1987;17:303-304.Crossref 9. Garabiol B, Touraine R. Syndrome de Lyell de l'adulte: éléments de pronostic et déductions thérapeutiques: étude de 27 cas . Ann Med Intern (Paris). 1976; 127:670-672. 10. Halebian PH, Corder VJ. Madden MR. et al. Improved burn center survival of patients with toxic epidermal necrolysis managed without corticosteroids . Ann Surg. 1986;204:503-512.Crossref 11. Kim PS, Goldfarb IW, Gaisford JC, et al. Stevens-Johnson syndrome and toxic epidermal necrolysis: a pathophysiologic review with recommendations for a treatment protocol . J Burn Care Rehabil. 1983;4:91-100.Crossref 12. Bastuji-Garin S, Rzany B, Stern RS, et al. A clinical classification of cases of toxic epidermal necrolysis, Stevens-Johnson syndrome, and erythema multiforme . Arch Dermatol. 1993;129:92-96.Crossref 13. Roujeau JC. The spectrum of Stevens-Johnson syndrome and toxic epidermal necrolysis: a clinical classification . J Invest Dermatol. 1994;102:28S-30S.Crossref 14. Roujeau JC, Guillaume JC, Fabre JP, et al. Toxic epidermal necrolysis (Lyell syndrome) . Arch Dermatol. 1990;126:37-42.Crossref 15. Williams GH, Dluhy RG. Diseases of the adrenal cortex . In: Braunwald E, lsselbacher KJ, Petersdorf RG, et al, eds. Harrison's Principles of Internal Medicine . New York, NY: McGraw-Hill International Book Co; 1991:1753-1774. 16. Moore N, Biour M, Paux G, et al. Adverse drug reaction monitoring: doing it the French way . Lancet. 1985;2:1056-1058.Crossref 17. Kaufman DW. Kelly JP, Levy M, Shapiro S. The drug etiology of agranulocytosis and aplastic anemia . In: Monographs in Epidemiology and Biostatistics . New York, NY: Oxford University Press; 1991;18:260-261. 18. Miyauchi H, Hosokawa H, Akaeda T, et al. T-cell subsets in drug-induced toxic epidermal necrolysis . Arch Dermatol. 1991;127:851-855.Crossref 19. Bagot M, Charue D, Heslan M, et al. Impaired antigen presentation in toxic epidermal necrolysis . Arch Dermatol. 1993;129:721-727.Crossref 20. Merot Y, Saurat JH. Clues to the pathogenesis of toxic epidermal necrolysis . Int J Dermatol. 1985;24:165-168.Crossref 21. Simons HN. Acute life-threatening dermatologic disorders . Med Clin North Am. 1981;65:227-243. 22. Renfro L, Grant-Kels JM, Feder HM, et al. Controversy: are systemic steroids indicated in the treatment of erythema multiforme? Pediatr Dermatol. 1989;6: 43-50.Crossref 23. Weston WL, Oranje AP, Rasmussen JE, et al. Corticosteroids for erythema multiforme? Pediatr Dermatol. 1989;6:229-250.Crossref
Buechner, Stanislaw A.;Lautenschlager, Stephan;Itin, Peter;Bircher, Andreas;Erb, Peter
doi: 10.1001/archderm.1995.01690180047008
Abstract Background and Design: Specific humoral and cell-mediated immune responses play an important role in the pathogenesis of Lyme borreliosis. Several previous studies demonstrated that a specific cellular immune response to Borrelia burgdorferi can occur independently of a diagnostic humoral response. Little is known about T-cell reactivities against B burgdorferi in early and late cutaneous manifestations of Lyme borreliosis. We studied the lymphoproliferative response of peripheral blood mononuclear cells to B burgdorferi antigen from 99 patients (25 with erythema migrans, 16 with acrodermatitis chronica atrophicans, 13 with lymphadenosis benigna cutis, and 45 with localized scleroderma) and 21 control subjects. The results are expressed as a stimulation index (SI) (mean count per minute of triplicate cultures with stimulant divided by mean count per minute without stimulant). The serum samples from all patients and control subjects were tested for antibodies to B burgdorferi by indirect immunofluorescence assay. Results: The 21 healthy seronegative controls had an SI of 3.3±2.0 (mean±SD). Compared with that of control subjects, the SIs were significantly elevated in patients with erythema migrans (9.8±9.1), acrodermatitis chronica atrophicans (11.8±8.2), and lymphadenosisbenigna cutis (7.2±6.2). The 45 patients with localized scleroderma had elevated proliferative responses, with an SI of 6.5±7.3, but these responses did not significantly differ from those of controls. Elevated titers of antibodies to B burgdorferi were present in six (24%) of 25 patients with erythema migrans, five (38%) of 13 patients with lymphadenosis benigna cutis, and 13 (29%) of 45 patients with localized scleroderma. All 16 patients with acrodermatitis chronica atrophicans had markedly elevated antibody titers. Conclusions: Our findings show that a significant lymphoproliferative response to B burgdorferi occurs in the majority of patients with cutaneous manifestations of Lyme borreliosis. The lymphocyte proliferation assay may be of diagnostic value in patients in whom Lyme borreliosis is strongly clinically suspected and who have nondiagnostic levels of antibodies against B burgdorferi.(Arch Dermatol. 1995;131:673-677) References 1. Asbrink E, Hovmark A. Cutaneous manifestations in Ixodes-borne Borrelia spirochetosis . Int J Dermatol. 1987;26:215-223.Crossref 2. Malane MS, Grant-Kels JM, Feder HM, Luger SW. Diagnosis of Lyme disease based on dermatologic manifestations . Ann Intern Med. 1991;114:490-498.Crossref 3. Asbrink E, Olsson I, Hovmark A. Clinical manifestations of erythema chronicum migrans Afzelius in Sweden: a study on 231 patients . Zentralbl Bakteriol Mikrobiol Hyg A. 1986;263:229-236. 4. Asbrink E, Olsson I. Clinical manifestations of erythema chronicum migrans Afzelius in 161 patients . Acta Derm Venereol (Stockh). 1985;65:43-52. 5. Hovmark A, Asbrink E, Olsson I. The spirochetal etiology of lymphadenosis benigna cutis solitaria . Acta Derm Venereol (Stockh). 1986;66:479-484. 6. Abele DC, Anders KH. The many faces and phases of borreliosis, I: Lyme disease . J Am Acad Dermatol. 1990;23:167-186.Crossref 7. Abele DC, Anders KH. The many faces and phases of borreliosis, II . J Am Acad Dermatol. 1990;23:401-410.Crossref 8. Asbrink E, Hovmark A. Lyme borreliosis: aspects of tick-borne Borrelia burgdorferiinfection from a dermatologic viewpoint . Semin Dermatol. 1990;9:277-291. 9. Strle F, Pleterski-Rigler D, Stanek G, Pejovnik-Pustinek A, Ruzic E, Cimperman J. Solitary borrelial lymphocytoma: report of 36 cases . Infection. 1992;20:201-206.Crossref 10. Asbrink E, Hovmark A, Olsson I. Clinical manifestations of acrodermatitis chronica atrophicans in 50 Swedish patients . Zentralbl Bakteriol Mikrobiol Hyg A. 1986; 263:253-261. 11. Aberer E, Stanek G, Ertl M, et al. Evidence for spirochetal origin of circumscribed scleroderma (morphea) . Acta Derm Venereol (Stockh). 1987;67:225-231. 12. Aberer E, Neumann R, Stanek G. Is localized scleroderma a Borrelia infection? Lancet. 1985;2:278.Crossref 13. Buechner SA, Winkelmann RK, Lautenschlager S, Gilli L, Rufli T. Localized scleroderma associated with Borrelia burgdorferi infection: clinical, histologic, and immunohistochemical observations . J Am Acad Dermatol. 1993;29:190-196.Crossref 14. Aberer E, Klade H, Stanek G, Gebhart W. Borrelia burgdorferi and different types of morphea . Dermatologica. 1991;182:145-154.Crossref 15. Schempp C, Bocklage H, Lange R, Kölmel HW, Orfanos CE, Gollnick H. Further evidence for Borrelia burgdorferi infection in morphea and lichen sclerosus et atrophicus confirmed by DNA amplification . J Invest Dermatol. 1993; 100:717-720.Crossref 16. Sigal LH. Immunopathogenesis of Lyme borreliosis . Clin Dermatol. 1993;11: 415-422.Crossref 17. Hansen K. Laboratory diagnostic methods in Lyme borreliosis . Clin Dermatol. 1993;11:407-414.Crossref 18. Dattwyler RJ, Volkman DJ, Luft BJ, Halperin JJ, Thomas J, Golightly MG. Seronegative Lyme disease: dissociation of specific Tand B-lymphocyte responses to Borrelia burgdorferi . N Engl J Med. 1988;319:1441-1446.Crossref 19. Dattwyler RJ, Thomas JA, Benach JL, Golightly MG. Cellular Immune response in Lyme disease: the response to mitogens, live Borrelia burgdorferi, NK cell function and lymphocyte subsets . Zentralbl Bakteriol Mikrobiol Hyg A. 1986;263:151-159. 20. Dressler F, Yoshinari NH, Steere AC. The T-cell proliferative assay in the diagnosis of Lyme disease . Ann Intern Med. 1991;115:533-539.Crossref 21. Krause A, Burmester GR, Rensing A, et al. Cellular immune reactivity to recombinant OspA and flagellin from Borrelia burgdorferi in patients with Lyme borreliosis: complexity of humoral and cellular immune responses . J Clin Invest. 1992;90:1077-1084.Crossref 22. Sigal LH, Steere AC, Freeman DH, Dwyer JM. Proliferative responses of mononuclear cells in Lyme disease: reactivity to Borrelia burgdorferi antigens is greater in joint fluid than in blood . Arthritis Rheum. 1986;29:761-769.Crossref 23. Krause A, Brade V, Schoerner C, Solbach W, Kalden JR, Burmester GR. T-cell proliferation induced by Borrelia burgdorferi in patients with Lyme borreliosis . Arthritis Rheum. 1991;34:393-402.Crossref 24. Zoschke DC, Skemp AA, Defosse DL. Lymphoproliferative responses to Borrelia burgdorferi in Lyme disease . Ann Intern Med. 1991;114:285-289.Crossref 25. Asbrink E, Hederstedt B, Hovmark A. The spirochetal etiology of erythema chronicum migrans Afzelius . Acta Derm Venereol (Stockh). 1984;64:291-295. 26. Weir DM. Handbook of Experimental Immunology . 3rd ed. Boston, Mass: Blackwell Scientific Publications Inc; 1978. 27. Sigal LH, Moffat CM, Steere AC, Dwyer JM. Cellular immune findings in Lyme disease . J Biol Med. 1984;57:595-598. 28. Miller LC, Isa S, Vannier E, Georgilis K, Steere AC, Dinarello CA. Live Borrelia burgdorferi preferentially activate interleukin-1 beta gene expression and protein synthesis over the interleukin-1 receptor antagonist . J Clin Invest. 1992; 90:906-912.Crossref 29. Büchner SA, Rufli T. Erythema chronicum migrans: evidence for cellular immune reaction in the skin lesion . Dermatologica. 1987;174:144-149.Crossref 30. Steere AC, Duray PH, Butcher EC. Spirochetal antigens and lymphoid cell surface markers in Lyme synovitis: comparison with rheumatoid synovium and tonsillar lymphoid tissue . Arthritis Rheum. 1988;31:487-495.Crossref 31. Baranton G, Postic D, Saint-Girons I, et al. Delineation of Borrelia burgdorferi sensu stricto, Borrelia garinii sp. nov., and group VS461 associated with Lyme borreliosis . Int J Syst Bacteriol. 1992;42:378-383.Crossref 32. van Dam AP, Kuiper H, Vos K, et al. Different genospecies of Borrelia burgdorferi are associated with distinct clinical manifestations of Lyme borreliosis . Clin Infect Dis. 1993;17:708-717.Crossref 33. Assous MV, Postic D, Paul G, Nivot P, Baranton G. Western blot analysis of sera from Lyme borreliosis patients according to the genomic species of the Borrelia strains used as antigens . Eur J Clin Microbiol Infect Dis. 1993;12: 261-268.Crossref 34. Sigal LH, Steere AC, Dwyer JM. In vivo and in vitro B-cell hyperactivity in Lyme disease . J Rheumatol. 1988;15:648-654. 35. Pachner AR, Steere AC, Sigal LH, et al. Antigen-specific proliferation of CSF lymphocytes in Lyme disease . Neurology. 1985;35:1642-1645.Crossref 36. Buechner SA, Rufli T, Erb P. Acrodermatitis chronica atrophicans: a chronic T-cell—mediated immune reaction against Borrelia burgdorferi? clinical, histologic, and immunohistochemical study of five cases . J Am Acad Dermatol. 1993;28:399-405.Crossref 37. Yssel H, Shanafelt MC, Soderberg C, Schneider PV, Anzola J, Peltz G. Borrelia burgdorferi activates a T-helper type 1—like T-cell subset in Lyme arthritis . J Exp Med. 1991;174:593-601.Crossref 38. Plörer A, Sepp N, Schmutzhard E, et al. Effects of adequate versus inadequate treatment of cutaneous manifestations of Lyme borreliosis on the incidence of late complications and late serologic status . J Invest Dermatol. 1993;100:103-109.Crossref 39. Breier F, Klade H, Aberer E. T-cell responses to Borrelia burgdorferi in circumscribed scleroderma . Arch Dermatol Res. 1992;284:21-22. 40. Büchner SA, Lautenschlager S, Itin P, Erb P, Rufli T. Lymphocyte proliferative response to Borrelia burgdorferi: new diagnostic test in borreliosis . Dermatologica. 1991;183:298-299.
doi: 10.1001/archderm.1995.01690180051009
This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables.
Muellegger, Robert R.;Zoechling, Natalie;Soyer, H. Peter;Hoedl, Stefan;Wienecke, Ralf;Volkenandt, Matthias;Kerl, Helmut
doi: 10.1001/archderm.1995.01690180052010
Abstract Background and Design: Early treatment of erythema migrans is important to prevent late complications. Minocycline possesses several attributes, making it potentially useful in the treatment of borrelial infections. In our study, minocycline was administered to 14 patients with erythema migrans. Punch biopsy specimens were obtained from the (affected) skin of all patients before and after therapy. The formalin-fixed, paraffin-embedded specimens were analyzed by polymerase chain reaction for the presence of Borrelia burgdorferi— specific DNA. Results: Polymerase chain reaction assay succeeded in amplifying B burgdorferi—specific DNA from the first biopsy specimen, obtained from the border of erythema migrans before initiating treatment, in eight (57%) of 14 patients. At the end of minocycline therapy, however, polymerase chain reaction analysis disclosed no B burgdorferi—specific DNA in any of the 14 patients. The good clinical response of our patients with erythema migrans substantiates our molecular findings. Conclusions: The presented polymerase chain reaction data, together with the clinical outcome, indicate that minocycline may be useful for treatment of early Lyme borreliosis.(Arch Dermatol. 1995;131:678-682) References 1. Steere AC, Hutchinson GJ, Rahn DW, et al. Treatment of the early manifestations of Lyme disease . Ann Intern Med. 1983;99:22-26.Crossref 2. Weber K, Preac-Mursic V, Neubert U, et al. Antibiotic therapy of early European Lyme borreliosis and acrodermatitis chronica atrophicans . Ann N Y Acad Sci. 1988;539:324-345.Crossref 3. Steere AC, Green J, Hutchinson GJ, et al. Treatment of Lyme disease . Zbl Bakteriol Hyg A. 1986;263:352-356. 4. Berger BW. Treating erythema chronicum migrans of Lyme disease . J Am Acad Dermatol. 1986;15:459-463.Crossref 5. Strle F, Preac-Mursic V, Cimperman J, Ruzic E, Maraspin V, Jereb M. Azithromycin versus doxycycline for treatment of erythema migrans: clinical and microbiologic findings . Infection. 1993;21:83-88.Crossref 6. Strle F, Ruzic E, Cimperman J. Erythema migrans: comparison of treatment with azithromycin, doxycycline and phenoxymethylpenicillin . J Antimicrob Chemother. 1992;30:543-550.Crossref 7. Nadelman RB, Luger SW, Frank E, Wisniewski M, Collins JJ, Wormser GP. Comparison of cefuroxime axetil and doxycycline in the treatment of early Lyme disease . Ann Intern Med. 1992;117:273-280.Crossref 8. Berger BW, Johnson RC, Kodner C, Coleman L. Failure of Borrelia burgdorferi to survive in the skin of patients with antibiotic-treated Lyme disease . J Am Acad Dermatol. 1992;27:34-37.Crossref 9. Sigal LH. Current recommendations for the treatment of Lyme disease . Drugs. 1992;43:683-699.Crossref 10. Steere AC, Grodzicki RL, Kornblatt AN, et al. The spirochetal etiology of Lyme disease . N Engl J Med. 1983;308:733-740.Crossref 11. Asbrink E, Olsson I, Hovmark A. Erythema chronicum migrans Afzelius in Sweden: a study of 231 patients . Zbl Bakteriol Hyg A. 1986;263:229-236. 12. Weber K, Preac-Mursic V, Wilske B, Thurmayr U, Neubert U, Scherwitz C. A randomized trial of ceftriaxone vs oral penicillin for the treatment of early European Lyme borreliosis . Infection. 1990;18:91-96.Crossref 13. Dattwyler RJ, Volkman DJ, Conaty SM, Platkin SP, Luft BJ. Amoxicillin plus probenecid versus doxycycline for treatment of erythema migrans borreliosis . Lancet. 1990;2:1404-1406.Crossref 14. Massarotti EM, Luger SW, Rahn DW, et al. Treatment of early Lyme disease . Am J Med. 1992;92:396-403.Crossref 15. Weber K, Neubert U, Thurmayr R. Antibiotic therapy in early erythema migrans disease and related disorders . Zbl Bakteriol Hyg A. 1986;263:377-388. 16. Johnson SE, Klein GC, Schmid GP, Feeley JC. Susceptibility of the Lyme disease spirochete to seven antimicrobial agents . Yale J Biol Med. 1984;57:549-553. 17. Wienecke R, Neubert U, Volkenandt R. Molecular detection of Borrelia burgdorferi in formalin-fixed, paraffin-embedded lesions of Lyme disease . J Cutan Pathol. 1993;20:385-388.Crossref 18. Berger BW. Cutaneous manifestations of Lyme borreliosis . Rheum Dis Clin North Am. 1989;15:627-633. 19. Rosa PA, Hogan D, Schwan TG. Polymerase chain reaction analyses identify two distinct classes of Borrelia burgdorferi . J Clin Microbiol. 1991;29:524-532. 20. Hansen K, Asbrink E. Serodiagnosis of erythema migrans and acrodermatitis chronica atrophicans by the Borrelia burgdorferi flagellum enzyme-linked immunosorbent assay . J Clin Microbiol. 1989;27:545-551. 21. Reik L Jr, Burgdorfer W, Donaldson JO. Neurologic abnormalities in Lyme disease without erythema chronicum migrans . Am J Med. 1986;81:73-78.Crossref 22. Preac-Mursic V, Wilske B, Schierz G, Holmburger M, Süss E. In vitro and in vivo susceptibility of Borrelia burgdorferi . Eur J Clin Microbiol. 1987;4:424-426.Crossref 23. Johnson RC. Isolation techniques for spirochetes and their sensitivities to antibiotics in vitro and in vivo . Rev Infect Dis. 1989;11( (suppl 6) ):1505-1510.Crossref 24. Dattwyler RJ, Halperin JJ. Failure of tetracycline therapy in early Lyme disease . Arthritis Rheum. 1987;30:448-450.Crossref 25. Luft BJ, Volkman DJ, Halperin JJ, Dattwyler RJ. New chemotherapeutic approaches in the treatment of Lyme borreliosis . Ann N Y Acad Sci. 1988;539: 352-561.Crossref 26. Brogden RN, Speight TM, Avery GS. Minocycline: a review of its antibacterial and pharmacokinetic properties and therapeutic use . Drugs. 1975;9:251-291.Crossref 27. Luft BJ, Steinman CR, Neimark HC, et al. Invasion of the central nervous system by Borrelia burgdorferi in acute disseminated infection . JAMA. 1992;267: 1364-1367.Crossref 28. Macdonald H, Kelly RG, Allen ES, Noble JF, Kanegis LA. Pharmacokinetic studies on minocycline in man . Clin Pharmacol Ther. 1973;14:852-861. 29. Pfister HW, Neubert U, Wilske B, Preac-Mursic V, Einhäupl KM, Borasio GD. Reinfection with Borrelia burgdorferi . Lancet. 1986;2:984-985.Crossref 30. Liegner KB. Minocycline in Lyme disease . J Am Acad Dermatol. 1992;26:263-264.Crossref 31. Weber K. Therapy of cutaneous manifestations . In Weber K, Burgdorfer W, eds. Aspects of Lyme Borreliosis . New York, NY: Springer-Verlag NY Inc; 1993; 312-327. 32. Berger BW, Johnson RC, Kodner C, Coleman L. Cultivation of Borrelia burgdorferi from erythema migrans lesions and perilesional skin . J Clin Microbiol. 1992;30:359-361. 33. Nadelman RB, Nowakowski J, Forseter G, et al. Failure to isolate Borrelia burgdorferi after antimicrobial therapy in culture-documented Lyme borreliosis associated with erythema migrans: report of a prospective study . Am J Med. 1993;94:583-588.Crossref 34. Preac-Mursic V, Weber K, Pfister HW. Survival of Borrelia burgdorferi in antibiotically treated patients with Lyme borreliosis . Infection. 1989;17:355-359.Crossref 35. Melchers W, Meis J, Rosa P, et al. Amplification of Borrelia burgdorferi DNA in skin biopsies from patients with Lyme disease . J Clin Microbiol. 1991;29: 2401-2406. 36. Schwartz I, Wormser GP, Schwartz JJ, et al. Diagnosis of early Lyme disease by polymerase chain reaction amplification and culture of skin biopsies from erythema migrans lesions . J Clin Microbiol. 1992;30:3082-3088.
Compton, Carolyn C.;Tong, Yiai;Trookman, Nathan;Zhao, Huifen;Roy, Dawn;Press, William
doi: 10.1001/archderm.1995.01690180057011
Abstract Background: Cultured human keratinocyte grafts have been shown to stimulate endogenous reepithelialization of both chronic nonhealing and acute partial-thickness wounds. This effect is most likely mediated by cytokines that stimulate keratinocyte growth, such as transforming growth factor alpha. The effect of cellular age on cytokine expression by cultured grafts used for this purpose is presently undefined. In this study, transforming growth factor alpha gene expression in cultured foreskin keratinocytes from donors varying in age from 2 to 82 years was analyzed semiquantitatively by two separate methods, ie, Northern hybridization and competitive polymerase chain reaction. Results: No pattern of decline in transforming growth factor alpha messenger RNA expression with increasing cellular age was observed by either analysis. Conclusion: The results indicate that expression of transforming growth factor alpha by cultured grafts may not be significantly affected by increasing cellular age and suggest that, even in the elderly, cultured autografts may be effective as pharmacologic agents for wound treatment.(Arch Dermatol. 1995;131:683-690) References 1. Derynck R. Transforming growth factor-α: structure and biological activities . J Cell Biochem. 1986;32:293-304.Crossref 2. Wong ST, Winchell LS, McCune BK, et al. The TGF-α precursor expressed on the cell surface binds to the EGF receptor on adjacent cells, leading to signal transduction . Cell. 1989;56:495-506.Crossref 3. Coffey RJ Jr, Derynck R, Wilcox JN, et al. Production and auto-induction of transforming growth factor-α in human keratinocytes . Nature. 1987;328:817-820.Crossref 4. Gottlieb AB, Chang CH, Posnett DN, Fanelli B, Tam JP. Detection of transforming growth factor α in normal, malignant, and hyperproliferative human keratinocytes . J Exp Med. 1988;167:670-675.Crossref 5. Ansel J, Perry P, Brown J, et al. Cytokine modulation of keratinocyte cytokines . J Invest Dermatol. 1990;94:101S-107S.Crossref 6. Elder JT, Fisher GJ, Linquist PB, et al. Overexpression of transforming growth factor α in psoriatic epidermis . Science. 1989;243:811-814.Crossref 7. Schultz GS, White M, Mitchell R, et al. Epithelial wound healing enhanced by transforming growth factor-α and vaccinia growth factor . Science. 1987;235: 350-352.Crossref 8. Leigh IM, Purkis PE. Cultured grafted leg ulcers . Clin Exp Dermatol. 1986;11: 650-652.Crossref 9. Leigh IM, Purkis PE, Navsaria HA, Phillips TJ. Treatment of chronic venous ulcers with sheets of cultured allogenic keratinocytes . Br J Dermatol. 1987; 117:591-597.Crossref 10. Pye RJ. Cultured keratinocytes as biological wound dressings . Eye. 1988;2: 172-178.Crossref 11. Clancy JM, Shehade SA, Blight AE, Young KE, Levick PL. Treatment of leg ulcers with cultured epithelial grafts . J Am Acad Dermatol. 1988;18:1356-1357.Crossref 12. Phillips TJ, Gilchrest BA. Cultured allogenic keratinocyte grafts in the management of wound healing: prognostic factors . J Dermatol Surg Oncol. 1989; 15:1169-1176.Crossref 13. Phillips TJ, Gilchrest BA. Cultured epidermal grafts in the treatment of leg ulcers . Adv Dermatol. 1990;5:33-50. 14. Teepe RGC, Koebrugge EJ, Vermeer BJ. Fresh versus cryopreserved cultured allografts for the treatment of chronic skin ulcer . Br J Dermatol. 1990;122: 81-89.Crossref 15. Brysk MM, Raimer SS, Pupo R, Bell T, Rajaraman S. Grafting of leg ulcers with undifferentiated keratinocytes . J Am Acad Dermatol. 1991;25:238-244.Crossref 16. Mol MAE, Nanninga PB, van Eendenburg JP, Westerhof W, Mekkes JR, van Ginkel CJW. Grafting of venous leg ulcers: an intraindividual comparison between cultured skin equivalents and full-thickness skin pinch grafts . J Am Acad Dermatol. 1991;24:77-82.Crossref 17. DeLuca M, Albanese E, Cancedda R, et al. Treatment of leg ulcers with cryopreserved allogeneic cultured epithelium: a multicenter study . Arch Dermatol. 1992;128:633-638.Crossref 18. Hefton JM, Madden MR, Finkelstein JL, Shires GT. Grafting of burn patients with allografts of cultured epidermal cells . Lancet 1983;2:428-430.Crossref 19. Madden MR, Finkelstein JL, Staiano-Coico L, et al. Grafting of cultured allogeneic epidermis on secondand third-degree burn wounds on 26 patients . J Trauma. 1986;26:955-962.Crossref 20. DeLuca M, Albanese E, Bondanza S, et al. Multicentre experience in the treatment of burns with autologous and allogenic cultured epithelium, fresh or preserved in a frozen state . Burns. 1989;15:303-309.Crossref 21. Blight A, Fatah MF, Datubo-Brown DD, Mountford EM, Cheshire IM. The treatment of donor sites with cultured epithelial grafts . Br J Plast Surg. 1991;44: 12-14.Crossref 22. Oliver AM, Kaawach W, Mithoff EW, Watt A, Abramovich DR, Rayner CR. The differentiation and proliferation of newly formed epidermis on wounds treated with cultured epithelial allografts . Br J Dermatol. 1991;125:147-154.Crossref 23. Phillips TJ, Gilchrest BA. Cultured epithelial allografts as biological wound dressings . In: Barbul A, ed. Clinical and Experimental Approaches to Dermal and Epidermal Repair: Normal and Chronic Wounds . New York, NY: Wiley-Liss Inc; 1991:77-94. 24. DeLuca M, Bondanza S, Cancedda R, et al. Permanent coverage of full skin thickness burns with autologous cultured epidermis and re-epithelialization of partial skin thickness lesions induced by allogeneic cultured epidermis: a multicentre study in the treatment of children . Burns. 1992;18:S16-S19.Crossref 25. Phillips TJ, Provan A, Colbert D, Easley KW. A randomized single-blind controlled study of cultured epithelial allografts in the treatment of split-thickness skin graft donor sites . Arch Dermatol. 1993;129:879-882.Crossref 26. Phillips TJ. Cultured skin grafts: past, present, future . Arch Dermatol. 1988; 124:1035-1038.Crossref 27. Limova M, Grekin RC. Synthetic membranes and cultured keratinocyte grafts . J Am Acad Dermatol. 1990;23:713-719.Crossref 28. Carver N, Leigh IM. Keratinocyte grafts and skin equivalents . Int J Dermatol. 1991;30:540-551.Crossref 29. Leigh IM, McKay I, Carver N, Navsaria H, Green C. Skin equivalents and cultured skin: from the Petri dish to the patient . Wounds. 1991;3:141-148. 30. Parenteau NL, Nolte CM, Bilbo P, et al. Epidermis generated in vitro: practical considerations and applications . J Cell Biochem. 1991;45:245-251.Crossref 31. Arons JA, Wainwright DJ, Jordon RE. The surgical applications and implications of cultured human epidermis: a comprehensive review . Surgery. 1992; 111:4-11. 32. Barrandon Y, Green H. Three clonal types of keratinocyte with different with different capacities for multiplication . Proc Natl Acad Sci U S A. 1987;84:2302-2306.Crossref 33. Stanulis-Praeger BM, Gilchrest BA. In-vitro studies of aging . Clin Geriatr Med. 1989;5:23-40. 34. Sauder DN, Stanulis-Praeger BM, Gilchrest BA. Autocrine growth stimulation of human keratinocytes by epidermal cell-derived thymocyte activating factor: implications for skin aging . Arch Dermatol Res. 1988;280:71-76.Crossref 35. Stanulis-Praeger BM, Gilchrest BA. Growth factor responsiveness declines during adulthood for human skin-derived cells . Mech Aging Dev. 1986;35:185-189.Crossref 36. Rheinwald JG, Green H. Serial cultivation of strains of human epidermal keratinocytes: the formation of keratinizing colonies from single cells . Cell. 1975; 6:331-343.Crossref 37. Barrandon Y, Li V, Green H. New techniques for the grafting of cultured human epidermal cells onto athymic animals . J Invest Dermatol. 1988;91:315-318.Crossref 38. Longley J, Ding TG, Cuono C, et al. Isolation, detection and amplification of intact mRNA from dermatome strips, epidermal sheets, and sorted epidermal cells . J Invest Dermatol. 1991;97:974-979.Crossref 39. Cathala G, Savouret J-F, Mendez B, et al. A method for isolation of intact, translationally active ribonucleic acid . DNA. 1983;2:329-335.Crossref 40. Ausubel FM, Brent R, Kingston RE, Moore DD, et al, eds. Current Protocols in Molecular Biology . New York, NY: Wiley Interscience; 1991; chap 4:4.0.1-4.10.9. 41. Derynck R, Roberts AB, Winkler ME, Chen EY, Goeddel DV. Human transforming growth factor-α precursor structure and expression in E coli. Cell. 1984; 38:287-297. 42. Feinberg AP, Vogelstein B. A technique for radiolabeling DNA restriction endonuclease fragments to high specific activity . Anal Biochem. 1983;132:6-13.Crossref 43. Giaid A, Gibson SJ, Steel JH, Polak JM. In situ detection of peptide messenger RNA using complementary RNA probes . In: Conn M, ed. Methods in Neurosciences . Orlando, Fla: Academic Press Inc; 1989:150-164. 44. Tong Y, Zhao HF, Simard J, Labrie F, Pelletier G. Electron microscopic autoradiographic localization of prolactin mRNA in rat pituitary . J Histochem Cytochem. 1989;37:567-571.Crossref 45. Holm R, Karlsen F, Nesland JM. In situ hybridization with nonisotopic probes using different detection systems . Mod Pathol. 1992;5:315-318. 46. Burt AM, Pallett CD, Sloane JP, et al. Survival of cultured allografts in patients with burns assessed with probe specific for Y chromosome . BMJ. 1989;298: 915-917.Crossref 47. Aubock J, Irschick E, Romani N, et al. Rejection, after a slightly prolonged survival time, of Langerhans cell-free allogeneic cultured epidermis used for wound coverage in humans . Transplantation. 1988;45:730-737.Crossref 48. Thivolet J, Faure M, Demidem A, Mauduit G. Long-term survival and immunological tolerance of human epidermal allografts produced in culture . Transplantation. 1986;42:274-280.Crossref 49. Compton CC, Gill JM, Bradford DA, Regauer S, Gallico GG, O'Connor NE. Skin regenerated from cultured epithelial autografts on full-thickness burn wounds from 6 days to 5 years after grafting: a light, electron microscopic and immunohistochemical study . Lab Invest. 1989;60:600-612. 50. Gielen V, Faure M, Maudit G, Thivolet J. Progressive replacement of human cultured epithelial allografts by recipient cells as evidenced by HLA class 1 antigen expression . Dermatologica. 1987;175:166-170.Crossref 51. Brain A, Purkis P, Coates P, Hackett M, Navsaria H, Leigh I. Survival of cultured allogeneic keratinocytes transplanted to deep dermal bed assessed with probe specific for Y chromosome . BMJ. 1989;298:917-919.Crossref 52. Philips TJ, Bhawan J, Leigh IM, Baum HJ, Gilchrest BA. Cultured epidermal autografts and allografts: a study of differentiation and allograft survival . J Am Acad Dermatol. 1990;23:189-198.Crossref 53. Yang-bing Z, Xiong-fei A, Ao(Ngao) L, et al. Clinical observation and methods for identifying the existence of cultured epidermal allografts . Burns. 1992;18: 408.Crossref 54. Kaawach WF, Oliver AM, Weiler-Mithoff E, Abramovich DR, Rayner CR. Survival assessment of cultured epidermal allografts applied onto partial-thickness burn wounds . Br J Plast Surg. 1991;44:321-324.Crossref 55. Kirsner RS, Falanga V, Eaglstein WH. The biology of skin grafts: skin grafts as pharmacological agents . Arch Dermatol. 1993;129:481-483.Crossref 56. Regauer S, Compton CC. Cultured keratinocyte sheets enhance spontaneous re-epithelialization in a dermal explant model of partial-thickness wound healing . J Invest Dermatol. 1990;95:341-346.Crossref 57. Hefton JM, Caldwell D, Biozes DG, Balin AK, Carter DM. Grafting of skin ulcers with cultured autologous epidermal cells . J Am Acad Dermatol. 1986;14:399-405.Crossref
Fazio, Michael J.;Zitelli, John A.
doi: 10.1001/archderm.1995.01690180065012
Abstract Background and Design: A recent animal study indicated that epinephrine in local anesthesia adversely affects the survival of full-thickness skin grafts. Because animal models do not always correlate to humans, we performed a prospective observational study to elucidate the clinical outcome of using epinephrine in local anesthesia of the donor site. Seventy-two patients had cutaneous tumors excised by the Mohs micrographic technique. The resultant surgical defects were repaired using full-thickness skin grafts. Patients were randomly divided into two groups based on the local anesthetic used at the donor site: (1) 1% lidocaine (Xylocaine) (n=33) or (2) 1% lidocaine with 1:100 000 epinephrine (n=39). Results: Assessment of the skin grafts at 1 week revealed a significantly increased risk of developing graft complications in the lidocaine with epinephrine group compared with the plain lidocaine group. The overall cosmetic outcome of the grafted site at 6 weeks revealed no significant difference between the two groups. Conclusions: Because there was only a minimal clinical effect of epinephrine on graft survival observed at 1 week and there was no effect on the 6-week cosmetic outcome, we do not recommend harvesting all full-thickness skin grafts with plain lidocaine. In certain clinical circumstances with compromised vascular supply or poor oxygenation, the use of plain lidocaine may be advantageous.(Arch Dermatol. 1995;131:691-694) References 1. Rudolph R, Fisher J, Ninnemann J. Skin Grafting . Boston, Mass: Little Brown & Co Inc; 1979. 2. Branham GH, Thomas JR. Skin grafts . Otolaryngol Clin North Am. 1990;23: 889-897. 3. Hill T. Enhancing the survival of full-thickness skin grafts . J Dermatol Surg Oncol. 1984;10:639-642.Crossref 4. Wolfort S, Rohrich RJ, Handren J, May JW. The effect of epinephrine on local anesthesia on survival of full- and split-thickness skin grafts: an experimental study . Plast Reconstr Surg. 1990;86:535-540.Crossref 5. Smahel J. The healing of skin grafts . Clin Plast Surg. 1977;4:409-424. 6. Smahel J. Biology of the stage of plasmatic imbibition . Br J Plast Surg. 1971; 24:140-143.Crossref 7. Converse JM, Uhlschmid CK, Ballantyne DL. 'Plasmatic circulation' in skin grafts: the phase of serum imbibition . Plast Reconstr Surg. 1969;43:495-499.Crossref 8. Converse JM, Smahel J, Ballantyne DL, Harper AD. Inosculation of vessels of skin graft and host bed: a fortuitous encounter . Br J Plast Surg. 1975;28:274-282.Crossref
Nelson, J. Stuart;Milner, Thomas E.;Anvari, Bahman;Tanenbaum, B. Samuel;Kimel, Sol;Svaasand, Lars O.;Jacques, Steven L.
doi: 10.1001/archderm.1995.01690180071013
Abstract Background and Design: The clinical objective in the treatment of a patient with port-wine stain (PWS) undergoing laser therapy is to maximize thermal damage to the PWS, while at the same time minimizing nonspecific injury to the normal overlying epidermis. With dynamic cooling, the epidermis can be cooled selectively. When a cryogen spurt is applied to the skin surface for an appropriately short period of time (on the order of tens of milliseconds), the cooling remains localized in the epidermis, while leaving the temperature of the deeper PWS vessels unchanged. Results: Comparative measurements obtained by a fast infrared imaging detector demonstrated that the surface temperature prior to laser exposure could be reduced by as much as 40°C using the dynamic cooling technique. No skin surface textural changes were noted on PWS test sites cooled with a 20- to 80-millisecond cryogen spurt after flashlamp-pumped pulsed dye laser (FLPPDL) exposure (λ=585 nm; τp=450 microseconds) at the maximum light dosage possible (10 J/cm2). In contrast, epidermal necrosis occurred on the uncooled sites after such exposure. Six months after laser exposure, clinically significant blanching on the cooled sites indicates laser photothermolysis of PWS blood vessels did occur. Conclusions: Our preliminary experiments demonstrate the feasibility of selectively cooling the normal overlying epidermis without affecting the temperature of the deeper PWS vessels. Furthermore, protection of the epidermis from thermal injury, produced by melanin light absorption at clinically relevant wavelengths, can be achieved effectively. An additional advantage of dynamic epidermal cooling is reduction of patient discomfort associated with FLPPDL therapy. Further studies are under way to determine an optimum strategy for applying this dynamic cooling technique during pulsed laser treatment of patients with PWS and others with selected dermatoses (dermal melanocytic lesions and tattoos).(Arch Dermatol. 1995;131:695-700) References 1. Anderson RR, Parrish JA. Selective photothermolysis: precise microsurgery by selective absorption of pulsed radiation . Science. 1983;220:524-527.Crossref 2. Garden JM, Polla LL, Tan OT. The treatment of port-wine stains by the pulsed dye laser . Arch Dermatol. 1988;124:889-896.Crossref 3. Tan OT, Sherwood K, Gilchrest BA. Treatment of children with port wine stains using the flashlamp-pumped tunable dye laser . N Engl J Med. 1989;320:416-421.Crossref 4. Reyes BA, Geronemus RG. Treatment of port-wine stains during childhood with the flashlamp-pumped dye laser . J Am Acad Dermatol. 1990;23:1142-1148.Crossref 5. Nelson JS, Applebaum J. Clinical management of port-wine stain in infants and young children using the flashlamp-pulsed dye laser . Clin Pediatr. 1990; 29:503-508.Crossref 6. Ashinoff R, Geronemus RG. Flashlamp-pumped pulsed dye laser for port wine stains in infancy: earlier versus later treatment . J Am Acad Dermatol. 1991;24:467-472.Crossref 7. Ashinoff R, Geronemus RG. Capillary hemangiomas and treatment with the flashlamp-pulsed dye laser . Arch Dermatol. 1991;127:202-205.Crossref 8. Gilchrest BA, Rosen S, Noe JM. Chilling port wine stains improves the response to argon laser therapy . Plast Reconstr Surg. 1982;69:278-283.Crossref 9. Manzer LE. The CFC-ozone issue: progress on the development of alternatives to CFCs . Science. 1990;249:31-36.Crossref 10. Nelson JS, Jacques SL, Wright WH. Determination of thermal and physical properties of port wine stain lesions using pulsed photothermal radiometry . Proceedings of Society of Photo-optical and Instrumentation Engineers . 1992; 1643:287-298. 11. Jacques SL, Nelson JS, Wright WH, Milner TE. Pulsed photothermal radiometry of port-wine-stain lesions . Appl Optics. 1993;32:2439-2446.Crossref 12. Milner TE, Norvang LT, Svaasand LO, Tran N, Tanenbaum BS, Nelson JS. Photothermal tomography of subcutaneous chromophores . Proceedings of Society of Photo-optical and Instrumentation Engineers . 1993;2077:228-236. 13. Carslaw HS, Jaeger JC. Conduction of Heat in Solids . New York, NY: Oxford University Press; 1959:57. 14. Cohen ML. Measurement of the thermal properties of human skin . J Invest Dermatol. 1977;69:333-338.Crossref 15. Barsky SH, Rosen S, Geer DE, Noe JM. The nature and evolution of port wine stains: a computer assisted study . J Invest Dermatol. 1980;74:154-157.Crossref 16. Anderson RR, Beck H, Bruggemann U, Farinelli W, Jacques SL, Parrish JA. Pulsed photothermal radiometry in turbid media: internal reflection of backscattered radiation strongly influences optical dosimetry . Appl Optics. 1989; 28:2256-2262.Crossref 17. Motamedi M, Rastegar S, LeCarpentier G, Welch AJ. Light and temperature distribution in laser irradiated tissue: the influence of anisotropic scattering and refractive index . Appl Optics. 1989;28;2230-2237.Crossref 18. Geronemus RG. Pulsed dye aser treatment of vascular lesions in children . J Dermatol Surg Oncol. 1993;19:303-310.Crossref
Weinstock, Martin A.;Coulter, Silvija;Bates, Jeannie;Bogaars, Hendrik A.;Larson, Pamela L.;Burmer, Glenna C.
doi: 10.1001/archderm.1995.01690180077014
Abstract Background: Oral psoralen with UV-A (PUVA) photochemotherapy is known to cause cutaneous malignancies and has been associated with cutaneous immunosuppression. Human papillomavirus infection has also been associated with cutaneous malignancies and with immunosuppressed individuals. We therefore sought evidence of human papillomavirus infection in a patient with a long history of PUVA therapy and multiple cutaneous malignancies. Observations: During a 15-year period, an otherwise healthy patient with psoriasis who had undergone a 10-year course of PUVA photochemotherapy developed 13 squamous cell carcinomas, eight lesions diagnosed as ''squamous cell carcinoma vs keratoacanthoma,'' 14 other keratoacanthomas, six basal cell carcinomas, one melanoma in situ, and 18 other keratinocytic dysplasias. Twenty-two of the 30 lesions tested for human papillomavirus DNA by polymerase chain reaction were positive for type 16/18, including six of the seven basal or squamous cell carcinomas tested. Conclusion: We hypothesize that PUVA therapy-induced immunosuppression may play an important role in PUVA-related carcinogenesis by affecting the extent and pathogenicity of human papillomavirus infection.(Arch Dermatol. 1995;131:701-704) References 1. Bauer HM, Manos MM. PCR detection of genital human papillomavirus . In: Persing H, Smith TF, Tenover FC, White TJ, eds. Diagnostic Molecular Microbiology: Principles and Applications . Washington DC: American Society for Microbiology; 1993:407-413. 2. Burmer GC, Parker JD, Bates J, East K, Kulander BG. Comparative analysis of human papillomavirus detection by polymerase chain reaction and Virapap/ Viratype kits . Am J Clin Pathol. 1990;94:554-560. 3. Burmer GC, True LD, Krieger JN. Squamous cell carcinoma of the scrotum associated with human papillomaviruses . J Urol. 1993;149:374-377. 4. Ting Y, Manos MM. Detection and typing of genital human papillomaviruses . In: Innis MA, Gelfand D, Sninsky JJ, White TJ, eds. PCR Protocols: A Guide to Methods and Applications . Orlando, Fla: Academic Press Inc; 1990:356-367. 5. Stern RS, Thibodeau LA, Kleinerman RA, et al. Risk of cutaneous carcinoma in patients treated with oral methoxsalen photochemotherapy for psoriasis . N Engl J Med. 1979;300:809-813.Crossref 6. Stern RS, Lange R, and members of the Photochemotherapy Follow-up Study. Non-melanoma skin cancer occurring in patients treated with PUVA five to ten years after first treatment . J Invest Dermatol. 1988;91:120-124.Crossref 7. Gupta AK, Stern RS, Swanson NA, Anderson TF, and members of the PUVA Follow-up Study. Cutaneous melanomas in patients treated with psoralens plus ultraviolet A: a case report and the experience of the PUVA Follow-up Study . J Am Acad Dermatol. 1988;19:67-76.Crossref 8. Ashworth J, Kahan MC, Breathnach SM. PUVA therapy decreases HLA-DR+ CDla+ Langerhans cells and epidermal cell antigen-presenting capacity in human skin, but flow cytometrically sorted residual HLA-DR+ CDla+ Langerhans cells exhibit normal alloantigen-presenting function . Br J Dermatol. 1989;120:329-339.Crossref 9. Strauss GH, Bridges BA, Greaves M, Hall-Smith P, Price M, Vella-Briffa D. Inhibition of delayed hypersensitivity reaction in skin (DNCB test) by 8-methoxypsoralen photochemotherapy: possible basis for pseudo-promoting action in skin carcinogenesis? Lancet. 1980;2:556-559.Crossref 10. Kripke ML, Morison WL, Parrish JA. Systemic suppression of contact hypersensitivity in mice by psoralen plus UVA radiation (PUVA) . J Invest Dermatol. 1983;81:87-92.Crossref 11. Morison WL, Wimberly J, Parrish JA, Bloch KJ. Abnormal lymphocyte function following long-term PUVA therapy for psoriasis . Br J Dermatol. 1983;108: 445-450.Crossref 12. Slaper H, Schothorst AA, van der Leun JC. Risk evaluation of UVB therapy for psoriasis: comparison of calculated risk for UVB therapy and observed risk in PUVA-treated patients . Photodermatology. 1986;3:271-283. 13. Maughan WZ, Muller SA, Perry HO, Pittelkow MR, O'Brien PC. Incidence of skin cancers in patients with atopic dermatitis treated with coal tar: a 25-year follow-up study . J Am Acad Dermatol. 1980;3:612-615.Crossref 14. Pittelkow MR, Perry HO, Muller SA, Maughan WZ, O'Brien PC. Skin cancer in patients with psoriasis treated with coal tar: a 25-year follow-up study . Arch Dermatol. 1981;117:465-468.Crossref 15. Quan MB, Moy RL. The role of human papillomavirus in carcinoma . J Am Acad Dermatol. 1991;25:698-705.Crossref 16. Piepkorn M, Kumasaka B, Krieger JN, Burmer GC. Development of human papillomavirus-associated Buschke-Löwenstein penile carcinoma during cyclosporin therapy for generalized pustular psoriasis . J Am Acad Dermatol. 1993; 29:321-325.Crossref 17. Kopelson PL, Nguyen QH, Moy RL. Verruca vulgaris and radiation exposure are associated with squamous cell carcinoma of the finger . J Dermatol Surg Oncol. 1994;20:38-41.Crossref 18. Vittorio CC, Schiffman MH, Weinstock MA. Epidemiology of human papillomaviruses . In: Weinstock MA, ed. Dermatoepidemiology . Philadelphia, Pa: WB Saunders Co. In press. 19. Boyle J, MacKie RM, Briggs JD, Junor BJR, Aitchison TC. Cancer, warts, and sunshine in renal transplant patients: a case control study . Lancet. 1984;1: 702-705.Crossref 20. Kelly GE, Mahony JF, Sheil AGR, Meikle WD, Tiller DS, Horvath J. Risk factors for skin carcinogenesis immunosuppressed kidney transplant recipients . Clin Transpl. 1987;1:271-277. 21. Barr BBB, Benton EC, McLaren K, et al. Human papilloma virus infection and skin cancer in renal allograft recipients . Lancet . 1989;1:124-129.Crossref 22. Cohen LM, Tyring SK, Rády P, Callen JP. Human papillomavirus type 11 in multiple squamous cell carcinomas in a patient with subacute lupus erythematosus . J Am Acad Dermatol. 1992;26:840-846.Crossref 23. Campo MS. Vaccination against papillomavirus . Cancer Cells . 1991;3:421-426.
Arbiser, Jack L.;Dzieczkowski, Jeffery S.;Harmon, James V.;Duncan, Lyn M.
doi: 10.1001/archderm.1995.01690180083015
Abstract Background: Protein A immunoadsorption is a novel therapy for the treatment of diseases mediated by pathogenic autoantibodies. This procedure consists of circulating patients' plasma through a column containing staphylococcal protein A, which binds to the Fc portion of IgG, enabling removal of IgG. Presently, protein A immunoadsorption is used in the treatment of idiopathic thrombocytopenic purpura, but may be more widely used as an immunomodulator in human immunodeficiency virus infection and metastatic carcinoma. Observations: We present two histologically documented cases of leukocytoclastic vasculitis in the setting of protein A immunoadsorption. This potentially severe adverse effect is probably more common than the literature reflects and should be recognized by physicians who are treating patients with protein A column pheresis. Conclusions: The pathogenesis of protein A therapy-associated leukocytoclastic vasculitis remains unclear. Further study of vasculitis in the setting of protein A column pheresis may lead to modifications of this therapy, resulting in fewer adverse effects. Protein A-associated leukocytoclastic vasculitis may serve as a useful model of the relation of immune complexes and vasculitis.(Arch Dermatol. 1995;131:707-709) References 1. Kessler SW. Rapid isolation of antigens from cells with Staphylococcus protein A antibody absorbent: parameters of the interaction of antibody-antigen complexes with protein A . J Immunol. 1975;115:1617-1624. 2. McDougal JS, Redecha PB, Inman RD, Christian CL. Binding of immunoglobulin G aggregates and immune complexes in human sera to staphylococci containing protein A . J Clin Invest. 1979;63:627-636.Crossref 3. Snyder HW, Ernst NR, Grosmire LS, Balint JP, Yoshida LH, Jones FR. Selective removal of antigen-complexed IgG from cat plasma by adsorption onto a protein A silica matrix . J Immunol Methods. 1987;101:209-217.Crossref 4. Langone JJ. Immune complex formation enhances the binding of staphylococcal protein A to immunoglobulin G . Biochem Biophys Res Commun. 1980;94:473-479.Crossref 5. Pinsky CM. Selective removal of plasma components to achieve immune modulations . Semin Hematol. 1989;26( (suppl 1) ):1-51. 6. 'Communicating With the Immune System' Using the PROSORBA Immunabsorption Treatment Column . Seattle, Wash: IMRÉ Corp; 1991. 7. Jones FR, Baliant JP, Snyder HW. Selective extracorporeal removal of immunoglobulin G and circulating immune complexes: a review . Plasma Ther Transfus Technol. 1986;7:333-339. 8. Cochran SK, Snyder HW, Balint JP, et al. Minimal toxicity during protein A immunoadsorption therapy (Prosorba column) for chronic refractory idiopathic thrombocytopenic purpura . Blood. 1990;76( (suppl 1) ):452a. 9. Handelsman H. Protein A Columns for the Treatment of Patients With Idiopathic Thrombocytopenic Purpura and Other Indications . Washington, DC: Agency for Health Care Policy and Research; (March) 1991. 10. Guthrie TH Jr, Oral A. Immune thrombocytopenia purpura: a pilot study of staphylococcal protein A immunomodulation in refractory patients . Semin Hematol. 1989;26:3-9. 11. Ainsworth SK, Pilia PA, Pepkowitz SH, O'Brien P. Toxicity following protein A treatment of metastatic breast adenocarcinoma . Cancer. 1988;61:1495-1500.Crossref 12. Snyder HW, Henry DH, Messerschmidt GL, et al. Minimal toxicity during protein A immunoadsorption treatment of malignant disease: an outpatient therapy . J Clin Apheresis. 1991;6:1-10.Crossref 13. Messerschmidt GL, Henry DH, Snyder HW Jr, et al. Protein A immunotherapy in the treatment of cancer: an update . Semin Hematol. 1989;26:19-24. 14. Mittelman A, Bertram J, Henry DH, et al. Treatment of patients with HIV thrombocytopenia and hemolytic uremic syndrome with protein A (Prosorba column) immunoadsorption . Semin Hematol. 1989;26:2615-2618. 15. Smith RE, Gottschall JL, Pisciotta AV. Life-threatening reaction to staphylococcal protein A immunomodulation . J Clin Apheresis. 1992;7:4-5.Crossref 16. Dzik WH, Duncan LM. Case records of the Massachusetts General Hospital . N Engl J Med. 1994;331:792-800. Case 35-1994.Crossref
Kanzler, Matthew H.;Dhillon, Inder;Headington, John T.
doi: 10.1001/archderm.1995.01690180086016
Abstract Background: Fibroblastic rheumatism was first described in the French literature in 1980. Since that time, 11 other patients with this disorder have been identified in the literature, mostly from France. This is a unique syndrome characterized by the sudden onset of symmetric polyarthritis and cutaneous nodules ranging from 5 to 20 mm in diameter, with predilection for the upper and lower extremities. While the cutaneous findings resolve spontaneously after several months, permanent joint sequelae are common. Observations: We present the first two patients with fibroblastic rheumatism reported in the United States. The clinical features and histologic findings were identical to those of patients described in the European literature. Conclusions: Fibroblastic rheumatism is a relatively rare syndrome characterized by the association of multiple cutaneous nodules with polyarthritis. The clustering of cases in France may, in part, be attributable to increased recognition by clinicians owing to prevalence of reports in the European literature. Perhaps, as clinicians in the United States become familiar with this disorder, further cases will be diagnosed, and the pathogenesis of the disorder will be elucidated.(Arch Dermatol. 1995;131:710-712) References 1. Chaouat Y, Aron-Brunetiere R, Faures B, et al. Une nouvelle entite: le rhumatisme fibroblastique: a propos d'une observation . Rev Rhum Ed Fr. 1980;47: 345-351. 2. Hernandez RJ, Headington JT, Kaufman RA, et al. Case report 511 . Skeletal Radiol. 1989;8:43-45.Crossref 3. Vignon-Pennamen M, Naveau B, Foldes C, et al. Fibroblastic rheumatism . J Am Acad Dermatol. 1986;14:1086-1087.Crossref 4. Barbaud A, Schmutz JL, Chemidling M, et al. Le rhumatisme fibroblastique . Ann Dermatol Venereol. 1990;117:828-830. 5. Crouzet J, Amouroux J, Duterque M, et al. Rhumatisme fibroblastique un cas avec etude de l'histologie synoviale . Rev Rhum Mal Osteoartic. 1982;49:469-472. 6. Leclech C, Croue A, Masson C, et al. Rhumatisme fibroblastique . Ann Dermatol Venereol. 1990;117:830-833. 7. Lacour JP, Maquart FX, Bellon G, et al. Fibroblastic rheumatism: clinical, histological, immunohistological, ultrastructural and biochemical study of a case . Br J Dermatol. 1993;128:194-202.Crossref 8. Levigne V, Perrot JL, Faisant M, et al. Rhumatisme fibroblastique . Ann Dermatol Venereol. 1990;117:199-202. 9. Ziegler G, Ortonne JP, Gagnerie F, et al. Le rhumatisme fibroblastique: a propos d'un cas avec etude de cultures de fibroblastes . Presented at the Seventh International Coference of Rheumatic Diseases; June 22-25, 1988; Aix-les-Bains, France. 10. Taccari E, Teodori S, Zoppini A. Le rheumatisme fibroblastique du sujet age . Rev Rhum Ed Fr. 1987;54:463-467. 11. Schiavon F, Punzi L, Fabiano F, et al. Sur un caso de rhumatismo fibroblastico: Ve Congres Latin de Rhumatologie, Florence, 1982 . Reumatismo . 1982; 34:226-227. 12. Ostlere LS, Stevens HP, Jarmulowicz M, et al. Fibroblastic rheumatism . Clin Exp Dermatol. 1994;19:268-270.Crossref 13. Crouzet J, Duterque M. Fibroblastic rheumatism: an 8-year follow-up . Clin Exp Rheumatol. 1990;8S:83.
doi: 10.1001/archderm.1995.01690180095017
Abstract REPORT OF A CASE A 3-year-old boy was examined because of a scalp mass that appeared 1 year earlier. Physical examination revealed a 0.6×0.8-cm, slightly erythematous nodule on the scalp (Figure 1). The biopsy specimen was stained with hematoxylin-eosin (Figure 2 and Figure 3).What is your diagnosis? DIAGNOSIS: Giant molluscum contagiosum. HISTOPATHOLOGIC FINDINGS Microscopic examination showed invagination of a keratotic column with an acanthotic epidermis having basophilic granular inclusion bodies as well as minute ovoid eosinophilic bodies. There was marked ulceration with acute nonspecific suppurative inflammation at the overhanging edge of the inverted keratotic column. DISCUSSION Molluscum contagiosum is a disease caused by the pox virus. Most commonly affected sites of typical molluscum contagiosum are the head, eyelids, trunk, and genitalia in temperate climates; the extremities are the most commonly affected sites in the tropics.1 Lesions in children commonly occur on the face, trunk References 1. Lowy DW. Muller's nodules, molluscum contagiosum . In: Fitzpatrick TB, Eisen AZ, Wolff K, et al. Dermatology in General Medicine , 3rd ed. New York, NY: McGraw-Hill International Book Co; 1987:2351-2352. 2. Linberg JV, Blaylock WK. Giant molluscum contagiosum following splenectomy . Arch Ophthalmol. 1990;108:1076.Crossref 3. Dickinson A, Tschen JA, Wolf JE. Giant molluscum contagiosum of the sole . Cutis. 1983;32:239-243. 4. Lever WF, Schaumburg-Lever G. Histopathology of the Skin. 7th ed. Philadelphia, Pa: JB Lippincott; 1989:409-411. 5. Arnold HL Jr, Odom RB, James WD. Andrews' Diseases of the Skin. 8th ed. Philadelphia, Pa: WB Saunders Co; 1990:461-463.
Guitart, Joan;Micali, Giuseppe;Norton, Scott A.
doi: 10.1001/archderm.1995.01690180097018pmid: 7778926
Abstract REPORT OF A CASE A 27-year-old man presented with a 2-year history of pruritic, scaly papules unresponsive to oral erythromycin. The papules began on his scalp and after a few months spread to his chest and upper arms. His personal and family history were negative for hair or scalp disorders, psoriasis, or cancer. The patient also complained of polydypsia and polyuria for the 4 to 5 months before presentation.Physical examination revealed numerous follicular-based erythematous crusted papules, mostly on the scalp (Figure 1 and Figure 2) with a few scattered on the trunk. Mild diffuse hair thinning of the scalp was present with no evidence of a scarring process or pustules. Otherwise, the physical and neurologic examination was unremarkable. The patient was treated with dicloxacillin, rifampin, topical clindamycin, and coal tar shampoo for a presumed diagnosis of acne necrotica miliaris, but his condition did not improve. The serum electrolytes, general References 1. Gianotti F, Caputo R. Histiocytic syndromes . J Am Acad Dermatol. 1985;13: 383-404.Crossref 2. Berry DH, Becton DL. Natural history of histiocytosis X . Hematol Oncol Clin North Am. 1987;1:23-34. 3. Favara BE, Jaffe R. Pathology of Langerhans cell histiocytosis . Hematol Oncol Clin North Am. 1987;1:75-97. 4. McLelland J, Chu AC. Comparison of peanut agglutinin and S100 stain in the paraffin tissue diagnosis of Langerhans cell histiocytosis . Br J Dermatol. 1988; 119:513-521.Crossref 5. Nethercott JR. Murray AH, Medwidsky W. Histiocytosis X in two adults . Arch Dermatol. 1983:119;157-161.Crossref 6. Lookingbill DP. Histiocytosis confined to the skin of the scalp . J Am Acad Dermatol. 1984:10;968-969.Crossref 7. Modi D, Schulz EJ. Skin ulceration as sole manifestation of Langerhans cell histiocytosis . Clin Exp Dermatol. 1990;16:212.Crossref
Clark, Johnson;Helm, Thomas N.;Bergfeld, Wilma F.
doi: 10.1001/archderm.1995.01690180099019
Abstract REPORT OF A CASE A 27-year-old well-nourished, anxious woman presented with a 6-year history of hair loss. She reported no significant medical problems and took no medications or extra vitamins. She had normal and regular menstrual periods. She described her mother and aunt as having thinning hair and her father as having male pattern baldness.The physical examination revealed a large irregular area of alopecia on the vertex and crown of her head (Figure 1 and Figure 2) with some residual hairs up to about 1 cm in length. There was no evidence of skin scaling, erythema, atrophy, or crusting on the scalp. Normal hair completely surrounded this alopecia. Eyebrows and eyelashes were normal. The skin on the rest of her body and inner fingernails was unremarkable. A biopsy specimen was obtained. Histologic findings are shown in Figure 3 and Figure 4.What is your diagnosis? Figure 1 . Figure 2 References 1. Muller S. Trichotillomania . Dermatol Clin. 1987:5:595-601. 2. Mehregan A. Trichotillomania . Arch Dermatol. 1970;102:129-133.Crossref 3. dimino-Emme L, Camisa G. Trichotillomania associated with the 'Friar Tuck sign' and nail biting . Cutis. 1991;47:107-110. 4. Slagle D, Martin T. Trichotillomania . Am Fam Pract. 1991;43:2019-2024. 5. Muller S. Trichotillomania . J Am Acad Dermatol. 1990;23:56-62.Crossref 6. Steck W. The clinical evaluation of pathologic hair loss . Cutis. 1979;24:293-301. 7. Bergfeld WF. Noninflammatory reactions of the pilosebaceous unit and disorders of the hair shaft . In: Farmer ER, Hood AF, eds. Pathology of the Skin. East Norwalk, Conn: Appleton & Lange; 1990:941-943. 8. Mehregan AH. Lesions of the hair and nail . In: Mehregan and Pinkus' Guide to Dermatohistopathology . 4th ed. East Norwalk, Conn: Appleton & Lange; 1986: 621. 9. Muller S, Winkleman R. Trichotillomania . Arch Dermatol. 1972;105:535-540.Crossref 10. Bergfeld W. Alopecia . Adv Dermatol. 1989;4:301-322. 11. Swedo S, Leonard H. A double-blind comparison of clomipramine and desipramine in the treatment of trichotillomania . N Engl J Med. 1989;321:497-501.Crossref
Bulengo-Ransby, Stella M.;Johnson, Carole;Metcalf, John S.
doi: 10.1001/archderm.1995.01690180101020
Abstract REPORT OF A CASE A 63-year-old man presented with a large nodule on his scalp. He reported the lesion to be present for 30 years; the lesion developed as an asymptomatic papule in a site of trauma. The lesion had slowly enlarged and recently ulcerated.On physical examination, a 5.5×5.0-cm ulcerated tumor draining purulent exudate was seen on the vertex of the scalp (Figure 1). There were hyperkeratotic columns and scale-crust on the surface of the tumor. No cervical or occipital lymphadenopathy was noted.An incisional biopsy and subsequent excision of the tumor with graft placement was performed (Figure 2 through Figure 4).What is your diagnosis? DIAGNOSIS: Proliferating trichilemmal cyst (PTC). HISTOPATHOLOGIC FINDINGS Compact hyperkeratosis and areas of scale-crust were seen. An intradermal tumor composed of lobulated, well-circumscribed squamous epithelium was seen extending to the subcutaneous fat. The lobules had a basaloid References 1. Mehregan AH, Lee KC. Malignant proliferative trichilemmal tumors . Dermatol Surg Oncol. 1987;13:1339-1342.Crossref 2. Lever WF, Schaumburg-Lever G. Histopathology of the Skin. 7th ed. Philadelphia, Pa: JB Lippincott Co; 1989;589-591. 3. Brownstein MH, Arluk DJ. Proliferating trichilemmal cyst . Cancer. 1981;48: 1207-1214.Crossref 4. Mehregan AH, Hardin I. Generalized follicular hamartoma, complicated by multiple proliferating trichilemmal cysts and palmar pits . Arch Dermatol. 1973; 107:435-438.Crossref
doi: 10.1001/archderm.1995.01690180106021
Abstract THIS ISSUE of the Archives contains a thought-provoking article describing 13 patients who developed druginduced toxic epidermal necrolysis (TEN), while they were receiving systemic corticosteroids. After reviewing the data on these 13 patients culled from the records of 179 patients with TEN, the authors conclude that ''longterm steroid therapy may delay the onset of TEN but does not halt its progression.''1 Most articles in the past 10 years confirm that steroids do not have any beneficial effect on TEN, yet the subject continues to be controversial. Since the more serious variants of erythema multiforme such as Stevens-Johnson syndrome (SJS) and TEN are among the most lifethreatening emergencies that a dermatologist is likely to see, a brief editorial on their treatment seems appropriate. Is there a standard of care? Should we be concerned about doing ''nothing''? What will produce the best results for our patients? To discuss therapy, we need References 1. Guibal F, Bastuji-Garin S, Chosidow O, Saiag P, Revuz J, Roujeau J-C. Characteristics of toxic epidermal necrolysis in patients undergoing long-term glucocorticoid therapy . Arch Dermatol. 1995;131:669-672.Crossref 2. von Hebra F. Erythema exudativum multiforme . In: On Diseases of the Skin . 2nd ed. London, England: New Sydenham Society; 1866:285. Reprinted by Charles C Thomas Publisher, 1970:105-109. 3. Roujeau JC, Chosidow O, Saiag P, Guillaume JC. Toxic epidermal necrolysis (Lyell syndrome) . J Am Acad Dermatol. 1990;23:1039-1058.Crossref 4. Ruiz-Maldonado R. Acute disseminated epidermal necrosis types 1, 2 and 3: a study of 60 cases . J Am Acad Dermatol. 1985;13:623-635.Crossref 5. Bastuji-Garin S, Rzany B, Stern RS, Shear NH, Naldi L, Roujeau JC. Clinical classification of cases of toxic epidermal necrolysis, Stevens-Johnson syndrome, and erythema multiforme . Arch Dermatol. 1993;129:92-96.Crossref 6. Guillaume JC, Roujeau JC, Revuz J, Penso D, Touraine R. The culprit drug in 87 cases of toxic epidermal necrolysis (Lyell syndrome) . Arch Dermatol. 1987; 123:1166-1170.Crossref 7. Kauppinen K, Stubb S. Drug eruptions: causative agents and clinical types: a series of inpatients during a ten year period . Acta Dermatol Venereol. 1984; 64:320-324. 8. Schopf E, Stuhmer A, Rzany B, Victor N, Zentgraf R, Kapp JF. Toxic epidermal necrolysis and Stevens-Johnson syndrome: an epidemiological study from West Germany . Arch Dermatol. 1991;127:839-842.Crossref 9. Chan HL, Stern RS, Arndt KA, et al. The incidence of erythema multiforme, Stevens-Johnson syndrome, and toxic epidermal necrolysis: a populationbased study with particular reference to reactions caused by drugs among outpatients . Arch Dermatol. 1990;126:43-47.Crossref 10. Strom BL, Carson JL, Halpern AC, et al. A population-based study of Stevens-Johnson syndrome: incidence and antecedent drug exposures . Arch Dermatol. 1991;127:831-838.Crossref 11. Leenutaphong V, Sivayathorn A, Suthipinittharn P, Sunthonpalin P. Stevens-Johnson syndrome and toxic epidermal necrolysis in Thailand . Int J Dermatol. 1993;32:428-431.Crossref 12. Correia O, Delgado L, Ramos JP, Resende C, Torrinha JAF. Cutaneous T-cell recruitment in toxic epidermal necrolysis: further evidence of CD8+ lymphocyte involvement . Arch Dermatol. 1993;129:466-468.Crossref 13. Friedmann PS, Strickland I, Pirmohamed M, Park BK. Investigation of mechanism in toxic epidermal necrolysis induced by carbamazepine . Arch Dermatol. 1994;130:598-604.Crossref 14. Roujeau JC, Bracq C, Huynh NT, Chaussalete F, Raffin C, Duedari N. HLA phenotypes and bullous cutaneous reactions to drugs . Tissue Antigens. 1986;28: 251-254. 15. Roujeau JC, Huynh N, Bracq C, Guillaume JC, Revuz J, Touraine R. Genetic susceptibility to toxic epidermal necrolysis . Arch Dermatol. 1987;123:1171-1173.Crossref 16. Sayama K, Watanabe Y, Tohyama M, Miki Y. Localization of perforin in viral vesicles and erythema multiforme . Dermatology. 1994;188:305-309.Crossref 17. Nickoloff BJ. Role of interferonγ in cutaneous trafficking of lymphocytes with emphasis on molecular and cellular adhesion events . Arch Dermatol. 1988; 124:1835-1843.Crossref 18. Wrone-Smith T, Johnson T, Nelson B, et al. Discordant expression of Bcl-x and Bcl-2 by keratinocytes in vitro and psoriatic keratinocytes in vivo . Am J Pathol. In press. 19. Haake AR, Polaskowska RR. Cell death by apoptosis and epidermal biology . J Invest Dermatol. 1993;101:107-112.Crossref 20. Foedinger D, Anhalt GJ, Boecskoer B, Elbe A, Wolff K, Rappersberger K. Autoantibodies to desmoplakin I and II in patients with erythema multiforme . J Exp Med. 1995;181:169-179.Crossref 21. Patterson R, Miller M, Kaplan M, et al. Effectiveness of early therapy with corticosteroids in Stevens-Johnson syndrome: experience with 41 cases and a hypothesis regarding pathogenesis . Ann Allergy. 1994;73:27-34.Crossref 22. Wilkel CS, McDonald CJ. Cyclosporine therapy for bullous erythema multiforme . Arch Dermatol. 1990;126:397-398.Crossref 23. Heng MCY, Allen SG. Efficacy of cyclophosphamide in toxic epidermal necrolysis: clinical and pathophysiological aspects . J Am Acad Dermatol. 1991;25: 778-786.Crossref 24. Parsons JM. Toxic epidermal necrolysis . Int J Dermatol. 1992;31:749-767.Crossref 25. Ruocco V, Bimonde D, Luongo C, et al. Hyperbaric oxygen treatment of toxic epidermal necrolysis . Cutis. 1986;38:267-271. 26. Tatnall FM, Schofield J, Proby C, Leigh IM. A double blind placebo controlled trial of continuous acyclovir in recurrent erythema multiforme . Br J Dermatol. 1991;125( (suppl 38) ):29. 27. Schofield JK, Tatnall FN, Leigh IM. Recurrent erythema multiforme: clinical features and treatment in a large series of patients . Br J Dermatol. 1993;128: 542-545.Crossref
Peñas, Pablo F.;Jones-Caballero, María;García-Díez, Amaro
doi: 10.1001/archderm.1995.01690180111022pmid: 7778931
Abstract We read with interest the article by Stone et al1 in the June 1994 issue of the Archives. They report two cases of rudimentary meningocele (type I or primary cutaneous meningioma2) that presented at birth with a prominent tuft of hair located on the scalp. The authors opine that primary cutaneous meningiomas are developmental defects similar to meningoceles. This has been the prevalent opinion in the literature, but we have described a patient with a congenital localized hypertrichosis on the left lumbar region that showed the histologic and immunohistochemical features of a primary cutaneous meningioma (with no connection to the central nervous system), making the meningocele mechanism unlikely.3 Theaker et al4 have suggested that these lesions represent the continued growth of meningeal cells, displaced with cutaneous nerves, within the perineural environment that normally supports the growth and development of a related cell type. A literature search References 1. Stone MS, Walker PS, Kennard CD. Rudimentary meningocele presenting with a scalp hair tuft . Arch Dermatol. 1994;130:775-777.Crossref 2. Lopez DA, Silvers DN, Helwig EB. Cutaneous meningiomas: a clinicopathologic study . Cancer. 1974;34:728-744.Crossref 3. Peñas PF, Jones-Caballero M, Amigo A, Aragüés M, García-Díez A. Cutaneous meningioma underlying congenital localized hypertrichosis . J Am Acad Dermatol. 1994;30:363-366.Crossref 4. Theaker JM, Fletcher CD, Tudway AJ. Cutaneous heterotopic meningeal nodules . Histopathology. 1990;16:475-479.Crossref 5. Daugaard S. Ectopic meningioma of a finger: case report . J Neurosurg. 1983; 58:778-780.Crossref 6. Tron V, Bellamy C, Wood W. Familial cutaneous heterotopic meningeal nodules . J Am Acad Dermatol. 1993;28:1015-1017.Crossref
doi: 10.1001/archderm.1995.01690180111023
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 Forgot to turn on the flash? Tired of red eyes, dead batteries, burned-out flash cubes, cumbersome flash units? Never got around to buying that expensive, bulky macro lens? Described is a simple photographic technique enabling one to take high-quality medical prints and/or slides without the use of either a flash or a macro lens. By employing a standard singlelens reflex (commonly known as SLR) camera, highspeed film, and inexpensive close-up lenses, one can obtain excellent photodocumentation with fluorescent office lighting. This is a technique that I have been utilizing over the past several years. The convenience is unsurpassed and results yield high-quality photographs suitable for publication. Materials and Methods. The trick is to utilize highspeed film, namely film with an ISO (International Standards Organization) of 1000 such as Kodak Ektar 1000, which is widely available at most photography stores. High-speed film obviates the need for both a tripod and a
Ishiko, Akira;Hashimoto, Takashi;Shimizu, Hiroshi;Masunaga, Takuji;Nishibori, Yukiko;Watanabe, Kyoko;Nishikawa, Takeji
doi: 10.1001/archderm.1995.01690180112024
Abstract Pemphigus foliaceus (PF) and bullous pemphigoid (BP) are blistering skin diseases caused by autoantibodies against the keratinocyte cell surface or the basement membrane zone (BMZ) of the epidermis, respectively. These diseases rarely coexist, with only three such cases reported.1-3 However, none has been studied by immunoelectron microscopy. In only one case was immunoprecipitation used to confirm the coexistence at the molecular level.3 We report coexistent PF and BP, in which a reactivity of the autoantibodies was studied by both immunoblot and immunoelectron micro scopic examination. Report of a Case. A 63-year-old Japanese man visited us complaining of blisters and erosions that involved almost the entire body. He had noticed crusted erythema on his back and had been treated under a diagnosis of PF for 6 years until tense vesicles and blisters developed rapidly on the trunk and extremities 3 months before his presenttion. Physical examination showed erythema with References 1. Harrington CI, Sneddon UB. Coexistence of bullous pemphigoid and pemphigus foliaceus . Br J Dermatol. 1979;100:441-445.Crossref 2. Rantanen T, Niemi KM. A further case of coexisting bullous pemphigoid and pemphigus foliaceus . Br J Dermatol. 1979;101:611-612. 3. Korman NJ, Stanley JR, Woodley DT. Coexistence of pemphigus foliaceus and bullous pemphigoid . Arch Dermatol. 1991;127:387-390.Crossref 4. Hashimoto T, Ogawa MM, Konohana A, Nishikawa T. Detection of pemphigus foliaceus antigens by immunoblot analysis using different antigen sources . J Invest Dermatol. 1990;94:327-331.Crossref 5. Shimizu H, McDonald JN, Kennedy AR, Eady RAJ. Demonstration of intraand extracellular localization of bullous pemphigoid antigen using cryofixation and freeze substitution for postembedding immunoelectron microscopy . Arch Dermatol Res. 1989;281:443-448.Crossref 6. Shimizu H, Masunaga T, Ishiko A, et al. Demonstration of desmosomal antigens by electron microscopy using cryofixed and cryosubstituted skin with silver-enhanced gold probe . J Histochem Cytochem. 1994;42:687-692.Crossref 7. Ishliko A, Shimizu H, Kikuchi A, Ebihara T, Hashimoto T, Nishikawa T. Human autoantibodies against the 230-kd bullous pemphigoid antigen (BPAG1) bind only to the intracellular domain of the hemidesmosome, whereas those against the 180-kd bullous pemphigoid antigen (BPAG2) bind along the plasma membrane of the hemidesmosome in normal human and swine skin . J Clin Invest. 1993;91:1608-1615.Crossref
Halder, Rebat M.;Battle, Eliot F.;Smith, Elaine M.
doi: 10.1001/archderm.1995.01690180114025
Abstract Vitiligo is an acquired, sometimes familial, depigmentation disorder of the skin and hair. Oral or topical psoralen photochemotherapy (PUVA) is the most popular and efficacious treatment currently available in the United States for repigmentation of vitiliginous patches.1 However, the long-term safety of this treatment is still under investigation, and further studies are warranted. There are limited published studies examining the long-term risk in patients with vitiligo who have been treated with oral PUVA therapy. We found no published studies examining the long-term risk in patients with vitiligo treated with topical PUVA therapy. A study of 59 patients with vitiligo, who received oral PUVA therapy from 1972 through 1986, reported no incidence of skin cancers, actinic keratoses, or lentigines.2 Likewise, a 1984 study examining 596 East Indian patients with vitiligo, who were treated with oral psoralen and sunlight (PUVASOL), reported that no increased risk of cutaneous carcinoma was apparent References 1. Nordlund JJ, Halder RM, Grimes P. Management of vitiligo . Dermatol Clin . 1993;11:27-33.Crossref 2. Wildfang IL,Jacobsen FK, Thestrup-Pedersen K. PUVA treatment of vitiligo: a retrospective study of 59 patients . Acta Derm Venereol (Stockh) . 1992;72: 305-306. 3. Harrist TJ, Pathak MA, Mosher DB, et al. Chronic cutaneous effects of longterm psoralen and ultraviolet radiation therapy in patients with vitiligo . Natl Cancer Inst Monogr. 1984;66:191-196. 4. Haider RM. Topical PUVA therapy for vitiligo . Dermatol Nurs. 1991;3:178-180. 5. Stern RS, Lange R. Nonmelanoma skin cancer occurring in patients treated with PUVA five to ten years after first treatment . J Invest Dermatol. 1988;91: 120-124.Crossref
doi: 10.1001/archderm.1995.01690180115026
Abstract Lentigo maligna can be defined as ''melanoma in situ,'' histologically showing atypical melanocytes confined to the epidermis and appendageal epithelium. The clinical appearance of lentigo maligna features inhomogeneously pigmented, polycyclic macules arising predominantly in sun-exposed areas in elderly whites (Figure, left). The lesions tend to enlarge slowly in a horizontal direction. They may, within years, give rise to metastatic disease. Complete but conservative excision should be the treatment of choice to achieve accurate microstaging and to reduce the likelihood of recurrence. In patients showing hazardous health conditions due to systemic diseases, malformations, or advanced age, or presenting with large lentigo maligna lesions in cosmetically precarious locations that require flaps or skin grafts, surgical excision may be not be possible. We performed carbon dioxide laser vaporization of histopathologically verified lentigo maligna lesions in four selected patients (Table). Materials and Methods. Carbon Dioxide Laser. The carbon dioxide laser emits invisible infrared light References 1. Coleman WP, Davis RS, Reed RJ, et al. Treatment of lentigo maligna and lentigo maligna melanoma . J Dermatol Surg Oncol. 1980;6:476-479.Crossref 2. Nazzarro-Porro M, Passi S, Balus L, et al. Effect of dicarboxylic acids on lentigo maligna . J Invest Dermatol. 1979;72:296-305.Crossref 3. Goldschmidt H, Breneman JC, Breneman DL. Ionizing radiation therapy in dermatology . J Am Acad Dermatol. 1994;30:157-182.Crossref 4. Arndt KA. New pigmented macule 4 years after argon laser treatment of lentigo maligna . J Am Acad Dermatol. 1986;14:1092.Crossref 5. Arndt KA, Noe JM. Lasers in dermatology . Arch Dermatol. 1982;118:293-295.Crossref
Lui, Harvey;Salasche, Stuart;Kollias, Nikiforos;Flotte, Thomas;McLean, David;Anderson, R. Rox
doi: 10.1001/archderm.1995.01690180117027
Abstract In dermatology, photodynamic therapy (PDT) has been used primarily for treating malignant skin tumors and involves the sequential administration of photosensitizing drugs and light to patients. Aminolevulinic acid is a naturally occurring porphyrin precursor that can photosensitize cutaneous neoplasms for destruction by light when applied topically in pharmacologic doses. Exogenous topical aminolevulinic acid appears to be taken up preferentially by tumors and metabolized in situ to protoporphyrin IX, a photosensitive compound.1,2 Kennedy et al1,2 reported first on the use of topical aminolevulinic acid and red light to photosensitize skin tumors in patients. There has been limited longterm clinical follow-up data concerning patients treated with aminolevulinic acid and light, and there is also a lack of detailed histologic studies assessing microscopic tumor responses to therapy. Subjects and Methods. Five patients with one or more biopsy-proven and previously untreated basal cell or squamous cell (in situ or invasive) carcinomas measuring References 1. Kennedy JC, Pottier RH, Pross DC. Photodynamic therapy with endogenous protoporphyrin, IX: basic principles and present clinical experience . J Photochem Photobiol B Biol. 1990;6:143-148.Crossref 2. Kennedy JC, Pottier RH. Endogenous protoporphyrin, IX: a clinically useful photosensitizer for photodynamic therapy . J Photochem Photobiol B Biol. 1992; 14:275-292.Crossref 3. Goff BA, Bachor R, Kollias N, Hasan T. Effects of photodynamic therapy with topical application of 5-aminolevulinic acid on normal skin of hairless guinea pigs . J Photochem Photobiol B Biol. 1992;15:239-251.Crossref 4. Wolf P, Rieger E, Kerl H. Topical photodynamic therapy with endogenous porphyrins after application of 5-aminolevulinic acid: an alternative treatment modality for solar keratoses, superficial squamous cell carcinomas, and basal cell carcinomas? J Am Acad Dermatol. 1993;28:17-21.Crossref 5. Cairnduff F, Stringer MR, Hudson EJ, Ash DV, Brown SB. Superficial photodynamic therapy with topical 5-aminolevulinic acid for superficial primary and secondary skin cancer . Br J Cancer. 1994;69:605-608.Crossref
Cambiaghi, Stefano;Tadini, Gianluca;Barbareschi, Mauro;Caputo, Ruggero
doi: 10.1001/archderm.1995.01690180118028
Abstract Olmsted syndrome is a rare disorder of keratinization appearing at birth or in early infancy that is characterized by the unusual association of palmoplantar keratoderma and periorificial hyperkeratosis, with possible involvement of other ectodermal derivatives.1-6 We report the second familial case, showing a progressive course unresponsive to conventional treatment. Report of a Case. The patients are monozygotic male twins, born at term to nonconsanguineous parents, aged 29 (father) and 25 (mother) years. At 4 months of age, both children developed bilateral palmoplantar keratoderma and keratotic lesions at the external acoustic meatus. Familial history was negative for any related skin disorders.Examination at age 15 months showed symmetrical, thick, sharply marginated, and yellowish areas of hyperkeratosis affecting the plantar surface of the forefeet and of the first and fifth toes. The lesions were surrounded by an erythematous border and extended onto the lateral aspects of the toes. A periodic complete References 1. Olmsted HC. Keratodermia palmaris et plantaris congenitalis: report of a case showing associated lesions of unusual location . AJDC. 1927;33:757-764. 2. Poulin Y, Perry HO, Muller SA. Olmsted syndrome: congenital palmoplantar and periorificial keratoderma . J Am Acad Dermatol. 1984;10:600-610.Crossref 3. Atherton DJ, Sutton C, Jones BM. Mutilating palmoplantar keratoderma with periorificial keratotic plaques (Olmsted's syndrome) . Br J Dermatol. 1990; 122:245-252.Crossref 4. Ueda M, Nakagawa K, Hayashi K, Shimizu R, Ichihashi M. Partial improvement of Olmsted syndrome with etretinate . Pediatr Dermatol. 1993;10:376-381.Crossref 5. Battini ML, Moretti S, Giovannucci Uzielli ML, Happle R. Olmsted syndrome: a case associated with severe corneal opacities . In: Caputo R, Gelmetti C, eds. Proceedings of the Fifth International Congress of Pediatric Dermatology; July 11-15, 1989; Milan, Italy . 6. Hauber I, Frantzmann Y, Anton-Lamprecht I, Estes S, Frosch PJ. Olmsted-Syndrom. Erfolgreiche Therapie durch behandlung mit Etretinat . Hautarzt. 1993;44:394-400.
Berger, Timothy G.;Kerschmann, Russell L.;Roth, Rudolph;Schulze, Karen;Zackheim, Herschel S.
doi: 10.1001/archderm.1995.01690180119029
Abstract We have followed a patient with human immunodeficiency virus (HIV) infection and erythrodermic cutaneous T-cell lymphoma (CTCL). He eventually developed tumor-stage disease and large numbers of circulating atypical helper T cells (Sézary's syndrome). He suffered progression of HIV disease to the acquired immunodeficiency syndrome with a rising helper T-cell count and no development of opportunistic infections. Report of a Case A 51-year-old black male airplane mechanic with frequent and long-term expsoure to chemicals and solvents presented in 1988 with widespread erythema, exfoliation, and scaling plaques on the trunk. A serologie test for syphilis was positive at 1:32 and confirmed with a reactive fluorescent treponemal antibody-absorption test. Treatment for syphilis led to no improvement of the eruption but return of the VDRL to negative in 1 year. Serologie testing for HIV was positive. At the time of the diagnosis of HIV, his helper T-cell count was 0.50×109/L and the helper-to-suppressor ratio was 1:1. Over the next 4 years, his skin eruption became more References 1. Fletcher V, Zackheim HS, Beckstead JH. Circulating Sézary cells: a new preparatory method for their identification and enumeration . Arch Pathol Lab Med. 1984;108:954-958. 2. Crane GA, Variakojis D, Rosen ST, et al. Cutaneous T-cell lymphoma in patients with human immunodeficiency virus infection . Arch Dermatol. 1991; 127:989-994.Crossref 3. Nahass GT, Kraffert CA, Penneys NS. Cutaneous T-cell lymphoma associated with the acquired immunodeficiency syndrome . Arch Dermatol. 1991; 127:1020-1022.Crossref 4. Parker SC, Fenton DA, McGibbon DH. Homme rouge and the acquired immunodeficiency syndrome . N Engl J Med. 1989;321:906-907. 5. Dreno B, Milpied-Homsi B, Moreau P, et al. Cutaneous anaplastic T-cell lymphoma in a patient with human immunodeficiency virus infection: detection of Epstein-Barr virus DNA . Br J Dermatol. 1993;129:77-81.Crossref 6. Burns MK, Cooper KD. Cutaneous T-cell lymphoma associated with HIV infection . J Am Acad Dermatol. 1993;29;394-399.Crossref 7. Heald P, Yan SL, Edelson R. Profound deficiency in normal circulating T cells in erythrodermic cutaneous T-cell lymphoma . Arch Dermatol. 1994; 130:198-203.Crossref 8. Pancake BA, Zucker-Franklin D. HTLV tax and mycosis fungoides . N Engl J Med. 1993;329:580.Crossref 9. Herndier BG, Shiramizu BT, Jewett NE, et al. Acquired immunodeficiency syndrome-associated T-cell lymphoma: evidence for human immunodeficiency virus type 1—associated T-cell transformation . Blood. 1992;79:1768-1774. 10. Shiramizu B, Herndier BG, McGrath MS. Identification of a common clonal human immunodeficiency virus integration site in human immunodeficiency virus—associated lymphomas . Cancer Res. 1994;54:2069-2072.
Guédénon, A.;Zinsou, C.;Josse, R.;Andélé, K.;Pritze, S.;Portaels, F.;Meyers, Wayne M.
doi: 10.1001/archderm.1995.01690180121030
Abstract After tuberculosis and leprosy, Mycobacterium ulcerans infection (Buruli ulcer) is the third most important and probably the third most common mycobacterial disease of immunocompetent human.1 Buruli ulcers often cause massive destruction of skin and subcutaneous tissue that, without appropriate therapy, often leave grossly deforming sequelae.2 Wide excision of the ulcers with subsequent skin grafting and physical therapy prevents many of these disastrous results. Buruli ulcers prevail in focal riverine and swampy localities of numerous tropical regions, including most countries of West Africa, and afflict many impoverished inhabitants, primarily children, of remote areas where the amenities of modern medical science are unavailable or too expensive. In 1988, Muelder3 was the first to describe a patient with Buruli ulcer in Bénin. Subsequent observations suggest a relatively high prevalence in Bénin.4 In 1993, for example, the dispensary of the Catholic Mission of Zangnanado, one of the few centers in References 1. Portaels F. Mycobacterioses . In: Janssens PG, Kivits M, Vuylsteke J, eds. Médecine et hygiène en Afrique Centrale de 1885 à nos jours . Brussels, Belgium: Fondation Roi Baudoin; 1992;1:1207. 2. Connor DH, Meyers WM, Krieg RE. Infection by Mycobacterium ulcerans . In: Binford CH, Connor DH, eds. Pathology of Tropical and Extraordinary Diseases . Washington, DC: Armed Forces Institute of Pathology; 1976;1:226. 3. Muelder K. Buruli ulcer in Bénin Trop Doctor . 1988;18:53. 4. Josse R, Lorenzo A, Zinsou C, et al. Etude clinique et épidémiologique de l'ulcère de Buruli chez le jeune au Bénin Cahiers Sante . 1992;2:23-27. 5. Meyers WM, Shelly WM, Connor DH, Meyers EK. Human Mycobacterium ulcerans infections developing at sites of trauma to skin . Am J Trop Med Hyg . 1974;23:919-923. 6. Mitchell PJ, Jerrett IV, Slee KJ. Skin ulcers caused by Mycobacterium ulcerans in koalas near Bairnsdale, Australia . Pathology . 1984;16:256-260.Crossref 7. Read RG, Heggie CM, Meyers WM, Connor DH. Cytotoxic activity of Mycobacterium ulcerans . Infect Immun . 1974;9:1114-1122. 8. Atherton DJ. Towards the safer use of traditional remedies . BMJ . 1994;308: 673-674.Crossref
Saff, Deborah M.;Taylor, James S.;Vidimos, Allison T.
doi: 10.1001/archderm.1995.01690180122031
Abstract Corticosteroids can sensitize patients when used orally, parenterally, or intralesionally. We report delayed-type hypersensitivity to intralesional sterile triamcinolone acetonide suspension USP (Kenalog-40), which is rarely reported in the literature. Report of a Case. A 60-year-old woman presented for treatment of an 18-cm sternal hypertrophic scar. Treatment of this scar with an intralesional corticoid 3 years earlier had resulted in erythema and pruritus along the entire length of the midline scar approximately 12 to 18 hours after injection. The reaction resolved in approximately 3 weeks without treatment.Because of the earlier reaction, a test dose of 0.2 mL of intralesional sterile triamcinolone acetonide suspension USP (Kenalog-40) was injected in a 2-cm chest tube scar inferior to her sternal scar. About 8 hours later, she noticed erythema and pruritus along the length of the horizontal scar and superior margin of the sternal scar, which resolved over a 2-week period. She denied any previous contact allergies. She had References 1. Rasanen L, Hasan T. Allergy to systemic and intralesional corticosteroids . Br J Dermatol. 1993;128:407-411.Crossref 2. Fisher AA. Allergic reactions to intralesional and multiple topical corticosteroids . Cutis. 1979;23:564, 708-709. 3. Karck E. Sensitivity to fluorinated steroids presenting as a delayed hypersensitivity . Contact Dermatitis. 1980;6:214-216.Crossref 4. Wilkinson SM. Hypersensitivity to topical corticosteroids . Clin Exp Dermatol. 1994;19:1-11.Crossref 5. Preuss L. Allergic reactions to systemic glucocorticoids: a review . Ann Allergy. 1985;55:772-775. 6. Mathias CG, Robertson DB. Delayed hypersensitivity to a corticosteroid suspension containing methylprednisolone . Arch Dermatol. 1985;121:258-261.Crossref
doi: 10.1001/archderm.1995.01690180123032
Abstract Herpetic whitlow is a herpes simplex virus (HSV) infection of a digit. Medical and dental personnel are at risk for herpetic whitlow because of exposure to oral secretions containing HSV,1 and patients with clinical HSV oral and genital infections are at risk because of autoinoculation.2,3 The following is a case report of an infant who contracted a herpetic whitlow without specific exposure to HSV. Report of a Case. An 8-month-old boy presented to his physician with a 1-day history of fever and irritability. Physical examination revealed erythema of the distal digit of his index finger with a blister at the finger tip. The patient was given oral cephalexin for cellulitis. Over the next 2 days, blisters developed proximally, and he was referred to the University of Connecticut Health Center, Farmington. At this time, the patient was irritable, febrile (rectal temperature, 38.3°C), and had erythema of Erythema and blisters of the References 1. Stern H, Elek SD, Millar DM, et al. Herpetic whitlow: a form of crossinfection in hospitals . Lancet. 1959;2:871-874.Crossref 2. Glogau R, Hanna L,Jawetz E. Herpetic whitlow as part of a genital virus infection . J Infect Dis. 1977;136:689-692.Crossref 3. Feder HM Jr, Long SS. Herpetic whitlow: epidemiology, clinical characteristics, diagnosis, and treatment . AJDC , 1983;137:861-863. 4. Gill MJ, Arlette J, Buchan K. Herpes simplex virus infection of the hand: a profile of 79 cases . Am J Med. 1988;84:89-93.Crossref 5. Berkowitz RL, Hentz VR. Herpetic whitlow: a non-surgical infection of the hand . Plast Reconstr Surg. 1977;60:125-127.Crossref 6. Haburchak DR. Recurrent herpetic whitlow due to herpes simplex virus type 2 . Arch Intern Med. 1978;138:1418-1419.Crossref 7. Schleiss MR, Fong W. Primary palmar herpes simplex virus 1 infection in a 10-year-old girl . Pediatr Infect Dis J. 1922;11:338-339.Crossref 8. Feder HM Jr, Geller RW. Herpetic whitlow of the great toe . N Engl J Med. 1922;326:1295-1296. 9. Gill MJ, Arlette J, Buhan KA. Herpes simplex virus infection of the hand . J Am Acad Dermatol. 1990;22:111-116.Crossref 10. Whitley RJ, Gnann JW, Acyclovir: a decade later . N Engl J Med. 1992;327: 782-789.Crossref 11. Laskin OL. Acyclovir and suppression of frequently recurring herpetic whitlow . Ann Intern Med. 1985;102:494-495.Crossref 12. Gill MJ, Arlette J, Tyrrell DL, Buchan KA. Herpes simplex virus infection of the hand: clinical features and management . Am J Med. 1988;85( (suppl 2A) ): 53-55.Crossref
Dereure, O.;Montes, B.;Guilhou, J. J.
doi: 10.1001/archderm.1995.01690180124033
Abstract Human parvovirus B19 has been recognized as the causative agent of a number of cutaneous eruptions, including classic erythema infectiosum or fifth disease; some less well-defined, often purpuric, acute exanthematous eruptions; vasculitis; and the recently described petechial glove-and-sock syndrome.1,2 On the other hand, acute infection with parvovirus B19 may trigger a number of visceral manifestations. We report a new cutaneous manifestation of parvovirus B19 as a primary infection with a striking generalized livedo reticularis, occurring simultaneously with an impressive myasthenialike muscular weakness. Report of a Case. A 29-year-old woman was first referred to our institution in December 1993 for the evaluation of a recent, generalized livedo reticularis with fever and general alteration in her health. Her medical history was unremarkable, and she denied taking any medication. The disease began about 4 days before her admission to the hospital; it had an acute onset, consisting of a temperature as high as 40°C and chills, rapidly followed by generalized and increasing muscular weakness, and, eventually, by an extensive livedo reticularis. Initial examination revealed an acutely ill, febrile patient (temperature, 38°C) with myalgias and impressive References 1. Anderson MJ, Jones SE, Fisher-Hoch SP, et al. Human parvorvirus: the cause of erythema infectiosum (fifth disease)? Lancet. 1983;1:1378.Crossref 2. Halasz CLG, Cormier D, Den M. Petechial glove and sock syndrome caused by parvovirus B19 . J Am Acad Dermatol. 1992;27:835-838.Crossref 3. Woolf AD, Campion GV, Chishick A, et al. Clinical manifestations of human parvovirus B19 in adults . Arch Intern Med. 1989;149:1153-1156.Crossref 4. Saint-Martin J, Choulot JJ, Bonnaud E, Morinet F. Myocarditis caused by parvovirus . J Pediatr. 1990;116:1007.Crossref 5. Walsh KJ, Armstrong RD, Turner AM. Brachial plexus neuropathy associated with human parvovirus infection . BMJ. 1988;296:896.Crossref
doi: 10.1001/archderm.1995.01690180128034
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 1986, I evaluated the first edition of Diseases of the Nails and Their Management (Dermatol Surg Oncol. 1986; 12:987-988). The review was mixed. In the second edition, Baran and Dawber consolidated new information, enhanced figures and tables, and completely renovated the original. Diseases is the best current reference text on the subject of nail diseases. Substantial time, energy, and effort went into preparation of this new edition. Coverage of onychology is complete, current, and balanced. Each chapter was written by one or both of the authors. The decision to write and edit each chapter achieved its intended result. The chapters are cohesive, well-organized, and uniform in writing style and format. Duplicate coverage of topics in different sections of the book occurred by design, not by chance. The index is encyclopedic, easy to use, and complete. Its brief perusal offers a comprehensive differential diagnosis of sundry disorders including clubbing, Beau's lines,