Archives of Dermatology

1988 Archives of Dermatology

doi: 10.1001/archderm.1988.01670060005001

Abstract Scabies in Health-Care Facilities—Iowa SCABIES continues to occur among residents and staff of Iowa nursing homes and hospitals. For the 8-year period July 1979-June 1987, the Iowa Department of Public Health confirmed scabies in 25 nursing homes, 1 hospital, 1 state institution, and 1 county residential care facility. Reports of scabies were received from 11 other facilities. A report of the investigation of this problem in three nursing homes follows. Facility 1. In September 1985, scabies mites were found on three of seven nursing home patients with lesions suggestive of the disease. Skin scrapings from one of these patients yielded mites and eggs. He was successfully treated with an appropriate regimen of lindane lotion. The three visiting physical therapists who had treated the patient were also evaluated. Two had pruritic lesions compatible with scabies. A live mite was recovered in skin scrapings from one therapist, who was referred to her References 1. Orkin M. Resurgence of scabies . JAMA 1971;217:593-7.Crossref 2. Orkin M, Maiback HI. Current concepts in parasitology: this scabies pandemic . N Engl J Med 1978;298:496-8.Crossref 3. Juranek DD, Currier RW, Millikan LE. Scabies control in institutions . In: Orkin M, Maiback HI, eds. Cutaneous infestations and insect bites . New York: Dekker, 1985:139-56. 4. Lerche NW, Currier RW, Juranek DD, Baer W, Dubay NJ. Atypical crusted "Norwegian" scabies: report of nosocomial transmission in a community hospital and an approach to control . Cutis 1983;31:637-42, 668, 684. 5. Cooper CL, Jackson MM. Outbreak of scabies in a small community hospital . Am J Infect Control 1986;14:173-9.Crossref 6. Currier RW. Scabies and pediculosis: hospitalized mites and lice . Asepsis—The Infection Control Forum 1984;6:13-21. 7. Use of trade names is for identification only and does not imply endorsement by the U.S. Department of Health and Human Services or the Public Health Service. 8. Use of trade names is for identification only and does not imply endorsement by the U.S. Department of Health and Human Services or the Public Health Service. 9. de la Cruz E, Sun S, Vangvanichyakorn K, Desposito F. Multiple congenital malformations associated with maternal isotretinoin therapy . Pediatrics 1984;74:428-30. 10. Rosa FW, Wilk AL, Kelsey FO. Teratogen update: vitamin A congeners . Teratology 1986; 33:355-64.Crossref 11. Lammer EJ, Chen DT, Hoar RM, et al. Retinoic acid embryopathy . N Engl J Med 1985; 313:837-41.Crossref 12. Rosa FW. Teratogenicity of isotretinoin (Letter) . Lancet 1983;2:513.Crossref 13. Food and Drug Administration. Etretinate approved . FDA Drug Bull 1986;16:16-7. 14. Roche Laboratories. Tegison brand of etretinate/Roche capsules (Package Insert) . Nutley , New Jersey: Hoffmann-La Roche, Roche Laboratories, 1986. 15. Medical Economics Company. Physicians' desk reference . 42nd ed. Oradell , New Jersey: Medical Economics Company, 1988:1705, 1746.

Fuchs, Jürgen

1988 Archives of Dermatology

doi: 10.1001/archderm.1988.01670060007002

Abstract To the Editor.— I would like to comment on the recent article by Schallreuter and Pittelkow1 on thioredoxin-reductase activity in psoriasis and its inhibition by anthralin. Schallreuter and Pittelkow present experimental data that thioredoxin-reductase activity in patients with psoriasis is elevated in involved, but not in uninvolved, skin. The measurements of thioredoxin-reductase activity in skin biopsy specimens are based on a bioassay, developed by Schallreuter et al.2 Using electron resonance spectroscopy (ESR), the signal loss of a membraneimpermeable, cationic nitroxide (free radical) is monitored in skin biopsy specimens and keratinocytes. The nitroxide is reduced in the epidermis to an ESR silent product. It is presumed that reduction of this particular nitroxide is specific for thioredoxin reductase in the epidermis. Indeed, under test tube conditions, nitroxides are reduced by mammalian and Escherichia coli thioredoxin reductase in the presence of nicotinamide-adenine dinucleotide phosphate (NADPH). There is, however, absolutely no rationale References 1. Schallreuter KU, Pittelkow MR: Anthralin inhibits elevated levels of thioredoxin reductase in psoriasis . Arch Dermatol 1987;123:1494-1498.Crossref 2. Schallreuter KU, Hordinsky MK, Wood JM: Thioredoxin reductase . Arch Dermatol 1987;123:615-619.Crossref 3. Belkin S, Mehlhorn RJ, Hideg K, et al: Reduction and destruction rates of nitroxide spin probes . Arch Biochem Biophys 1987;256:232-243.Crossref 4. Chen KY, McLaughlin MG: Differences in the reduction kinetics of incorporated spin labels in undifferentiated and differentiated mouse neuroblastoma cells . Biochim Biophys Acta 1985;845:189-195.Crossref

Schallreuter, Karin U.;Pittelkow, Mark R.;Wood, John M.

1988 Archives of Dermatology

doi: 10.1001/archderm.1988.01670060007003

Abstract In Reply.— It is our belief that a critical review of the literature, including your references 3 and 4, on the thioredoxin reductase (TR) bioassay, provides sufficient information to confirm our results. A most important feature of our spin-labeled substrate is its inability to penetrate the plasma membranes of keratinocytes and melanocytes. Therefore, the nitroxide radical reduction that we measure is catalyzed by an enzyme acting at the outer membrane surface.1 We understand your criticism that nitroxide radicals are easily reduced to the electron resonance spectroscopy-silent hydroxylamine product by many biological redox systems (your reference 3), but in our bioassay we have shown that the nitroxide radical is reduced at the cell surface to a secondary amine.2 The inability of our spin-labeled substrate to penetrate the plasma membrane rules out nonspecific reactions that would undoubtedly occur in the cytosol or on mitochondrial membranes. Indeed, if substrate transport occurred, References 1. Schallreuter KU, Schulz KH, Wood JM: Induction of contact dermatitis in guinea pigs by quarternary ammonium compounds: The mechanisms of antigen formation . Environ Health Perspect 1986;70:229-237.Crossref 2. Schallreuter KU, Wood JM: The role of thioredoxin reductase in the reduction of free radicals at the surface of the epidermis . Biochem Biophys Res Commun 1986;136:630-637.Crossref 3. Hansson HA, Holmgren A, Rozell B, et al: Localization of thioredoxin, thioredoxin reductase, and ribonucleotide reductase in cells: Immunohistochemical aspects , in Holmgren A, Branden C-I, Jornvall H, et al (eds): Thioredoxin and Glutaredoxin Systems . New York, Raven Press, 1986, pp 177-187. 4. Schallreuter KU, Pittelkow MR, Gleason FK, et al: The role of calcium in the regulation of free radical reduction by thioredoxin reductase at the surface of the skin . Inorgan Biochem 1986; 28:227-238.Crossref 5. Schallreuter KU, Wood JM: Azelaic acid as a competitive inhibitor of thioredoxin reductase in human melanoma cells . Cancer Lett 1987;36:297-305.Crossref 6. O'Donnell M, Williams CH Jr: Mechanism of Escherichia coli thioredoxin reductase , in Holmgren A, Branden C-I, Jornvall H, et al (eds): Thioredoxin and Glutaredoxin Systems . New York, Raven Press, 1986, pp 131-141. 7. Schallreuter KU, Pittelkow MR: Anthralin inhibits elevated levels of thioredoxin reductase in psoriasis . Arch Dermatol 1987;123:1494-1498.Crossref

Kato, Taizo;Saijyo, Shinobu;Hatchome, Naohiro;Tagami, Hachiro;Kawashima, Makoto

1988 Archives of Dermatology

doi: 10.1001/archderm.1988.01670060009004

Abstract To the Editor.— Human papillomavirus (HPV) type 16 (HPV-16) has been found in lesions of bowenoid papulosis, Bowen's disease, and cervical intraepithelial neoplasia, as well as anogenital carcinoma. Although bowenoid papulosis is well known to occur in patients who had been treated for cervical carcinoma,1 the progression of bowenoid papules themselves to invasive carcinoma is not well documented. In the present report we describe a woman with a previous history of treated carcinoma of the cervix who developed invasive carcinoma of Bowen's type, apparently arising from bowenoid papulosis on her perianal region, and regional lymph node metastasis; in both lesions of the invasive carcinoma and of bowenoid papulosis we found the presence of HPV-16 DNA. This case presents strong evidence for a causal relationship between HPV-16 and cancer derived from its precursor lesion. Report of a Case.— A 56-year-old woman was first seen by us in May 1986, with a complaint of a nodule of ten months' duration on the left side of her perianal References 1. Zachow KR, Ostrow RS, Bender M: Detection of human papillomavirus DNA in anogenital neoplasias . Nature 1982; 300:771-773.Crossref 2. Yoshikawa H, Mizuno M, Yoshiike K: Occurrence of human papillomavirus types 16 and 18 DNA in cervical carcinomas from Japan . Gann 1985;76:667-671.

Luber, Howard;Amornsiripanitch, Somnuk;Lucky, Anne W.

1988 Archives of Dermatology

doi: 10.1001/archderm.1988.01670060011005

Abstract To the Editor.— Cutaneous colonization and infection with Staphylococcus aureus are well-recognized complications of atopic dermatitis.1 Topical and systemic antibiotics are administered for the treatment of these infections as well as the chronic suppression of bacterial growth of these heavily colonized individuals. As a result of long-term antibiotic therapy, resistant bacterial strains emerge, requiring development of new antibiotic agents for therapeutic success.We report the case of a 4-year-old boy with severe atopic dermatitis and recurrent methicillin-resistant S aureus infection of his skin as well as distal phalangeal osteomyelitis. A full report of his course of osteomyelitis has been submitted for publication. Report of a Case.— A 4-year-old boy was diagnosed with atopic dermatitis at 21 months of age. He was treated with 2½% hydrocortisone ointment, 5% liquor carbonis detergens, hydroxyzine, and intermittent oral antibiotic therapy (erythromycin ethyl succinate, dicloxacillin, and cephalexin monohydrate). He was chronically colonized with S References 1. Dahl M: Staphylococcus aureus and atopic dermatitis . Arch Dermatol 1983;119:840-846.Crossref 2. Boyce J, Causey W: Increasing occurrence of methicillinresistant Staphylococcus aureus in the United States . Infect Control 1982;3:377-383. 3. Dacre J, Emmerson A, Jenner E: Nasal carriage of gentamicin and methicillin resistant Staphylococcus aureus treated with topical pseudomonic acid . Lancet 1983;2:1036.Crossref 4. Eells L, Mertz PM, Piovanetti Y, et al: Topical antibiotic treatment of impetigo with mupirocin . Arch Dermatol 1986;122:1273-1276.Crossref 5. Wuite J, Davies B, Go M, et al: Pseudomonic acid: A new antibiotic for topical therapy . J Am Acad Dermatol 1985;12:1026-1031.Crossref

Fisher, David A.;Elias, Peter M.;LeBoit, Philip L.

1988 Archives of Dermatology

doi: 10.1001/archderm.1988.01670060012006

Abstract To the Editor.— Elicitation or exacerbation of psoriasis has occurred following administration of the psychopharmacologic agents,1 β-blockers,2 nonsteroidal anti-inflammatory agents,3 antimalarials,4 isotretinoin,5 and chlorthalidone.6 Abel and coworkers7 have extensively analyzed and discussed the entire subject of drug-induced psoriasis in an excellent recent review.We report herein a case of psoriasis exacerbated by gemfibrozil, a hypolipidemic fibric acid derivative, in the same category as clofibrate. Gemfibrozil decreases production of very-low-density lipoprotein (VLDL) triglycerides and enhances its clearance, but does not decrease plasma cholesterol.8 It does, however, increase high-density lipoprotein (HDL) cholesterol levels.8,9 Its mechanism of action, as discussed below, is unclear.8 There are no previous reports of psoriasis exacerbated by gemfibrozil (Lopid, Parke-Davis). Moreover, a recent computer search by the American Academy of Dermatology Adverse Drug Reporting Center (Evanston, Ill) failed to reveal any prior reports of this phenomenon. Report of References 1. Sarantides D, Waters B: A review and controlled study of cutaneous conditions associated with lithium carbonate . Br J Psychiatry 1983;143:42-50.Crossref 2. Neuman HAM, Van Joost T: Adverse reactions of the skin to metaprolol and β-adrenergic-blocking agents . Dermatologia 1981;163:330-335.Crossref 3. Meyerhoff JO: Exacerbation of psoriasis with meclofenamate . N Engl J Med 1983;309:496. 4. Luza MJ: Hydrochloroquine in psoriatic arthropathy: Exacerbation of psoriatic skin lesions . J Rheumatol 1982;9:462-464. 5. Davis TL, Hayes TJ: Isotretinoin-induced psoriasis: A case of Koebner's phenomenon . J Assoc Milit Dermatol 1987;12:23-26. 6. Wolf R, Dorfman B, Krakowski A: Psoriasiform eruption induced by captopril and chlorthalidone . Cutis 1987;40:162-164. 7. Abel EA, Diciccio LM, Orenberg EK, et al: Drugs in exacerbation of psoriasis . J Am Acad Dermatol 1986;15:1007-1022.Crossref 8. Gemfibrozil: A new lipid lowering agent: A symposium . Proc R Soc Med 1976;69( (suppl 2) ): 1-120. 9. Grass A, Lehner B, Haberosch W, et al: Effect of gemfibrozil on lipids, apoproteins, and postheparin lipolytic activities in normolipidemic subjects . Metabolism 1986;35:382-393. 10. Williams ML, Feingold KR, Grubauer G, et al: Ichthyosis induced by cholesterol-lowering drugs: Implications for epidermal cholesterol homeostasis . Arch Dermatol 1987;123:1535-1538.Crossref 11. Wolfe BM, Kane JP, Howel RJ, et al: Mechanism of the hypolipidemic effect of clofibrate in post-absorptive man . J Clin Invest 1973;52:2146-2155.Crossref 12. Williams ML, Elias PM: Genetically transmitted generalized disorders of cornification (the ichthyosis) . Dermatol Clin 1987;5:155-178.

Kossard, Steven;Commens, C. A.

1988 Archives of Dermatology

doi: 10.1001/archderm.1988.01670060013007

Abstract To the Editor.— A number of reports have dealt with unexpected disorders secondary to radiotherapy. Most of these have emphasized the development of follicular-based acneform eruptions characterized by comedones, papules, pustules, and cysts,1-3 but more recently, Burns4 described a patient in whom multiple digitate keratoses appeared after radiotherapy.We describe a patient in whom a miliarialike eruption developed confined to the radiotherapy field, which showed extensive keratinization concentrated in the eccrine ducts and their openings. This appears to be a distinct radiotherapy-induced keratotic disorder that may have been conditioned by previous chemotherapy. Report of a Case.— A 48-year-old man underwent a laparotomy in May 1981 for abdominal pain thought to be due to a pseudocyst of the pancreas. Biopsies and subsequent staging revealed stage 2E non-Hodgkin's lymphoma of a poorly differentiated lymphocytic type. He was treated with nine courses of doxorubicin hydrochloride, teniposide, cyclophosphamide, References 1. Bluefarb SM: Comedos following roentgen ray therapy . Arch Dermatol 1947;56:537-538.Crossref 2. Trunnell TN, Baer RL, Michaelides P: Acneform changes in areas of cobalt irradiation . Arch Dermatol 1972;106:73-75.Crossref 3. Stein KM, Leyden JJ, Goldschmidt H: Localised acneform eruption following cobalt irradiation . Br J Dermatol 1972;87:274-279.Crossref 4. Burns DA: Postirradiation digitate keratoses . Clin Exp Dermatol 1986;11:646-649.Crossref 5. Harrist TJ, Fine JD, Berman RS, et al: Neutrophilic eccrine hidradenitis . Arch Dermatol 1982;118:263-267.Crossref 6. Lerner TH, Barr RJ, Dolezal JF, et al: Syringomatous hyperplasia and eccrine squamous syringometaplasia associated with benoxaprofen therapy . Arch Dermatol 1987;123:1202-1204.Crossref 7. Bronner AK, Hood AF: Cutaneous complications of chemotherapeutic agents . J Am Acad Dermatol 1983;9:645-663.Crossref

Fitzpatrick, Thomas B.

1988 Archives of Dermatology

doi: 10.1001/archderm.1988.01670060015008

Abstract The concept of sun-reactive "skin typing" was created in 19751 for a specific need: to be able to classify persons with white skin in order to select the correct initial doses of ultraviolet A (UVA) (in joules per cubic centimeter) in the application of the then newly developed technique for the treatment of psoriasis—oral methoxsalen photochemotherapy (PUVA).2 The need arose as a result of experience with several patients who were a "dark" phenotype (brown or even black hair, and some with brown eyes) but, to our surprise, developed severe phototoxic reactions following oral ingestion of 0.6 mg/kg of methoxsalen and then, two hours later, were exposed to 4 to 6 J/cm2. These initial doses were obviously too high, and it was then understood that the estimation of the white-skinned person's tolerance level to oral PUVA could not be based solely on the phenotype (hair and eye color). References 1. Fitzpatrick TB: Soleil et peau . J Med Esthet 1975;2:33-34. 2. Parrish JA, Fitzpatrick TB, Tanenbaum L, et al: Photochemotherapy of psoriasis with oral methoxsalen and long-wave ultraviolet light . N Engl J Med 1974;291:1207-1211.Crossref 3. Melski JW, Tanenbaum L, Parrish JA, et al: Oral methoxsalen photochemotherapy for the treatment of psoriasis: A cooperative clinical trial . J Invest Dermatol 1977;68:328-335.Crossref 4. Roenigk HH, Martin JS: Photochemotherapy for psoriasis . Arch Dermatol 1977;113:1667-1670.Crossref 5. Pathak MA, Jimbow K, Szabo G, et al: Sunlight and melanin pigmentation , in Smith KC (ed): Photochemical and Photobiological Reviews . New York, Plenum Press, 1976, pp 211-239. 6. Fitzpatrick TB: Ultraviolet-induced pigmentary changes: Benefits and hazards . Curr Probl Dermatol 1986;15:25-38. 7. Pathak MA, Fanselow DL: Photobiology of melanin pigmentation: Dose response of skin to sunlight and its contents . J Am Acad Dermatol 1983;9:724-732.Crossref 8. Stern RS, Momtaz K: Skin typing for assessment of skin cancer risk and acute response to UV-B and oral methoxsalen photochemotherapy . Arch Dermatol 1984;120:869-873.Crossref 9. Amblard P, Beani JC, Gautron R, et al: Statistical study of individual variations in sunburn sensitivity in 303 volunteers without photodermatosis . Arch Dermatol Res 1982;274:195-206.Crossref 10. Sayre RM, Desrochers DL, Wilson CJ, et al: Skin type, minimum erythema dose (MED), and sunlight acclimatization . J Am Acad Dermatol 1981;2:439-443.Crossref 11. Agin PP, Desrochers DL, Sayre RM: The relationship of immediate pigmentation darkening to minimal erythema dose and eye color . Photodermatology 1985;2:288-294. 12. Sunscreen drug products for over-the-counter human drugs: Proposed safety, effective, and labeling conditions . Federal Register 1978;43( (Aug 25) ):38206-38207. 13. Rampen FHJ, Fleuren BAM, de Boo ThM, et al: Unreliability of self-reported burning tendency and tanning ability . Arch Dermatol 1988;124:885-888.Crossref 14. Wolff K, Honigsmann H, Gschnait FD, et al: Photochemotherapie bei Psoriasis: Klinische Erfahrungen bei 152 Patienten . Dtsch Med Wochenschr 1975;100:2471-2477.Crossref 15. Schulze R: Einige Versuche und Bemerkungen zum Problem der handelsublichen Lichtschutzmittel . Parf Kosmetik 1956; 37:310-365. 16. Simoni S, Perotti R, Fimiami M, et al: Evaluation of cutaneous pigmentation in skin cancer patients . Program and abstracts of the First Meeting of the European Society for Pigment Cell Research, Sorrento (Naples), Oct 11-14, 1987 , p 57. 17. Kollias N, Baqer, Chedekel MR: In vivo spectroscopic observation of melanogenesis . Program and abstracts of the First Meeting of the European Society for Pigment Cell Research, Sorrento (Naples), Oct 11-14, 1987 , p 1.

Falanga, Vincent

1988 Archives of Dermatology

doi: 10.1001/archderm.1988.01670060018009

Abstract For more than a century, the practice of dressing a wound has had as one of its major rationales the prevention of infection. Dressings can theoretically protect the wound from gross microbial contamination and help to prevent the spread of infection to other patients on the surgical ward. In this setting, one thinks of dressings as a barrier between the wound and the outside world. It is a relatively novel idea that the composition and properties of the dressing itself can play a major role in modifying the wound microenvironment. In the span of a decade, three key observations have helped physicians think of dressings as pharmacologic agents. Odland1 first observed in 1958 that a blister healed faster if left unbroken. Then, in a 1962 landmark article, Winter2 showed that occlusion of wounds with a polyethylene film (Polythene) more than doubled wound epithelialization in domestic pigs. Finally, Hinman References 1. Odland G: The fine structure of the interrelationship of cells in the human epidermis . J Biophys Biochem Cytol 1958;4:529-535.Crossref 2. Winter GD: Formation of scab and the rate of epithelialization of superficial wounds in the skin of the young domestic pig . Nature 1962;193:293-294.Crossref 3. Hinman CD, Maibach H: Effect of air exposure and occlusion on experimental human skin wounds . Nature 1963;200:377-378.Crossref 4. Eaglstein WH, Mertz PM, Falanga V: Occlusive dressings . Am Fam Physician 1987;35:211-216. 5. Eaglstein WH, Mertz PM: New method for assessing epidermal wound healing: The effects of triamcinolone acetonide and polyethelene film occlusion . J Invest Dermatol 1978;71:382-384.Crossref 6. Rovee DT: Effect of local wound environment on epidermal healing , in Maibach HL, Rovee DT (eds): Epidermal Wound Healing . Chicago, Year Book Medical Publishers Inc, 1972, pp 159-181. 7. Barnett A, Berkowitz RL, Mills R, et al: Comparison of synthetic adhesive moisture vapor permeable and fine mesh gauze dressings for split-thickness skin graft donor sites . Am J Surg 1983;145:379-381.Crossref 8. Mandy SH: A new primary wound dressing made of polyethylene oxide gel . J Dermatol Surg Oncol 1983;9:153-155.Crossref 9. Linsky CB, Rovee DT, Dow T: Effect of dressing on wound inflammation and scar tissue , in Dineen P, Hildick-Smith G (eds): The Surgical Wound . Philadelphia, Lea & Febiger, 1981, pp 191-206. 10. Winter GD: Epidermal regeneration studied in the domestic pig , in Maibach HL, Rovee DT (eds): Epidermal Wound Healing . Chicago, Year Book Medical Publishers Inc, 1972, pp 71-112. 11. Alvarez OM, Mertz PM, Eaglstein WH: The effect of occlusive dressings on collagen synthesis and re-epithelialization in superficial wounds . J Surg Res 1983;35:142-148.Crossref 12. Leipziger LS, Glushko V, DiBernardo B, et al: Dermal wound repair: Role of collagen matrix implants and synthetic polymer dressings . J Am Acad Dermatol 1985;12:409-419.Crossref 13. Douglas DM: Factors affecting the gain of tensile strength in healing wounds , in Illingworth C (ed): Wound Healing . Boston, Little Brown & Co Inc, 1966, pp 233-241. 14. Eaton AC: A controlled trial to evaluate and compare a sutureless skin closure technique (Op-Site skin closure) with conventional skin suturing and clipping in abdominal surgery . Br J Surg 1980;67:857-860.Crossref 15. Buchan IA, Andrews JK, Lang SM: Laboratory investigation of the composition and properties of pigskin wound exudate under Op-Site . Burns 1981;8:39-46.Crossref 16. Nemeth AJ, Hebda PA, Eaglstein WH: Stimulatory effect of human wound fluid on epidermal outgrowth from porcine skin explant cultures, abstracted . J Invest Dermatol 1986;86:497. 17. Mertz PM, Eaglstein WH: The effect of a semiocclusive dressing on the microbial population in superficial wounds . Arch Surg 1984;119:287-289.Crossref 18. Katz S, McGinley K, Leyden JJ: Semipermeable occlusive dressings . Arch Dermatol 1986;122:58-62.Crossref 19. Eaglstein WH: Experiences with biosynthetic dressings . J Am Acad Dermatol 1985;12:434-440.Crossref 20. May SR: Physiology, immunology, and clinical efficacy of an adherent polyurethane wound dressing: Op-Site , in Wise DL (ed): Burn Wound Coverings . Boca Raton, Fla, CRC Press, 1984, pp 53-78. 21. Holland KT, Davis W, Ingham E, et al: A comparison of the in vitro antibacterial and complement activating effect of Op-Site and Tegaderm dressings . J Hosp Infect 1984;5:323-328.Crossref 22. Mertz PM, Marshall DA, Eaglstein WH: Occlusive wound dressings to prevent bacterial invasion and wound infection . J Am Acad Dermatol 1985;12:662-668.Crossref 23. Jaffe LF, Vanable JW: Electric fields and wound healing , in Eaglstein WH (ed): Clinics in Dermatology: Wound Healing . Philadelphia, JB Lippincott, 1984, pp 34-44. 24. Falanga V, Bourguignon GJ, Bourguignon LYW: Electrical stimulation increases the expression of fibroblast receptors for transforming growth factor-beta, abstracted . J Invest Dermatol 1987;88:488. 25. Eaglstein WH, Davis SC, Mehle AL, et al: Optimal use of an occlusive dressing to enhance healing: Effect of delayed application and early removal on wound healing . Arch Dermatol 1988;124:392-395.Crossref 26. Alper JC, Tibbetts LL, Sarazen AA: The in vitro response of fibroblasts to the fluid that accumulates under a vapor-permeable membrane . J Invest Dermatol 1985;84:513-515.Crossref 27. Friedman SJ, Su WPD: Management of leg ulcers with hydrocolloid occlusive dressing . Arch Dermatol 1984;120:1329-1336.Crossref 28. Alper JC, Welch EA, Ginsberg M, et al: Moist wound healing under a vapor permeable membrane . J Am Acad Dermatol 1983;8:347-353.Crossref 29. Angermeier MC, Alper JC, Urbaniak HS: Vapor-permeable membrane therapy for ulcers of osteomyelitis . J Dermatol Surg Oncol 1984;10:384-388.Crossref 30. Gorse GJ, Messner RL: Improved pressure sore healing with hydrocolloid dressings . Arch Dermatol 1987;123:766-771.Crossref 31. Mallory SB: Adjunctive therapy for epidermolysis bullosa . J Am Acad Dermatol 1982;6:951-952.Crossref 32. Eisenberg M: The effect of occlusive dressings on reepithelializations of wounds in children with epidermolysis bullosa . J Pediatr Surg 1986;21:892-894.Crossref 33. Alper JC, Welch EA, Maguire P: Use of the vapor permeable membrane for cutaneous ulcers: Details of application and side effects . J Am Acad Dermatol 1984;11:858-866.Crossref 34. Zitelli JA: Delayed wound healing with adhesive wound dressings . J Dermatol Surg Oncol 1984;10:709-710.Crossref 35. Varghese MC, Balin AK, Carter DM, et al: Local environment of chronic wounds under synthetic dressings . Arch Dermatol 1986;122:52-57.Crossref 36. Gilmore WA, Wheeland RG: Treatment of ulcers on legs by pinch grafts and a supportive dressing of polyurethane . J Dermatol Surg Oncol 1982;8:177-183.Crossref 37. Mertz PM, Marshall DA, Kuglar MA: Povidone-iodine in polyethylene oxide hydrogel dressing . Arch Dermatol 1986; 122:1133-1138.Crossref 38. Richmond JD, Sutherland AB: A new approach to the problems encountered with Op-Site as a donor site dressing: Systemic ethamsylate . Br J Plast Surg 1986;39:516-518.Crossref

Shea, Thomas C.;Antman, Karen H.;Eder, J. Paul;Elias, Anthony;Peters, William P.;Schryber, Susan;Henner, William D.;Schoenfeld, David A.;Schnipper, Lowell E.;Frei, Emil

1988 Archives of Dermatology

doi: 10.1001/archderm.1988.01670060024010

Abstract • Nineteen patients with metastatic malignant melanoma were treated with 20 courses of high-dose combination alkylating agent chemotherapy and autologous bone marrow support. All 20 treatment courses were evaluable for toxic reactions and 17 of 20 were assessable for response. Twelve of the 20 courses were given at the phase 2 dose per square meter of cyclophosphamide (5.625 g), cisplatin (165 mg), and carmustine (600 mg). Marrow reconstitution occurred with a median time to recovery of 21 and 24 days for more than 500 neutrophils and more than 20 000 platelets, respectively. The overall response rate was 65%, with one patient achieving a complete response with chemotherapy alone. Ten additional patients achieved partial responses following chemotherapy, of which three were subsequently rendered disease free by surgical resection of single areas of residual tumor. Two of these patients are alive and disease free more than 22 months following chemotherapy and one remains relapse free. The median survival for responding patients was 15.2 months and 8.6 months for the entire group. (Arch Dermatol 1988;124:878-884) References 1. DeVita VT, Carbone PP, Owens AH, et al: Clinical trials with 1,3-bis(L-chloroethyl)-1-nitrosourea, NSC 409962 . Cancer Res 1965;25:1876-1881. 2. Costanza ME, Nathanson L, Lenhard R, et al: Therapy of malignant melanoma with an imidazole carboxamide and bischloroethyl nitrosourea . Cancer 1972;30:1457-1461.Crossref 3. Costanza ME, Nathanson L, Schoenfeld D, et al: Results with methyl-CCNU and DTIC in metastatic melanoma . Cancer 1977; 40:1010-1015.Crossref 4. Comis RL: DTIC (NSC-45388) in malignant melanoma: A perspective . Cancer Treat Rep 1976;60:165-176. 5. Young DW, Lever RS, English JS, et al: The use of BELD combination chemotherapy (bleomycin, vindisine, CCNU and DTIC) in advanced malignant melanoma . Cancer 1985;55:1879-1881.Crossref 6. Del Prete SA, Maurer CH, O'Donnell J: Combination chemotherapy with cisplatin, carmustine, decarbazine and tamoxifen in metastatic melanoma . Cancer Treat Rep 1985;68:1403-1405. 7. Bajetta E, Roue R, Vaglini M, et al: Treatment of advanced malignant melanoma with vinblastine, bleomycin and cisplatin . Cancer Treat Rep 1982;66:1299-1302. 8. Johnson DH, Presant C, Einhorn L, et al: Cisplatin, vinblastine and bleomycin in the treatment of metastatic melanoma: A phase II study of the southeastern cancer study group . Cancer Treat Rep 1985;69:821-824. 9. Ariel IM, Pack GT: Treatment of disseminated melanoma with phenylalanine mustard (melaphalan) and autogenous bone marrow transplants . Surgery 1962;51:582-591. 10. Thomas MR, Robinson WA, Glode LM, et al: Treatment of advanced malignant melanoma with high-dose chemotherapy and autologous bone marrow transplantation: Preliminary results— phase I study . Am J Clin Oncol 1982;5:611-622.Crossref 11. 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