Volume 24 Number 4 April 1991
in reducing all forms of ache lesions analyzed, by one formulation, and the maintenance of numeric superiority by the same formulation over the duration of the study may prove meaningful to the objective observer. There is no reference 16. Table I appeared in both the February and March articles with an asterisk. In the February 1990 article it was stated that the asterisk denoted that the grading scale is modified from the Cook method. In the March article, about which Dr. Sweren wrote, indeed the typesetting gremlins have seemingly substituted "reference 16" for the explanation the asterisk denoted. Lest our correspondent, Dr. Sweren, didn't have sufficient angst, I feel a tinge of guilt to point out that he missed the fact there are no references 11 through 15 either.
Lawrence Sehachner, AID, and Arm Pestana, AID Department of Dermatology and Cutaneous Surgery, P. O. Box 016250 (R-250), Miami, FL 33101
REFERENCES 1. Hollander M, Wolfe DA. Nonparametric statistical methods. New York: John Wiley & Sons, 1973:69-74. 2. BrownBW, Hollander M. Statistics: a biomedicalintroduction. New York: John Wiley & Sons, 1977:456. 3. Schachner L, Eaglstein W, Kitties C, et al. Topical erythromycin and zinc therapy for acne. J AM ACADDERMATOL 1990;22:253-60. 4. Schachner L, Pestana A, Kitties C. A clinical trial comparing the safety and efficacy of a topical erythromycin-zinc formulation with a topical elindamycin formulation. J AM ACADDERMATOL1990;22:489-95.
"Cello scrotum" questioned To the Editor: I applaud the comprehensive, excellent recent review of"Derrnatologic Problems of Musicians" by Rimmer and Spielvogel (J AM AcaI3 DERMATOL 1990;22:657-63). As a former professional cellist, I appredate the descriptions of "cellist's chest" and "cello knee." However, I question the accuracy of the information under the designation of "cello scrotum." The authors cite just one case, which is not their own (Br Med J 1974;2:335). That case consists of a brief (9-line) letter to the editor in which the author states that a professional cellist had "cello scrotum" caused by "irritation from the body of the cello." I find this a bit puzzling. When the cello is held in typical playing position, the body of the instrument is not near the scrotum. Contact of the body of the cello with the scrotum would require an extremely awkward playing position, which I have never seen a playing cellist assume. If the scrotal dermatitis of the cellist in question was truly associated with cello playing, I think it more likely was associated with irritation from the forward edge of the chair; this is a location with which a cellist's scrotum
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typically comes into contact. However, because even this is speculation and because this problem would not be unique to the cellist but could occur in anyone who does not sit still in his chair, I think it would be best to expunge the term "cdlo scrotum" from the dermatologic literature.
Philip E. Shapiro, MD Department of Dermatology, Yale University New Haven, Connecticut
Use of griseofulvin To the Editor: At the end of his report of oral contraceptive failure apparently caused by the concurrent use of griseofulvin (J AM ACAD DERMATOL 1990;22:124-5), Dr. C6t6 says that he favors ketoconazole as a noninteracting substitute for treatment periods of more than 3 months. However, the use of ketoeonazole is controversial. One study found that 7 of 147 women taking low-dose oral contraceptives (Ovidon, Rigevidon, Anteovin) experienced break-through bleeding within 2 to 5 days of starting a 5-day course of 400 mg ketoconazole daffy.~No pregnancies occurred but intermenstrual bleeding is a sign of a decrease in the effectiveness of the oral contraceptives. I do not know of any direct evidence of total contraceptive failure caused by ketoconazole, but it may not be a safe substitute for griseofulvin. Ivan 1-1.Stockley, PhD, MRPharm S The University of Nottingham Medical School Nottingham, NG7 2UH, U.K.
REFERENCE l. Kovacs L, Somos P, Hamori M. Examination of the potential interaction between ketoconazole (Nizoral) and oral contraceptives with special regard to products of low hormone content (Rigevidon, Anteovin). Ther Hung 1986; 34:167.
Short-contact anthralin therapy To the Editor."Short-contact anthralin therapy (SCAT) involves the removal of anthralin by washing after a short period of contact. Logic dictates that either all the anthralin is thereby removed from the tissue (in which case there is no need for further neutralization by amines or anything else) or, if there is residual, active anthralin within the tissue, such active anthralin cannot be ignored when considering the reasons for the demonstrable effectiveness of SCAT. The relative inhibitory effects on anthralin-induced inflammation, postulated for primary, secondary, and tertiary amines, make interesting reading insofar as they
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demonstrate comparative lipid solubility and confirm the known susceptibility of anthralin to oxidize or dimerize in the presence of bases. However, the deduction that amines could be used after short-contact anthralin therapy "to reduce perilesional inflammation, without diminishing the therapeutic effect" seems to be without evidence. Ramsay et al. (J AM ACAD DI~RMATOL1990;22:76572) suggest that lipid-soluble amines may penetrate the cell membrane and exert a direct effect on the bound anthratin. Paradoxically, whereas the potentially inflammatory role of such anthralin is recognized by the investigators, its therapeutic role is all but ignored. The presumption that "the therapeutic effect of anthralin requires only short contact with the skin" implicitly denies the potentially therapeutic role of the same membrane-bound anthralin that the authors seek to neutralize with topical amines. In earlier work, with K O H used to oxidize anthralin, three of the same investigators conceded the possibility that "[either] anthralin is rapidly bound at a site inaccessible to K O H but accessible to its site of therapeutic action. "t The underlying assumption for the latest work (which used amines) is what was previously only stated to be "more probable," namely, that anthralin's "therapeutic action is initiated rapidly, within 40 minutes." Perhaps the question that deserves attention is whether the therapeutic action is completed within 40 minutes as far as any membrane-bound anthralin is concerned. Put another way, the procedure for removing anthralin after SCAT usually involves a simple process of washing. In practice, although the surplus is thereby removed from the stratum corneum, there is no evidence to suggest that the small amount that has penetrated cell membranes is also removed. On the contrary, it is this very presence, which may be therapeutically critical to SCAT, that the authors have targeted for neutralization by lipidsoluble amines. Accepting the hypothesis that anthralin may reside in the tissue to cause irritation, this cannot be dissociated from its therapeutic function--unless and until either it is demonstrated that all anthralin is removed by washing off after SCAT (in which case, the need for topical amines is questionable) or the use of such topical amines is shown in a controlled, clinical study to be without detriment to the actual effectiveness of SCAT (and, of course, without any additional side effects of its own, such as those reported from the use of KOH). Whereas Ramsay et al. dissolve anthralin in chloroform for study precision, the clinical practice of SCAT involves pharmaceutical vehicles (usually applied for more than 5 minutes), which, in comparison, may complicate both the physical and chemical processes of removal. Much of the initial work on SCAT used traditional ointment/paste formulations of anthralin, which are necessarily difficult to confine within the plaque
perimeter and hard to remove by ordinary washing. The recent availability of aqueous, vanishing creams of anthralin has dramatically improved and popularized the patients' attitude to anthralin therapy in general and SCAT in particular. Because anthralin is water washable, the efficiency of anthralin removal is likely to be much more complete when such creams are used; they can also be accurately located and rubbed into the plaques so as to avoid the unnecessary spread and perilesional inflammation that concerns the authors.
Michael Yarrow, President American Dermal Corporation Plumsteadville, PA 18949
REFERENCE 1. Lawrence CM, Shuster S, Collins M, et al. Reductionofanthralin inflammation by potassiumhydroxideand Teepol. Br J Dermatol/987;116:171-7.
Six children with malignant melanoma To the Editor: [ read with interest the report of Roth et al. (J AM ACAD DERMATOL1990;22:265-74) about four children with malignant melanoma. Although there have been cases of malignant melanoma reported in prepubertal children, the magnitude of the risk seems small and it may not be necessary or realistic to expect dermatologists to do a better job of detection. It has been well established that giant congenital nevo9 cytic nevi carry an increased risk for the development of melanoma before puberty.l-3 The transplacental spread of metastatic melanoma to fetuses whose mothers have malignant melanoma is also well documented. An increased risk for melanoma among peripubertal children who have a dysplastic nevus syndrome is not well established but would not be surprising. Outside of these predisposing conditions, the most disturbing feature of malignant melanoma in children appears to be the lack of clinical indicators that suggest malignancy. One patient reported in the article by Roth et al. had a "pedunculated, crusted, nonpigmented growth." None of the clinical features described was suggestive of melanoma. The lesion was subjected to biopsy because the patient had been concerned about an increase in size and a change in color. In many cases reported in detail in the literature,4-7 the presenting lesion was typical ofa pyogenic granuloma, was amelanotic, or had other features that would not suggest the possibility of a melanoma. Counted among the world's literature of children with malignant melanoma are several cases of metastatic melanoma without a primary lesion. In the review of Boddie et al., 4 melanoma in prepubertal children (younger than 12 years of age) was responsible for 0.4% of all melanomas at their institution, accumulated over 31