Letters will be published as space permits and at the discretion of the editor. They typewritten, double-spaced, with not more than five references and two figures in duplicate; they should not exceed 500 words in length. Three copies of all letters are required and they are subject to editing. Letters are not acknowledged. For other details, including copyright procedure, see "Instructions for Authors." must be

PUVA, Pruritus, and the Loss of the Axon Flare

To the Editor.\p=m-\Severepruritus, espeover the buttocks, was seen in two middle-aged men who were approaching a maintenance-schedule program (7 joules/sq cm) of psoralens and ultraviolet-A light (PUVA). Both men failed to exhibit the axon-flare response with the intradermal injection of 0.1 mL of histamine phosphate (0.1 mg/mL) into the buttock. Both men demonstrated the axon-flare response in less symptomatic areas. A neurology consultant, unaware of the histamine skin test, examined the first man and diagnosed a peripheral neuropathy of mainly unmyelinated fibers that affected the hands, feet, nose, and buttocks. There was hyperesthesia of the buttock. The PUVA program was stopped, and the flare had returned when the patient was tested three months later. The histamine intradermal test should prove useful in evaluating pruritus associated with PUVA. Loss of axon-flare reflex vasodilation should end any dilemma about treating the patient with antipruritic drugs during this

cially

period.

Jordan, MD Richmond, Va William P.

Note.—This letter was previously published in the Archives (114:1552-1553, 1978) but is being republished under its corrected title to facilitate proper indexing.

Vitiligo and Melanoma To the Editor.\p=m-\Dr David Paslin is

correct when he states in his letter in the October Archives (114:1551, 1978) that he missed our point on the relationship between vitiligo and melanomas.

Patients with melanomas and

metastases to the skin, lymph nodes, or internal organs have a life expec-

tancy of a few years. Vitiligo develops

in some of these patients. Those patients with metastatic melanomas in whom vitiligo develops live for

many years or, in a few instances, for several decades. In patients with vitiligo there is destruction of normal pigment cells in the skin or the eyes. It is our hypothesis that those factors that cause vitiligo may also destroy malignant pigment cells or at least retard their growth. If our hypothesis is correct, patients who have vitiligo in association with their melanomas would be expected to survive for longer periods of time or might even be cured of their disease. The mechanism by which vitiligo causes the destruction of malignant pigment cells is unknown. Phenolic agents, such as monobenzylether of hydroquinone, when applied to the skin for prolonged periods of time can induce a vitiligo-like condition in the subjects. If we could use such agents to produce a vitíligo in patients with melanomas, especially when the mela¬ noma is first discovered and when the tumor load within the host is small, we might intensify the host defense against the malignancy. The proposal is based on the possibility that the processes that cause vitíligo might destroy the malignant cells but not by the direct toxic effect of phenolic agents on the melanin-producing cells. The negative results of Dr Paslin's own experiments in which he injected phenols and catechols into hamsters bearing melanomas are disappointing to be sure. His experiments depended on a toxic effect of the chemicals on the malignant cells. Had he been able to induce vitíligo by any method, he may have found positive results. We should add that hamsters could be poor models in which to study the induction of vitíligo. Most rodents covered with fur have few epidermal pigment cells, the target of attack for

vitíligo. We hope these comments clarify Dr Paslin's difficulty in trying to under¬ stand why our proposed therapy to

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induce vitíligo may be a much more effective and specific way of destroy¬ ing malignant pigment cells than

merely by administering phenolic

or

catecholic agents.

James J. Nordlund, MD Aaron B. Lerner, MD New Haven, Conn

Thalidomide in the Treatment of Recurrent, Necrotic, and Giant Mucocutaneous Aphthae and Aphthosis

To the Editor.\p=m-\The treatment of recurrent and necrotic mucocutaneous aphthae is usually unsatisfactory. In six cases (men aged 30 to 39), we obtained an excellent result with thalidomide. The cutaneous symptoms in five of the patients consisted of large, deep, necrotic, painful ulcerations in the mouth and on the scrotum, and pustular lesions scattered on different parts of the body. The sixth patient

had giant, deep, necrotic, mutilating lesions in the mouth, as in so-called

periadenitis

mucosa

necrotica

recur-

rens; he had not been free of these

lesions for the past year and was having enormous difficulties with his nutrition. One of the patients had had uveitis, orchitis, and epididymitis (inactive during the treatment with thalidomide), and two had active arthritis at the time of treatment. The daily administration of 100 mg of thalidomide gave us spectacularly good results. On the second or third day, the aphthae were painless and they healed in seven to ten days, depending on their diameter. The patient with periadenitis mucosa necrotia recurrens showed an equally quick and good response and had no recurrences during the time in which he received the drug. The others (man¬ ifesting only occasional recurrences) could stop the medication after seven

days. patients with arthritis showed improvement in their joint symp-

to 12

The no