636 Thomsen and Wantzin

Journal of the American Academy of

Dermatology

one patient complete remission was observed, al- though methotrexate had to be continued in low dosage,

Although clinically atypical lesions and abnor- mal DNA histograms were not associated with an increased risk of 1.ymphoma within the limits of our current follow-up, continued long-term obser- vation will be important to determine if such pa- rameters will ultimately identify a subset of !ym- phomatoid papulosis patients who are at increased risk for malignancy.

REFERENCES

1. Macaulay WL Lymphomatold papulosis. A continuing self-healing eruption, clinically benign--histologically malignant. Arch Dermatol 1968;97:23-30.

2. Weinman VF, Ackerman AB. Lymphomatoid papulosis. A critical review and new findings. Am J Dermatopathol 1981 ;3:129-63.

3. Lange Wantzin G, Thomsen K, Larsen JK, Christensen IJ, Rasmussen BB. DNA analysis by flow cytometry in lymphomatoid papulosis. Clin Exp Dermatol 1983;8: 505-18,

4. Lange Wantzin G, Thomsen K, Hou-Jensen K. Lym- phomatoid papulosis. A follow-up study. Acta Derm Ve- nereol (Stockh) 1984;64:46-51.

5. Ralfkiaer E, Stein H, Lange Wantzin G, Thomsen K, Ralfkiaer N, Mason DY. Lymphomatoid papulosis. Characterization of skin infiltrates by monoclonal anti- bodies. Am J Clin Pathol 1985;87:587-93.

6. Lange Wantzin G, Saxinger WC, Woods A, Larsen JK, Thomsen K, Gallo RC. Human T-cell leukemia virus in cutaneous T-cell lymphorna in Denmark. Acta Derm Ve- nereol (Stockh) 1984;64:395-9.

7. Willemze R, Scheffer E, Ruitter DJ, van Vloten WA, Meijer CJL. Immunological, cytochemical and ultra- structural studies in lymphomatoid papulosis. Br J Der- matol 1983;108:381-94.

8. Lange Wantzin G, Thomsen K. PUVA-treatmeat in lym- phomatoid papulosis. Br J Dermatol 1982;107:687-90.

9. Lange Wantzin G, Thomsen K. Methotrexate in lym- phomatoid papulosis. Br J Dermatol 1984;111:93-5.

10. Black MM. "Classical" lymphomatoid papulosis. A vari- ant o f pityriasis !ichenoides. Am J Dermatopathol 1981;3: i75-6.

11. Lange Wantzin G, Thomsen K, Brandrup F, Larsen JK. Lymphomatoid papulosis. Development into cutaneous T-cell lymphoma. Arch Dermatol 1985;12!:792-4,

A B S T R A C T S

Relation of oral hairy leukoplakia to infection with the human immunodeficiency virus and the risk of developing AIDS

.Greenspan D, Greenspan IS, Hearst NG, et al: J Infect Dis 1987;155:475-81

Oral hairy leukoplakia appears as raised white areas, often with a corrugated or "hairy" surface, usually on the lateral margin of the tongue and occasionally on the buecal mucosa. Histologically, there is excessive keratinization, without inflammation; intraepithelial Lan- gerhans cells are reduced or absent. Papil!omalike virus and Epstein- Barr virus have been detected in these lesions. Almost all patients with hairy leukoplakia are immunosuppressed homosexual men with a high incidence of antibodies to human immunodeficiency virus (HIV); their probability of developing acquired immunodeficiency syndrome (AIDS) was 48% by 16 months and 83% by 31 months. These men develop AIDS at what appears to be the highest rate yet reported for any of the AIDS-associated conditions. A request by a dermatologist for a patient to "please stick out your tongue" should be neither humorous, onerous, nor numinous.

"teven R. Kohn, M.D.

Retroviruses as carcinogens and pathogens: expectations and reality

Duesberg PH: Cancer Res 1987;47:1199-1220

Seventeen pages of complex argument and 278 references lead to the conclusions that: (1) because the percentage of symptomatic car- tiers of the lymphotropic retrovirus proposed to cause acquired im- munodeficiency syndrome (AIDS) is low, (2) because the 5-year latent period for AIDS is incompatible with the short latent period

of virus replication, and (3) because there is .no gene with a late AIDS function, the AIDS vires is not sufficient to cause AIDS and there is no evidence, besides its presence in a latent form, that it is necessary for AIDS. However, the virus may be directly responsible for the early, mononucleosislike disease observed in several infections prior to antiviral immunity. In a person who belongs t ° the high-risk group for AIDS, antibody against the AIDS virus serves as an in- dicator of an annual risk for AIDS that averages 013% and may reach 5%, but in a person who does not belong to this group antibody to the virus signals no apparent risk for AIDS. Since nearly all virus carriers have antiviral immunity including neutralizing antibody, vac- cination is ~aot likely to benefit virus carriers with or without AIDS.

Steven R. Kohn, M.D.

Cover and cover legend

Anonymous: Cancer Res 1987;47(8):cover and cover legend

The cover portraits of Wallace H. Clark, Jr., M.D., Mark H. Greene, M.D., Susan B., and Richard K. of the "'B-K mole sy n- drome" celebrate the wedding of clinic to laboratory. These nuptials led to insights into the etiology an d pathogenesis of human neoplastic disease: hypermutable dysplastic nevi, with their disorderly arChitec- ture and cytologic atypia, are the most common and best characterized precursors of malignant melanoma. Malignant melanoma and dys- plastic nevi traits are consistent with autosomal dominant inheritance, representing the ple!otropic effects of a single, highly penetrant gene that might be located on the short arm of chromosome 1, near the Rh blood group gene. The progeny of the marriage of examination table and researc h bench will lead to proper management of patients with dysplastic nevi and thereby to reduced incidence and mortality from malignant melanoma.

Steven R. Kohn, M.D.