522
Journal of the American Academy of Dermatology
Correspondence
REFERENCES
REFERENCES
1. Herd J-K. Nailfold capillary microscopy made easy [Letter]. Arthritis Rheum 1976;19:1370-1. 2. Minkin W, Rabhan NB. Office nail fold capillary microscopy using ophthalmoscope, ff AM AChD DE~TOL 1982;7:190-3. 3. Sedlaeek TV, Cunnane M, Carpiniello V. Colposcopy in the diagnosis of penile condyloma. Am J Obstet Gynecol 1986;154:494-6.
1. Norrlind R. A contribution to the problem of the etiology and pathogenesis of psoriasis. Acta Derm Venereol (Stockh) 1948;28:571-84. 2. Rosenberg EW, Brew PW. Role of microbial factors in psoriasis. In: Farber EM, Cox AY, eds. Psoriasis: Proceedings of the Third International Symposium. New York: Grune & Stratton, 1982;343-4. 3. Landry M, Muller SA. Generalized pustular psoriasis. Observations on the course of the disease in a familial occurrence. Arch Dermatol 1972;105:711-6. 4. Henocq E. Psoriasis and allergy. In: Sidi E, Zagula-Mally ZW, Hincky M, eds. Psoriasis. Springfield,IL: Charles C Thomas, 1968:140-72. 5. Hill HR, Gerrard JH, Hogan NA, Quie PG. Hyperactivity of neutrophit leukotactic resonses during active bacterial infection. J Clin Invest 1974;53:996-1002. 6. Lazarus GS, Gi/gor RS. Psoriasis, polymorphonuclear leukocytes, and lithium carbonate [Editorial]. Arch Dermatol 1979;115:1183-4. 7. Ternowitz T. Monocyte and neutrophil chemotaxis in psoriasis. J AM Ac~a3DERMAXOL1986;15:1191-9. 8. Wahba A, Cohen H. Therapeutic trials with oral colchieine in psoriasis. Acta Derm Venereol (Stockh) 1980;60:515-520. 9. Walsdorfer U, Christopher E, Sehroder JM. Methotrexate inhibits polymorphonuclear leukocyte chemotaxis in psoriasis. Br J Dermatol 1983;108:451-6. 10. Ternowitz T, Herlin T. Neutrophil and monocyte chemotaxis in methotrexate-treated psorisiasis patients. Acta Derm Venereol [SuppI] (Stockh) 1985;120:23-6.
Psoriasis: Neutrophil chemotaxis and microbial factors To the Editor: It was with great interest and attention that I read the commentary, "The Koebner Phenomenon and the Microbial Basis of Psoriasis" by Drs. Rosenberg and Noah (J A M ACAD DERMATOL 1988;18:151-8). The observation that psoriasis can be induced or exacerbated by bacterial or yeast infections is well documented?.2 Furthermore, exacerbations of psoriasis can be induced by the inoculation of skin-test quantities of different bacterial antigens. 3,4 1 completely agree with the authors' opinion that the role of bacterial infection in the pathogenesis of psoriasis is unique and that it is not just another form of the Koebner phenomenon. In this context I would like to draw attention to a possible mechanism through which microbial infection can induce psoriatic flares. Patients with active bacterial infection are known to have hyperactive chemotactic responses of circulating neutrophils, which appear to be an early and a sensitive event in the inflammatory cycle stimulated by infection? Furthermore, preincubation of normal leukocytes in vitro with bacterial endotoxin causes a brisk and significant increase in their chemotactic activity? Increased ehemotactic activity has been implicated in the initiation and perpetuation of the psoriatic lesion. Lithium carbonate increases migrational activity of polymorphonuelear cells and is known either to induce psoriasis or to complicate its course? Exacerbation of psoriasis was observed to be preceded by a rapid increase of polymorphonuclear chemotaxis, whereas improvement of the cutaneous lesions was noticed after decline of the chemotactic responsesJ Drugs that inhibit chemotaxis have a beneficial effect in psoriasis, a and a profound depression of the enhanced polymorphonuclear cell and monocyte chemotaxis has been found within the first 48 hours after intake of methotrexate.9,t0 Thus it seems reasonable to assume that induction or exacerbation of psoriasis as a result of bacterial infection is at least partially mediated through stimulation of the leukotactic response. Asher Wahba-Yahav, MD Ramot 271, Jerusalem 97725, Israel
Melanocytic nevus counts and melanoma To the Editor: We found very interesting the report by Dr. Holly and associates (J AM ACAD DERMATOL 1987;17:459-68) on the relationship between melanocytic nevus counts and cutaneous melanoma. The authors' findings agree with results from other studies, in some of which less extensive nevus data were obtained by examination of the arms or by interview with the subjects themselves~-S;in others data were from "wholebody" nevus counts by dermatologists or other trained health personnel. 6,7 It is clearly important to explore the relationship further, and clarification of the relationship between the site of nevi and the site of melanoma will require data on large numbers of subjects. Also, however, given the substantial and growing evidence for an association, it appears appropriate now to consider whether and how attempts should be made to identify persons in the highest risk groups and what supervisory action or advice should be offered to them. A. J. Swerdlow," J. English," R. M. MacKied C. J. O'Doherty,b J. A. A. Hunter) J. Clark," and D. J. Hole? University of Glasgow," University of Edinburgh) and West of Scotland Cancer Surveillance Unit? Glasgow and Edinburgh, Scotland