© 2002 by Oxford University Press
Journal of the National Cancer Institute, Vol. 94, No. 22, 1712-1718,
November 20, 2002
© 2002 Oxford University Press
ARTICLE |
Risk Factors for Classical Kaposi’s Sarcoma
The Classical Kaposi’s Sarcoma Working Group
J. J. Goedert, E. E. Brown, Viral Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD; F. Vitale, N. Romano, Dipartimento di Igiene e Microbiologia "Giuseppe D’Alessandro," Universitá degli studi di Palermo, Palermo, Italy; C. Lauria, L. Gafá, Lega Italiana per la lotta contro i tumori-sez. Ragusa, Ragusa, Italy; D. Serraino, Dipartimento di Epidemiologia, Istituto Nazionale per le Malattie Infettive Lazzaro Spallanzani, Istituti di Ricovero e Cura a Carattere Scientifico (IRCCS), Rome, Italy; M. Tamburini, M. Montella, Servizio di Epidemiologia e Prevenzione, Istituto Tumori "Fondazione G. Pascale," Napoli, Italy; A. Messina, Dipartimento di Scienze Biomediche, Universitá degli studi di Catania, Catania, Italy; G. Rezza, Laboratorio di Epidemiologia e Biostatistica, Istituto Superiore di Sanità, Rome.
Correspondence to: James J. Goedert, M.D., National Cancer Institute, 6120 Executive Blvd., Suite 8012, Rockville, MD 20892 (e-mail: goedertj{at}mail.nih.gov).
Background: Classical Kaposi’s sarcoma (KS) is a malignancy of lymphatic endothelial skin cells. Although all forms of KS are associated with the KS-associated herpesvirus (KSHV), classical KS occurs in a small fraction of KSHV-infected people. We sought to identify risk factors for classical KS in KSHV-infected individuals. Methods: Lifestyle and medical history data from case patients with biopsy-proven non-AIDS (non-acquired immunodeficiency syndrome) KS in Italy were compared by logistic regression analysis with data from population-based KSHV-seropositive control subjects of comparable age and sex. After KSHV immunofluorescence testing, randomly selected patients on the rosters of local physicians were identified as control subjects. Risk of KS was estimated by odds ratios (ORs) and 95% confidence intervals (CIs). All statistical tests were two-sided. Results: From April 13, 1998, through October 8, 2001, we enrolled 141 classical KS case patients and 192 KSHV-seropositive control subjects of similar age (mean = 72 years for case patients and 73 years for control subjects) and sex (30% female case patients and 35% female control subjects). The strongest association was a reduced risk of KS with cigarette smoking (OR = 0.25, 95% CI = 0.14 to 0.45). Cigarette smoking intensity and duration could be evaluated for men, among whom the risk for KS was inversely related to the amount of cumulative smoking (Ptrend<.001). KS risk decreased approximately 20% (OR = 0.81, 95% CI = 0.74 to 0.89) for each 10 pack-years reported, and it was decreased sevenfold (OR = 0.14, 95% CI = 0.07 to 0.30) with more than 40 pack-years. In multivariable analysis, a decreased KS risk was associated with smoking (OR = 0.23, 95% CI = 0.12 to 0.44); but an increased KS risk was associated with topical corticosteroid use (OR = 2.73, 95% CI = 1.35 to 5.51), infrequent bathing (OR = 1.85, 95% CI = 1.04 to 3.33), and a history of asthma (OR = 2.18, 95% CI = 0.95 to 4.97) or of allergy among men (OR = 2.59, 95% CI = 1.15 to 5.83) but not among women (OR = 0.09, 95% CI = 0.003 to 2.76). KS was not related to other exposures or illnesses examined. Conclusion: Risk for classical KS was approximately fourfold lower in cigarette smokers, a result that requires confirmation by other studies. Identification of how smoking affects KS risk may lead to a better understanding of the pathogenesis of this malignancy and interventions for its prevention.
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