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The Journal of Clinical Endocrinology & Metabolism Vol. 85, No. 7 2483-2487
Copyright © 2000 by The Endocrine Society

Original Studies

Increased Leptin Levels in Serum and Peritoneal Fluid of Patients with Pelvic Endometriosis1

Giuseppe Matarese2,3, Carlo Alviggi2, Veronica Sanna4, Jane K. Howard5, Graham M. Lord5, Carlo Carravetta, Silvia Fontana, Robert I. Lechler, Stephen R. Bloom and Giuseppe De Placido

Laboratorio di Immunologia, Dipartimento di Biologia e Patologia Cellulare e Molecolare (G.M.) and Dipartimento di Ginecologia e Ostetricia, Area Funzionale di Medicina della Riproduzione ed Endoscopia Ginecologica (C.A., C.C., G.D.P.), Università degli Studi di Napoli "Federico II", 80131, Napoli, Italy; Centro di Endocrinologia ed Oncologia Sperimentale, CNR, Napoli (V.S., S.F.), 80131, Napoli, Italy; and Department of Immunology (G.M.L., R.I.L.) and Endocrine Unit (J.K.H., S.R.B.), Imperial College School of Medicine, Hammersmith Hospital, London W12 ONN, United Kingdom

Address correspondence and requests for reprints to: Dr. Giuseppe Matarese, Laboratorio di Immunologia, Dipartimento di Biologia e Patologia Cellulare e Molecolare - Università degli Studi di Napoli "Federico II"- via S. Pansini 5, 80131, Napoli, Italy. E-mail: gmatarese{at}napoli.com

Pelvic endometriosis is an immune-related chronic inflammatory disease, characterized by ectopic implants of endometrium in the peritoneal cavity and associated with increased secretion of proinflammatory cytokines and neoangiogenesis. Leptin, the adipocyte-derived hormone, has been shown to have a role in food intake, basal metabolism, and reproductive function. Leptin levels are dynamically regulated, being elevated by inflammatory mediators and reduced by starvation. Leptin itself can influence the proinflammatory immune responses of CD4+ T lymphocytes, and reports have also shown this hormone to be an angiogenic factor in vitro and in vivo. We investigated whether leptin concentrations in serum and peritoneal fluid (PF) differed between 13 patients with different stages of endometriosis and 15 age- and body mass index-matched controls. We found a statistically significant (P < 0.05) increase in leptin levels in serum (30.3 ± 14.8 ng/mL) and PF (35.9 ± 17.4 ng/mL) of patients with endometriosis, compared with our control population (serum, 15.6 ± 8.4; PF, 17.5 ± 7.2 ng/mL). Regression equations, relating leptin to body mass index, were also significantly different in endometriosis patients, compared with controls. Higher levels of leptin were observed in the earlier stages of endometriosis than advanced-stage disease.

These data suggest that the proinflammatory and neoangiogenic actions of leptin may contribute to the pathogenesis of endometriosis.




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