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Human Reproduction, Vol. 10, No. 4, pp. 815-817, 1995
© 1995 European Society of Human Reproduction and Embryology

research-article

Immunology: Mitogen-induced lymphocyte proliferation and peripheral blood mononuclear cell {beta}-endorphin concentrations in primary dysmenorrhoea

Maurizio Marchini1, Barbara Manfredi2, Luca Tozzi1, Paola Sacerdote2, Alberto Panerai2 and Luigi Fedele1,3

1Department of Obstetrics and Gynecology, University of Milan Milan, Italy 2Department of Pharmacology, University of Milan Milan, Italy

Correspondence: 3To whom correspondance should be addressed at: Clinica Ostetrica e Ginecologica L. Mangiagalli, Via della Commenda 12, 20122 Milano, Italy

Dysmenorrhoea is a recurrent painful disease which causes physical and psychological stress. The purpose of the present study was to investigate whether there was a measurable derangement of immune cells and immune responses in women with severe primary dysmenorrhoea. On day 26 of one cycle and on days 1 and 3 of the following cycle we measured polyclonal, mitogen-induced lymphocyte proliferation and {beta}-endorphin concentration in peripheral blood mononuclear cells obtained from 16 infertile women with normal pelvis, of whom eight had and eight did not have the disorder. In women with dysmenorrhoea, polyclonal mitogen-induced lymphocyte proliferation was lower than in controls on all 3 days considered, but the difference was statistically significant only on day 26 (43 605 ± 9876 µg/ml versus 67 305 ± 15 249 µg/ml; P < 0.01). Monocyte {beta}-endorphin concentrations in the patients with dysmenorrhoea were significantly elevated on day 3 compared to controls (67.8 ± 24.3 pg/106 cells versus 29.7 ± 6.9 pg/106 cells; P < 0.05). Our results demonstrate that immune responses are modified in patients with primary dysmenorrhoea. These effects are independent of circulating hormone concentrations and are consistent with the role of dysmenorrhoea as a stressful event.

Key words: dysmenorrhoea/{beta}-endorphin/immune function/lymphocyte/neuroimmunomodulation


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