Immune dysfunction--a potential target for treatment in endometriosis.

The treatment approach towards endometriosis has been traditionally either surgical or hormonal in nature. Since endometriosis is, to a large extent, a microscopic disease, a surgical approach cannot be expected to eradicate the disease. Treatment is, therefore, generally attempted by hormonal manipulation, an approach based on the known oestrogen sensitivity of endometriosis. Hormonal manipulation can only temporarily affect endometriosis, and quite clearly does not address the underlying aetiology and/or pathophysiology of the disease. Since neither is, at present, well understood, one can only speculate as to the treatment approach that would, in fact, affect the pathophysiology of the condition. Endometriosis has, in recent years, been characterized by a large number of immunological abnormalities in the host. It is, therefore, very tempting to speculate that an immunological defect represents the basic abnormality which later leads to the occurrence of the disease. This assumption is supported by the observation that those immunological defects are already present in the mildest forms of the disease. In fact, if one believes that many cases of unexplained infertility represent undiagnosed microscopic endometriosis, then evidence suggests that this precursor stage of the disease is basically characterized by an identical immunological profile to that of endometriosis. An immunological aetiology and/or pathophysiology of endometriosis should lead to an immunological treatment approach toward the disease. Specifically, a number of non-specific immunomodulators, presently utilized in a variety of medical conditions with immunological aetiologies, would seem to represent promising new therapeutic strategies to conquer endometriosis at its roots. A new treatment approach to endometriosis appears urgently needed since, at least with regard to the effects of endometriosis on fertility and pregnancy loss, present approaches have proven ineffective.