Adil Omar Bahathiq
Embryo implantation is necessary for the successful formation of pregnancy. Ectopic implantation external the uterine cavity and the growth of ectopic pregnancy (EP) is a major cause of maternal morbidity and occasionally mortality during the first trimester. EP may be encouraged by failure of tubal transport and/or increased tubal receptivity. Activin A and related proteins (inhibins, follistatin [FS], follistatin-related gene [FLRG], endometrial bleeding associated factors [ebaf]) are involved in the complex mechanisms letting the formation and the upkeep of pregnancy. Pathological expression of activins and their binding protein, follistatin, was observed in tissue and serum samples collected from EP. Numerous studies with different designs studied the diagnostic value of a single measurement of serum activin-A in the differentiation between normal intrauterine and failing early pregnancy and the results are controversial. Nevertheless, the diagnostic value of activins in EP, including the other activin isoforms (activin-B and -AB) and follistatin, merits further research. The local derangement of activin A pathway in some pregnancy disorders (incomplete and complete miscarriages, recurrent abortion, and ectopic pregnancy [EP]) further sustains the hypothesis that activin A and its related proteins play a relevant role in the formation of pregnancy. This review appraises the data to date researching the role of activins or inhibin dimers in the formation of normal pregnancy and, pathogenesis and diagnosis of tubal EP.
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