Background and Aims

Premature ovarian insufficiency (POI) refers to a continuum of decreasing ovarian function in women before the age of 40. To date, the cause of POI in the majority of cases remain unresolved. Many cases has been linked to genetic, toxic, infections, enzymatic and iatrogenic causes.

A key function of the immune system is to identify and differentiate “self” and “non self” i.e. tolerance. Loss of self-tolerance results in an immune response against self-tissues and thus autoimmunity. Various investigations have highlighted the role of autoimmunity and its pertinence to POI. Several potential immune antigenic targets in the ovary have been reported to be involved in autoantibody induced autoimmune attack. The presence of lymphocytic oöphorits in ovarian samples of patients with POI provides histopathological evidence of autoimmune ovarian involvement. Finally, POI is strongly associated with other autoimmune conditions including for instance Addison disease, autoimmune polyglandular syndrome (APS) −1, APS-4, hypothyroidism, and diabetes mellitus among other autoimmune diseases. Taken together, these lines of evidence provide strong basis that support the role of autoimmunity as a potential cause of disease etiopathogenesis. Continuing research is increasingly providing more insight into the complex disease process. The aim of this review is to summarize the current literature related to the autoimmune nature of POI.

Methods

this is a review

Results

this is a review

Conclusions

this is a review

Background and Aims

The loss of the ability of the immune system to recognize “self” antigens mounts an immune response against one’s own tissues and cells, hence autoimmunity. Specific environmental triggers include both intrinsic and extrinsic factors. Of those factors; dietary factors, infections, smoking, stress, and chemicals have been shown to influence disease etiopathogenesis.

Heavy metals are naturally occurring elements with high atomic density. Their wide distribution stems from their widespread use in industry, medical and technological fields. Heavy metals exert an important biochemical and physiological function in the human body. They are considered important constituents of several key enzymes and thus play an important role in oxidation-reduction reactions. Nevertheless, at high doses, heavy metals could have detrimental effects resulting in epigenetic modifications, reactive oxygen species production, activation of the innate and adaptive immune cells, and shifting the cytokine expression to proinflammatory profile. Current scientific evidence points towards the role of heavy metals in the exacerbation of various autoimmune diseases including systemic lupus erythematosus, rheumatoid arthritis, and multiple sclerosis. Similarly, heavy metals were shown to be associated with the induction of autoimmune disease in animal models. Interestingly, Aluminum which has been used as an adjuvant was shown to activate both arms of the immune system thus resulting in a hyperinflammatory response. Aluminum accumulation has been shown to be associated with autoimmune diseases including inflammatory bowel disease, system lupus erythematosus, multiple sclerosis among others.

Methods

This is a review

Results

This is a review

Conclusions

This is a review