Abstract
Premature ovarian insufficiency (POI), previously known as premature ovarian failure or premature menopause, is defined as loss of ovarian function before the age of 40 years. The risk of POI before the age of 40 is 1%. Clinical symptoms develop as a result of estrogen deficiency and may include amenorrhea, oligomenorrhea, vasomotor instability (hot flushes, night sweats), sleep disturbances, vulvovaginal atrophy, altered urinary frequency, dyspareunia, low libido, and lack of energy. Most causes of POI remain undefined, however, it is estimated that anywhere from 4–30% of cases are autoimmune in origin. As the ovaries are a common target for autoimmune attacks, an autoimmune etiology of POI should always be considered, especially in the presence of anti-oocyte antibodies (AOAs), autoimmune diseases, or lymphocytic oophoritis in biopsy. POI can occur in isolation, but is often associated with other autoimmune conditions. Concordant thyroid disorders such as hypothyroidism, Hashimoto thyroiditis, and Grave’s disease are most commonly seen. Adrenal autoimmune disorders are the second most common disorders associated with POI. Among women with diabetes mellitus, POI develops in roughly 2.5%. Additionally, autoimmune-related POI can also present as part of autoimmune polyglandular syndrome (APS), a condition in which autoimmune activity causes specific endocrine organ damage. In its most common presentation (type-3), APS is associated with Hashomoto’s type thyroid antibodies and has a prevalence of 10–40%. 21OH-Antibodies in Addison’s disease (AD) can develop in association to APS-2.
Highlights
Clinical symptoms of Premature ovarian insufficiency (POI) are largely the result of estrogen deficiency and may include amenorrhea, oligomennorhea, vasomotor instability, sleep disturbances, vulvovaginal atrophy, altered urinary frequency and recurrent infections, mood disorders including irritability and emotional lability
Associated autoimmune POI should always be considered in the presence of a primary diseases such as autoimmune thyroiditis, diabetes type 1, celiac disease, myasthenia gravis, systemic lupus erythematosus, or any family history of autoimmune diseases [4,15]
Difficulties in establishing a diagnosis is thought to be due to the transient state and biphasic nature of POI which only leads to atrophy in its final stage [20]
Summary
The exists a wide variety of causes leading to POI. Potential etiologies can be subdivided into different groups: idiopathic, genetics, autoimmune; iatrogenic, and environmental. Idiopathic cases are reported is as high as 74–90% of POI patients. The extent to which genetics play a role in the development of POI remains unclear. Autoimmune-related diseases are estimated to drive anywhere from 4–30% of POI cases [10]. Up to 10–20% of patients suffering with Addison’s disease will develop POI. Patients with cancer in childhood and during adolescence are at higher risk of development POI in later life. POI in this group is most often a result of ovarian surgery, chemotherapy, and/or pelvic radiotherapy. Among those receiving chemotherapy, ovarian damage depends largely on the age of patient during treatment, chemotherapeutic agent(s) received, dose and duration of treatment [13]. There is a well-documented correlation in the literature between POI and incidence of recurrent viral infections [14]
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