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Premature/Primary Ovarian Insufficiency (POI)
Published in S Paige Hertweck, Maggie L Dwiggins, Clinical Protocols in Pediatric and Adolescent Gynecology, 2022
Christina N. Davis-Kankanamge, Alla Vash-Margita
Associated with other autoimmune statesMyasthenia gravis, diabetes mellitus, pernicious anemia, vitiligo, celiac disease, rheumatoid arthritis, systemic lupus erythematosus, congenital thymic aplasia, and IgA deficiencyAutoimmune oophoritis occurs in autoimmune polyendocrine syndromes (APS) I and II
Immunopathogenesis and Therapy of Gonadal Disorders and Infertility
Published in George S. Eisenbarth, Immunotherapy of Diabetes and Selected Autoimmune Diseases, 2019
One patient in Irvine’s 1968 study had an ovarian biopsy which demonstrated a lymphocytic and plasma cell infiltrate, destruction of developing follicles, and sparing of primordial follicles. Few reported cases of autoimmune oophoritis have included histologic studies of the ovaries. Immunologic characterization of the lymphocytic infiltrate has been performed on only two occasions.15,23 In only one of those instances was nonembedded tissue used for analysis. The lymphoplasmacytic infiltrate in that case was confined to developing, cystic, and atretic follicles, sparing primordial follicles. The mononuclear infiltrate included B cells and plasma cells, T cells of both CD4 + (helper) and CD8 + (suppressor-cytotoxic) phenotype, and a small number of natural killer (NK) cells and macrophages.
Endocrinology
Published in Fazal-I-Akbar Danish, Essential Lists of Differential Diagnoses for MRCP with diagnostic hints, 2017
Hypogonadism in females:1 Gonadotrophin failure: a Hypothalamic–pituitary disease.b Kallman’s syndrome.2 Complete ovarian failure: a Dysgenesis; Turner’s syndrome; Swyer’s syndrome.12b Autoimmune oophoritis; oophorectomy/radiotherapy/chemotherapy.3 Partial ovarian failure: a PCOS.b Resistant ovary syndrome.4 Adrenal pathology: 17a-hydroxylase deficiency.5 Iatrogenic: cytotoxic drug therapy.
Association of forkhead box P3 gene polymorphisms with premature ovarian insufficiency in Chinese women
Published in Gynecological Endocrinology, 2021
Chenyi Zhong, Wanyue Wang, Danhua Pu, Huiyuan Wang, Rongrong Tan, Jie Wu
POI presents as highly heterogeneous clinical manifestations and a heterogeneous etiology. According to the experts, autoimmune dysfunction contributes to the pathogenesis of 10–30% of premature ovarian failure (POF) cases, as evidenced by autoimmune oophoritis complicated with other autoimmune disorders [13]. The immune system attacks the ovary during the normal physiological activities of follicle formation, ovulation, luteum formation, or dysgenesis, similar to other various autoimmune diseases [14]. Changes in the infiltration of Treg cells may disturb the immune balance, negatively affecting these processes [8], and the sustained expression of FOXP3 is required for the development of Treg cells [15]. As previously described in a study by our group [7], the proportions of CD4 + CD25 + FOXP3 + Treg cells and expression of the FOXP3 mRNA in the peripheral blood are decreased in patients with POI, suggesting that the immunological equilibrium has been disrupted during the ovarian cycle of patients with POI.
Ovarian reserve in young juvenile idiopathic arthritis patients
Published in Modern Rheumatology, 2019
Gabriela R. V. Ferreira, Renato B. Tomioka, Nadia E. Aikawa, Elaine P. Leon, Gustavo A. R. Maciel, Paulo C. Serafini, Edmund C. Baracat, Claudia Goldenstein-Schainberg, Rosa M. R. Pereira, Eloisa Bonfá, Clovis A. Silva
DOR in JIA patients may be triggered by autoimmune mechanisms. Autoimmune oophoritis may impact developing follicles, sparing primordial follicles during early phase due to CD4+ T cells activation, inducing progressive decrease of ovarian function in mice. In humans, there are several reported target antigens involved in autoimmune oophoritis, such as zona pellucida/oocyte, granulosa cells, theca cells, steroidogenic enzymes and corpus luteum (anti-Col) [7]. The presence of anti-Col was rarely observed in our JIA patients, contrasting with a prevalence of 16–22% in adult and cSLE populations [8,18].
Evaluation of CD4+CD25+FOXP3+ regulatory T cells and FOXP3 mRNA in premature ovarian insufficiency
Published in Climacteric, 2020
J. Xiong, R. Tan, W. Wang, H. Wang, D. Pu, J. Wu
The anti-inflammatory cytokine TGF-β induces the proliferation of Treg cells and the differentiation of initial T cells into Treg cells and maintains the expression level and immunosuppressive activity of FOXP3. TGF-β sustains regulatory networks through the modulation of FOXP3 expression and development of ectopic Treg cells28. In the case of an immunological abnormality, more pro-inflammatory cytokine IFN-γ molecules are secreted by type 1 T helper cells; however, Treg cells inhibit the proliferation of type 1 T helper cells, thereby inhibiting the production of IFN-γ and maintaining immune tolerance29. In the present study, the POI patients had lower levels of TGF-β1 than the controls and increased IFN-γ levels compared to those of the controls, which may be attributable to the decreased frequency of CD4+CD25+FOXP3+ Treg cells and FOXP3 gene expression in the peripheral blood of women with POI. Thyroid autoimmunity is the most commonly associated endocrine autoimmune abnormality reported in POI patients (25–60%)30. Moreover, 20% of women with POI were positive for anti-TPO and/or anti-TG in the present study. The ovary is a common target of autoimmune attack in organ-specific and systemic autoimmune diseases, and positivity for circulating autoantibodies against ovarian tissue has been demonstrated in women with POI, at an incidence of 30–67% of patients17. Moreover, it has been reported that all women identified with histological evidence of autoimmune oophoritis by ovarian biopsy are positive for AAA31. Therefore, AAA is considered the best marker of POI associated with steroid cell autoimmunity4. Consistent with the findings of previous reports, the levels of AAA were significantly increased in the POI patients compared with the controls. Thus, while a specific non-invasive reliable diagnostic test for ovarian autoimmunity is still unavailable, patients should be tested for thyroid, adrenal, and ovarian autoantibodies.