The inflammatory markers in gonadal failure association with chromosomal abnormalities and autoimmune antibodies

Abstract

Objective: Gonadal failure in young women is related with genetic factor and autoimmunity, however, most of cases are unknown of etiology. The role of autoimmunity in primary ovarian insufficiency (POI) and the presence of autoimmune oophoritis were demonstrated. The inflammatory markers studied in chronic disorders is a paucity in gonadal failure. The aim of this study was to investigate the inflammatory markers in gonadal failure and compared regarding to chromosomal abnormalities and autoimmune antibodies. Design: Total 128 women complained of amenorrhea were enrolled in this cross sectional study. One hundred four women having hypergonadotropic hypogonadism diagnosed as gonadal failure, and evaluated the chromosomal abnormalities, autoimmune antibodies such as antithyroglobluin antibody, antimicrosomal antibody, antinuclear antibody, rheumatic factor, anti-smooth muscle antibody, and anti-acetylcholin receptor antibody. Twenty four women with hypogonadotropic hypogonadism were also included as control. The inflammatory markers were leukocyte count, neutrophil to lymphocyte ratio (NLR), platelet to lymphocyte ratio (PLR), and red cell distribution width to platelet ratio (RPR). Results: Mean age of women with gonadal failure was 22.34 ± 4.55, and FSH and AMH were 66.22 ± 33.61 mIU/mL, and 0.24 ± 0.86 ng/mL separately. Gonadal failure group had higher RPR than those of controls (0.06 ± 0.03, 0.04 ± 0.01, p = 0.04). Leukocyte count, NLR, and PLR were similar between two groups. Among 104 women with gonadal failure, 73 women were diagnosed as POI and 31 women had chromosomal abnormalities such as 45 X, 46 X Del(X)(q22q26), etc. In women with POI, leukocyte count, neutrophil count, lymphocyte count, NLR, PLR, and RPR were not different with those of gonadal failure related with chromosomal abnormalities. Twenty two women (30.1%) of POI and 8 (25.8%) women of gonadal failure related with chromosomal abnormalities had autoantibodies. Regarding the presence of autoantibodies, leukocyte count, NLR, PLR, and RPR were not different. AMH, FSH, or estradiol were not correlated with inflammatory markers either. Conclusion: RPR was increased in gonadal failure. However, NLR, PLR, and RPR were not different by POI or presence of autoantibodies. The inflammatory markers were not correlated with ovarian reserve either. Further larger studies are needed.