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Asprosin is a novel peptide hormone produced and secreted by white adipose tissues. Asprosin associated with insulin resistance and promotes hepatic glucose production. Previous studies showed that serum asprosin was raised in the general population with polycystic ovary syndrome (PCOS). However, there were studies supporting the opposite. Also, there were studies that showed the highest levels of asprosin was due to insulin resistance, as well as in type 2 diabetes patients. PCOS is one of the metabolic disorders related to insulin resistance. Therefore, the current study aims to evaluate the levels of asprosin in the blood serum of women with PCOS compared to the healthy women who resident in Duhok in the Kurdistan Region of Iraq. A cross-sectional study was conducted from 20th of June, 2020 to 11th of January, 2021 at Obstetrics and Gynecology Hospital and Mazi medical clinics. Serum asprosin level was determined in 75 women with PCOS (18-44 years) and 96 healthy women. SPSS software was utilized for analyzing the study data. The (means ± SD) of demographic parameters (body mass index (BMI) and waist circumference (WC)) in women with PCOS were significantly highest in comparison to healthy women. The biochemical parameters (serum asprosin, fasting blood sugar (FBS), fasting insulin (FI), total cholesterol (TC), and triglyceride (TG)) in women with PCOS also were remarkably higher compared to healthy women with the exception of high-density lipoprotein- cholesterol (HDL-C). The current data show that serum asprosin variance significantly between WC, BMI, FBS, FI, TC, TG and HDL-C. The study confirms that serum asprosin in women with PCOS was higher than in the healthy women. In addition in women with PCOS it was found that serum asprosin was positively correlated with BMI, WC, FBS, FI, HOMA-IR, TC and TG (P<0.05). Except, HDL-C was negatively correlated with serum asprosin (P<0.01).

Methotrexate (MTX) is still one of the gold standard treatments for rheumatoid arthritis (RA). It shows diverse outcomes in blood level and clinical response, this was demonstrated by its relation to the genetic polymorphism in the pharmacogenetic study. This study aimed to investigate the role of methylenetetrahydrofolate reductase (MTHFR) gene polymorphisms in relation to MTX efficacy and toxicity in Iraqi Kurdish RA patients. Sixty-four RA patients were involved in this study with an average age of 47.78 ±14.08 and female to male ratio of (8.1). Diagnosis and disease activity were confirmed. Blood analyses, including those of laboratory markers of disease activity, were done. The 28 joint disease activity score (DAS28-CRP) was calculated.  MTHFR gene polymorphisms were analyzed by real-time polymerase chain reaction. The most frequent genotypes which were identified in RA patients were the CT genotype of the C677T single nucleotide polymorphism (SNP) (51.6%) and the AC genotype of the A1298C SNP (48.4%). Patients with non-response to treatment had high frequencies of genotypes CT and TT (58.0% and 12.0%) of the C677T SNP respectively, as compared to those in the responder group; 28.6% and 0.0%); T-allele was associated with drug non-responding OR=4.17, P value=.0.009, meanwhile; genotypes AC and CC of the A1298C SNP were seen in (54.0% and 16.0%) in non-responder group. Patients with active RA had increased frequencies of CT and TT genotypes of the C677T SNP (60.0% and16.0%) respectively as compared to those who were in remission (26.6% and 0.0%); T-allele was associated with high disease activity; OR = 5.11. No association was found between C677T SNP and A1298C SNP, and MTX level status (P> 0.05). However, the variant alleles (T and C) were associated with the MTX toxic level (OR: 2.05, 95% CI [0.97 – 4.32]) and (OR: 1.99, 95% CI [0.96 – 4.18]) respectively. This study suggests that genetic polymorphisms of MTHFR SNP (C677T and A1298C) are associated with MTX efficacy but not toxicity in RA patients. This may assist the physicians in personalizing RA treatment in Iraqi patients.

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