Psoriasis is a chronic inflammatory skin condition and angiotensin‐converting enzyme (ACE) is a key circulating enzyme converting angiotensin (Ang) I to the vasoactive peptide Ang II. The exact role of ACE insertion (I)/deletion (D) polymorphism (rs106180) in psoriasis is not clear. We aimed to examine whether the ACE I/D and Ang II type 1 receptor (AT1R) A1166C‐polymorphisms (rs106165), lipid profile, and stress oxidative are associated with susceptibility to psoriasis. One hundred patients with psoriasis and 100 sex‐ and age‐matched unrelated healthy controls were recruited for this case‐control study. ACE I/D and AT1R A1166C polymorphisms were identified by the polymerase chain reaction (PCR) and PCR‐restriction fragment length polymorphism, respectively, malondialdehyde (MDA) was detected by the high‐performance liquid chromatography, serum arylesterase (ARE) activity of paraoxonase and catalase activities were detected by the spectrophotometry, superoxide dismutase (SOD) activity and vascular adhesion protein (VAP)‐1 were measured by ELISA. The presence of C allele of AT1R A1166C and I allele of ACE considerably increased the risk of psoriasis by 6.42‐fold (P < 0.001). The distribution of II‐genotype of ACE was significantly higher in psoriasis patients than in control group and increased the risk of disease by 3.11‐times (P = 0.023). The higher levels of MDA in patients and the higher activity of SOD, ARE, and CAT was observed in healthy controls with I/D+I/I‐genotype of ACE I/D. This study for the first time demonstrated that the ACE I/D and AT1R A 1166C genes polymorphisms robustly increases the risk of developing psoriasis in population from west of Iran. In addition, these individuals had significantly higher VAP‐1 and MDA concentration and lower enzymatic and nonenzymatic antioxidant‐status, suggesting that psoriatic patients carrying C allele of AT1R1166 polymorphism may be more susceptible to cardiovascular disease and myocardial infarction compared with A allele.

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Introduction Sickle cell disease (SCD) patients are susceptible to the development of vitamin D deficiency (VDD). Vitamin D through binding to vitamin D receptor (VDR) exerts its function and affects gene transcription in target tissues. VDR gene variants affect bone mineral density. Methods In a case‐control study, 101 SCD patients including 61 sickle cell anemia (SCA), 39 S/β‐thalassemia, and 1 HbS/HbD (SD) along with 110 healthy individuals from Kurdistan of Iraq were studied. The lipid profile, vitamin D level, FokI, and TaqI variants of VDR and group‐specific component (GC) were detected using the standard enzymatic method, the immunodiagnostic systems limited EIA kit and PCR‐RFLP methods, respectively. Results Around 93% and 82% of SCA and S/β‐thalassemia patients, respectively, had VDD compared to 83% of healthy individuals. Severe VDD (<10 ng/ml) was detected in 78.7% of patients with HbSS. Plasma levels of total cholesterol, HDL‐C, and LDL‐C in SCD patients were significantly lower compared to controls. Vitamin D levels were negatively correlated to TG and positively correlated to total cholesterol and HDL‐C. The frequencies of the C allele of FokI were 81.7% (p = 0.003), 80.3% (p = 0.034), and 84.6% (p = 0.011) in all SCD, SCA, and S/β‐thalassemia patients, respectively, compared to 69.1% in controls. However, no significant difference was detected comparing the frequencies of VDR TaqI and GC polymorphisms between SCD patients and controls. Conclusion In the present study, we found hypocholesterolemia, high prevalence of VDR FokI C allele, and low vitamin D levels among children and adults with SCD from Kurdistan of Iraq.