Polymorphisms in the TNF-α and IL-10 gene promoters and risk of psoriasis and correlation with disease severity.

Several cytokines were assumed to play an essential role in the induction and the pathogenesis of psoriasis. The aim of this work was to investigate the role of TNF-α-308 and IL-10-1082 polymorphisms and their serum levels in the pathogenesis of psoriasis and determine their relation to disease severity. 110 Psoriasis patients and 120 healthy volunteers were genotyped for TNF-α-308 and IL-10-1082 polymorphism by polymerase chain reaction. Serum level of TNF-α and IL-10 were measured by ELISA. Our study demonstrated an association of IL-10-1082 polymorphism and psoriasis and between TNF α-308 polymorphism and psoriasis disease and severity. Serum TNF α increased in patients, while serum IL-10 decreased in patients with significant correlation between serum TNF-α and psoriasis severity. These results indicated that TNF-α-308 and IL-10-1082 polymorphisms imparted significant risk towards the development of psoriasis.

Risk and severity of psoriasis vulgaris in relation to angiotensin II type 1 receptor gene polymorphism and metabolic syndrome.

BACKGROUND: Psoriasis vulgaris is a chronic inflammatory and proliferative skin disease, characterized by the formation of itchy, erythematous skin patches or plaques. Patients with psoriasis are at an increased risk of developing metabolic syndrome, including obesity, hypertension, diabetes, and atherosclerosis. Recently, angiotensin II (Ang II) has been reported to be associated with the development of psoriasis. Ang II not only increases the blood pressure but is also a potent proinflammatory modulator and functions through interaction with angiotensin II type 1 receptor (AT1R). Moreover, it is hypothesized that the AT1R gene expression could be correlated with the severity of psoriasis and/or metabolic syndrome. AIM: We examined the association of Ang II type 1 receptor (AT1R) A1166C gene polymorphisms and metabolic syndrome with the severity of psoriasis. PATIENTS AND METHODS: The present case-control study included 25 patients with psoriasis vulgaris and 25 healthy subjects in Egypt. The psoriasis lesions in the patient group were assessed using the psoriasis area and severity index (PASI) score. The AT1R polymorphism A1166C (rs5186) was studied using restriction fragment length polymorphism (RFLP) and polymerase chain reaction (PCR) amplification of the gene from the whole blood sample in both groups. Serum lipid profile and blood sugar levels were assessed post 12 h and 8 h fasting, respectively, in both groups. The severity of metabolic syndrome was evaluated using the severity score. RESULTS: The results of the present study demonstrated that the AT1R A1166C gene polymorphisms increased the risk of developing psoriasis in the Egyptian population. We found that 70% of patients with AC genotype and 100% of patients CC genotype reported a PASI score >20 and were considered to be severe cases with a statistically significant difference as compared with patients with AA genotype (p=0.003). In addition, a high statistically significant difference (p=0.001) existed among AT1R genotypes with respect to the percentage of metabolic syndrome in psoriasis patients. Similarly, a statistically significant difference (p=0.004) among AT1R genotypes with respect to metabolic score was found, with the highest level of score and percentage observed in patients with CC genotype than in patients with AC genotype. The lowest level was present among those with AA genotype. CONCLUSION: Patients with psoriasis expressing the C allele of AT1R1166 are susceptible to developing metabolic syndrome and have higher PASI scores as compared with patients carrying the A allele.