Varicocele is the most common cause of male infertility. Several theories have been proposed to explain how varicocele induces infertility. The role of epididymis in male infertility is not fully well established. Fibrinogen‐like protein 2 is one of serine proteases and is a potent coagulant in membranous form and immune‐modulator in soluble form (sFGL‐2) and expressed in the epididymis. There are no previous reports about its possible role in varicocele. This case‐controlled study aimed to evaluate the seminal level of sFGL‐2 in infertile men with varicocele and in men with idiopathic infertility. This study included 85 participants divided into three groups; 25 normal fertile men, 30 infertile men with varicocele and 30 infertile men of idiopathic cause. Clinical examination, Doppler ultrasound, semen analysis and measurement of seminal level of sFGL‐2 were done to all participants. Seminal level of sFGL‐2 was significantly elevated in infertile than normal fertile men. Seminal level of sFGL‐2 showed negative correlations with sperm concentration, motility and normal morphology. Seminal level of sFGL‐2 had a positive correlation with seminal liquefaction time. This study concluded that seminal level of sFGL‐2 is increased in infertile men with idiopathic cause and with varicocele induced infertility and affects seminal liquefaction.

Varicocele is an abnormal enlargement of the pampiniform venous plexus in the scrotum. The adverse effect of varicocele on spermatogenesis can be attributed to many factors such as an increased testicular temperature, increased intratesticular pressure, hypoxia due to attenuation of blood flow, reflux of toxic metabolites from the adrenal glands and hormonal profile abnormalities. FGL2 might play a protective role during sperm maturation in epididymis. FGL2 was found to be secreted from the principal cells into the tubule lumen where sFGL2 binds specifically to the nonviable, but not the viable, spermatozoa. This process forms sFGL2-protein complex that coats and envelops dying sperms to restrict release and spread of detrimental enzymes and immunogenic molecules from defective spermatozoa. The aim of study is to evaluate FGL2 in semen of patients with varicocele. We determined the presence of fgl2 in the seminal plasma via enzyme-linked immunosorbent assay [ELISA], whereas semen analysis was done as a routine investigation before separation of seminal plasma.fgl2 values in 55 infertile patients were significantly higher than in 25 healthy volunteers [p >0.001]. this result demonstrated strong association between infertility and level of fgl2 in the semen, fgl2 level are increased in infertility.

Background: Psoriatic arthritis is a chronic, immune-mediated, inflammatory arthropathy that presents with inflammation of the joints and entheses, including those of the axial skeleton, and is associated with increased mortality from cardiovascular disease. The aim of the work is to evaluate serum level of sclerostin in patients with psoriatic arthritis and to correlats its level with the severity and activity of psoriatic arthritis. Methods: This case control study included ( 50) subjects classified into two groups: Group I: 30 patients with psoriatic arthritis. Group II: 20 healthy age and sex matched individuals as a control group. Results: there were no statistically significant differences between case group and control group, with a mean value of 42.45±12.90 vs 41.05±9.84 respectively. Regarding sclerostin , it found that there were no statistically significant differences between case group and control group with a mean value of 2787.92±1838.06 vs 2235.53±1830.67 respectively, And it found that there were highly statistically significant differences between groups with high mean value in patients with psoriasis group of 4276.72±1239.7 when it compared with other groups. Conclusion: The significantly higher serum sclerostin levels in PsA patients, compared with controls; there was positive significant correlation between sclerostin and each of age and PASI score. Sclerostin plays an important role in the pathogenesis of PsA and its associated bone damage, either systemic or localized.