The female to male ratio was 0.8 and 0.7 in permanent and transient CH respectively. The female to male ratio of permanent hypothyroidism is similar 
to a study by Hashemipour et al. Other studies reported a higher incidence among females compared with males. This finding could be explained by the high parental consanguinity in our region and the undiagnosed family history of CH as reported also by Castanet et al. The median TSH levels before treatment were significantly higher in patients with permanent CH than those with transient CH. Similar findings were reported by Hashemipour et al in the study from Iran and by Nair et al in the study from India. The median T4 levels before starting treatment were not significantly different among patients with permanent and transient CH. This was reported also by Hashemipour et al, while in other reports initial T4 levels correlated with the etiology of CH. It was conducted from these findings that the first TSH and T4 levels may have predictive role for identifying permanent forms of CH from the transient forms. The most common cause of permanent CH is thyroid dysgenesis. In this study thyroid dysgenesis was the main cause of permanent CH accounting for 79% of cases and dyshormonogenesis accounts for the remaining 21%. These results were similar to other studies reported by Nair et al from india and Ordookhani et al from Iran. We concluded that the incidences of CH as well as the permanent form were similar to the worldwide reported ones. Although the high incidence of transient CH in our study could be explained by iodine deficiency further studies are needed to confirm the etiology and plan the treatment strategies. Interleukin 1 is a major contributor to the development of immune mediated arthritis. This cytokine is expressed by macrophages, monocytes and synovial fibroblasts. Its action is in part regulated by the IL-1 receptor antagonist protein which is the product of the Il1rn gene. The importance of IL-1RA in regulation of IL-1 activity has been established by generating mice deficient in IL-1RA. These IL-1RA deficient mice develop spontaneous arthritis as first described by Horai and colleagues. BALB/c mice that are homozygous for the deficiency develop inflammation in the hind limbs beginning at about 6 weeks of age and achieving an incidence approaching 100% by 3 months of age. Histopathologic examination of the joints of these mice shows infiltration of inflammatory cells and synovial proliferation. The development of disease is in part dependent upon genetic background since DBA/1 mice with a similar deficiency in IL-1RA do not develop spontaneous arthritis. Deficiency of IL-1RA as a result of IL1RN mutation has also been identified in humans and results in a rare autosomal AbMole Diperodon recessive autoinflammatory syndrome. DIRA is manifested by systemic inflammation including rash, painful movement, joint swelling and bone involvement.