**7. Psoriatic arthritis**

vitiligo susceptibility is inconsistent [25–28]. It has been reported to be a risk factor for vitiligo in English, Romanian, North American, Mexican, and South Indian Tamil populations [20, 25, 29, 30]. PTPN22 C1858T polymorphism is strongly associated with vitiligo susceptibility in Saudis also [in press]. A genome-wide association study indicates that PTPN22 C1858T is associated with vitiligo in European-derived white patients [Jin et al. 2010]. A meta-analysis utilizing data from different ethnicities shows an association of PTPN22 C1858T with vitiligo in

In contrast, no significant association of PTPN22 C1858T polymorphism with susceptibility to generalized vitiligo was found in Indian Gujarat population, Jordanian, Egyptian female, and Turkish population [27, 32–34]. Available literature shows that the variant of PTPN22 C1858T is responsible for increased risk of vitiligo in Caucasian patients; however, among non-Caucasians/Asians, inconsistency exits, and even the two populations of same country differ in association of PTPN22 C1858T with vitiligo indicating the role of ethnicity. The heterozygous CT genotype of the PTPN22 C1858T has a strong association with non-segmental vitiligo in South Indian Tamils, while there is no association of this polymorphism in Indian Gujarat population [25, 32]. This difference in the results of this polymorphism in Asians or

AA is a dermatological condition in which hair is lost from certain or all areas of the body, typically from certain areas of the scalp, more frequent in young ones [35]. The characteristic feature of AA is circular or oval bald spots which may progress and spread to the entire scalp (alopecia totalis) or entire body (alopecia universalis). Sometimes hair loss is localized to the sides and lower back of the scalp which is known as alopecia ophiasis [36]. The prevalence of AA in the general population varies between 0.1 and 6.9% depending on the ethnic group [37].

Alopecia areata is an autoimmune disease mediated by T cells to the hair follicles. There are enough evidences indicating that AA is a complex multigenetic trait with components of inherited predisposition. Molecular biology studies have led to the identification of a number of candidate genes in humans that confer susceptibility to AA. Recently, PTPN22 gene has been reported to be an additional immunoregulatory gene associated with AA. PTPN22 C1858T polymorphism has been associated with susceptibility of AA in Belgian, English, Egyptian, German, and Mexican populations (**Table 2**) [38–43]. Two meta-analyses have also indicated an association with AA susceptibility [42, 43]. However, no association of PTPN22

Psoriasis is a chronic, complex autoimmune disease with characteristic reddish patches covered by silvery-white scales. It affects approximately 120–180 million people worldwide [45]. The prevalence of psoriasis varies significantly depending mainly on race, geographical location, genetics, environmental factors, and ethnic-

The etiology of psoriasis involves both genetic and environmental factors indicating a multifactorial nature. Moreover, a number of characteristic features of psoriasis are also found in other autoimmune diseases indicating a common

European but not in Asian population [28].

*The Recent Topics in Genetic Polymorphisms*

non-Caucasians can be attributed to ethnic differences.

C1858T has been found in Iranian patients [44].

**5. Alopecia areata (AA)**

**6. Psoriasis**

ity [46–50].

**92**

etiology [51, 52].

PsA is a chronic inflammatory arthritis associated with psoriasis. PsA is a chronic skin and joint condition that considerably affects patient's quality of life. PsA is a complex disease with environmental and genetic risk factors contributing to it. Several studies have demonstrated different associations of genetic polymorphisms in the pathogenic process of PsA.

PTPN22 C1858T polymorphism has also been strongly associated with PsA (**Table 4**) in Toronto admix and Swedish population [61, 62]. Several non-HLA loci including *PTPN22* have been suggested to affect the susceptibility to PsA [63, 64]. A complete genetic overlap has been suggested between psoriasis and PsA susceptibility loci as about a third of people who have psoriasis gets PsA. It has been noticed that subjects with severe psoriasis have a greater chance of getting PsA and about 40% of patients with PsA have relatives with it or with psoriasis, while other earlier studies reported no association of PTPN22 C1858T polymorphism and PsA in Newfoundland, the UK, and German Caucasian [57, 61, 65]. Though no significant differences were observed in allele distribution with different manifestations of disease, there is gender difference, and male PsA patients has higher frequency of T-allele than in the subgroup of female patients [66].
