Graves disease is an autoimmune disorder in which antibodies to the thyroid-stimulating hormone receptors (TSHR) are formed by the patient's body, and therefore, resulting in hyperthyroidism. As the antibodies bind to the TSHR, these receptors will be activated causing abnormal growing of the thyroid gland and excessive production of thyroid hormone (thyrotoxicosis).
Susceptibility to Graves disease is found to be associated with the human leukocyte antigen (HLA) alleles, however, HLA haplotypes vary among the different ethnic groups. Genetic studies have shown that polymorphisms in the cytotoxic T-lymphocyte antigen 4 (CTLA-4) gene have a role in causing the symptoms of Graves disease. In addition, alterations in the vitamin D-binding protein (DBP) gene may increase the susceptibility to Graves disease.
Isseh and Al-Sharkawy (1998) undertook a retrospective (1984-1991) study of thyrotoxic patients in Qatar. Of the total of 179 patients, 62 of whom were Qatari and 60 others from other Arab nationalities, 151 patients were found to have Grave's Disease, making it the most common cause of thyrotoxicosis in Qatar.
[Isseh N, Al-Sharkawy W. Thyrotoxicosis in Qatar. Qatar Med J. 1998; 7(1):39-41.]
Malabu et al. (2008) conducted a retrospective review study of patients diagnosed with Grave’s Disease between years 1995 and 2004 in a large tertiary care center in Saudi Arabia.
Using case-control and family-based designs in a sample from Tunisia, and microsatellite markers, Hadj Kacem et al. (2003) found evidence that SLC26A4 may be a susceptibility gene for AITDs, with varying contributions in Graves disease.