Newman et al. (1991) demonstrated that the form of Glanzmann thrombasthenia frequent in Iraqi Jews is due to a truncated GP IIIa lacking a transmembrane domain as a result of an 11-bp deletion within exon 12 of the ITGB3 gene (identified in six unrelated Iraqi-Jewish patients), whereas the form of the disease frequent in Arabs in the Occupied Territories is due to a 13-bp deletion that spans the intron/exon boundary of exon 4 of the ITGA2B gene.

Rosenberg et al. (1997) identified an 11.2-kb deletion between an Alu sequence in intron 9 and exon 13 in the GP3A gene in three unrelated Iraqi-Jewish families with Glanzmann thrombasthenia. They showed that in the general Iraqi-Jewish population living in the Occupied Territories, the frequency of heterozygotes for an 11-bp deletion is 1 in 114 and that for the 11.2-kb deletion is less than 1 in 700. Haplotype analyses indicated that each mutation originated in a distinct founder.

Abu-Amero et al. (2004) studied the PI(A1) and PI(A2) allele frequencies of the ITGB3 gene among the Saudi population, and tried to assess if they could act as independent gene factors for Coronary Artery Disease (CAD) in this population.  Among 509 healthy Saudi blood donors (485 males and 24 females), 71% were homozygous PI(A1)/PI(A1), 27% were PI(A1)/ PI(A2), and 2% were PI(A2)/ PI(A2).  Among 451 Saudi patients with CAD (422 males, 29 females), 77% were homozygous PI(A1)/PI(A1), 20% were PI(A1)/PI(A2), and 3% were PI(A2)/PI(A2).  Although the PI(A1) allele was the most prominent in both groups, its allele frequency was higher in the CAD group (0.87) than in the control (0.84), indicating a possible association of this allele with the condition in this population.  Abu-Amero and colleagues (2004) noted that this was in variance with the documented association of the PI(A2) allele with CAD in other ethnic groups.

Al-Ali et al. (2008) determined the prevalence of glycoprotein (GP) IIb/IIIa among end stage renal disease (ESRD) patients on hemodialysis in the Eastern Province of Saudi Arabia.  Genotypes were analyzed by a reverse-hybridization assay and were confirmed by restriction fragment length polymorphism procedures.  A total of 91 individuals (42 patients and 49 controls) were conducted in the study.  The PI^A2 allele frequency among the control samples was 29%, while it was significantly higher among the hemodialysis samples accounting for 50% (two were homozygous for PI^A2, two were homozygous for PI^A1, and 38 were heterozygous for PI^A1/A2).  The findings suggested that the PI^A2 polymorphism may contribute to the etiology of cardiovascular diseases in ESRD patients.