A study conducted by Haider et al. (2001) on the pattern of exon deletion in SMN in Spinal Muscular Dystrophy included three SMA patients from Bahrain [See Kuwait > Haider et al., 2001].

Samilchuk et al. (1996) carried out deletion analysis of the SMN and NAIP genes in 11 cases of type I SMA and in 4 type II SMA cases. The patients were of Kuwaiti origin. All type II patients analyzed belonged to a single kinship. They also analyzed samples from 41 healthy relatives of these patients and 44 control individuals of Arabic origin. They found homozygous deletions of exons 7 and 8 of the SMN gene in all SMA patients studied. All of the control individuals had normal SMN and NAIP.

Haider and Moosa (1997) investigated the presence of survival motor neuron gene and neuronal apoptosis inhibitory protein gene deletions in 17 Arab and 1 Indian families with spinal muscular atrophy (15 type I and 3 type II). Homologous deletions were detected in exons 7 and 8 of the survival motor neuron gene and exon 5 of the neuronal apoptosis inhibitory protein gene in all patients with type I spinal muscular atrophy. In two patients with type II spinal muscular atrophy, only exons 7 and 8 of the survival motor neuron gene were deleted whereas exons 5 and 13 of the neuronal apoptosis inhibitory protein gene were present. In another patient with spinal muscular atrophy type II, exons 7 and 8 of the survival motor neuron gene and exon 5 of the neuronal apoptosis inhibitory protein gene were deleted. This latter patient also had the Pierre Robin syndrome. No deletion was detected in healthy siblings or the parents.

Haider et al. (2001) investigated the pattern of exon deletion in survival motor neuron (SMN) genes in 46 patients with different phenotypes of spinal muscular atrophy from different ethnic backgrounds, which included 26 Kuwaiti patients. DNA from affected patients and 62 unaffected control subjects was subjected to PCR amplification of both exons 7 and 8 of SMN gene which were then digested with the restriction enzymes DraI and DdeI, respectively. Absence of the DdeI enzyme restriction site in exon 8 of SMN1 gene made it possible to distinguish between SMN1 and SMN2 genes. In all the patients with type I SMA, both exons 7 and 8 of SMN gene showed deletions. All patients with type II SMA showed deletion in exon 7, while exon 8 showed deletion in almost all patients. Both patients with Type III SMA were Kuwaitis, and were found to have deletion in both exons 7 and 8. None of the controls were found to have deletions in either SMN gene. In addition, the authors also checked for the presence of two polymorphisms, an A-G transition in exon 7 and the presence of an ATGGCT sequence in exon 8, by using the restriction enzymes BsmAI and HaeIII respectively. The BsmAI polymorphism showed similar results as earlier reported from Spain, with 97% of the tested chromosomes showing allele 1. However, the HaeIII polymorphism differed from earlier reports from Spain and Taiwan, with again about 97% of chromosomes harboring allele 1.

In his study of single gene disorders in Kuwait, Samilchuk (2005) found that SMA was common in the country. All SMA patients studied had a homozygous deletion of both exons 7 and 8 of the SMN1 gene.

A study conducted by Haider et al. (2001) on the pattern of exon deletion in SMN in Spinal Muscular Dystrophy included five Omani SMA patients [See Kuwait > Haider et al., 2001].

A study conducted by Haider et al. (2001) on the pattern of exon deletion in SMN in Spinal Muscular Dystrophy included one Saudi SMA patient [See Kuwait > Haider et al., 2001].