Using fluorescence-assisted mismatch analysis (FAMA) and cycle sequencing of the PCR products, Alif et al. (1999) screened for mutations in the IDUA gene in a group of 13 Moroccan patients with MPS I and their families, including three sibs and twin sibs. The p.P553R mutation, which is rare in Europeans, was identified in 92% of mutant alleles (24 of 26). This was said to be the highest frequency of this mutation detected in patients with Hurler syndrome. None of the patients carried the p.W402X or the p.Q70X allele, the most common MPS I mutations in Europeans.

Schaap and Bach (1980) found 13 Arab patients with Hurler syndrome. The patients came from eight families, five of which were Druze and three Muslim. Bach et al. (1993) found homozygosity for three different mutations distributed in seven families, five of them Druze: mutations in exon 2 (p.TYR64TER), exon 7 (p.GLN310TER), and exon 8 (p.THR366PRO). Transfection of mutagenized cDNA into COS-1 cells showed that the missense mutation p.THR366PRO permitted the expression of only trace amounts of alpha-L-iduronidase activity. The nonsense mutations were associated with abnormalities of RNA processing. The p.TYR64TER mutation was accompanied by a very low level of mRNA and skipping of exon 2. Utilization of a cryptic splice site was observed with the p.GLN310TER mutation. Bach et al. (1993) anticipated that MPS in the Druze population would be caused by one founder mutation which might or might not be shared with the Muslim patients residing in the surrounding area. They were surprised to find that, in fact, there were three different mutations and that none of which had been found in Europeans.