Tamary et al. (2000) studied an Ashkenazi/Egyptian Fanconi anemia patient. However, the mutation in one FANCA allele could not be identified.

Tamary et al. (2000) studied an Iraqi-Jewish Fanconi anemia patient. They could not identify any mutations in the two FANCA alleles of this patient.

[See also: Morocco > Tamary et al., 2000].

Mohammed (1994) described a girl child with Fanconi Anemia born to consanguineous parents. The child had multiple congenital anomalies including microcephaly, short neck, high arched palate, VSD, polydactyly, and bilateral simian creases. Bone marrow biopsy suggested acute lymhoblastic leukemia. Karyotype analysis of peripheral blood revealed multiple chromosomal abnormalities, mostly in chromosomes 1, 3, and 9, including breakages, fragile X, hypo- and hyper-diploidy, breaks exchange, translocations, and ring chromosomes.

[Mohammed FM. Chromosomal abnormalities in Fanconi anaemia. Kuwait Med J. 1994; 26(1):43-7.]

Tamary et al. (2000) studied an Iraqi-Jewish Fanconi anemia patient. They could not identify any mutations in the two FANCA alleles of this patient.

[See also: Morocco > Tamary et al., 2000].

Kannan et al. (2003) reported a case of pancytopenia which was confirmed by an aplastic bone marrow on biopsy. The presence of a rudimentary thumb on the right hand with its absence on the left hand raised the suspicion of Fanconi anemia, which was confirmed by stress induced chromosome fragility test on peripheral blood lymphocytes. He received an allogenic bone marrow transplant and his blood counts improved.

Tamary et al. (2004) described the genotype (FANCA and FANCG) and phenotype of three consanguineous families with nine FA patients and one additional unrelated patient, all of Arab origin. Tamary et al. (2004) identified three novel disease-causing mutations: FANCA gross deletion of exons 6-31; FANCA splice-site mutation IVS 42-2A>C; and FANCG splice-site mutation IVS4+3A>G. Of the four patients from the first family with the FANCA deletion of exons 6-31, three had malformations (microcephaly, Klippel-feil disease) and developed bone marrow failure at a median age of 10.75 yr. One developed acute myelobalstic leukemia and two died of bone marrow transplantation (BMT) complications. The three patients from the second family with FANCA IVS42-2A>C had several malformations (hypoplastic thumbs, left pelvic kidney with reflux, absent left kidney, deafness, microcephaly, mental retardation). All developed bone marrow failure at an early age (median age=8.5 yr), and two developed squamous cell carcinoma at the ages of 26 and 30 yr. Two patients from the third family with FANCG IVS4+3A>G were available for evaluation. One patient had malformations (rotated left kidney, hypoplastic thumbs), and both patients developed bone marrow failure at age 12-13 yr and are currently well at age 18-21 yr (the 21 years old patient post-BMT). The clinical condition of eight patients with FANCA mutations was found severe. Tamary et al. (2004) concluded that further analysis of FA mutations and genotype-phenotype correlations may facilitate prenatal diagnosis of FA and allow for a more rational therapeutic approach, including frequent monitoring, early bone marrow transplantation, and eventually gene therapy.

In the year 2000, Habib et al. reported a 4-year-old boy from Saudi Arabia with an established diagnosis of Fanconi anemia. Ultrasonography and a renal nuclide scan showed a solitary kidney on the left side a micturating cystourethrogram showed gross vesicoureteral reflux. The findings observed in the patient are consistent with a diagnosis of solitary crossed renal ectopia (SCRE). In addition, the patient had hypospadias and unilateral undescended testis with absent vas deferens.

Al-Hwiesh et al. (2005) reported two Saudi brothers with Fanconi Syndrome in comorbidity with familial tuberous sclerosis. In both cases, there were histories of failure to thrive and mental retardation associated with hypokalemic metabolic acidosis.

Bouchlaka et al. (2003) investigated FANCA ANEMIA gene mutations in 49 patients from different regions in Tunisia. Nearly, 96% of the patients presented mainly with skeletal malformations while 92% presented abnormal skin pigmentations. In 43% of the cases, profound aplastic anemia had developed. The families were mostly consanguineous 60% of which were first cousins and 25% second cousins.

[See also: Morocco > Tamary et al., 2000].

Revesz et al. (1993) reviewed the occurrence of rare congenital forms of aplastic anemias in the United Arab Emirates. They concluded that Fanconi anemia is the most frequently diagnosed form of aplastic anemias in the UAE population.