Benabadji et al. (1978) indicated that glucose-6-phosphate dehydrogenase (G6PD) deficiency is found in 3.2% of the male population living in the urban area of Algiers. Deficient subjects originated from multiple geographic regions of Northern Algeria, with prevalence of individuals of Berber-Kabyle origin. Red blood cell G6PD was partially purified and characterized in deficient males from 17 families, and six different variants were found. Among them, only one, the Gd(-) Kabyle variant, had been previously described. It was detected in nine families. The other five variants were new: Gd(-) Laghouat (four cases), Gd(-) Blida (one case), Gd(-) Thenia (one case), Gd(-) Titteri (one case), and Gd(-) Alger (two brothers). Strikingly, the common G6PD*Mediterranean variant was not found.

Nafa et al. (1993) identified a T-to-C transition at nucleotide 143 converting codon 48 from ATC (ile) to ACC (thr) in an Algerian boy who presented to the hospital with acute hemolytic anemia associated with 7 to 10% of G6PD residual activity. The mutation was associated with favism.

In a study performed in Abu Dhabi, Anvery (1980) identified 121 cases with G6PD deficiency in which about 4% of them were Bahrainis [Anvery SM. Glucose-6-phosphate dehydrogenase deficiency in Abu Dhabi. Emirates Med J. 1980; 1:24-6.]

In 1987, Bhagwat and Bapat carried out the first study on the prevalence of G6PD deficiency in Bahraini blood donors. Between March 1986 and February 1987, 2680 male Bahraini blood donors visiting Salmaniya Medical Center were screened for G6PD deficiency by using the qualitative dye reduction test of Bernstein. Of those blood donors, 709 individuals were found to be G6PD deficient. That result showed a high prevalence of G6PD deficiency in Bahraini male blood donors (26%). It was suggested that G6PD deficient blood transfused to G6PD deficient individuals might cause an increase in hemolysis, particularly during the exchange transfusion of G6PD deficient infants. [Bhagwat GT, Bapat JP. Glucose -6- phosphate dehydrogenase deficiency in Bahraini blood donors. Bahrain Med Bull. 1987; 9(3):120-2.]

Mohammed et al. (1992) conducted a cord blood screening program to determine the frequency of G6PD Deficiency in Bahrain. A total of 10,327 cord blood samples, representing over 80% of all Bahraini neonates born in 1985 were analyzed in the study. The incidence of G6PD Deficiency was found to be 21%.

Ardati et al. (1995) performed the first study in Bahrain to identify the extent and severity of G6PD deficiency and to define the phenotypes by the use of quantitative enzyme analysis and electrophoretic mobility. Cord blood samples were collected from 100 Bahraini neonates (54 males and 46 females). Phenotyping of the G6PD variants was done by electrophoresis on cellulose acetate plates and the enzyme bands were visualized using isoenzyme reagent. Sixty- one neonates (32 males and 29 females) had normal enzyme activity. Of those, one had a fast moving band (G6PD-A+), another one was heterozygous (G6PD-A+B+), and the remaining had the band in the normal position (G6PD-B+). There were 29 neonates with severe deficiency, 25 of them (18 males and seven females) had undetectable activity. All eight neonates with moderate deficiency had the electrophoretic band in the normal position (G6PD-B+); seven of those were females. The two neonates with increased activity had their band in the normal position. Accordingly, six putative phenotypes were noted in the study. Ardati et al. (1995) suggested that the G6PD*Mediterranean variant were the most common in Bahraini neonates with severe G6PD. [Ardati KO, Bajakian KM, Mohammad AM, Coe EL. Glucose-6-phosphate dehydrogenase phenotypes in Bahrain: quantitative analysis and electrophoretic characterization. Saudi Med J. 1995; 16(2):102-4.]

During the study of the incidence of cystic fibrosis in Bahrain, Al Arrayed and Abdulla (1996) detected 27 patients with cystic fibrosis (25 were Bahrainis). Of those, 98% had G6PD deficiency. [Al Arrayed SS, Abdulla F. Incidence of cystic fibrosis in Bahrain. J Bahrain Med Soc. 1996; 8(3):157-60.]

Mohammad et al. (1998) studied the coexistence of sickle cell disease with G6PD deficiency in Bahrain. Blood samples from 310 Bahraini individuals (152 males and 158 females) attending four major health centers were collected and underwent hemoglobin and G6PD electrophoresis. The subjects were of ages ranging between five to 74 years. One-hundred-and-twenty-five individuals had either sickle cell disease or sickle cell trait. Severe G6PD deficiency (Gd-) was present in 47% of individuals with HbS, while only 19% of those with only HbA had such a deficiency, indicating a significant statistical difference between the two groups. [Mohammad AM, Ardatl KO, Bajakian KM. Sickle cell disease in Bahrain: coexistence and interaction with glucose-6-phosphate dehydrogenase (G6PD) deficiency. J Trop Pediatr. 1998; 44:70-2.]

Al Arrayed et al. (1999) analyzed 500 formats for 500 clients taken at random. About 23.2% of the parents were first cousins, 1.5% were second cousins, and 3% were far relatives. G6PD deficiency was found in 26% of samples and 8% of attended couples were found to be at risk of having affected offspring. The consanguinity rate among them was 15%. [Al Arrayed SS, Hafadh N, Serafi S. Premarital counseling, an experience from Bahrain. Bahrain Med Bull. 1999; 21(4)]

Al Momen et al. (2004) were the first to study the molecular basis of G6PD deficiency in Bahrain with further emphasis on the genetic polymorphism c.1311C>T for both normal and deficient subjects. DNA extraction was done for 83 Bahraini patients (64 males and 19 females) and 80 normal Bahraini controls (43 males and 37 females). A combination of PCR-RFLP and PCR-DGGE procedures were employed to uncover the sequence variations at c.563C>T (G6PD*Mediterranean; p.Ser188Phe) and at the c.1311C>T polymorphism in both groups. G6PD*Mediterranean mutation was identified in 93 of the 102 X chromosomes (91.2%) from G6PD deficient subjects. The c.1311C>T silent polymorphism was found to be associated with the c.563C>T mutation in 89 of the 93 X chromosomes (95.7%) that harbor this mutation. The c.563C>T mutation was found to be associated with cytosine in two X chromosomes (2.15%), however two other X chromosomes (2.15%) could not be ascertained whether having cytosine or thymine at nt position 1311. Of the 117 normal chromosomes, 82 (70%) showed cytosine at nt position 1311, while it was thymine in 35 of the X chromosomes (30%). [Al Momen A, Al Arrayed S, Al Alawi AA. Molecular homogeneity of G6PD deficiency. Bahrain Med Bull. 2004; 26(4):139-42.]

Badens et al. (2000) identified the frequency of G6PD deficiency in the Comorian community by screening blood samples of 467 Comorian newborns (246 females and 221 males). G6PD activity was determined by spectrophotometry. Of the 221 males, 21 were G6PD-deficient (G6PD activity < 10% of normal) resulting in an allele frequency of 9.5%. G6PD mutations were characterized in 17 chromosomes from 11 male and three female patients. The G6PD A(-) variant was found in 14 chromosomes, while G6PD*Mediterranean was detected in three chromosomes. Two females carried both mutations and one was homozygous for G6PD A(-).

Sidrak et al. (1991) investigated the prevalence of glucose-6-phosphate dehydrogenase (G-6-PD) deficiency among the inhabitants of the east African Republic of Djibouti. The study included the analysis of the methemoglobin reduction test in the blood of 170 Djiboutian males, 81 Afars and 89 Somalis. Eight subjects were found to be G-6-PD deficient, 1 Afar and 7 Somalis (1.2% versus 8%; P = 0.02).

Ragab et al. (1966) studied the occurrence of G6PD deficiency in Egypt by employing methemoglobin reduction test on 500 adult males from the army recruits blood donation centers. G6PD deficiency was found in 132 of 500 adult males, the total incidence was found to be 26.4%. The study found that G6PD deficiency had lower incidence rate (15.8%) in metropolitan regions than in rural regions (29.7%) possibly due to mixed genetic make-up and low incidence rates of malaria.

McCurdy et al. (1974) studied the heterogeneity of red cell glucose-6-phosphate dehydrogenase (G-6-PD) deficiency in Egypt and described several variants including G6PD El-Fayoum, G6PD El-Kharga, G6PD Siwa, and G6PD Tahta.

Usanga and Ameen (2000) investigated the frequency of G6PD deficiency, the level of enzyme activity and the phenotype distribution in 3,501 male subjects living in Kuwait, 409 of which are Egyptians. Of the ethnicities discussed in the study, Egypt presented the lowest frequency for G6PD deficiency (1%). The enzyme activity was of 6.4 ± 1.2 IU/g Hb and the prevalent phenotype was G6PD B, but G6PD A and G6PD B- were also present with very low frequencies (97.1%, 1.9%, and 1% respectively). Usanga and Ameen (2000) used the fluorescent spot method for detection and electrophoresis to determine the phenotype.

Al-Ani et al. (2008) reviewed the incidence rates of favism in Arab countries, and reported that in Egypt, 1% of all neonates screened had G6PD deficiency.

Geerdink et al. (1973) described an Iraqi Jewish family with the red cell glucose-6-phosphate dehydrogenase variant (G6PD-Bagdad) and kernicterus.

Gutman et al. (1978) described two maternal male cousins in a Jewish Iraqi family with dyskeratosis congenita and megaloblastic bone marrow. The kindred displayed a deficiency of glucose-6-phosphate dehydrogenase (G6PD) and a beta-thalassemia trait.

In 1980, Anvery described a 16-year-old Iraqi boy who was residing in Abu Dhabi with marked G6PD deficiency. He had multiple congenital abnormalities, including a grossly deformed bony thorax, and an enlarged heart. He died within 24 hours of admission with heart failure. [Anvery SM. Glucose-6-phosphate dehydrogenase deficiency in Abu Dhabi. Emirates Med J. 1980; 1:24-6.]

Kurdi-Haidar et al. (1990) studied 21 unrelated individuals with G6PD*Mediterranean from Saudi Arabia, Iraq, Iran, Jordan, Lebanon, and Palestine. All but one had the c.563C>T (p.Ser188Phe), and, of these, all but one had the silent C-to-T change at nucleotide 1311. Among another 24 unrelated Middle Eastern persons with normal G6PD activity, 4 had the silent c.1311C>T mutation in the absence of the deficiency c.563C>T mutation. Kurdi-Haidar et al. (1990) concluded that most Middle Eastern subjects with the G6PD*Mediterranean phenotype have the same mutation as that found in Italy; that the silent mutation is an independent polymorphism in the Middle East, with a frequency of about 0.13; and that the mutation leading to G6PD*Mediterranean deficiency probably arose on a chromosome that already carried the silent mutation.

Al-Allawi et al. (2010) carried out a molecular study to determine the prevalence of G6PD deficiency in a random sample of healthy Iraqi Kurdish males attending a regional premarital screening center and to define the molecular basis of G6PD deficiency among a sample of G6PD deficient males in the same region. A total of 580 randomly selected healthy male Kurdish Iraqis were screened for G6PD deficiency using methemoglobin reduction test and results were confirmed by quantitative enzyme assay for the cases that showed G6PD deficiency. DNA analysis was performed on 115 G6PD deficient subjects, 50 from the premarital screening group and 65 unrelated Kurdish male patients with documented acute hemolytic episodes due to G6PD deficiency. Analysis was performed using polymerase chain reaction/restriction fragment length polymorphism for the five most common deficient molecular variants reported in Iraq's surrounding countries, namely G6PD*Mediterranean (c.563C>T), G6PD*Chatham (c.1003G>A), G6PD*A- (c.202G>A), G6PD*Aures (c.143T>C; p.lle48Thr) and G6PD Cosenza (c.1376G>C), as well as the silent c.1311C>T mutation. Among 580 random Iraqi male Kurds, 63 (11%) were found to have G6PD deficiency. Molecular studies were performed on a total of 115 G6PD deficient males revealed that the G6PD*Mediterranean variant (c.563C>T) was the most common and was detected in 101 of 115 individuals (88%), followed by G6PD*Chatham variant (c.1003G>A) that was detected in 10 (9%). No cases of G6PD A-, G6PD*Aures or G6PD Cosenza were identified, leaving 4 cases (3%) uncharacterized. Further molecular screening revealed that the silent c.1311C>T mutation was present in 93/95 (98%) of the Mediterranean deficient variants, in 1/10 of the Chatham cases and in one of the three uncharacterized variants. The current study revealed a high prevalence of G6PD deficiency among Iraqi Kurdish population of Northern Iraq (11%), which is higher than that reported from neighboring Iranian Kurdish population. This study, which is the first molecular study on G6PD deficient variants from Iraq, documented that G6PD*Mediterranean and Chatham constitute the large majority of the deficient variants. These results were found to be similar to those reported from neighboring Iran and Turkey and to lesser extent other Mediterranean countries.

Shaker et al. (1966) examined the appearance of G6PD deficiency through analyzing peripheral blood samples that were collected from Sabah Hospital for both Kuwaiti and non-Kuwaiti populations. The estimated frequency of non-Kuwaitis showed that Iraqis (36.4% newborn males and 31.3% adult males) had the highest rate of G6PD deficiency, followed by Jordanians with 23.6% newborn males and 22.9% adult males. 

Karadsheh et al. (1986) studied two glucose-6-phosphate dehydrogenase (G6PD) variants. G6PD Amman-1 was partially purified from the red cells of a patient suffering from recurrent jaundice and spontaneous episodic attacks of severe hemolysis in the absence of oxidant drugs, infection, or fava beans. The enzymatic characteristics of G6PD Amman-1 were markedly reduced activity, fast eletrophoretic mobility, slightly increased km for NADP, normal km for G-6-P, normal heat stability, normal utilization of substrate analogues 2-deoxy G-6-P and deamino-NADP, and a monophasic pH curve with a peak at 8.5 to 9.3. The second variant, G6PD Amman-2, was partially purified from the red cells of a patient suffering from recurrent jaundice with episodic mild hemolysis caused by infection or unknown factors. G6PD Amman-2 characteristics were severely reduced activity, slow electrophoretic mobility, normal km for NADP, decreased km for G-6-P, decreased heat stability, increased utilization of substrate analogues, and a monophasic pH curve with a narrow peak at pH 9.5. The red cell level of reduced glutathione was markedly decreased with twofold increase in the activity of glutathione reductase in the patient with G6PD Amman-2.

Usanga and Ameen (2000) calculated the frequency of G6PD to be 3.6% in 333 male Jordanians living in Kuwait. The phenotypes identified were predominantly G6PD B and G6PD B- and G6PD A- with very low frequency. The phenotype G6PD A could not be identified in this group.

Karadsheh et al. (2005) identified six different G6PD mutations in two Jordanian populations. Blood samples were collected from 875 males in Amman area and 106 males in Jordan Valley. Quantitative G6PD deficiency assays were performed in individuals with positive fluorescent spot screening test. The incidence of G6PD deficiency in Jordan Valley was 8.5% (9/106), while it was 3.2% in Amman area. The higher incidence of G6PD deficiency in the Valley might be explained by historically higher rates of malaria in that region. The most common mutation found among the subjects was the G6PD*Mediterranean mutation (c.563C>T) which consisted 53.3% of the total mutations. Interestingly, the frequency of G6PD*A- (c.376A>G+202G>A; p.Asn126Asp+Val68Met) mutation was higher in Jordan Valley and that could be attributed to the African ancestry of its population. The other four variants were the G6PD*Chatham (c.1003G>A), G6PD*Valladolid (c.406C>T), G6PD*Aures (c.143T>C; p.lle48Thr), and G6PD*Asahi (c.202G>A); however, the last three variants were found only in Amman area. The mutation could not be identified in four cases. By observing the clinical findings of the subjects with G6PD*Valladolid and G6PD*Asahi, Karadsheh et al. (2005) suggested that the clinical expression of G6PD deficiency was the result of interaction of the molecular properties of each G6PD variant with exogenous factors and possibly with additional population-specific genetic factors.

Al-Ani et al. (2008) reviewed the incidence rates of favism in Arab countries, and reported that in Jordan, 3.6% of all neonates screened had G6PD deficiency.

Kurdi-Haidar et al. (1990) studied 21 unrelated individuals with G6PD*Mediterranean from Saudi Arabia, Iraq, Iran, Jordan, Lebanon, and Palestine. All but one had the c.563C>T (p.Ser188Phe), and, of these, all but one had the silent C-to-T change at nucleotide 1311. Among another 24 unrelated Middle Eastern persons with normal G6PD activity, 4 had the silent c.1311C>T mutation in the absence of the deficiency c.563C>T mutation. Kurdi-Haidar et al. (1990) concluded that most Middle Eastern subjects with the G6PD*Mediterranean phenotype have the same mutation as that found in Italy; that the silent mutation is an independent polymorphism in the Middle East, with a frequency of about 0.13; and that the mutation leading to G6PD*Mediterranean deficiency probably arose on a chromosome that already carried the silent mutation.

Shaker et al. (1966) examined the appearance of G6PD deficiency through analyzing peripheral blood samples that were collected from Sabah Hospital for both Kuwaiti and non-Kuwaiti populations. A total of 206 newborn males (where 93 are Kuwaiti and 113 non-Kuwaiti) and 255 adult males (where 118 are Kuwaiti and 137 non-Kuwaiti) were employed for the field screening and the methemoglobin reduction tests. Estimation of the incidence of G6PD deficiency showed that 18 Kuwaiti and 28 non-Kuwaiti out of 206 newborn males, and 22 Kuwaiti and 30 non-Kuwaiti out of 461 adult males had G6PD deficiency. The total resulted in 22.3% newborn males and 20.4% adult males with G6PD deficiency, observing that the frequency is somewhat higher in non-Kuwaiti populations than in Kuwaitis. The estimated frequency of non-Kuwaitis showed that Iraqis (36.4% newborn males and 31.3% adult males) had the highest rate of G6PD deficiency, followed by Jordanians with 23.6% newborn males and 22.9% adult males. Shaker et al. (1966) concluded that in Kuwait the gene for G6PD deficiency is rather common, with an average mean of 21.3%.

In 15 male newborns with glucose-6-phosphate dehydrogenase deficiency, Kandil et al (1996) investigated the effect of family members applying henna (Lawsonia inermis Linn.) on the patients' bodies. Patients were admitted to Al-Jahra Hospital in Kuwait presenting significant anemia, reticulocytosis and indirect hyperbilirubinemia. Kandil et al. (1996) reaffirmed the nocuous effect of henna on G6PD deficient red blood cells and that the use of henna on infants is prevented by a health education program in the region.

D'Souza et al. (1998) conducted a study in Kuwaiti to analyze the population and haplotype for the c.563C>T mutation. The study included a population group that consisted of 110 unrelated native Kuwaitis and Bedouins residing in Kuwait and 20 family members of probands with G6PDMed. Peripheral blood was collected from the subjects who consisted of 63 males and 47 females. In the population group, seven subjects were identified having the c.563C>T mutation (4 hemizygotes, 2 heterozygotes and 1 homozygote) revealing a G6PDMed frequency of 0.0509 in Kuwait. Haplotype analysis was performed and was found to be informative for all subjects except for a heterozygous female. The seven unrelated subjects from Kuwait with the G6PDMed chromosomes consisted of six Mediterranean and one Asian haplotypes. [D'Souza B, Samilchuck E, Al-Awadi S. Molecular analysis of the G6PD-Mediterranean mutation in Kuwait. Med Principles Pract. 1998; 7:209-4.]

Samilchuk et al. (1999) conducted a population study to determine the common G6PD mutations in Kuwait. The study included 200 random samples for Kuwaitis (122 males and 78 females) that were employed in DNA extraction and 6 G6PD deficient probands that were examined for G6PD mutations. Initially, all samples were examined for the presence of the c.563C>T and 367A-G mutations, subsequently the samples that were found positive for c.376A>G were additionally tested for three other mutations (c.202G>A, 680G-T, and 968T-C). Samilchuk et al. (1999) found that in the Kuwaiti population, three mutations (c.563C>T, c.376A>G, and c.202G>A) were common and their polymorphic frequencies were found to be 0.053, 0.0215 and 0.0111, respectively. Judging by the c.1311C>T polymorphism, Samilchuk et al. (1999) noticed that out of 20 unrelated Kuwaiti chromosomes with c.563C>T, 19 were found to have the Mediterranean haplotype. The study also showed that the frequency of the G6PD deficient genotype was found to be 4.5% showing 5.73% for males and 2.56% for females.

Usanga and Ameen (2000) conducted a study on a group of 3,501 male donors living in Kuwait, 1,307 of which are of Kuwaiti ethnicity, to identify the frequency of the G6PD deficiency, the enzyme activity, and the distribution of the phenotype. Other analyzed ethnicities included Egyptians, Jordanians, Lebanese, and Syrian. With the fluorescent spot method, Usanga and Ameen (2000) determined the G6PD prevalence to be of 5.5%, the highest when compared to the other ethnicities considered in this study group, but the lowest compared to other Gulf countries. G6PD activity was of 6.5 ± 1.1 IU/g Hb and the phenotypes observed were predominantly G6PD B followed by very low frequencies for G6PD B- and G6PD A-. G6PD A could not be found in these individuals.

Samilchuk et al. (2003) screened for G6PD in 1, 080 Kuwaiti male blood donors and found 70 cases of G6PD. They also found the following mutations: c.563C>T (Mediterranean; 72.9%), c.202G>A (G6PD*A-; 14.3%), c.1003G>A (G6PD*Chatham; 7.1%), c.143T>C (G6PD*Aures; 1.4%), and 4.3% of the samples remained with unknown mutations. G6PD cases were genotyped for UDO-glucuronosyltransferase 1 (UDPGT1) gene promoter polymorphisms and resulted in the following alleles: (ta)6/(ta)6 [38.6%], (ta)7/(ta)7 [15.7%], (ta)6/(ta)7 [44.3%], and (ta)7/(ta)8 [1.4%]. Samilchuk et al. (2003) concluded that 4% of the Kuwaiti males possess G6PD deficiency coexisting with low activity of the UDPGT1 promoter.

AlFadhli et al. (2005) determined the allele frequencies of G6PD variants in 82 G6PD deficient subjects (75 males and 7 females) and 1,209 randomly selected individuals (660 males and 549 females) all within the Kuwaiti population with minimal recent non-Kuwaiti admixture. According to AlFadhli et al. (2005), the highest allele frequency in the G6PD deficient subjects was that of the G6PD*Mediterranean c.563C>T (0.742) followed by G6PD*A- c.376A>G+202G>A (0.124). The two other mutations, G6PD*Chatham c.1003G>A and G6PD*Aures c.143T>C were found to be at lower allele frequencies in the G6PD deficient group. With these findings, AlFadhli et al. (2005) suggested a gene flow from the Indian sub-continent, sub-Saharan Africa and the Mediterranean region contributing to the mutations characterized in the Kuwaiti population.

In a study of single gene disorders in Kuwait, Samilchuk (2005) found that G6PD deficiency was common in Kuwait with 6.5% of Kuwaiti males being affected with the condition. Four mutations in the G6PD gene were shown to be causative for the condition in this population; c.563C>T, c.202G>A, c.1003G>A, and 143T>C.

Al-Ani et al. (2008) reviewed the incidence rates of favism in Arab countries, and reported that in Kuwait, 5.5% of all neonates screened had G6PD deficiency.

In a study conducted in 1964 on 549 Lebanese male blood samples, Taleb et al. concluded that the disorder is present in many of the ethnic groups in the country except in the Druze and Aramians. Most likely, this is due to the fact that these groups used to live in the areas which were not infested by malaria. Since G6PD deficiency is considered to be a mutation surviving in the regions where malaria is endemic, these groups, thus, had no reason, evolutionary speaking, to develop or maintain the mutant trait.

Usanga and Ameen (2000) established the prevalence of G6PD in 282 Lebanese male subjects to be as low as 2.13% by means of the fluorescent spot method. 

Al-Ani et al. (2008) reviewed the incidence rates of favism in Arab countries, and reported that in Lebanon, 1% of male and 2.1% of all neonates screened had G6PD deficiency.

Kurdi-Haidar et al. (1990) studied 21 unrelated individuals with G6PD*Mediterranean from Saudi Arabia, Iraq, Iran, Jordan, Lebanon, and Palestine. All but one had the c.563C>T (p.Ser188Phe), and, of these, all but one had the silent C-to-T change at nucleotide 1311. Among another 24 unrelated Middle Eastern persons with normal G6PD activity, 4 had the silent c.1311C>T mutation in the absence of the deficiency c.563C>T mutation. Kurdi-Haidar et al. (1990) concluded that most Middle Eastern subjects with the G6PD*Mediterranean phenotype have the same mutation as that found in Italy; that the silent mutation is an independent polymorphism in the Middle East, with a frequency of about 0.13; and that the mutation leading to G6PD*Mediterranean deficiency probably arose on a chromosome that already carried the silent mutation.

Mir et al. (1985) studied 120 cord and 320 venous blood samples collected from Libyan newborns and adults respectively for the estimation of glucose-6-phosphate dehydrogenase (G-6-PD) activity by a screening technique and by quantitative estimation. The mean (S.D.) enzyme activity in the non-deficient neonates and adults was 1.13 (0.23) and 0.87 (0.21) IU/ml RBC/min, respectively. The incidence of G-6-PD deficiency in the male population was 2.8%. The enzyme activity in the deficient male population ranged from 0-19.5%; none of them was symptomatic or had a hematological abnormality. Of the female subjects 1.8% had enzyme activity of 50-65%. Mir et al. (1985) indicated that the frequency of G6PD deficiency appears to be low in Libya compared with that found in other Arab populations and is comparable with the incidence in other Mediterranean countries.

Anvery (1980) performed a study on 476 consecutive patients for whom requests for screening were received at the hematology department of the Central Hospital, Abu Dhabi. More than 25% of these cases were found to have G6PD deficiency (121 patients). Nearly half of the cases were five years of age or less and nine patients were females (7%). Of the affected individuals, it was found that more than 20% were Omani patients. Three adult Omani women had border-line positive results on the screening tests, intermediate assay levels. They showed hepatosplenomegaly and moderate anemia. One of those women had ancylostomiasis and all had had repeated attacks of malaria in the past. In addition, a 5-year-old Omani girl had acute severe hemolysis after eating raw fava beans which indicated positive results of G6PD deficiency. Presentation, in most cases, was with well defined hemolytic episodes and about one quarter required blood transfusion. [Anvery SM. Glucose-6-phosphate dehydrogenase deficiency in Abu Dhabi. Emirates Med J. 1980; 1:24-6.]

[See also: United Arab Emirates > Anvery, 1980].

White et al. (1986) analyzed 5000 subjects from three major Peninsular Arab States and determined the frequency of glucose-6-phosphate dehydrogenase deficiency in Oman to be 3%. Later, White et al. (1993) re-estimated the frequency of G6PD Deficiency in Oman by studying 1,000 Omani subjects. The frequency this condition was found to be 0.27 for males and 0.11 for females in this population, which indicates that nearly 400,000 people are G6PD deficient in Oman. In spite of this high frequency, however, oxidative hemolytic syndromes were very uncommon.

Ahmed and Farooqui (2000) described a 12-year old G6PD deficient boy, who developed an episode of acute intravascular hemolysis, upon ingestion of moth balls, as prescribed by a traditional healer, for treating a rectal ulcer. The patient was managed conservatively with intravenous fluids, alkalinisation of urine, and transfusions, when needed. [Ahmed A, Farooqui MA. Naphthalene-associated severe intravascular hemolysis in a G6PD deficient patient. Oman Med J. 2000; 17(2):33-5.]

Al-Riyami et al. (2001) estimated the prevalence of hemoglobinopathies in Oman by interviewing members of households (6600 with response rate of 92.5%) randomly selected from a list prepared from a sample of 264 units chosen from all Oman districts. The 1993 national population census was used as a frame for the two-stage stratified probability sampling. Blood was withdrawn from 6342 children (aged 0-5 years) and analyzed for G6PD activity. The prevalence of G6PD deficiency was found to be 18.8% and it showed significant association with gender (26.6% males versus 10.6% females), mild anemia (in 24.2%) and history of blood transfusion during the year that preceded this study (34% had transfusions). However, no association with age was detected. It also showed significant regional variation, being more common in Al Dakhiliyah (29%) and South Batinah (26.1%), and least common in Dhofar (2.1%). The prevalence of first cousin consanguinity was determined as 33.6%, and it was associated significantly with homozygous blood disorders. Upon comparison of the prevalence with that of other countries of the Gulf Cooperation Council (GCC), Oman had the highest prevalence compared to United Arab Emirates (8.7%) and Saudi Arabia (6.2%). On combing these results with the 1993 census, it was calculated that in Oman, 44,733 children under the age of five years had G6PD deficiency. The number of children born yearly with a major hemoglobinopathy according to the authors' results and the Hardy-Weinberg equation, was 2 per 1000 live births, which increased to 3 per 1000 live births upon correction for consanguinity. Therefore, with a birth rate of 42,000/year, 125 children with a major hemoglobinopathy were calculated to be born yearly. As these numbers would increase the burden on health services, Al-Riyami et al. (2001) suggested that future health planning for Oman should be undertaken by improving and strengthening the national programs for detection, genetic counseling and health education.

Nair and Al-Khusaiby (2003) undertook a retrospective study of all babies with significant jaundice admitted at an Omani hospital during a 6-year period (1995-2001). Of the total of 258 patients, 87 were found to have G6PD Deficiency. Kernicterus developed in 14 of these babies, ten of which were G6PD deficient. In three of these G6PD deficient babies, the crisis was preceded by henna application. No increase in hemoglobin levels or decrease in reticulocyte counts were noted. Nair and Al-Khusaiby (2003) suggested that babies known to be G6PD deficient should be monitored for early detection of jaundice.

Kurdi-Haidar et al. (1990) studied 21 unrelated individuals with G6PD*Mediterranean from Saudi Arabia, Iraq, Iran, Jordan, Lebanon, and Palestine. All but one had the c.563C>T (p.Ser188Phe), and, of these, all but one had the silent C-to-T change at nucleotide 1311. Among another 24 unrelated Middle Eastern persons with normal G6PD activity, 4 had the silent c.1311C>T mutation in the absence of the deficiency c.563C>T mutation. Kurdi-Haidar et al. (1990) concluded that most Middle Eastern subjects with the G6PD*Mediterranean phenotype have the same mutation as that found in Italy; that the silent mutation is an independent polymorphism in the Middle East, with a frequency of about 0.13; and that the mutation leading to G6PD*Mediterranean deficiency probably arose on a chromosome that already carried the silent mutation.

Al-Jawadi and Al-Hilali (1998) carried out a study on 43 non-thalassemic G6PD-deficient patients ranging in age from 1 to 62 years (35 males and 8 females) and 52 G6PD normal subjects as controls ranging in age from 1 to 56 years (40 males and 12 females) of different nationalities (including Qataris) living in Qatar, to compare the levels of HbA2 in both groups. Al-Jawadi and Al-Hilali (1998) measured the concentration of HbA2 and estimated qualitatively and quantitatively G6PD activities in all subjects, and then compared the results of the two groups by using Student's t test. Al-Jawadi and Al-Hilali (1998) observed a close numerical similarity between HbA2 levels in the two groups studied and found no significant statistical difference, leading them to conclude that HbA2 has no relationship with G6PD activity in the red cells.

Gelpi (1967) analyzed the frequency of G6PD deficiency and sickle cell disease in the population of Saudi Arabia residing along the Gulf perimeter through employing Motulsky brilliant cresyl blue screening test (BCB) and a colorimetric test to calculate the enzyme activity. The study resulted in finding a close association among sickle cell disease and enzyme deficiency, showing a correlation among the sickling trait and G6PD deficiency in the oasis regions and demonstrated the presence of more than one type of mutants in Saudi males with enzyme deficiency.

In Saudi Arabia, Mallouh and Abu-Osba (1987) reviewed the G6PD status of all children aged 1 month to 14 years who were treated for meningitis, septicemia, osteomyelitis, or typhoid fever during a 9-year period. The observed frequency of G6PD deficiency was significantly higher than expected for the entire group, for females with both catalase-positive and catalase-negative infection, and for males with catalase-positive infections.

In Saudi Arabia, Niazi et al. (1996) described G6PD*Aures (c.143T>C; p.lle48Thr) in 7 of 20 children (35%) with severe G6PD deficiency and in a 16-year-old boy with a history of passing dark urine after eating fava beans at the age of 5 years. Of the 20 children, 12 were positive for G6PD*Mediterranean and the mutation in 1 child remained unidentified. [Niazi G, Adeyokunu A, Westwood B, Beutler E. G6PD Aures: a rare mutant of G6PD in Saudi Arabia: molecular and clinical presentations. Saudi Med J. 1996; 17:311-4.]

As part of the hemoglobinopathies' neonatal screening program in the provinces of Qatif and Al Hasa, Nasserullah et al. (1998) carried out a molecular study on a total of 12,220 infants, including 11,313 (92.6%) Saudis, to estimate the frequency of G6PD. The study group included 4,744 males (4,410 Saudis and 334 non-Saudis) and 4,722 females (4,378 Saudis and 344 non-Saudis); and 1,370 males (1,254 Saudis and 116 non-Saudis) and 1,279 females (1,172 Saudis and 107 non-Saudis), in Al Hasa and Qatif, respectively. This target population included all babies born in Qatif Central hospital, Qatif, and King Fahad Hospital, Al Hasa, from December 1992 to December 1993. In addition, babies delivered at home in the Qatif and Al Hasa areas, and coming to primary health care centers for vaccination, were also included. The diagnosis of G6PD was confirmed by fluorescent spot test. High prevalence of G6PD deficiency was found among Saudi infants, in Qatif (30.6%) Al Hasa (14.6%). In contrast, low frequencies were found among non-Saudi infants, in Qatif (5.8%) and Al Hasa (2.6%). In Qatif, the deficiency was found in 35% of the male and in 21% of the female subjects. These were found to be lower in Al Hasa infants, with 19.4% in male and 8.2% in female subjects. Nasserullah et al. (1998) concluded that the Saudi populations in Qatif and Al Hasa are at risk for G6PD.

Al-Ani et al. (2008) reviewed the incidence rates of favism in Arab countries, and reported that in Yanbu, Saudi Arabia, 3.1% of all male and 0.9% of all female neonates screened had G6PD deficiency.

Kurdi-Haidar et al. (1990) studied 21 unrelated individuals with G6PD*Mediterranean from Saudi Arabia, Iraq, Iran, Jordan, Lebanon, and Palestine. All but one had the c.563C>T (p.Ser188Phe), and, of these, all but one had the silent C-to-T change at nucleotide 1311. Among another 24 unrelated Middle Eastern persons with normal G6PD activity, 4 had the silent c.1311C>T mutation in the absence of the deficiency c.563C>T mutation. Kurdi-Haidar et al. (1990) concluded that most Middle Eastern subjects with the G6PD*Mediterranean phenotype have the same mutation as that found in Italy; that the silent mutation is an independent polymorphism in the Middle East, with a frequency of about 0.13; and that the mutation leading to G6PD*Mediterranean deficiency probably arose on a chromosome that already carried the silent mutation.

Sidrak et al. (1991) investigated the prevalence of glucose-6-phosphate dehydrogenase (G-6-PD) deficiency among the inhabitants of the east African Republic of Djibouti. The study included the analysis of the methemoglobin reduction test in the blood of 170 Djiboutian males, 81 Afars and 89 Somalis. Eight subjects were found to be G-6-PD deficient, 1 Afar and 7 Somalis (1.2% versus 8%; P = 0.02).

Omer et al. (1972) studied the incidence of G6PD deficiency among five indigenous and two immigrant groups in Sudan. The indigenous groups were consisting of Nubians (Northern Sudan), Kalakla (central), Dinka (Southern), Ingassena (South Eastern), and Beja (Eastern). The two immigrant groups were Nigerians (Western bank of the Blue Nile) and Tchiendians (central Sudan). Blood samples were collected from unrelated males and screening tests for G6PD deficiency was performed by the methemoglobin reduction test. The highest frequency of G6PD deficiency was observed in Nigerians (21%) followed by Dinka populations (14%). Techiendians had the frequency of 11% and Nubians had 3%. Both Ingassena and Beja groups showed no G6PD deficient subjects. Therefore, the indigenous groups appeared to have low or no incidence for G6PD, with the exception of Dinka.

Samuel et al. (1981) studied 597 unrelated persons, comprising of 401 males and 196 females, for glucose-6-phosphate dehydrogenase (G6PD) and hemoglobin phenotypes by starch gel electrophoresis. The levels of G6PD activity were assayed in order to study the quantitative expression of G6PD phenotypes and the influence of hemoglobin phenotypes on such expression. There was no significant different in the levels of G6PD activity in subjects with GdA or GdB. The mean levels of the enzyme activity were 165.5 +/- 33.7 and 164.8 +/- 33.8 IU/10(12) red cells in males and 159.3 +/- 27.8 and 163.4 +/- 33.5 IU/10(12) red cells in females, respectively. 14 subjects with Gd(+) "Khartoum" had significantly (p less than 0.001) higher level of enzyme activity with a mean above 200 IU/10(12) red cells. On the other hand, 20 subjects with GdB(int) (demonstrated by visual comparison of starch gel) showed significantly (p less than 0.001) lower levels of enzyme activity (107.6 +/- 23.5 IU/10(12) red cells). The heterozygotes GdAB also had slightly, but not significantly lower levels of enzyme activity than either GdA or GdB. The mean level of activity for GdAB was 140.1 +/- 29.4 IU/10(12) red cells.

Vulliamy et al. (1988) have cloned and sequenced several mutant G6PD alleles. They described the G6PD*Chatham (c.1003G>A; p.Ala335Thr) mutations in a man from Syria. They suggested that this mutation may be polymorphic and that it causes class 2 enzyme derangement with no change in restriction sites.

Usanga and Ameen (2000) identified the frequency of G6PD in 737 Syrian male donors living in Kuwait with fluorescent spot method to be of 2.98%. Samples were assayed for enzyme activity, which was as high as 6.5 ± 0.9 IU/g Hb and electrophoresis revealed the phenotypes G6PD B and B-. The phenotypes G6PD A and A- could not be determined in these subjects.

Al-Ani et al. (2008) reviewed the incidence rates of favism in Arab countries, and reported that in Syria, 2.9% of all neonates screened had G6PD deficiency.

Blibech et al. (1989) screened male students originating from several towns in Tunisia to identify the incidence of G6PD deficiency in the country. Three hundred and twenty five assays were made and the incidence of the deficiency was calculated at 1.84%. G6PD electrophoresis in 54 subjects revealed that the majority (96.2%) were of the B+ type, whereas only 1.96% presented the A+ type. Three deficient subjects showed an electrophotetic mobility identical to that of the A+ type of G6PD.

Anvery (1980) performed a study on 476 consecutive patients for whom requests for screening were received at the hematology department of the Central Hospital, Abu Dhabi, in order to identify the prevalence of G6PD deficiency in Abu Dhabi. More than 25% of these cases were found to have G6PD deficiency (121 patients). Nearly half of the cases were five years of age or less and nine patients were females (7%). UAE national patients with G6PD deficiency comprised more than 40% of the cases with at least two affected females. Presentation, in most cases, was with well defined hemolytic episodes and about one quarter required blood transfusion. [Anvery SM. Glucose-6-phosphate dehydrogenase deficiency in Abu Dhabi. Emirates Med J. 1980; 1:24-6.]

In the same year, Kamel et al. (1980) indicated that the indigenous population of Abu Dhabi had a high rate of G6PD deficiency.

White et al. (1986) analyzed 5000 subjects from three major Peninsular Arab States and determined the frequency of glucose-6-phosphate dehydrogenase deficiency in the UAE to be 0.9%.

Miller et al. (2003) carried out a cross-sectional community clinic-based capillary blood survey to produce a hematological profile of preschool national children of the United Arab Emirates. The sample included 1-5-year-old Emirati children attending a Primary Health Care Center in Al-Ain from April 2000 to October 2000. Those children with capillary hemoglobin (Hb) and mean corpuscular volume (MCV) values below predetermined cutoffs were offered venous blood hematological workup. A random sample of children with values above those cutoffs was also offered the same workup. In total, 496 children were surveyed. The mean Hb and adjusted MCV rose with increasing age but were not significantly different by gender. Two hundred and sixty-two children with Hb or MCV below the cutoffs and 50 children above the cutoffs were venous blood tested. The estimated abnormalities for this population of children were as follows: anemia 36.1%; iron deficiency anemia 9.9%; glucose-6-phosphate dehydrogenase (G6PD) deficiency 9.1%; sickle cell trait 4.6%; and beta thalassemia 8.7%. Miller et al. (2003) further indicated that there was likely to be a high prevalence of alpha-thalassemia in the population and emphasized the importance of DNA studies in this regard.

Al-Ani et al. (2008) evaluated the prevalence of G6PD deficicnecy in Khorfakkan, UAE, by studying the cord blood samples of all neonates born in a 6-month time period between 2006 and 2007. Good quality cord blood samples were collected from 254 neonates (123 males, 131 females); 202 of these neonates were Emiratis. G6PD deficiency was identified in 20 of these samples; providing a prevalence rate of 7.9%. Of these 20, 13 were males, giving a gender specific prevalence rate of 5.1% for male neonates and 2.8% for female neonates.

White et al. (1986) analyzed 5000 subjects from three major Peninsular Arab States and determined the frequency of glucose-6-phosphate dehydrogenase deficiency in Yemen to be 0.6%.