Biomedical subjects

Khaled K Abu-Amero

Publications and source records attributed to Khaled K Abu-Amero.

At least 19 recordsLinked to original sources

PubMed2006

E-selectin S128R polymorphism and severe coronary artery disease in Arabs.

BACKGROUND: The E-selectin p. S128R (g. A561C) polymorphism has been associated with the presence of angiographic coronary artery disease (CAD) in some populations, but no data is currently available on its association with CAD in Arabs. METHODS: In the present study, we determined the potential relevance of the E-selectin S128R polymorphism for severe CAD and its associated risk factors among Arabs. We genotyped Saudi Arabs for this polymorphism by PCR, followed by restriction enzyme digestion. RESULTS: The polymorphism was determined in 556 angiographically confirmed severe CAD patients and 237 control subjects with no CAD as established angiographically (CON). Frequencies of the S/S, S/R and R/R genotypes were found as 81.1%, 16.6% and 2.3% in CAD patients and 87.8%, 11.8%, and 0.4% in CON subjects, respectively. The frequency of the mutant 128R allele was higher among CAD patients compared to CON group (11% vs. 6%; odds ratio = 1.76; 95% CI 1.14 - 2.72; p = .007), thus indicating a significant association of the 128R allele with CAD among our population. However, the stepwise logistic regression for the 128R allele and different CAD risk factors showed no significant association. CONCLUSION: Among the Saudi population, The E-selectin p. S128R (g. A561C) polymorphism was associated with angiographic CAD in Univariate analysis, but lost its association in multivariate analysis.

Amino Acid Substitution↗

PubMed2006

T null and M null genotypes of the glutathione S-transferase gene are risk factor for CAD independent of smoking.

BACKGROUND: The association of the deletion in GSTT1 and GSTM1 genes with coronary artery disease (CAD) among smokers is controversial. In addition, no such investigation has previously been conducted among Arabs. METHODS: We genotyped 1054 CAD patients and 762 controls for GSTT1 and GSTM1 deletion by multiplex polymerase chain reaction. Both CAD and controls were Saudi Arabs. RESULTS: In the control group (n = 762), 82.3% had the T wild M wildgenotype, 9% had the Twild M null, 2.4% had the Tnull M wild and 6.3% had the Tnull M null genotype. Among the CAD group (n = 1054), 29.5% had the Twild M wild genotype, 26.6% (p < .001) had the Twild M null, 8.3% (p < .001) had the Tnull M wild and 35.6% (p < .001) had the Tnull M null genotype, indicating a significant association of the Twild M null, Tnull M wild and Tnull M null genotypes with CAD. Univariate analysis also showed that smoking, age, hypercholesterolemia and hypertriglyceridemia, diabetes mellitus, family history of CAD, hypertension and obesity are all associated with CAD, whereas gender and myocardial infarction are not. Binary logistic regression for smoking and genotypes indicated that only M null and Tnullare interacting with smoking. However, further subgroup analysis stratifying the data by smoking status suggested that genotype-smoking interactions have no effect on the development of CAD. CONCLUSION: GSTT1 and GSTM1 null-genotypes are risk factor for CAD independent of genotype-smoking interaction.

Arabs↗

PubMed2006

The Glu27 genotypes of the beta2-adrenergic receptor are predictors for severe coronary artery disease.

BACKGROUND: The role of the Beta2-adrenoceptor (beta2-AR) Gln27Glu polymorphism in the manifestation of cardiovascular diseases is still unclear. METHODS: In the present study, we evaluated the potential relevance of the c.79 C>G (p.Gln27Glu) polymorphism of this receptor gene for coronary artery disease (CAD) and its associated risk factors in Saudi Arabs. Genotyping was performed by PCR using the confronting two-pair primer (PCR-CTPP) method. RESULTS: In the general population group (BD) (n = 895), 68.5% were homozygous wild-type C/C, 28.3% were heterozygous C/G and 3.2% were homozygous mutant G/G. Among the CAD patients (n = 773), 50.6% were homozygous wild-type C/C, 43.6% were heterozygous C/G and 5.8% were homozygous mutant G/G, while in the angiographed control group (CON) (n = 528), 71.8% were C/C, 24.4% C/G and 3.8% G/G genotypes. These results indicate that both the C/G (p = or < .001) and G/G (p = .005) genotypes are significantly associated with CAD, when compared to the CON group. In addition, C/G (p = or < .001) and G/G (p = or < .001) were significantly associated with CAD, when compared to the BD group. Furthermore, stepwise logistic regression showed that the genotype [C/G (p < .001) and G/G (p < .001)] increase the risk of CAD. CONCLUSION: These results shows that the Gln27Glu genotypes (homo- or heterozygous) of the beta2-AR may be independent predictors of severe CAD.

Arabs↗

PubMed2006

Mitochondrial abnormalities in patients with primary open-angle glaucoma.

PURPOSE: Primary open-angle glaucoma (POAG) is the second most common cause of blindness. It has been linked to mutations in the myocilin (MYOC) and optineurin (OPTN) genes, although mutations have been found in <5% of patients. The pathologic mechanism(s) of POAG remain unknown but may include retinal ganglion cell apoptosis, which causes progressive damage to axons at the optic nerve head. METHODS: In 27 patients with definite POAG, the MYOC and OPTN genes were sequenced, the entire mitochondrial (mt)DNA coding region was sequenced, relative mtDNA content was investigated, and mitochondrial respiratory function was assessed. RESULTS: Only three benign polymorphisms were identified in MYOC and OPTN in patients with POAG and in control subjects. Conversely, 27 different novel nonsynonymous mtDNA changes were found, only in patients with POAG (not control subjects), 22 of which (found in 14 patients) were potentially pathogenic. Unlike Leber hereditary optic neuropathy, most mtDNA sequence alterations in patients with POAG were transversions-sequence changes that alter the purine/pyrimidine orientation and imply oxidative stress. mtDNA content was relatively increased in 17 patients with POAG compared with age-matched control subjects, also implying a possible response to oxidative stress. Mean mitochondrial respiratory activity was decreased by 21% in patients with glaucoma compared with control subjects (P<0.001). CONCLUSIONS: These results reveal a spectrum of mitochondrial abnormalities in patients with POAG, implicating oxidative stress and implying that mitochondria dysfunction may be a risk factor for POAG. This concept may open up new experimental and therapeutic opportunities.

Adult↗

PubMed2006

Mitochondrial abnormalities in patients with LHON-like optic neuropathies.

PURPOSE: To investigate certain biochemical and molecular characteristics of mitochondria in patients with Leber hereditary optic neuropathy (LHON)-like optic neuropathies. METHODS: Patients who had LHON-like optic neuropathies in both eyes were selected from neuro-ophthalmology clinics. Evaluation included clinical examination, neuroimaging, and assessment of several mitochondrial parameters in the blood, including sequencing the entire mitochondrial (mt)DNA coding region, measuring relative mtDNA content, studying mitochondrial respiratory function in some patients, and sequencing the OPA1 and OPA3 genes. RESULTS: Thirty-five patients (21 men and 14 women; average age at onset 19.0 +/- 8.7 years) met inclusion and exclusion criteria for LHON-like optic neuropathies with median visual acuity approximately 20/200. Other hereditary retinopathies and optic neuropathies were unlikely because of inclusion and exclusion criteria, because ERGs were normal, and because no patient had pathogenic sequence changes in the OPA1 or OPA3 genes. Compared with control subjects, these patients had more potentially pathogenic nonsynonymous mtDNA changes, greater relative mtDNA content (P < 0.001), and less mitochondrial respiratory activity (P < 0.001). Only six patients (17%) had primary LHON mutations; however, even the 29 patients without primary LHON mutations had significant evidence of mitochondrial abnormalities. Mitochondrial haplogroup distribution was similar in patients and control subjects. CONCLUSIONS: Primary LHON mutations are less common in patients with LHON-like optic neuropathy selected from a clinical setting than in patients with LHON from multigenerational families. The results suggest that mitochondrial dysfunction plays a role in this type of optic neuropathy whether or not primary LHON mutations are present. This information has implications for diagnostic testing and for future investigations into mechanisms of disease.

Adolescent↗

PubMed2006

Novel mitochondrial DNA transversion mutation in transfer ribonucleic acid for leucine 2 (CUN) in a patient with the clinical features of MELAS.

We describe an 11-year-old Saudi boy who had an encephalopathy suggestive of mitochondrial encephalomyopathy with lactic acidosis and strokelike episodes (MELAS). We screened his entire mitochondrial DNA coding region and detected one novel transversion point mutation at nt-12299 A > C in the transfer ribonucleic acid for leucine 2 (CUN) that is located in the anticodon loop. We believe that this mutation is the cause of his disease condition.

Anticodon↗

PubMed2005

High frequency of somatic mitochondrial DNA mutations in human thyroid carcinomas and complex I respiratory defect in thyroid cancer cell lines.

Significant progress has been made to elucidate the molecular mechanisms that determine thyroid tumor development and progression. However, most investigations have mainly focused on the genetic alterations of nuclear DNA. The potential role of mitochondrial DNA (mtDNA) mutations in thyroid tumorigenesis is not well defined. In the present study, we investigated the frequency of mtDNA mutations in 24 thyroid tumor specimens (19 primary papillary thyroid carcinomas (PTC), one follicular thyroid carcinoma, and four multinodular hyperplasias) and four thyroid cancer cell lines by sequencing the entire coding regions of mitochondrial genome. Among the 19 PTC samples tested, seven (36.8%) had somatic mutations. Somatic mtDNA mutations were also detected in one of four multinodular hyperplasias examined. All the thyroid tumor cell lines carried sequence variations that change amino acid and have not been reported previously as normal sequence variants. Flow cytometry analysis of mitochondria respiratory function in the thyroid tumor cell lines revealed a severe defect in mitochondrial complex I activity. The majority of the mutations was involved in genes located in the complex I of the mitochondrial genome. The mutations were either A --> G or C --> T transitions, often resulting in a change of a moderately or highly conserved amino acid of their corresponding protein. These data suggest that mtDNA mutations may play an important role in the thyroid tumorigenesis. Given that mtDNA mutation is present in the benign multinodular hyperplasia, it might be involved in the early stage of tumor development.

Carcinoma↗

PubMed2005

Mitochondrial T9957C mutation in association with NAION and seizures but not MELAS.

PURPOSE: To assess the functional significance of the mitochondrial nt-9957 mutation in a man with non-arteritic ischemic optic neuropathy (NAION). This nt-9957 mutation has been previously reported in association with mitochondrial encephalopathy, lactic acidosis, and stroke-like events (MELAS). METHODS: The patient was examined clinically and with magnetic resonance imaging and spectroscopy. The entire coding region of the mitochondrial genome was sequenced, and mitochondrial function was assessed by flow cytometry after staining with fluorescent dihydroethidium. RESULTS: This 76-year-old man had optic nerve disease bilaterally and seizures, but no clinical or radiological evidence of MELAS. He had no mitochondrial DNA mutation other than the 9957. Functional testing revealed a severe defect in mitochondrial complex III activity. CONCLUSIONS: This patient had a mitochondrial functional deficit consistent with his 9957 mutation. It seems quite likely that this mutation may be responsible for optic nerve and brain injuries.

Case-Control Studies↗

PubMed2005

Beta 3 adrenergic receptor Trp64Arg polymorphism and manifestation of coronary artery disease in Arabs.

The substitution of tryptophan (Trp) by arginine (Arg) at position 64 in the beta3-adrenoceptor (beta3-AR) gene has been associated with obesity, diabetes mellitus, and coronary artery disease (CAD). We have investigated whether the Trp64Arg polymorphism is associated with the manifestation of CAD or one of its important risk factors, such as obesity, diabetes mellitus, elevated cholesterol and triglyceride levels, or hypertension in the Arab population. All participating subjects were genotyped for this polymorphism using the polymerase chain reaction followed by enzymatic digestion and sequencing. In the angiographed normal control subjects (n=495), 90.3% were homozygous Trp/Trp, 9.5% were heterozygous Trp/Arg, and 0.2% were homozygous for the Arg/Arg genotype, compared to 87%, 12.3%, and 0.7%, respectively, among angiographically confirmed CAD patients (n=981). There was no statistical difference in the distribution of genotypes or allele frequencies between the CAD and control groups. We carried out a stepwise logistic regression analysis to study the possible combined effect of the genotypes and other risk factors on CAD. All variables were retained in the model, with p values of 0.014, 0.006, 0.005, < 0.001, 0.045, 0.002, < 0.001, and 0.016 for genotype, diabetes mellitus, sex, family history of CAD, obesity, myocardial infarction, smoking, and age, respectively. In conclusion, the Trp64Arg polymorphism of the beta3-AR gene does not represent an independent risk factor for CAD in Arabs. However, in the presence of other CAD risk factors, this polymorphism may be used as a predictor of CAD.

Adult↗

PubMed2005

Detection of mitochondrial respiratory dysfunction in circulating lymphocytes using resazurin.

CONTEXT: Laboratory methods currently available for detecting mitochondrial respiratory dysfunction are labor-intensive, require large amounts of isolated mitochondrial protein, invasive (require a skeletal muscle biopsy), and usually produce conflicting results. OBJECTIVE: To develop a rapid, reliable, and noninvasive method for detecting oxidative phosphorylation activity without the need to isolate mitochondrial fractions. DESIGN: Lymphocytes from 6 patients with mitochondrial disorders (3 with mitochondrial myopathy and 3 with Leber hereditary optic neuropathy) and 51 normal control subjects were incubated with 6 microM resazurin without and with mitochondrial inhibition by amiodarone (200 microM), and the fluorescence intensity resulting from resazurin reduction was monitored spectrofluorometrically over time. Mitochondrial respiratory activity was calculated as the difference between uninhibited and inhibited measurements. RESULTS: Mitochondrial respiratory activity was established for 51 normal control subjects and was decreased in all 6 patients with mitochondrial syndromes. Mitochondrial respiratory activity values for patients 1 through 6 compared to the control group after 240 minutes' incubation with resazurin were 55%, 71%, 49%, 61%, 68%, and 59%, respectively (mean mitochondrial respiratory activity of patients, 13.6% or 60.5% of control mean; P < .001). CONCLUSION: This resazurin-based technique proved to be a fast and reproducible method for quantifying mitochondrial activity and identifying respiratory functional defects in patients with mitochondrial disorders.

Adolescent↗

PubMed2004

Mitochondrial DNA nucleotide changes in non-arteritic ischemic optic neuropathy.

The authors sequenced the entire mitochondrial DNA coding region in a group of 19 patients with non-arteritic anterior ischemic optic neuropathy (NAION) and in 100 controls. Synonymous and nonsynonymous nucleotide changes were more common in NAION patients (p < 0.001). Twelve of these (11 novel) were potentially pathologic, nine of which altered moderately or highly conserved amino acids in the functional domain of the affected protein. Mitochondrial malfunction may be a risk factor for NAION.

Adult↗

PubMed2004

Association of the platelet glycoprotein receptor IIIa (PlA1/PlA1) genotype with coronary artery disease in Arabs.

The PlA2 allele (heterozygotes or homozygotes) resulting from a genetic polymorphism in the glycoprotein IIIa gene has been proposed as a potential genetic factor linked to platelet hyperaggregability and increased risk of coronary artery disease (CAD). Such an association could only be established in some ethnic groups. There were no previous reports investigating the distribution of this allele and its possible link to CAD in Arabs. We used the polymerase chain reaction and allele-specific restriction digestion for determining the prevalence of this allele in 509 healthy blood donors (BD) and 451 angiographically confirmed CAD patients of Arabic ethnic background. For the BD group (n = 509), 70.7% were homozygous PlA1/PlA1, 26.9% were heterozygous PlA1/PlA2 and 2.4% were homozygous PlA2/PlA2. Within the CAD group (n = 451), 77.2% were homozygous PlA1/PlA1, 19.5% were heterozygous PlA1/PlA2 and 3.3% were homozygous PlA2/PlA2. The PlA1 allele frequency was 0.84 and 0.87, and for the PlA2 was 0.16 and 0.13 for the BD and CAD groups, respectively. In conclusion, our results suggest that the PlA1/PlA1 genotype (P = 0.029) is associated with CAD in Saudi Arabs.

Alleles↗

PubMed2004

A novel splice site mutation in the WAS gene causes Wiskott-Aldrich syndrome in two siblings of a Saudi family.

We report here on a Saudi family with two affected males with Wiskott-Aldrich syndrome (WAS), which includes mild to moderate bleeding and a low platelet count. A novel splice donor-site mutation (811 + 5 G <-- C) in intron 8 of the WAS gene (Genbank accession number NM_000377) was detected in a hemizygous status in both index cases, heterozygous in their mother and absent in the father. RNA from both index cases was transcribed and amplified with primers complementary to sequences in exons 7 and 10. A reverse transcription-polymerase chain reaction (RT-PCR) product of 688 bp (approximately 82%) was produced in addition to the normal RT-PCR product of 485 bp (approximately 18%). cDNA sequence analysis reveals an inclusion of full intron 8 sequence in the final transcript. The resultant protein is predicted to have 68 missense codons and a pre-mature stop codon at amino acid 260. This novel splice donor-site mutation was not detected in 80 normal controls (56 females and 24 males) from the same ethnic background as the index cases. Since no other mutation was detected in the WAS gene and the patients have classical symptoms of WAS, we concluded that it is highly likely that this novel mutation is responsible for the phenotype observed in these patients.

Base Sequence↗

PubMed2003

Homozygous protein C deficiency with purpura fulminans: report of a new case and a description of a novel mutation.

We report here a quite rare case of severe homozygous protein C deficiency. The index case is a 9-month-old Saudi boy who was born after an uneventful pregnancy at 39 weeks. The diagnosis of epidermoloysis bullosa and the appearance of scrotal haematoma raised the diagnosis of thrombosis due to protein C deficiency. The clinical presentation and extremely low level of protein C activity (< 0.01 U/ml) in the index case suggested a severe case of protein C deficiency. The father is 28 years old and the mother is 25 years old and are consanguineous. Neither had a personal or family history of thrombosis. Genomic DNA was extracted from peripheral blood of the patient and both parents, exons of protein C were amplified by polymerase chain reaction and sequenced. Sequencing revealed the presence of a novel CCTG duplicate nucleotide (effective insertion) after nucleotide 8826 in exon 9 of the protein C gene. This insertion is found in the homozygous state in the patient and in the heterozygous state in both parents. It results in a frame-shift mutation, which introduces a stop-codon, thereby generating a prematurely truncated protein. These molecular findings agree with the presence of quantitative protein C deficiency in the index case.

Codon, Terminator↗

PubMed2003

Lack of association of lipoprotein lipase gene polymorphisms with coronary artery disease in the Saudi Arab population.

CONTEXT: Previous studies reported an association of certain polymorphisms in the lipoprotein lipase (LPL) gene with the risk of coronary artery disease (CAD); however, these studies were small and inconsistent. In addition, none of these studies attempted to establish such an association in the Arab population. OBJECTIVE: To determine whether 2 LPL polymorphisms (LPL-HindIII and LPL-PvuII located on introns 8 and 6, respectively, of the LPL gene) can be considered as independent risk factors or as predictors for CAD in Arabs. DESIGN: We used polymerase chain reaction and restriction enzyme digestion to determine the distribution of the LPL-HindIII and LPL-PvuII polymorphisms among healthy blood donors of Arabic origin (BD group) and angiographically confirmed CAD patients (CAD group) with identical ethnic backgrounds. RESULTS: For the HindIII genotypes, within the BD group (n = 410), the +/+ genotype was found in 206 individuals (50.2%), 173 (42.2%) carried the +/- genotype, and 31 (7.6%) carried the -/- genotype. Within the CAD group (n = 352), the +/+ genotype was found in 189 individuals (53.7%), 138 (39.2%) carried the +/- genotype, and 25 (7.1%) carried the -/- genotype. P values of.38,.45, and.92 were obtained for the +/+, +/-, and -/- genotypes, respectively. For the PvuII genotypes, within the BD group (n = 511), the +/+ genotype was found in 182 individuals (35.6%), 248 (48.5%) carried the +/- genotype, and 81 (15.9%) carried the -/- genotype. Within the CAD group (n = 431), the +/+ genotype was found in 138 individuals (32%), 225 (52.2%) carried the +/- genotype, and 68 (15.8%) carried the -/- genotype. P values of.28,.29, and.98 were obtained for the +/+, +/-, and -/- genotypes, respectively. The distribution and the allele frequency of these 2 LPL variants were similar in CAD and BD study groups and followed the Hardy-Weinberg equilibrium. CONCLUSION: There was no difference in the distribution of both LPL polymorphisms between the healthy group and the CAD group. Therefore, these 2 LPL polymorphisms cannot be considered as independent risk factors or as predictors for CAD in this population.

Adult↗

PubMed2003

Prevalence and role of methylenetetrahydrofolate reductase 677 C-->T and 1298 A-->C polymorphisms in coronary artery disease in Arabs.

CONTEXT: Previous studies reported an association of 677 C-->T and 1298 A-->C methylenetetrahydrofolate reductase (MTHFR) variants with coronary artery disease (CAD). No previous studies concerning the prevalence of these 2 MTHFR variants or their possible association with CAD in Arabs are currently available in the literature. OBJECTIVE: To determine the prevalence of MTHFR variants and their potential relevance to CAD among Arabs. DESIGN: We used polymerase chain reaction and restriction enzyme digestion to determine the prevalence of these 2 MTHFR polymorphisms in 625 healthy blood donors (BDs) and 545 angiographically confirmed CAD patients of Arab origin. RESULTS: For the 677 C-->T variant within the CAD group, 64.2% were homozygous wild-type C/C, 32.1% were heterozygous C/T, and 3.7% were homozygous T/T genotype. Within the BD group tested for the 677 C-->T variant, 72.2% were homozygous wild-type C/C, 25.8% were heterozygous C/T, and 2% were homozygous T/T genotype. Within the CAD group tested for the 1298 A-->C variant (n = 540), 45.7% were homozygous wild-type A/A, 46.9% were heterozygous A/C, and 7.4% were homozygous C/C genotype. Within the BD group tested for the 1298 A-->C variant (n = 625), 39.4% were homozygous wild-type A/A, 51.5% were heterozygous A/C, and 9.1% were homozygous C/C genotype. The distribution and allele frequency of these 2 MTHFR variants followed the Hardy-Weinberg equilibrium and were similar in the CAD and BD study groups. The prevalence of the 677 C-->T and 1298 A-->C compound heterozygosity was 9.6% for the BD group and 12.3% for the CAD group. CONCLUSION: The 2 MTHFR variants tested in this study, individually or compound, are not associated with CAD. Therefore, neither of these 2 variants can be considered an independent risk factor or a predictor for CAD in this population.

Adult↗

PubMed2003

A new era for preventive genetic programs in the Arabian Peninsula.

In the Arabian Peninsula, high percentages of consanguineous marriages and the tribal nature of marriages have resulted in high incidence of genetically based disorders. The successful management of these disorders incurs a high financial cost, which is a great burden on the health care system. The practical solution to this problem is through prevention. Prevention of genetic disorders should be the utmost public health concern especially where these disorders are prevalent. Preventive genetics became possible with the advent of biochemical and molecular technologies. Biochemical neonatal screening based on tandem mass spectrometry technology and molecular technologies such as sequencing, DNA microarray and nucleic acid hybridization techniques are steadily being transferred to clinical practice. Preventive genetics could be best achieved through establishment of databases for common genetic disorders, premarital diagnosis, and pre-implantation genetic diagnosis and by genetic counseling. These preventive measures must take into account the social and cultural aspects.

Adult↗

PubMed2002

Prevalence of the 20210 G-->A prothrombin variant and its association with coronary artery disease in a Middle Eastern Arab population.

BACKGROUND: No reports are available on the distribution of the 20210 G-->A prothrombin variant among Middle Eastern Arabs. Additionally, to date, studies that attempt to establish this polymorphism as an independent risk factor or as a predictor for coronary artery disease (CAD) have yielded conflicting results. OBJECTIVE: To determine the prevalence of the 20210 G-->A prothrombin variant among Middle Eastern Arabs and to evaluate the potential relevance of this variant to Arab patients with angiographically documented CAD. METHODS AND RESULTS: We used the polymerase chain reaction and restriction enzyme digestion to determine the prevalence of this polymorphism in 613 individuals from Arabic ethnic origin with CAD and from 593 healthy blood donors (BDs) from an identical ethnic background. Within the BD group (n = 593), 10 individuals (1.7%) were heterozygous, 583 individuals (98.3%) were normal, and none were homozygous for the 20210 G-->A prothrombin variant. Within the CAD group (n = 613), 13 individuals (2.1%) were heterozygous, 600 individuals (97.9%) were normal, and none were homozygous for the 20210 G-->A prothrombin variant. A chi(2) analysis was used to evaluate any significance in the distribution of genotypes. A value of 1.23 was obtained. Values less than 3.84 indicate no statistically significant difference between the heterozygous carriers of the 20210A allele in both study groups. CONCLUSIONS: In our population of Middle Eastern Arabs, the presence of the 20210 G-->A prothrombin variant is not associated with patients with angiographically documented CAD. Therefore, this variant cannot be considered as an independent risk factor or as a predictor for CAD in this population.

Adult↗