Neuro-meningeal cryptococcal infection revealing a multiple myeloma.

Rare cases of Cryptococcus have been documented in patients living with multiple myeloma. To date there has been no documented evidence of cryptococcosis revealing multiple myeloma. We reported a 63-year-old man who had a 2-months history continuous holocranial headaches, morning vomiting, complaining of blurred vision and fever. The biologic and the imaging showed a Cryptococcus meningoencephalitis. The search for a cause of immunodeficiency revealed a multiple myeloma. The diagnosis for Cryptococcus was confirmed according to an India ink stain, blood and cerebrospinal fluid culture. The patient's treatment for multiple myeloma was initiated with a chemotherapy regimen. The evolution was good without complication. Cryptococcosis, especially in the neuro-meningeal form, is a serious, deadly opportunistic infection. The search of an underlining immunodeficiency must be systematic. In this case, it was associated with early stage multiple myeloma.

[Disseminated intravascular coagulation: role of the International Society on Thrombosis and Haemostasis (ISTH) diagnostic scoring system]. / La coagulation intravasculaire disséminée: intérêt du score de la société internationale sur la thrombose et l´hémostase.

Disseminated intravascular coagulation (DIC) is a life-threatening event during resuscitation. The International Society on Thrombosis and Haemostasis (ISTH) diagnostic scoring system enables early diagnosis of DIC. We here report three clinical cases of DIC characterized by several etiologies: prostatic adenocarcinoma, septic shock and retroplacental hematoma. The tests of hemostasis needed to calculate international society on thrombosis and haemostasis (ISTH) score (platelet count, prothrombin ratio, values of fibrinogen and D-dimer levels) were performed regularly. Additional, complementary tests (soluble complexes test, euglobulin lysis test, antithrombin level dosing, activated protein C and factor V dosing) were also performed. ISTH score enables early diagnosis of DIC.

Association of FV G1691A Polymorphism but not A4070G With Coronary Artery Disease.

Coronary artery disease (CAD) is one of the chief causes of death in the world. Several hypotheses have been promoted as for the origin of the disease, among which are genetic predispositions and/or environmental factors. The aim of this study was to determine the effect of factor V (FV) gene polymorphisms (Leiden, G1691A [FVL] and HR2 A4070G) and to analyze their association with traditional risk factors in assessing the risk of CAD. Our study population included 200 Tunisian patients with symptomatic CAD and a control group of 300 participants matched for age and sex. All participants were genotyped for the FVL and HR2 polymorphisms. Multivariate logistic regression was applied to analyze independent factors associated with the risk of CAD. Our analysis showed that the FVL A allele frequency ( P < 10-3, odds ratio [OR] = 2.81, 95% confidence interval [CI] = 1.6-4.9) and GA genotype ( P < 10-3, OR = 4.03, 95% CI = 2.1-7.6) are significantly more prevalent among patients with CAD compared to those controls and may be predisposing to CAD. We further found that the FVL mutation is an independent risk factor whose effect is not modified by other factors (smoking, diabetes, hypertension, dyslipidemia, and a family history of CAD) in increasing the risk of the disease. However, analysis of FV HR2 variation does not show any statistically significant association with CAD. The FVL polymorphism may be an independent risk factor for CAD. However, further investigations on these polymorphisms and their possible synergisms with traditional risk factors for CAD could help to ascertain better predictability for CAD susceptibility.

The Effect of ACE I/D Polymorphisms Alone and With Concomitant Risk Factors on Coronary Artery Disease.

BACKGROUND: Coronary artery disease (CAD), also known as atherosclerotic heart disease, is a leading cause of mortality and morbidity throughout the world. The role of insertion/deletion (I/D) polymorphisms of the angiotensin-converting enzyme (ACE) gene in the etiology of CAD remains to be more completely clarified. The aim of this study was to determine the role of the ACE I/D polymorphism in patients with CAD and to study the association together with traditional risk factors in assessing the risk of CAD. METHODS: Our study population included 145 Tunisian patients with symptomatic CAD and a control group of 300 people matched for age and sex. All participants in the study were genotyped for the ACE I/D polymorphisms obtained by polymerase chain reaction amplification on genomic DNA. RESULTS: Our analysis showed that the ACE D allele frequency ( P < 10-3; odds ratio [OR] = 5.2; 95% confidence interval [CI] = 3.6-7.6) and DD genotype ( P < 10-3; OR = 6.8; 95% CI = 4.4-10) are significantly more prevalent among patients with CAD than in controls and may be predisposing to CAD. We further found that the risk of CAD is greatly potentiated by several concomitant risk factors (smoking, diabetes, hypertension, dyslipidemia, and a family history of CAD). CONCLUSION: The ACE D allele may be predictive in individuals who may be at risk of developing CAD. Further investigations of these polymorphisms and their possible synergisms with traditional risk factors for CAD could help to ascertain better predictability for CAD susceptibility.

Association between an angiotensin-converting enzyme gene polymorphism and Alzheimer's disease in a Tunisian population.

BACKGROUND: The angiotensin-converting enzyme gene (ACE) insertion/deletion (I/D or indel) polymorphism has long been linked to Alzheimer's disease (AD), but the interpretation of established data remains controversial. The aim of this study was to determine whether the angiotensin-converting enzyme is associated with the risk of Alzheimer's disease in Tunisian patients. METHODS: We analyzed the genotype and allele frequency distribution of the ACE I/D gene polymorphism in 60 Tunisian AD patients and 120 healthy controls. RESULTS: There is a significantly increased risk of AD in carriers of the D/D genotype (51.67% in patients vs. 31.67% in controls; p = .008, OR = 2.32). The D allele was also more frequently found in patients compared with controls (71.67% vs. 56.25%; p = .003, OR = 2.0). Moreover, as assessed by the Mini-Mental State Examination, patient D/D carriers were more frequently found to score in the severe category of dementia (65%) as compared to the moderate category (32%) or mild category (3%). CONCLUSIONS: The D/D genotype and D allele of the ACE I/D polymorphism were associated with an increased risk in the development of AD in a Tunisian population. Furthermore, at the time of patient evaluation (average age 75 years), patients suffering with severe dementia were found predominantly in D/D carriers and, conversely, the D/D genotype and D allele were more frequently found in AD patients with severe dementia. These preliminary exploratory results should be confirmed in larger studies and further work is required to explore and interpret possible alternative findings in diverse populations.

The Plasminogen Activator Inhibitor 1 4G/5G Polymorphism and the Risk of Alzheimer's Disease.

OBJECTIVE: The aim of this study was to determine whether plasminogen activator inhibitor 1 (PAI-1) is associated with the risk of Alzheimer's disease (AD) in Tunisian patients. DESIGN AND METHODS: We analyzed the genotype and allele frequency distribution of the PAI-1 polymorphism in 60 Tunisian patients with AD and 120 healthy controls. RESULTS: The results show a significantly increased risk of AD in carriers of the 4G/4G and 4G/5G genotypes versus the wild-type 5G/5G genotype (4G/4G: 28.33% in patients vs 10.0% in controls; P < 10-3; OR = 8.78; 4G/5G: 55.0% in patients vs 38.33% in controls; OR = 4.45; P < 10-3). The 4G allele was also more frequently found in patients compared with controls; P < 10-3; OR = 3.07. For all participants and by gender, homozygotic carriers (4G/4G) were at an increased risk of AD over heterozygotes and women were at an increased risk over their male genotype counterparts. The odds ratio for AD among 4G/4G carriers for any group was approximately twice that of heterozygotes in the same group. Women homozygotes ranked highest for AD risk (OR = 20.8) and, in fact, women heterozygotes (OR = 9.03) ranked higher for risk than male homozygotes (OR = 6.12). CONCLUSION: These preliminary exploratory results should be confirmed in a larger study.

HLA DRB1*03 as a possible common etiology of schizophrenia, Graves' disease, and type 2 diabetes.

BACKGROUND: Autoimmune diseases and schizophrenia share many common features. Association studies confirm a shared genetic association in the human leukocyte antigen (HLA) region between schizophrenia and most autoimmune diseases. To our knowledge, the simultaneous syndromes of Graves' disease (GD) and type 2 diabetes (T2D) in schizophrenia are rare in Tunisia. CASE PRESENTATION: We report a case of a 42-year-old woman admitted to the department of psychiatry for an acute relapse of chronic schizophrenia. Her medical history revealed that she was followed for Graves' disease and for a type 2 diabetes mellitus. A low-resolution HLA typing was performed by polymerase chain reaction sequence-specific primer (PCR-SSP) techniques according to determine the patient's haplotype. CONCLUSIONS: Our study suggests that the HLA DRB1*03 allele may explain a common etiology underlying the co-morbidity of Graves' disease, type 2 diabetes, and schizophrenia in our patient.

Role of the Apolipoprotein E Polymorphisms in the Development of Retinal Vein Occlusion in a Tunisian Population: A Case-Control Study.

Apolipoprotein E ( APOE) is a member of the apolipoprotein gene family. APOE is polymorphic with 3 main allelic types: ∊2, ∊3, and ∊4. Certain of these alleles have been associated with higher vascular risk. However, the association of APOE genotypes with retinal biomarkers and risk of retinal stroke is less clear. This study evaluated the role of APOE polymorphisms in retinal vein occlusion (RVO). In the present study, 2-point mutations coding amino acid residues 112 and 158 were amplified using the polymerase chain reaction (PCR) from DNA extracted from Tunisian participants. APOE genotypes were determined by multiplex PCR followed by molecular hybridization. Eighty-eight patients (26 women and 62 men) and 100 age- and gender-matched healthy participants were enrolled. The statistical study revealed a higher frequency of the ∊4 allele in patients as compared to controls (27.3% vs 9%) with a significant association of the ∊4 allele with the disease ( P < 10-3, Pa < 10-3, odds ratio [OR] = 3.8, 95% confidence interval [CI] = 2.1-6.8). The frequency of the ∊3 allele was significantly lower in the patients with RVO compared to the controls (60.2% vs 82.5%, respectively; P < 10-3, Pa < 10-3, OR = 0.32, 95% CI = 0.19-0.53). The ∊3 allele seems to be protective against the disease. There was no association between the APO ∊2 allele and RVO. The association of APOE allele and genotype with RVO requires further investigation in different populations.

Association Between Thrombophilic Gene Mutations and the Risk of Vascular Access Thrombosis in Hemodialysis Patients.

The cause of thrombosis in hemodialysis vascular access is considered to be of a multifactorial nature, including stenosis of the venous or arterial connection. Therefore, identification of relevant thrombotic risk factors could lead to an improved antithrombotic therapy. This case control study was performed to evaluate the relationship between Factor V (G1691A and A4070G) and Factor II polymorphisms and vascular access thrombosis in hemodialysis patients. One hundred and twenty-one patients undergoing dialysis were selected as subjects. This sample was divided into two groups; a case group of 60 patients who had sustained one or more thrombotic events that resulted in vascular access failure and a control group of 61 patients, who never had a thrombotic occlusion of a functioning permanent dialysis access. Our data demonstrated a significantly increased risk of vascular access thrombosis in carriers of the mutant FV (G1691A and A4070G) polymorphisms (P < 0.05).Further studies on a large-scale population and other genetic variants will be needed to find candidate genes for vascular access thrombosis in hemodialysis patients.

Methylenetetrahydrofolate reductase (C677T and A1298C) polymorphisms, hyperhomocysteinemia, and ischemic stroke in Tunisian patients.

OBJECTIVE: The present study evaluated the role of the methylenetetrahydrofolate reductase (MTHFR) C677T and A1298C gene polymorphisms and correlated these results with plasma homocysteine (Hcy) levels in Tunisian ischemic stroke (IS) patients. METHODS: Overall, 84 patients with IS were included and compared with 100 healthy controls. The most common stroke risk factors were investigated. Fasting plasma Hcy levels were measured. Genotyping of the MTHFR C677T and A1298 polymorphisms was studied by polymerase chain reaction. RESULTS: Aside from tobacco and alcohol use, the other studied factors were significant risk factors for IS. Mean plasma Hcy levels were significantly higher in IS patients than in controls (16.1 ± 8.28 µmol/L versus 8.76 ± 3.48 µmol/L, P < 10(-3)). Significant associations were found with both the MTHFR 677(CT + TT) and 1298 (AC + CC) genotypes in comparison with controls (P < 10(-3)). A significant synergistic interaction was also found with the double heterozygote MTHFR 677CT/1298AC (P < 10(-3)). Homocysteine levels were significantly higher in IS patients with the MTHFR C677T variant (CT and TT genotypes) (P < 10(-3)); however, the difference was not significant with the MTHFR A1298C variant (AC and CC genotypes) (P = .31). CONCLUSION: The MTHFR C677T and A1298 polymorphisms (individually or in concert) and hyperhomocysteinemia represent important risk factors for IS. Elevated Hcy levels were found to be associated with the MTHFR C677T variant; however, no significant association was found with the MTHFR A1298C variant.

Association of methylenetetrahydrofolate reductase A1298C polymorphism but not of C677T with multiple sclerosis in Tunisian patients.

BACKGROUND AND OBJECTIVE: Multiple sclerosis (MS) is a chronic neurological disease characterized by central nervous system (CNS) inflammation and demyelination of nerve axons. The aim of this study was to investigate a possible association between the methylenetetrahydrofolate reductase (MTHFR) gene and multiple sclerosis in Tunisian patients. PATIENTS AND METHODS: The genotyping of two missense variants of the methylenetetrahydrofolate reductase (MTHFR) gene, C677T and A1298C was performed in 80 multiple sclerosis patients and 200 healthy controls. RESULTS: No significant differences were found in the frequency of the MTHFR C677T polymorphism between MS patients and healthy controls. However, the genotype prevalence of the missense variant MTHFR A1298C was significantly different between patients and controls (A/C: 55% versus 7%, p<10(-3); C/C: 13.75% versus 0%, p<10(-3), respectively). CONCLUSION: Although our preliminary findings suggest no association between the MTHFR C677T variants and MS, there is evidence to suggest a significant association between the MTHFR A1298C polymorphisms and MS.

Association of HLA-DR-DQ polymorphisms with diabetes in Tunisian patients.

OBJECTIVE: Type 1 diabetes (T1D) is a polygenic disease whose principal locus is the human leukocytes antigen (HLA) region. The aim of this study was to evaluate HLA DR-DQ alleles and to asses them as risk factors for type 1 diabetes in the Tunisian population. MATERIALS AND METHODS: A total of 119 subjects with diabetes were tested for HLA class II alleles and compared with 292 healthy controls. HLA DRB1 and DQB1 alleles were genotyped using polymerase chain reaction sequence-specific primers (PCR-SSPs). RESULTS: The results revealed that the most susceptible haplotypes are the DRB1(*)03-DQB1(*)02 (pc<10(-3)) and DRB1(*)0401-DQB1(*)0302 (pc=0.001). (pc denotes Bonferroni corrected probability values.) The most protective haplotypes are DRB1(*)11-DQB1(*)03, DRB1(*)07-DQB1(*)02, and DRB1(*)13-DQB1(*)06 (pc=0.0026, pc=0.0065, and pc=0.02 respectively). Our results showed some particularities unique to Tunisians, there was a lack of a significant protective effect of the DRB1(*)15-DQB1(*)06 haplotype that usually is the dominant combination associated with protection in most other populations. CONCLUSION: Tunisian diabetic patients share the most susceptible and protective HLA haplotypes with Caucasians and those in neighbor Mediterranean countries. This is most likely explained by the history and admixture events of Tunisia and North Africa.

Role of methylenetetrahydrofolate reductase A1298C polymorphism in cerebral venous thrombosis.

The association between the methylenetetrahydrofolate reductase (MTHFR) gene and cerebral venous thrombosis (CVT) remains controversial. This study principally investigated the potential role of the MTHFR A1298C variant and CVT. The genotyping of the A1298C variant of the MTHFR gene was performed in 35 CVT patients and 200 healthy controls. The frequency of A1298C genotype among CVT patients was significantly higher compared with controls (P < 10(-3)), suggesting an association between this polymorphism and CVT. To our knowledge, there are no previous reports assessing the correlation between the MTHFR A1298C variant and CVT. Large study populations would be required to understand the contribution of this marker in the risk of CVT.

Factor VII levels, R353Q and -323P0/10 Factor VII variants, and the risk of acute coronary syndrome among Arab-African Tunisians.

The importance of the extrinsic haemostatic system, of which factor VII/VIIa (FVII/FVIIa) is a key constituent, in acute coronary syndrome (ACS) is well recognized. The contribution of FVII gene variants R353Q and -323P0/10, and altered FVII plasma levels to the risk of ACS was investigated in a North African Tunisian Arab cohort consisting of 308 ACS cases and 312 age-, gender- and ethnically-matched control subjects; FVII antigen levels were determined by ELISA. Regression analysis was used in assessing the association of FVII variants and changes in FVII levels to the overall risk of ACS. Significantly higher FVII antigen levels were seen in ACS patients (P < 0.001), and were associated with ACS and with ACS severity, and this association was confirmed by multivariate regression analysis, after adjusting for a number of confounders (BMI, smoking, systolic blood pressure, hypertension, diabetes, and glucose, cholesterol, and triglycerides levels). While the carriage of 353Q allele, was associated with significant reduction in FVII plasma levels, the distribution of the R353Q genotypes was comparable between cases and control subjects, thereby indicating that altered FVII levels, independent of R353 variant, were associated with increased risk of ACS. In contrast, the -323Ins variant, while not associated with altered FVII plasma levels, was associated with ACS, following adjustment for BMI, smoking, systolic blood pressure, hypertension, diabetes, and glucose, cholesterol, triglycerides and FVII levels. In summary, elevated FVII levels, and the -323P0/10 but not R353Q polymorphism, constitute risk factors for ACS.

Lack of association between factor V Leiden and prothrombin G20210A polymorphisms in Tunisian subjects with a history of myocardial infarction.

BACKGROUND: Myocardial infarction is a multifactorial disease. It is provoked by occlusions in the coronary arteries resulting from exposure to multiple risk factors. OBJECTIVE: To study the risk of myocardial infarction associated with the gene polymorphisms of factor V Leiden and factor II (G20210A). MATERIALS AND METHODS: Cases consisted of 100 myocardial infarction patients who were hospitalized in the Principal Military Hospital of Tunis and 200 control subjects with no history of myocardial infarction. RESULTS: The prevalence of the factor V Leiden was higher in myocardial infarction patients (9%) than in control subjects (6%) with an OR=1.55 (95% CI=0.58-4.12), whereas the prevalence of prothrombin G20210A mutation was 3% and 2.5% in the patient and control groups, respectively [OR=1.21 (95% CI=0.22-5.94)]. CONCLUSION: Our results indicate that neither factor V Leiden nor the prothrombin G20210A contributed to the risk factors for myocardial infarction.

Contribution of JAK2 and STAT3 variants to the genetic susceptibility of recurrent miscarriage among Bahraini and Tunisian Arabs.

We investigated the contribution of JAK2 rs2203724 and STAT3 rs1053023 and rs1053004 to the susceptibility of idiopathic recurrent miscarriage (IRM) in Bahraini (246 cases and 279 controls) and Tunisian (235 cases and 235 controls) Arabs. The distribution of JAK2 rs2203724 and STAT3 rs1053023 genotypes were in Hardy-Weinberg equilibrium (HWE) in both communities, while mild deviation from HWE was noted for rs1053004 in Tunisians but not Bahraini. JAK2 rs2203724 was not associated with IRM in either community, while STAT3 rs1053023 was positively associated with IRM in both Bahraini and Tunisian women. STAT3 rs1053004 displayed mixed association: it was positively associated with IRM in Bahraini (P < 0.001), but not Tunisian women (P = 0.10). Genotype association confirmed the association of both STAT3 variants with IRM under additive, dominant, and recessive models, while the association of STAT3 rs1053023 was seen under additive and dominant, but not recessive models in Tunisians. The contribution of JAK2 and STAT3 variants to IRM susceptibility must be evaluated regarding specific variants, and the ethnic/racial background.

Association of MTHFR A1298C polymorphism (but not of MTHFR C677T) with elevated homocysteine levels and placental vasculopathies.

Our aim in this study was to investigate the association between elevated homocysteine levels and the two MTHFR polymorphisms, C677T and A1298C, with several pregnancy complications such as recurrent pregnancy loss, preeclampsia, placental abruption and intrauterine growth retardation. In 203 women with different placental vasculopathies, we determined the MTHFR C677T and the A1298C prevalence and their relative association to elevated homocysteine levels. The mean plasma homocysteine level was significantly higher in the pathologic groups when compared with the control group. We identified the carriage of the MTHFR A1298C polymorphism as a significant risk factor for vascular-related pregnancy complications. Women with MTHFR A1298C polymorphism or elevated homocysteine levels have an increased risk of placental vasculopathies. The MTHFR A1298C mutation also had a positive impact on elevated homocysteine levels. The lack of association between the MTHFR C677T polymorphism and pregnancy morbidities needs further studies.

-174G>C interleukin-6 gene polymorphism in Tunisian patients with coronary artery disease.

BACKGROUND AND OBJECTIVES: A state of low-grade inflammation accompanies the pathogenesis of atherosclerotic events. Interleukin-6 (IL-6) is a pleotropic pro-inflammatory cytokine that modulates the development of acute coronary syndromes (ACSs), partly by destabilizing coronary atherosclerotic plaques. We have examined the contribution of the -174G>C IL-6 promoter variant on the risk of coronary artery disease (CAD) among Tunisians. PATIENTS AND METHODS: Study subjects included 418 CAD patients and 406 age- and sex-matched controls. IL-6 genotyping was done by PCR-restriction fragment length polymorphism. RESULTS: The frequency of the -174C allele (mutant) was lower in Tunisians than in Europeans, and the distribution of -174 G>C genotypes was similar between CAD patients and control subjects. Moreover, compared to GG genotype carriers, -174C allele carriage did not increase the CAD relative risk (odds ratio and 95% confidence interval=1.09 and 0.80-1.49), which remained nonsignificant after adjusting for traditional risk factors for CAD (age, smoking, hypertension, diabetes and obesity). CONCLUSION: The -174G>C IL-6 promoter variant is not associated with an increased risk of CAD among Tunisians.

Human platelet alloantigens HPA-1, HPA-2, and HPA-3 polymorphisms associated with extent of severe coronary artery disease.

The contribution of human platelet antigen (HPA)-1 (GPIIb/IIIa), HPA-2 (GPIb/IX), and HPA-3 (GPIIb/IIIa) polymorphisms to the risk of coronary artery disease (CAD) was investigated in 341 CAD patients and 316 matched control subjects. HPA genotyping was performed by PCR-SSP. Regression analysis was employed in assessing the contribution of these variants to CAD risk. The frequency of HPA-1b (P = .009) and HPA-3b (P = .004) alleles, and HPA-1a/1b (P = .045), HPA-1b/1b (P = .007), and HPA-3b/3b (P = .008) genotypes were higher in patients than control subjects. No significant association was demonstrated between the HPA variants and 1-, 2- and 3-vessel disease. HPA-1b/2a/3b (Pc = .021) and HPA-1b/2b/3a (Pc = .002) haplotypes were positively associated with CAD, thereby conferring a disease susceptibility nature to these haplotypes. Multivariate analysis confirmed the positive association of HPA-1b/2a/3b (aOR = 3.72; 95% CI = 1.49-9.28), and in addition identified HPA-1b/2a/3a (aOR = 2.49; 95% CI = 1.06-5.86) to be positively associated with CAD, after adjusting for a number of covariates. Our results demonstrate positive association of HPA variants and specific HPA-1/HPA-2/HPA-3 haplotypes with CAD in Tunisians.

Distinct association of factor V-Leiden and prothrombin G20210A mutations with deep venous thrombosis in Tunisia and Lebanon.

Factor V G1691A (FV-Leiden) and prothrombin (PRT) G20210A single nucleotide polymorphisms (SNPs) were associated with venous thrombosis among Caucasians. We assessed the contribution of both SNPs to the genetic susceptibility of deep venous thrombosis (DVT) among Lebanese and Tunisian patients. Subjects comprised 198 DVT patients and 540 healthy controls from Lebanon and 126 Tunisian DVT patients and 197 control subjects; FV-Leiden (MnlI) and PRT G20210A (HindIII) genotyping was done by PCR-RFLP. While the prevalence of FV-Leiden mutant A allele and the G/A and A/A genotypes were significantly higher among DVT patients from Lebanon and Tunisia, the association of PRT G20210A with DVT was pronounced among Lebanese but not Tunisian patients. The prevalence of PRT G20210A mutant A allele (P < 0.001 vs. P = 181) and G/A genotype (P < 0.001 vs. P = 0.994) was significantly higher among Lebanese but not Tunisians, respectively. While FV-Leiden was a common genetic risk factor for DVT in both communities, the contribution of PRT G20210A to the genetic susceptibility of DVT differed among Lebanese and Tunisians, which underscores the need to determine prothrombotic gene polymorphisms associated with DVT among Arab and Mediterranean basin communities.