Interplay of LncRNAs NEAT1 and TUG1 in Incidence of Cytokine Storm in Appraisal of COVID-19 Infection.

Background: In 2019, the coronavirus pandemic emerged, resulting in the highest mortality and morbidity rate globally. It has a prevailing transmission rate and continues to be a global burden. There is a paucity of data regarding the role of long non-coding RNAs (lncRNAs) in COVID-19. Therefore, the current study aimed to investigate lncRNAs, particularly NEAT1 and TUG1, and their association with IL-6, CCL2, and TNF-α in COVID-19 patients with moderate and severe disease. Methods: The study was conducted on 80 COVID-19 patients (35 with severe and 45 with moderate infection) and 40 control subjects. Complete blood count (CBC), D-dimer assay, serum ferritin, and CRP were assayed. qRT-PCR was used to measure RNAs and lncRNAs. Results: NEAT1 and TUG1 expression levels were higher in COVID-19 patients compared with controls (P<0.001). Furthermore, CCL2, IL-6, and TNF-α expressions were higher in COVID-19 patients compared to controls (P<0.001). CCL2 and IL-6 expression levels were significantly higher in patients with severe compared to those with moderate COVID-19 infection (P<0.001). IL-6 had the highest accuracy in distinguishing COVID-19 patients (AUC=1, P<0.001 at a cutoff of 0.359), followed by TUG1 (AUC=0.999, P<0.001 at a cutoff of 2.28). NEAT1 and TUG1 had significant correlations with the measured cytokines, and based on the multivariate regression analysis, NEAT1 is the independent predictor for survival in COVID-19 patients (P=0.02). Conclusion: In COVID-19 patients, significant overexpression of NEAT1 and TUG1 was observed, consistent with cytokine storm. TUG1 could be an efficient diagnostic biomarker, whereas NEAT1 was an independent predictor for overall survival.

Deregulation of CircANXA2, Circ0075001, and CircFBXW7 Gene Expressions and Their Predictive Value in Egyptian Acute Myeloid Leukemia Patients.

Background: Acute myeloid leukemia (AML) is of heterogeneous pathogenesis and caused by alterations of multiple genes. CircRNAs act as oncogenes or tumor suppressors in numerous tumors and could be novel diagnostic and prognostic biomarkers. Few studies had incorporated circRNAs in AML. Aim of the Work: Assessment of circANXA2, circ0075001, and circFBXW7 gene expressions in AML patients. Evaluation of their relations with clinical, cytogenetic, and overall survival outcome to emphasize their diagnostic role and prognostic impact. Methods: This study was carried out on 120 subjects (66 AML patients and 54 controls). All subjects were subjected to gene expressions assay for circANXA2, circ0075001, circFBXW7 by quantitative real-time polymerase chain reaction. Results: Prominent overexpression of circANAX2 and circ0075001 in patients than control (P < 0.001), whereas circFBXW7 was markedly downregulated in patients than in control (P < 0.001). Moreover, circANXA2 with AUC 0.824, P <0.001, had a sensitivity of 74.24%, specificity 88.89% whereas circ0075001 with AUC 0.855, P < 0.001, had the highest sensitivity of 83.33% and specificity 79.63%, and circFBXW7 with AUC 0.826, P < 0.001, had a sensitivity of 75.76% and specificity 74.07% in the distinction of AML patients from controls. Additionally, we find out that high expression of circANXA2 and circ0075001 correlated significantly with splenomegaly, hepatomegaly, less differentiated FAB subtypes (M5, M7), short overall survival, and had an adverse cytogenetic pattern. Conclusion: CircANXA2, circ0075001, and circFBXW7 gene expressions could serve as potential diagnostic biomarkers for AML disease. Moreover, CircANXA2 and circ0075001 exert poor prognostic effects on AML patients.

Prognostic Impact of Genetic Variants of MECP2 and TIRAP on Clinical Outcomes of Systemic Lupus Erythematosus with and without Nephritis.

Systemic lupus erythematosus (SLE) is a chronic autoimmune illness with a growing prevalence in many populations. Few studies have examined genetic predisposition to SLE, so we aimed to examine the clinical impact of the genetic polymorphisms MECP2 rs2734647and TIRAP rs8177374 on the outcomes and therapeutic precision of SLE with and without nephritis. This study included 110 SLE patients-divided into 63 with lupus nephritis (LN), and 47 without nephritis-and 100 controls. Laboratory measurements including CRP, ESR, ACR, CBC, anti-ds-DNA, vitamin A, C3, and C4 were carried out, along with genotyping of MECP2 rs2734647and TIRAP rs8177374 by real-time PCR and sequencing. Treg %, vitamin A, C3, and C4 were lower, whereas Th17 % was higher, in patients vs. controls (p < 0.001). The T allele of MECP2 rs2734647 was higher in LN than in non-nephritis and control subjects. Moreover, the T allele of TIRAP rs8177374 was higher in LN than in non-nephritis and control subjects. The MECP2 and TIRAP genes could play a role in predisposition to SLE, and can also predict disease progress to nephritis, helping to personalize medicine.

Evaluation of MicroRNA-122 as a Biomarker for Chronic Hepatitis C Infection and as a Predictor for Treatment Response to Direct-Acting Antivirals.

BACKGROUND: Treatment response to antiviral drugs is a challenging issue in patients with chronic hepatitis C virus (HCV) infection. Although microRNA-122 represents the majority of the microRNA content in hepatic tissues, few studies have evaluated its role in the treatment response, so we aimed to study its role in chronic HCV patients and in predicting the treatment response to direct-acting antivirals (DAAs). METHODS: The study included 125 chronic HCV patients (89 naïve and 36 with a prior failed peginterferon/ribavirin response) and 50 apparently healthy subjects. Complete blood count, liver function, α-fetoprotein, lipid profiles, serum creatinine, abdominal ultrasound, and FibroScan® were assessed. Viral markers, HCV antibodies, and hepatitis B surface antigen were measured by enzyme-linked fluorescent immunoassay, with quantitative estimation of HCV RNA and microRNA-122 levels by real-time PCR. RESULTS: The microRNA-122 level in HCV patients (those with a sustained virologic response 12 weeks after finishing therapy [SVR12] and non-responders) was significantly increased compared with controls and expressed more in non-responders versus SVR12 (p=0.042). ROC curve analysis of microRNA-122 for differentiating HCV patients from healthy controls revealed that a cut-off point of >1.45 had a sensitivity of 67.20%, specificity of 94.0%, AUC=0.861, and p<0.001; and for predicting response to treatment a cut-off point ≤5.66 could significantly (p=0.022) predict the occurrence of SVR, with a sensitivity of 60.34%, specificity of 66.67%, and AUC=0.729. Logistic regression analysis showed significant values for microRNA-122 in multivariate and univariate analysis for the prediction of response to DAAs. CONCLUSION: The results demonstrated the possible function of microRNA-122 as an indicative tool for distinguishing chronic HCV patients from controls and in the assessment of the therapeutic reaction to DAAs.

Differential expression of long noncoding RNA in hepatocellular carcinoma on top of chronic HCV and HBV infections.

Aim of the study: The task of long noncoding RNAs (lncRNAs) as a prospective goal for hepatocellular carcinoma (HCC) is a candidate for research. Several lncRNAs are involved in signal transduction, directing gene expression and epigenetic alteration in normal and cancer cells. Dysregulation of diverse lncRNAs has been involved in the pathogenesis and progression of different cancers including HCC. We aimed to investigate the differential expression of lncRNAs (aHIF, hPVT1, ANRIL) in HCC on top of chronic hepatitis C virus (HCV) and hepatitis B virus (HBV) infections. Material and methods: 182 participants were included: 85 patients with HCC in addition to 50 patients with cirrhosis on top of chronic HCV or HBV, and 47 healthy subjects as controls. HCC was diagnosed by triphasic computed tomography (CT). Detection of α-fetoprotein (AFP) and serological markers of HCVAb and HBsAg by enzyme-linked fluorescent immunoassay (ELFA) and quantitation of lncRNAs by real time PCR were applied. Results: Upregulation of ANRIL and hPVT1 and downregulation of aHIF were observed in patients with HCC on top of HCV and HBV vs. controls. Circulating aHIF could be of major diagnostic importance to discriminate HCC on top of HCV from cirrhotic patients with sensitivity 86.67% and specificity 91.89% whereas circulating hPVT1 had sensitivity 85.0% and specificity 84.62%; moreover ANRIL had AUC 0.902 and could discriminate HCC on top of HBV from cirrhotic patients. Conclusions: The differential expression of lncRNAs (ANRIL, hPVT1 and aHIF) might be of major worth in predicting the occurrence of HCC in cirrhotic patients related to chronic viral hepatitis and could be beneficial in the early management.

Role of Adiponectin Gene and Receptor Polymorphisms and Their mRNA Levels with Serum Adiponectin Level in Myocardial Infarction.

BACKGROUND AND AIM: Genetic factors are vital participants in the development and progression of myocardial infarction (MI). Adiponectin has been assumed to have a protective role in MI and adiponectin receptors variants could be a determinant for atherosclerosis. We aimed to evaluate the prevalence of ADIPOQ (rs2241766) and ADIPOR2 (rs10773989) polymorphisms and their association with mRNA levels and circulatory adiponectin levels in patients with MI. SUBJECTS AND METHODS: A total of 220 participants were classified into two groups: group 1 included 120 patients with MI, and group 2 involved 100 healthy participants as controls. Genotyping of ADIPOQ (rs2241766) and ADIPOR2 (rs10773989) polymorphisms were analyzed using an allele discrimination assay with real-time PCR and their relative expression or mRNA levels were determined by real-time PCR. Serum adiponectin level was determined using an ELISA technique. RESULTS: The ADIPOQ rs2241766 GG genotype and G allele and the CC genotype and C allele of ADIPOR2 rs10773989 were significantly prevalent in patients with MI and associated with increased risk of MI. We detected a marked reduction in serum adiponectin, ADIPOQ and ADIPOR2 mRNA levels in patients than control. The GG genotype of ADIPOQ rs2241766 and the CC genotype of ADIPOR2 rs10773989 had the lowest levels of their mRNA and adiponectin level in both patients and controls. CONCLUSION: Adiponectin gene and receptor variants are potentially related to MI risk; furthermore, their expressions were markedly depressed in MI which suggests their use as potential biomarkers for MI.

Biochemical study on modifying role of variants of leptin gene and its receptor on serum leptin levels in breast cancer.

The leptin is discharged from breast adipose tissue and is overexpressed in breast cancer (BC). Conflicting relation of leptin with BC was reported. We investigated this association and its impact on leptin level and disease characteristics. The study included 70 females (40 women with pathological proof of invasive BC patients and 30 controls). LEP and LEPR polymorphisms were evaluated by real-time PCR. Serum leptin was estimated by ELISA. Both LEPR and LEP disturbances increase the danger of BC where GG genotype and G allele frequencies of LEPR were higher in patients vs. control. GG genotype increases BC risk with OR (9.1) while G allele predisposes to disease with OR (3.8). Furthermore, LEP A allele was uniquely elevated in patients than healthy ones with OR (2.06). Precise relation of circulating leptin and its polymorphisms with predicting BC may authorize its utilization in early screening.

Simultaneous Assessment of MicroRNAs 126 and 192 in Diabetic Nephropathy Patients and the Relation of these MicroRNAs with Urinary Albumin.

BACKGROUND AND OBJECTIVE: Diabetic nephropathy (DN) is a major determinant of end-stage renal disease (ESRD). Altered microRNA levels lead to serious chronic diseases, such as diabetes. We aimed to measure the expression levels of two microRNAs, microRNA126 and 192 in DN and investigate their connection with albuminuria levels. METHODS: This study included 229 subjects (134 DN patients and 95 controls). Serum lipid profiles, glucose levels, glycated haemoglobin (HbA1c) levels, and renal functions were assayed. The microRNA126 and microRNA192 expression levels were determined by real-time PCR. RESULTS: Patients with DN had higher weights, BMI values, glucose levels (P<0.001), HbA1c levels (P<0.001), urinary albumin-creatinine ratio (ACR) values (P<0.001), urea levels (P=0.002), and creatinine levels (P=0.004) and lower expression levels of both microRNA192 (P<0.001) and microRNA126 (P<0.001) than controls. MicroRNA126 expression was positively correlated with age, estimated glomerular filtration rate (eGFR) and microRNA192 expression but negatively correlated with blood sugar, HbA1c, urea, creatinine and ACR. MicroRNA192 had higher sensitivity (91%), specificity (94%), and area under the curve (AUC) (0.967) values than microRNA126 (sensitivity, 90%; specificity, 68%; AUC, 0.897) and thus can precisely diagnose DN. CONCLUSION: Both MicroRNA126 and microRNA192 expression were obviously associated with DN and might determine the progression of the disease owing to prominent relation with macroalbuminuria.

The Genetic Variants of IKZF1 Gene Linked with the Growing Risk of Childhood Acute Lymphoblastic Leukaemia.

BACKGROUND: The zinc finger protein IKAROS (IKZF1) is an essential transcription factor in haematopoiesis that is involved primarily in lymphoid tissue differentiation. Many studies have indicated that IKZF1 alterations may be associated with acute lymphoblastic leukaemia, but the results remain controversial. OBJECTIVE: We aimed to investigate the association of the rs4132601 T/G and rs10272724 T/C IKZF1 gene polymorphisms with the risk of childhood acute lymphoblastic leukaemia and to determine whether these genetic variants affect the clinical parameters and the iron profiles of these children cohort. METHODS: This case control study was conducted on 170 Egyptian children comprising of two groups: group (I) included 90 children diagnosed with acute lymphoblastic leukaemia and group (II) comprised of 80 ages and sex-matched healthy control children. The studied polymorphisms were genotyped using PCR restriction fragment length polymorphism (PCR-RFLP). RESULTS: A higher frequency of the mutant GG genotype and G allele of rs4132601 was found in the patient group than in the control group. The results also showed a significant difference among the rs10272724 genotypes, with a higher frequency of the mutant CC genotype and C allele in the patients than in controls. The mutant GG genotype of rs4132601 and the mutant CC genotype of rs10272724 were associated with a higher serum ferritin level and transferrin saturation and an older age at diagnosis of acute lymphoblastic leukaemia than the other genotypes. CONCLUSION: IKZF1 rs4132601 and rs10272724 could be considered significant risk contributors to childhood acute lymphoblastic leukaemia and may impact the iron profiles in these children.

Potential role of MicroRNA 200c gene expression in assessment of colorectal cancer.

BACKGROUND AND AIM: Colorectal cancer (CRC) is a common cancer worldwide that affects men and women of all racial and ethnic groups. Recent evidence supports the role of microRNAs in CRC. We planned to investigate microRNA200c expression and its relation with diagnosis, prognosis, metastasis and overall survival in CRC patients. This study enrolled 90 subjects (3'0 CRC patients, 30 patients with benign colorectal polyps and 30 healthy control subjects). METHODS: Laboratory investigations included measurement of serum CA19-9 and CEA by enzyme linked immunosorbent assay (ELISA) method and relative quantitation (RQ) of microRNA200c gene expression by real time PCR technique. RESULTS: Significant higher MicroRNA200c expression levels in CRC patients versus both benign (P < 0.011) and control groups (P < 0.001), additionally, benign group had elevated levels versus control (P < 0.001). MicroRNA 200c at cutoff >4.56 had sensitivity 86.67% and specificity 73.33% (P < 0.001) for CRC discrimination. Kaplan-Meier survival analysis revealed significant association (P = 0.028) of high expression of microRNA200c with decreased overall survival. CONCLUSION: Noticeable up-regulation of microRNA200c in CRC and its remarkable relation with unfavorable survival suggesting its potential dual use as a diagnostic and prognostic biomarker for CRC.

Vitamin D deficiency and vitamin D receptor variants in mothers and their neonates are risk factors for neonatal sepsis.

BACKGROUND AND AIM: Increasing prevalence of neonatal sepsis in recent years catch attention to early prevention and management. Vitamin D receptor (VDR) polymorphism can modulate VDR expression level that greatly influences immunity and susceptibility to microbial infections. We aimed to investigate the association of VDR polymorphism at FokI, rs2228570 T/C, and TaqI, rs731236 C/T gene with serum 25-hydroxyvitamin D level and risk of neonatal sepsis. METHODS: This work carried on 160 subjects classified into 80 cases (40 mothers and their 40 septic neonates) and 80 healthy controls (40 volunteer mothers and their 40 healthy neonates). Genotyping of VDR polymorphisms were assayed by real-time PCR and serum 25-hydroxyvitamin D level and hs-CRP were measured by ELISA. RESULTS: Vitamin D deficiency was observed in mothers of cases compared with healthy ones (p = <0.001) and in septic neonates versus healthy ones (p = <0.001). Septic neonates had much higher VDR FokI TT genotype (p = 0.014) and T allele (p = 0.003) versus healthy ones. TT genotype and T allele could increase the risk of sepsis with OR 95% CI [4.804 (1.4-16.4)] and [2.786 (1.4-5.7)] respectively while VDR TaqI showed no association with sepsis. There was a strong LD between FokI and TaqI in sepsis cases. In sepsis, T/T genotype at FokI had significantly lower vitamin D (p = <0.001). CONCLUSION: Vitamin D deficiency in mothers/neonates is a risk factor for neonatal sepsis. VDR FokI T allele had lower 25-hydroxyvitamin D level that may predispose to sepsis hazards.

Biochemical and molecular study on interleukin-1ß gene expression and relation of single nucleotide polymorphism in promoter region with Type 2 diabetes mellitus.

Interleukin-1ß (IL-1ß) assumes a centric role in the regulation of immune and inflammatory responses and thus has been recognized in immune mediated diseases like type 2 diabetes mellitus (T2DM). We aimed to investigate expressed level of IL-1ß and its relation with IL-1ß -511T>C polymorphism in T2DM patients. This study enrolled 80 subjects (50 patients with T2DM and 30 healthy control subjects). Laboratory investigations included fasting (FBG) and 2 h postprandial blood sugar (2 h PBG), HBA1c, lipid profile, and renal function tests. Genotyping of IL-1ß -511T>C (rs16944) SNP assay by real-time PCR and relative quantitation of IL-1ß gene expression transcript by real-time PCR. RESULTS: T2DM patients had significantly higher FBG and 2 h PBG, HBA1c, LDLc, TC, TG, systolic, and diastolic BP while lower HDLc compared with control group. IL 1- ß -511 T>C, CC genotype and C allele were significantly associated with risk of T2DM with odds ratio (OR) 4.73, 95%CI (1.21-18.39) and OR 2.27, 95%CI (1.72-4.40), respectively. Moreover, diabetic patients had significantly higher IL 1- ß gene transcript compared with control group (P < 0.001). CC genotype of IL 1- ß -511 T > C had the highest significant level of IL 1- ß gene transcript demonstrated compared with C/T and T/T genotypes (P < 0.001) in patients. CONCLUSION: C allele of IL-1 ß -511 T >C could be considered risk factor contributor to T2DM and excess level of IL-1 ß transcript may disclose to some degree the inflammatory role of cytokines in T2DM.

Association of stem cell factor gene expression with severity and atopic state in patients with bronchial asthma.

BACKGROUND: Bronchial asthma is a chronic inflammatory and remodeling disorder of the airways, in which many cells, cellular elements, and cytokines play important roles. Stem cell factor (SCF) may contribute to the inflammatory changes occurring in asthma. We aimed to show the expression of SCF gene in patients with asthma as a means of diagnosis and its association with severity and atopic state in these patients. METHODS: This study was carried out on 80 subjects, 50 asthmatic patients and 30 age and gender matched healthy control persons. They were subjected to full history taking, general and local chest examination, spirometric measurements (pre and post broncodilators) using a spirometer, serum IgE, and real time PCR for assessment of SCF mRNA expression. RESULTS: This study showed significant difference between the studied groups regarding pulmonary function tests (P < 0.001). Asthmatic patients had significant higher SCF expression compared to control (P < 0.001), also atopic patients vs non atopic (P = 0.03) and severe asthmatic patients vs mild ones (P < 0.001). SCF expression at cut off point (0.528) is sufficient to discriminate asthmatic patients from control while at cut off point (1.84) for discrimination of atopic patients from non-atopic patients and at cut off point (1.395) for discrimination of severe asthmatic patients from mild ones. A significant negative correlation between SCF expression and inhaled steroid while significant positive correlation with serum IgE was found. CONCLUSION: Measuring SCF mRNA expression can be used as an efficient marker for evaluation of atopy and detection of severity of bronchial asthma.

Association of genetic variants of pentraxin 3 rs3816527 with hypertension in Chronic kidney disease patients.

Hypertension is a nearly constant feature and both a cause and a consequence of chronic kidney disease (CKD). Atherosclerotic lesions showed a marked expression of pentraxin 3 on the surface of lumen and in the plaque. The aim was to assess the correlation of exon 2 of pentraxin 3 gene SNP rs3816527 with hypertension with CKD. The study was conducted on 110 CKD patients (60 patients with and 50 patients without hypertension) and 40 healthy subjects as control. Laboratory investigations including the measurement of fasting blood glucose, lipid profile, and indices of oxidative stress, liver function tests, and renal function tests were done. Genotyping of pentraxin 3 gene SNP rs3816527 was done by real-time PCR. There was a significant difference between CKD patients with hypertension and the subjects in the control group regarding systolic and diastolic BP, urea, creatinine, GFR, TG, cholesterol, LDL, HDL, and total antioxidant levels (p < 0.001). There is a statistically significant difference between CKD patients with hypertension and the other studied groups regarding the frequencies of AA genotype and A allele of exon 2 SNP of pentraxin 3 gene compared to CC genotype and C allele (wild type) (p < 0.001), while there was significant difference between CKD patients without hypertension and control (p > 0.05). Pentraxin 3 AA genotype SNP rs3816527 can be considered as a potential biomarker and a risk factor for CKD patients, especially hypertensive patients, and specifically as an independent predictor of hypertension in CKD.

Association of factor V Leiden, Janus kinase 2, prothrombin, and MTHFR mutations with primary Budd-Chiari syndrome in Egyptian patients.

BACKGROUND AND AIM: Budd-Chiari syndrome (BCS) is defined as obstruction of hepatic venous outflow anywhere from the small hepatic veins to the suprahepatic inferior vena cava. The pathogenesis of BCS is still not fully understood. This study aimed to evaluate the association of factor V Leiden (FVL), Janus kinase 2 (JAK2), prothrombin, and methylene tetrahydrofolate reductase (MTHFR) mutations with primary BCS. METHODS: The study was carried out on 35 patients with primary BCS and 15 age and gender matched healthy individuals as a control group. Genotyping of FVL, prothrombin, and MTHFR mutations was determined by GENEQUALITY AB-THROMBO TYPE kit based on the reverse hybridization principle. JAK2 mutation was determined by polymerase chain reaction-restriction fragment length polymorphism. RESULTS: There was a statistically significant difference between patients and controls regarding FVL, MTHFR C677T, and MTHFR A1298C mutations with odds ratio of 1.83, 2.0, and 1.79, respectively. Hetero MTHFR C677T, hetero FVL, and hetero MTHFR A1298C were the most common etiological factors being responsible for 57.1, 42.9, and 42.9% of primary BCS cases, respectively. CONCLUSION: It could be concluded that BCS is a multifactorial disease; in the current study, MTHFR C677T mutation was the most common cause of disease. Identification of one cause of BCS should not eliminate investigations for detection of other etiological factors.

Association of deletion allele of insertion/deletion polymorphism in α2B adrenoceptor gene and hypertension with or without type 2 diabetes mellitus.

BACKGROUND: Vascular α2B-adrenoreceptors have the potential to increase blood pressure by mediating vasoconstriction. A nine-nucleotide deletion in the receptor enhances vasoconstriction and exacerbates hypertension. The aim of this study was to determine the association between insertion/deletion (I/D) polymorphism of the α2B-adrenoceptor and hypertension with and without diabetes. METHODS: The study was carried out in 35 hypertensive patients with diabetes, 35 hypertensive patients without diabetes, and 30 healthy controls. Clinical data, blood lipid profiles, and I/D polymorphism were assessed. RESULTS: Hypertensive patients were significantly older, with significantly higher systolic/diastolic blood pressures and worse plasma lipid profiles than controls. The frequency of the DD genotype was significantly higher in both hypertensive patients with (77.14%, P < 0.01) and without (71.43%, P < 0.05) diabetes versus controls (40%). Also, the D allele was significantly more common in both hypertensive patients with (84.29%, P < 0.01) and without (80%, P < 0.05) diabetes versus controls (58.33%). Hypertensive patients were more likely to have the D allele with (3.83-fold) and without (2.85-fold) diabetes. The frequencies of the DD genotype and the D allele were not significantly (P > 0.05) different between the patient groups. The DD genotype was associated with significantly lower high-density lipoprotein (P = 0.001) and significantly higher low-density lipoprotein (P = 0.017) levels versus the II and ID genotypes in the hypertensive group without diabetes. CONCLUSION: A marked and statistically significant association between DD genotype and D allele of I/D polymorphism in the α2B-adrenoceptor gene may be a risk factor for hypertension ± diabetes. The association between the DD genotype and dyslipidemia may partially explain its role in precipitating hypertension.