Detection of VIM- and IMP-type Metallo-Beta-Lactamase Genes in Acinetobacter baumannii Isolates from Patients in Two Hospitals in Tehran.

BACKGROUND: Acinetobacter baumannii, is an opportunistic pathogen and is responsible for numerous nosocomial infections. In recent years, this microorganism has been resistant to a wide range of antibiotics. One of the most important mechanisms of resistance in this microorganism is production of metallo-beta-lactamases (MBLs). OBJECTIVES: The aim of this study was to detect VIM- and IMP-type metallo-beta-lactamase genes in Acinetobacter baumanniiisolates from patients in two Hospitals in Tehran. MATERIALS AND METHODS: 104 isolates were tested using the PCR method for the identification of VIM- and IMP-type genes. RESULTS: vim1, vim2, imp1 and imp2 genes were detected in 6.7%, 41.7%, 50% and 1.7% of the isolates from Tehran Heart Center, and in 29.5%, 38.6%, 4.5% and 4.5% of the isolates from Shahid Mutahhari Hospital respectively. DISCUSSIONS: Our analysis revealed that the majority of the isolates had at least one of these genes, indicating that MBLs production is an important resistance mechanism in Acinetobacter baumannii.

Investigation of association between donors' and recipients' NADPH oxidase p22(phox) C242T polymorphism and acute rejection, delayed graft function and blood pressure in renal allograft recipients.

BACKGROUND: Production of reactive oxygen species (ROS) and thereby induction of oxidative stress seem to be one of the major mediators of inflammatory adverse outcomes after renal transplantation. p22(phox) is a polymorphic subunit of NAD(P)H-oxidase that is critical for activation and stabilization of the enzyme. This enzyme is involved in the production of superoxide that triggers inflammatory injuries to the kidney. So in this study, the association between donors and recipients' C242T polymorphism of p22(phox) and acute rejection (AR), delayed graft function (DGF), creatinine clearance (CrCl), and blood pressure in renal-allograft recipients was studied. METHODS: One hundred ninety six donor-recipient pairs were studied. The C242T polymorphism of p22(phox) was determined using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). According to p22 genotype, the subjects were divided in wild-type (CC) and T allele carriers (CT+TT). Transplantation outcomes were determined using acute rejection and delayed graft function criteria. The mean arterial pressure was also measured monthly after transplantation. RESULTS: There was a significant association between the recipients' p22(phox) polymorphism and DGF occurrence (OR=2.5, CI: 1.2-4.9, p=0.0009). No significant association was detected between donors' p22(phox) polymorphism and AR and DGF events. CrCl during the six months follow-up after transplantation was lower in the patients who received allograft from donors carrying 242T allele (B=-12.8, CI: -22.9-12.8 (-22.9 to -2.6)). Changes in the blood pressure were not different among the patients having different genotypes of p22(phox). CONCLUSION: These results suggest that the recipients' p22(phox) C242T polymorphism may be a major risk factor for DGF in renal transplantation. Moreover, the donors' 242T allele seems to affect the rate of CrCl in the renal allograft recipients.

The Kalirin Gene rs9289231 Polymorphism as a Novel Predisposing Marker for Coronary Artery Disease.

BACKGROUND: Atherosclerosis is the leading cause of death and disability worldwide. Genetic variations play a major role in the process of atherosclerosis. Recently, rs9289231 genetic variations of the Kalirin gene (KALRN) on chromosome 3q21.2 have been introduced as potential genetic markers for coronary artery disease (CAD). OBJECTIVE: In this case-control study, we investigated the association between genetic susceptibility to CAD and rs9289231 G/T polymorphism, located on the KALRN gene, in an Iranian population. METHODS: Our cohort consisted of 1486 individuals undergoing coronary angiography. Of these, we considered the 1007 patients with CAD to be case individuals and the 479 individuals with normal coronary conditions to be control individuals. We performed single-nucleotide polymorphism (SNP) genotyping via the high resolution melting (HRM) technique. RESULTS: Our data showed that the minor allele (G) frequency of rs9289231 SNP was higher in our CAD group than that in our control group (odds ratio, 1:37; confidence interval, 1.07-1.74; P = .01). The results of our data analysis highlighted a genetic association between rs9289231 polymorphism and severity and development of CAD. CONCLUSIONS: We consider the GG genotype and the G allele of rs9289231 polymorphism of KALRN to be genetic risk factors for CAD in an Iranian population, especially in early-stage atherosclerotic vascular disease.

The association between Factor V Leiden with the presence and severity of coronary artery disease.

OBJECTIVES: The presence of Factor V Leiden (FVL) is proposed to be associated with a higher risk for arterial thrombosis. The aim of this study was to examine a relationship between FVL with the presence and severity of angiographically determined coronary artery disease (CAD). DESIGN AND METHODS: In this case-control study, 1083 patients having angiographic evidence of atherosclerosis with ≥50% luminal stenosis in their epicardial coronary tree were compared with patients with no luminal stenosis (n=320) or with luminal stenosis <50% (n=191) at coronary angiography as reference group. The severity of CAD was determined by vessel score and also a semi-quantitative scoring system (Gensini score). The presence of Factor V polymorphisms was analyzed using polymerase chain reaction-based restriction fragment length polymorphism (PCR-RFLP). RESULTS: FVL was found to be independently associated with the occurrence of CAD (p=0.020). As compared to wild genotype, heterozygote or homozygote mutant genotypes were more likely associated with a trend towards more severe CAD (adjusted OR=1.85, 95% CI=1.26 to 2.72; p=0.002, and adjusted OR=3.70, 95% CI=1.71 to 8.00; p=0.001; respectively). In addition, the median and inter-quartile range for Gensini score were significantly different among the GG (27.8, 3 to 66.5), GA (53.5, 10 to 104.1), and AA (92.8, 48.1 to 125.9) genotypes (p<0.001). CONCLUSIONS: Our results confirmed the hypothesis that FVL mutation is a significant determinant of CAD risk. Furthermore, we observed that FVL is independently associated with increasing CAD severity.

Association between R353Q polymorphism for coagulative factor VII and severity of coronary artery disease in Iranian population.

BACKGROUND: Recent research has supported the central role of coagulative factors in advancing atherosclerosis and causing coronary artery disease (CAD). The present study, for the first time, aimed to clarify the relationship between R353Q polymorphism for factor VII and the occurrence and severity of CAD in a large sample of Iranian population. METHODS: Nine hundred and nineteen consecutive patients with suspected CAD, who candidated for coronary angiography in the Tehran Heart Center between January 2006 and March 2007, were examined. The number of diseased coronary vessels was determined, and the severity of CAD was assessed by the Gensini score. Genotyping was done via the PCR-RFLP method. RESULTS: The frequency of Q and R alleles was 74.1% and 25.9% in the patients with CADand 75.2% and 24.8% in those without CAD, with an insignificant difference (p = 0.625). The frequency of Q allele in the patients with single-vessel, two-vessel, and three-vessel diseases was 72.8%, 71.5%, and 76.4%, respectively; the difference was also insignificant (p = 0.379). No relationship was observed between the distribution of the genotypes and the number of the involved coronary vessels. The average of the Gensini score was 43.39 ± 46.18 in the patients with QQ genotype, 38.87 ± 42.89 in those with QR genotype, and 55.61 ± 53.80 in the ones with RR genotype, with the difference not constituting any statistical significance (p = 0.084). CONCLUSIONS: The results suggest no association between R353Q polymorphism for factor VII and the presence or progression of CAD in the Iranian population.

Detection of vim- and ipm-type metallo-beta-lactamases in Pseudomonas aeruginosa clinical isolates.

BACKGROUND: Pseudomonas aeruginosa is the most important bacterium isolated from burn wounds, and its resistance to imipenem due to metallo-beta-lactamases is increasing. This study was designed to detect vim1, vim2, ipm1 and ipm2 metallo-beta-lactamases genes between Pseudomonas aeruginosa isolates isolated from Shahid Motahari Burns Hospital, Iran. METHODS: To that end, we isolated 483 nonduplicate consecutive isolates of P. aeruginosa from burn infections; and after biochemical confirmation, we examined the imipenem susceptibility via the Kirby-Bauer method. All the imipenem-resistant and imipenem-intermediate isolates were screened for vim1, vim2, ipm1 and ipm2 genes through the PCR method. RESULTS: From the 483 isolates, 272 (56%) and 63 (13%) isolates had resistant and intermediate zones in their imipenem antibiogram pattern, respectively. Fifty-four (16.1%), 7 (2.1%), 22 (6.6%), and 11 (3.3%) of the resistant and intermediate isolates had vim1, vim2, ipm1 and ipm2 genes in their PCR results, respectively. CONCLUSION: MBL-mediated imipenem resistance in P. aeruginosa is a cause for concern in the treatment of infective burn patients. The rate of imipenem resistance due to MBL was increased dramatically and newer versions of MBL families were detected for the first time. These results suggest that an effective method should be provided to fight MBL production in clinical isolates.

Minimal Inhibitory Concentration of Ceftazidime and Co-trimoxazole for Stenotrophomonas Maltophilia using E-test.

BACKGROUND: Stenotrophomonas maltophilia, previously named as Pseudomonas or Xanthomonas maltophilia, is an important nosocomial pathogen AIM: The purpose of the present study was to investigate the prevalence of S. maltophilia in Iranian hospitals and its susceptibility to available antimicrobial agents. SETTING AND DESIGN: A cross-sectional study in Imam Khomeini Hospital affiliated to Tehran University of Medical Sciences. MATERIALS AND METHODS: All blood specimens were sent to the laboratory for blood culture and biochemical analysis. One hundred samples were positive for S. maltophilia. We used disk diffusion and E-test in order to determine minimal inhibitory concentration (MIC) of ceftazidime and co-trimoxazole as the first line antibiotics for S. maltophilia. The tests were performed and interpreted according to the guidelines of Clinical Laboratory Standards Institute (CLSI). STATISTICAL ANALYSIS: Chi-square test and Kappa measurement of agreement were applied as appropriate. RESULTS: S. maltophilia was the most frequent pathogen (895 specimens; 38.9%) isolated from the samples which were mostly from emergency ward (780 specimens; 33.9%). Ceftazidime MIC(50) and MIC(90) were 2 and 32 µg/ml, respectively (sensitive ≤8 µg/ml and resistant ≥32 µg/ml according to CLSI guideline). MIC(50) and MIC(90) for co-trimoxazole were 0.5 and 2 µg/ml, respectively (sensitive ≤2 µg/ml and resistant ≥4 µg/ml according to CLSI guideline). CONCLUSION: S. maltophilia is the most frequent pathogen in our hospital with a high susceptibility to both ceftazidime and co-trimoxazole.

Potential link of microalbuminuria with metabolic syndrome in patients undergoing coronary angiography.

BACKGROUND AND AIMS: Microalbuminuria and metabolic syndrome (MetS) are both risk factors for cardiovascular disease.We sought to examine the relationship between microalbuminuria and MetS in patients undergoing coronary angiography. METHODS: From August 2007 to March 2008, we studied 531 patients (354 men, 66.7%) undergoing elective coronary angiography due to symptoms related to coronary artery disease. MetS was defined based on the adapted Adult Treatment Panel III (ATP-III A) proposed by the American Heart Association/National Heart, Lung, and Blood Institute, and microalbuminuria was defined as urinary albumin-to-creatinine ratio (ACR) between 30 mg/g and 300 mg/g. RESULTS: MetS was detected in 39.7% of participants, 62.1% of women and 28.5% of men. Microalbuminuria was detected in 109 (20.5%) of participants, in 41 (12.8%) of non-MetS individuals, and in 68 (32.2%) of the MetS individuals. There was a significant positive association between the number of components of MetS and the corresponding prevalence of microalbuminuria (p<0.001). In patients with MetS compared to those without any component of MetS, multivariable-adjusted OR (95% CI) of microalbuminuria was 2.71 (1.71-4.29). Multiple logistic regression analyses revealed higher fasting blood glucose and lower HDL-cholesterol are independently associated with microalbuminuria. CONCLUSIONS: Our study demonstrated that microalbuminuria is strongly associated with MetS and that among the components of MetS high fasting blood glucose had the largest power to determine the risk of microalbuminuria in Iranian patients undergoing coronary angiography.

Lipid profile and inflammatory markers associated with estrogen receptor alpha PvuII and XbaI gene polymorphisms.

Estrogen is established to influence lipoprotein metabolism and inflammatory markers. Alternations in estrogen receptor alpha (ESR1) expression and function may affect the role of estrogen in this regard. The aim of this study was to determine whether ESR1 PvuII and XbaI gene polymorphisms have effects on lipoprotein (a) as well as inflammatory variables in an Iranian population. Three hundred and ninety seven consecutive participants (228 men, 57.4%) who were admitted at our center for elective coronary angiography because of symptoms related to coronary artery disease (CAD) were enrolled in our study. Total cholesterol, high-density lipoprotein (HDL)-cholesterol, and triglyceride levels were determined by standard methods using commercial kits. Low-density lipoprotein (LDL)-cholesterol was calculated according to the Friedewald formula. The lipoprotein (a) levels were measured by ELISA method using Biopool kit, and the CRP concentrations were determined by Latex Immunoturbidometry. The presence of PvuII and XbaI polymorphisms within the ESR gene were analyzed using polymerase chain reaction-based restriction fragment length polymorphism (PCR-RFLP). The frequency of homozygous and heterozygous were 25.9% and 50.1%, for PvuII genotypes, and the frequency was 23.7% and 48.6%, for XbaI genotypes, respectively. After adjusting for CAD and age, no impacts of ESR1 PvuII and XbaI polymorphisms were found on lipid profile, lipoprotein (a) level, and quantitative CRP either in total population or in subgroups stratified by gender. In conclusion, our data demonstrate that ESR1 PvuII and XbaI gene polymorphisms did not seem to have an effect on lipoprotein metabolism or on inflammatory variables such as CRP.

Association of estrogen receptor alpha gene polymorphism with the presence of coronary artery disease documented by coronary angiography.

OBJECTIVES: To examine the relationship between PvuII and XbaI polymorphisms, with the presence of angiographically determined CAD in an Iranian population. DESIGN AND METHODS: Patients having angiographic evidence of atherosclerosis (Gensini score > 6) in their epicardial coronary tree (CAD(+) case group) were compared with Patients with Gensini score < or = 6 (CAD(-) control group). The presence of PvuII and XbaI polymorphisms was analyzed using polymerase chain reaction-based restriction fragment length polymorphism (PCR-RFLP). RESULTS: The PvuIIota genotype distributions were not statistically different in CAD groups, and subgroups stratified by gender. For the XbaI polymorphism, after controlling for age, male sex, cigarette smoking and hyperlipidemia, XbaI GG genotype was not also found to be an independent predictor for CAD occurrence (OR=1.65; 95% CI: 0.90-3.03; P=0.10). CONCLUSIONS: We did not observe an association between ESR1 PvuII and XbaI gene polymorphisms with CAD in the risk of CAD in an Iranian population.