Sequence analysis of rpoB mutations in rifampin-resistant clinical Mycobacterium tuberculosis isolates from Turkey

Drug-resistant tuberculosis is a serious problem throughout the world. Resistance to Rifampicin (RIF) is mainly caused by the mutations in the rpoB gene coding the beta-subunit of RNA polymerase. In this study, we aimed to detect the distribution of rpoB gene mutations in 80 RIF-resistant clinical Mycobacterium tuberculosis (MTB) isolates from Turkey. The rpoB gene was amplified by PCR and mutations leading to RIF resistance were determined by automated sequence analysis. A total of 72 of the 80 isolates (90%) were found to carry mutations in the amplified region, whereas eight isolates (10%) carried no mutations. Overall, 24 different missense mutations affecting 14 codons, and two deletion mutants were identified. Nine new mutations, six in the hot-spot region and three outside this region, were found. The codon numbers of the most frequently encountered mutations were 531 (51.4%), 526 (18.1%), 516 (13.9%), and 513 (12.5%). As a result, 90% of the RIF-resistant MTB isolates from the Turkish patients were found to carry a mutation in the rpoB gene, Ser531Leu being the most frequent one. Although molecular methods identify mutations leading to RIF resistance very quickly, results of the antimycobacterial susceptibility tests must be taken into consideration for the patients carrying no mutations in this region.     

Preoperative embolization in surgical treatment of a primary hemangiopericytoma of the rib: a case report

Primary hemangiopericytoma of the rib is extremely rare and only a few cases have been reported. A 62-yr-old man presented with an aching chest pain and dyspnea. Thoracic computed tomography revealed a homogenous mass expanding the right seventh rib. A diagnosis of hemangiopericytoma was established by percutaneous needle biopsy. Preoperative embolization of the feeding vessels of the tumor was performed in order to prevent perioperative bleeding. There was no significant bleeding during the surgery, where complete resection of the tumor with 7th to 9th ribs with a surgical margin of 5 cm was performed. Postoperative course was uneventful and there has been no recurrence for thirteen months. To our knowledge, there has been no report to apply a preoperative embolization of a primary hemangiopericytoma of the rib.     

A cluster of nosocomial Klebsiella oxytoca bloodstream infections in a university hospital.

BACKGROUND: On February 19, 2003, four patients (patients 1-4) in the neurology ward underwent cranial magnetic resonance angiography (MRA) and developed fever within 1 hour afterward. Klebsiella oxytoca was isolated from blood cultures of patients 1 through 3. OBJECTIVE: To identify the source of this cluster of nosocomial K. oxytoca bloodstream infections. DESIGN: Outbreak investigation. SETTING: A 1,000-bed university hospital. METHODS: The infection control team reviewed patient charts and interviewed nursing staff about the preparation and administration of parenteral fluids. The procedure of cranial MRA was observed. Arbitrarily primed polymerase chain reaction (AP-PCR) was performed to show the clonal relationship among these three strains. RESULTS: AP-PCR revealed that three K. oxytoca isolates had the same molecular profile. Cranial MRA was found to be the only common source among these patients. During MRA, before injection of the contrast medium, normal saline solution was infused to check the functioning of the intravenous catheter. Use of the solution for multiple patients was routine, but the access diaphragm of the bottle was not cleansed. The bottle of normal saline solution used on February 19 had already been discarded and the culture sample taken from the solution on the day of observation was sterile. CONCLUSIONS: We speculate that normal saline solution became contaminated during manipulation and that successive uses might have been responsible for this cluster. Poor aseptic techniques employed during successive uses appear to be the most likely route of contamination. Use of parenteral solutions for multiple patients was discontinued.     

Impedance cardiographic monitoring during pericardiocentesis: comparison with echocardiography

OBJECTIVE: Thoracic impedance cardiography (TIC) is a noninvasive method which has proved to be useful in monitoring the haemodynamic status of the patients. In this study, we evaluated the TIC findings in patients with pericardial effusion and cardiac tamponade. METHODS AND RESULTS: The study consisted of patients with pericardial effusion with (group A) or without (group B) cardiac tamponade (CT). The stroke volume, cardiac output and ejection fraction was measured by both echocardiography and TIC. The measurements were done at baseline in both groups and following pericardiocentesis in group A. The variables were compared by linear regression analysis, paired sample's t test and chi-square test. The study included 32 patients. Group A consisted of 16 patients and group B of 14 patients. Two patients were excluded from comparisons because of insufficient quality of the echocardiographic examination. There were no significant differences between group A and B with regard to demographic features. Both echocardiographic and TIC measurements at baseline revealed decreased cardiac output, EDV and SV in group A and EF was not different. Linear regression analysis revealed that echocardiography and TIC were in significant correlation with regard to cardiac output, enddiastolic volume, stroke volume (p < 0.01) but not ejection fraction (p = 0.8910). The correlation was also present after pericardiocentesis. CONCLUSIONS: TIC can be safely used in patients with pericardial effusion. It provides suggestive data for the diagnosis of CT and can be used as a means of monitoring the results of the pericardiocentesis.     

Cardiac troponin I levels in patients with left heart failure and cor pulmonale

Cardiac troponin levels are regarded as the most specific of currently available biochemical markers of myocardial damage. Elevated levels of troponin have been previously reported in patients with left heart failure, reflecting small areas of undetected myocardial cell death. The aim of this study was to compare the levels of the cardiac troponin I (cTnI) in patients with left- and right-sided heart failure. Cardiac troponin I levels were studied with immunochemical methods in patients with right heart failure (n = 17) resulting from chronic obstructive pulmonary disease, ischemic left heart failure (n = 23), and nonischemic left heart failure (n = 18) who were admitted to departments of cardiology and chest diseases. Also, cTnI levels were measured in 32 healthy subjects as control group. Protein markers of myocardial injury (cTnI and myoglobin) in patients with left and right heart failure were collected approximately 12 to 36 hours after onset of obvious symptoms. Serum creatine kinase MB band was determined on admission and thereafter twice a day during the first 3 days. Elevated levels of serum cTnI were found in patients with nonischemic (0.83 +/- 0.6 ng/mL, p<0.01) and ischemic left heart failure (0.9 +/- 0.5 ng/mL, p<0.01) when compared to healthy subjects, whereas serum cTnI levels in patients with right heart failure due to chronic obstructive pulmonary disease were not significantly different from those of control subjects (0.22 +/- 0.1 vs 0.16 +/- 0.1 ng/mL, p>0.05). In addition, creatine kinase MB band and myoglobin levels were not significantly different between patient and healthy groups. The mean of cTnI levels in ischemic and even nonischemic left heart failure were increased compared to the mean of values in healthy individuals but without significant creatine kinase MB band and myoglobin elevations. But cTnI levels were not increased in patients with right heart failure due to chronic obstructive pulmonary disease. These data indicate that the cTnI levels are abnormal in left heart failure but not in cor pulmonale.     

The role of angiotensin converting enzyme genotype in coronary artery ectasia

Coronary artery ectasia (CAE) is characterised by irregular, diffuse, saccular, or fusiform dilatation of the coronary arteries. Although the underlying mechanisms are not fully understood, CAE is considered to be an original form of vascular remodelling in response to atherosclerosis. However, it is not clear why some patients develop CAE while most do not. Experimental data suggest that activation of the renin angiotensin system may lead to an increased inflammatory response in the vessel wall or to an activation of matrix metalloproteinases. In addition, an insertion/deletion (ID) polymorphism of angiotensin converting enzyme (ACE) has been associated with coronary vascular tone and the development of aneurysms. Accordingly, we hypothesised that the gene polymorphism of ACE may be a potential factor influencing the genesis of CAE. We retrospectively evaluated 112 patients who underwent coronary angiography. ACE ID genotype was determined in two groups of patients. Group 1 consisted of 56 patients who were found to have CAE. Group 2 consisted of 56 patients with significant coronary artery disease (CAD) (> 50% stenosis in any of the major epicardial coronary arteries or their branches) but without any evidence of coronary ectasia. Polymerase Chain Reaction (PCR) was used to detect ACE genotype. The ratio of DD genotype was found to be greater in group 1 than group in 2 (39% versus 18%, respectively, P < 0.05). When assessed according to the presence of the I allele, it was greater was greater in group 2 than in group 1 (82.1% versus 60.7%, respectively, P < 0.05). The results indicate that an ACE DD genotype may be a risk factor for CAE.     

Evaluation of serum zonulin level in prediabetic patients

BackgroundThis study aimed to investigate the relationship between lipopolysaccharide (LPS) and zonulin levels and also to show the effect of acute hyperglycemic stress induced by oral glucose tolerance testing (OGTT) on zonulin levels in pre-diabetic patients.MethodsFour groups were constituted according to the criteria of the American Diabetes Association (ADA), based on OGTT results: control group (n:40); prediabetic group (n:56), divided into two subgroups: impaired fasting glucose group (IFG) (n:36), and impaired glucose tolerance (IGT) + IFG group (n:20) and type-2 diabetes mellitus (T2DM) group (n:45).ResultsZonulin and LPS did not significantly differ between the prediabetes and control groups, but were significantly higher in the T2DM group compared to both the prediabetic and the control group (P < 0.001). After OGTT, zonulin and LPS were significantly higher in the prediabetes group compared to the control group (P < 0.01 and P < 0.05, respectively), and significantly lower in the IFG and IFG + IGT groups compared to the T2DM group (P < 0.001, P < 0.001 and P < 0.001, P < 0.001, respectively). A positive correlation was detected between fasting zonulin and 2-hour zonulin (r = 0.727, P < 0.001) and between fasting LPS (r = 0.555, P < 0.001) and 2-hour LPS (r = 0.567, P < 0.001) in the prediabetic group. Increased zonulin and LPS levels and the positive correlation between these levels during the prediabetic period although non significant suggests onset of intestinal permeability.ConclusionsDuring acute hyperglycemia in prediabetic patients, up-regulation of zonulin and LPS may affect intestinal function. The intestines may play a key role in up-regulation of glucose and the pathogenesis of diabetes.