Antibacterial Resistance in Lower Respiratory Tract Bacterial Pathogens: A Multicenter Analysis from Turkey.

INTRODUCTION: This study aimed to evaluate the etiology of lower respiratory tract infections (LRTIs) and their antibiotic resistance. METHODOLOGY: Bacterial culture results of LRT samples from 17 hospitals between 2016-2019 were included in the study. All isolates were identified and AST were performed by automated microbiology systems. AST was performed according to EUCAST. RESULTS: Non-duplicate 30,051 (26,890 HA and 3156 CA) isolates detected as causative pathogen. LRTIs are caused by 85.1% Gram-negative bacterial pathogens and 14.9% Gram-positive. The most common isolates among HA pathogens were Acinetobacter spp. (27.4%), P.aeruginosa (22.2%), K.pneumoniae (17.9%); among CA pathogen S.pneumoniae (19.9%), P. aeruginosa (18.9%), H.influenzae (14.6%). ESBL rate was 62.5% in K.penumoniae; 53.1% in E.coli; 19.1% in Klebsiella spp; 13.9% in Enterobacter spp.; 8.6% in Proteus spp.; 6.3% in Citrobacter spp.; and 4.3% in Serratia spp. Resistance rates to carbapenems and colistin were 92.8% and 12.8% in A baumannii, 39.8% and 7.5% in P.aeruginosa, 47.3% and 18.5% in K.penumoniae. Among staphylococci, 27.3% of S. aureus and 82.4% of CoNS were methicillin resistant. 7.6% of E.faecium and 0.9% of E.faecalis were vancomycin resistant.  Linezolid resistant S. aureus, CoNS, E.faecalis and E.faecium rates were 0.3%, 2.9%, 0.0% and 4.6%. Inducible clindamycin resistant rate was 17.2% in S. aureus 38.2% in CoNS. Non-susceptible S.pneumoniae isolate rate to penicillin was 37.0%. 6.5% of S.maltophilia and 4.4% of B.cepacia isolates were resistant to trimethoprim/sulfamethoxazole. CONCLUSIONS: Antibiotic resistance was mainly observed among A.baumannii and K.pneumoniae and continuous surveillance of antimicrobial resistance patterns in the management of LRTIs is important.

DNA repair gene XRCC1 polymorphisms and the risk of asthma in a Turkish population.

Polymorphisms have been identified in several DNA damage repair genes. These polymorphisms may effect DNA repair capacity and modulate asthma susceptibility. In this study, we aimed to determine the two polymorphisms in DNA repair gene, x-ray repair cross-complementing group 1 (XRCC1), in a sample of Turkish patients with asthma, and evaluate their association with asthma development. We used polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) to analyze XRCC1 Arg194Trp and XRCC1 Arg399Gln polymorphisms in 116 patients with asthma and in 180 disease-free controls. Our data showed a positive association between the polymorphisms of codons 194 (odds ratio [OR] = 1.97, 95% confidence interval [CI] = 1.06-3.66, and p = 0.03 for Arg/Trp genotype) and 399 (OR = 1.87, 95% CI = 1.12-3.13, and p = 0.02 for Arg/Gln genotype, and OR = 2.59, 95% CI = 1.24-5.43, and p = 0.01 for Gln/Gln genotype) and asthma risk. No statistically significant difference was found for the allelic and genotypic distributions of the polymorphisms in XRCC1 gene between mild and moderate asthmatic patients. A combined analysis of the effect of XRCC1 codons 194 and 399 revealed the highest risk (OR = 4.17, 95% CI = 1.77-9.83, and p = 0.001) for carriers of the polymorphic alleles in both of these codons. These results suggest that the risk of asthma may be associated with DNA repair mechanisms, and understanding these mechanisms will help identify individuals at increased risk of developing asthma and should lead to improved treatment of asthma.

The Ala allele at Val762Ala polymorphism in poly(ADP-ribose) polymerase-1 (PARP-1) gene is associated with a decreased risk of asthma in a Turkish population.

BACKGROUND AND OBJECTIVE: It has been suggested that inhibition of poly (ADP-ribose) polymerase-1 (PARP-1), either pharmacologically or by a gene knockout provides significant protection against systemic or tissue inflammation in animal models. The aim of this study was to analyze the association of the PARP-1 Val762Ala polymorphism, which has beenreported to be associated with decreased enzymatic activity, in Turkish patients with adult asthma. METHODS: A total of 112 subjects with stable asthma and 180 normal controls from the same geographic region were studied and polymerase chain reaction-based restriction analysis was used to identify Val762Ala polymorphism of the PARP-1. RESULTS: In univariate analysis, PARP-1 762 AA genotype conferred a 3.4 fold reduction in risk (OR = 0.297, 95% CI = 0.105-0.813; P = 0.014), while heterozygous VA genotype conferred an even greater level of protection (OR = 0.06; 95%CI, 0.026-0.14; P < 10(-6)). In addition, wild type PARP-1 762 V allele had 5 times the risk of developing asthma than those without the allele (OR 0.199, CI 0.118-0.334, P = 10(-6)). CONCLUSIONS: These findings suggest that PARP-1 V762A variants may be one of the factors participating in protection or susceptibility to asthma in our population.

FEF(25-75)/FVC measurements and extrathoracic airway obstruction in obstructive sleep apnea patients.

The aims of this study were to evaluate patients with obstructive sleep apnea syndrome (OSAS) with regards to dysanapsis (airway size relative to lung size) and to demonstrate the differences between the patients with and without extrathoracic airway obstruction. The study population consisted of 15 patients with OSAS and 14 age and body mass index (BMI) matched control subjects. OSAS patients and control subjects showed similar characteristics in FEV(1), FEV(1)/FVC, FEF(25-75), and FEF(25-75)/FVC ratios. Expiration reserve volume was significantly higher in the control group than in OSAS patients (p<0.01). Six patients exhibited extrathoracic airway obstruction while awake. Of these, three had also a sawtooth pattern in their flow-volume curves. The remaining nine patients had no extrathoracic airway obstruction and had lower apnea-hypopnea indexes (AHI) than the obstruction group (p<0.05). OSAS patients and age- and BMI-matched healthy controls had similar characteristics in terms of dysanapsis. In addition, there was no relation between the FEF(25-75)/FVC ratio and AHI, MinO(2), and MeanO(2). Extrathoracic airway obstruction may be a feature of only severe OSAS patients.

Cardiopulmonary responses to exercise in moderate-to-severe obstructive sleep apnea.

Information regarding the safety of maximal cardiopulmonary exercise testing (CPET) or the mechanisms of exercise limitation in obstructive sleep apnea (OSA) patients is fairly limited. In the present study, we addressed the problem of exercise capacity in moderate-to-severe OSA patients. Nineteen non-consecutive patients (three female, 16 male) with moderate-to-severe OSA and 11 age and body mass index matched control subjects (four female, seven male) underwent respiratory function tests during pre-exercise resting period and volitionally limited cardiopulmonary exercise testing on an electronically braked cycle ergometer. All participants completed CPET without any complication. Control subjects were exercise limited due to deconditioning. None of the patients revealed mechanical ventilatory limitation to exercise or had evidence of cardiac ischaemia. Five patients had no limitation to exercise. Six patients had low VO2peak, low anaerobic treshold (AT), and low peak O2 pulse, a pattern consistent with ventricular dysfunction. Six patients had low VO2peak, low AT, and peak heart rate less than 85% predicted. This pattern is consistent with exercise limitation due to peripheral vascular disease. Two patients had low VO2peak, low AT without peak oxygen pulse and peak heart rate abnormalities consistent with deconditioning. We concluded that moderate-to-severe OSA patients have impaired exercise capacity. Exercise limitation seems to originate from cardiovascular reasons namely left ventricular dysfunction and/or peripheral vascular impairment; and finally, maximal CPET can be tolerated by these patient group without serious complications.

Platelet function and fibrinolytic activity in patients with bronchial asthma.

Platelets have the capacity to release mediators with potent inflammatory or anaphylactic properties. Platelet factor-4 (PF4) and beta-thromboglobulin (BTG) are two of these mediators. On the other hand, plasminogen activator inhibitor-1 (PAI-1) and tissue plasminogen activator (tPA) are two important mediators of fibrinolysis. Both mediators are secreted mainly by vascular endothelium. Plasma levels of PF4, BTG, PAI-1, and tPA may show changes in chronic inflammatory diseases such as asthma. This study examined the role of thrombocytes and the function of the endothelium in asthmatic patients during an attack and during a stable phase. Eighteen patients with known allergic asthma who came to our emergency department with an asthma attack and 14 control subjects were included in the study. Blood samples were taken after starting therapy with salbutamol inhalation. Lung function tests were performed after receiving the first emergency therapy for asthma. Plasma levels of PF4, BTG, PAI-1, tPA were determined before starting steroid therapy and after receiving 1 week of steroid therapy. Plasma levels of PF4 among patients with an asthma attack were significantly higher than those of controls (150.5+/-8.92 IU/mL vs. 92.5+/-7.63 IU/mL, p<0.001). A further increase in plasma PF4 levels was detected after steroid therapy (163.5+/-9.16 IU/mL). Plasma BTG levels of patients on admission were not statistically different from those in the control group (140.4+/-6.34 IU/mL vs. 152.2+/-8.71 IU/mL). An increase was detected after therapy (171.6+/-7.27 IU/mL) and post-treatment plasma levels were statistically meaningful versus the controls. Plasma levels of tPA and PAI were statistically higher than those in controls in asthmatic patients on admission (6.01+/-2.72 vs. 5.4+/-2.3 ng/mL for tPA and 75.2+/-27.2 ng/mL vs. 32.7+/-14.3 ng/mL for PAI-1). Further increases were detected in two parameters after 1 week of therapy with steroids (tPA levels were 6.85+/-2.96 ng/mL and PAI-1 levels were 83.5+/-29.6 ng/mL). There seems to be an increased activity of platelets during an asthma attack. Elevated PAI-1 and tPA levels may also indicate the activated endothelium in asthma. Increases of plasma levels of PAI-1 and tPA after steroid therapy need further investigation because elevated PAI-1 levels enhance airway remodeling.

[One-year follow up results of Smoking Cessation Outpatient Clinic]. / Sigara Birakma Poliklinigimizin bir yillik izlem sonuçlari.

In this study we investigated the five-year-results of our smoking cessation outpatient clinic retrospectively. Out of 839 subjects admitted to our clinic during this time period 634 of them completed the one-year follow up period. 318 (50.2%) of these subjects were male and 316 (49.8%) of them were female. Subjects were divided into two groups. While one group received nicotine patch therapy, education and motivation the other group received just education and motivation. Mean age was 43.5 +/- 12 years. Nicotine patch therapy administered to 297 subjects and smoking cessation rates in this group were 46.8% at 15th day and 33.6% at the end of first year. The other group had smoking cessation rates of 11.8% at 15th day and 10.9% at the end of one year. Out of 185 subjects who did not smoke at the end of 15th day 98 of them were also not smoking at the end of one year. 449 subjects were smoking at the end of 15th day and just 26 (5.7%) of them gave up smoking at the end of first year. Therapy compliance was 82.2% at the 15th day and 23.2% at 12th week. Most frequent side effects were local skin reactions (13.8%) due to nicotine patches, irritability and nervousness (8.5%) and concentration difficulties (7.4%). In this retrospective analysis we concluded that nicotine replacement therapy in conjunction with education and motivation may be an effective method for helping individuals in giving up smoking. We also observed that smoking situation in first 15 days is a good predictor of long-term success.