Background:Chronic obstructive pulmonary disease (COPD) is one of the most important causes of disability and mortality in the world. Although cigarette smoking and environmental pollutants have been recognized as the major causes of COPD, the role of infection in the pathogenesis and progression of COPD has also been reported.Objectives:The aim of the present study was to find the relationship between Helicobacter Pylori infection and COPD through anti H. pylori IgG serology, real time PCR of bronchoalveolar lavage and trans bronchial biopsy urease tests.Patients and Methods:This descriptive cross-sectional study was carried out on 60 adults with COPD. After obtaining the patient’s history, physical examination, spirometry and confirmation of COPD diagnosis by pulmonologist, subjects were selected through convenience sampling. In order to determine the severity and prognosis of disease, the global initiative for chronic obstructive lung disease (GOLD) criteria and BODE index were used. Subjects underwent bronchoscopy for obtaining bronchoalveolar lavage (BAL) samples and biopsy was performed. Biopsy and BAL samples were investigated respectively by urease test and real time PCR. Moreover, patients’ serum samples were serologically studied for detection of anti H. pylori IgG.Results:Mean age of the participants was 60.65 ± 9.15 years, and 25% were female and 75% were male. The prevalence rate of H. pylori in COPD patients was 10% according to real time PCR, 88.3% according to the serology test and 0% based on the urease test. According to the results of PCR and considering the severity of disease based on the GOLD criteria, from those with a positive PCR, one patient (16.6%) had very severe obstruction, three (50%) had severe obstruction and two patients (33.3%) had moderate obstruction. The relationship between H. pylori presence (based on PCR) and disease severity and prognosis was not statistically significant.Conclusions:These findings can justify the hypothesis of direct injury and chronic inflammation via inhalation and aspiration resulting in H. pylori colonization. In fact, it is thought that H. Pylori infection, beside the host genetic vulnerability and other environmental risk factors might make the patient susceptible to COPD or lead to COPD worsening. Although we found H. pylori infection in some patients with COPD, the results of this study, could not explain the pathogenic mechanisms of COPD.

BackgroundLung cancer is one of the most common causes of death worldwide. Although smoking and environmental pollutants are the most important risk factors of lung cancer, the role of infectious causes should also be considered in the pathogenesis and progress of lung cancer.ObjectivesThis study examined the relationship between Helicobacter pylori and lung cancer through serology, real-time PCR, and urease tests.MethodsThis descriptive cross-sectional study was conducted on 52 adult patients with lung cancer who were selected after having their history taken and being physically examined by a pulmonologist. Then, the patients underwent a bronchoscopy, a BAL, and biopsy sampling. A urease test was run for each biopsy sample, real-time PCR was used for each BAL sample, and H. pylori serology was used for each patient’s serum.ResultsThe patients’ average age was 60.65 ± 9.15 years; 11.5% were female and 88.5% were male. The prevalence of H. pylori in lung cancer patients was 11.5% according to the BAL PCR test, 92.3% according to the serology test, and 3.8% according to the urease test.ConclusionsThe results demonstrated an association between of lung cancer and H. Pylori infection via the hypothesis of direct damage and chronic inflammation through inhalation and aspiration and the systematic immune response induced by H. pylori colonization. Helicobacter pylori, together with a host’s genetic predisposition and other environmental risk factors, could be attributed to the induction of lung cancer.

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Background: COVID-19 is an infectious disease caused by SARS-CoV-2 and can lead to acute respiratory distress. Objective: We aimed to investigate the association between COVID-19 severity and serum apelin-17 and inflammatory mediator levels. Method: This cross-sectional study was conducted on patients with COVID-19. COVID-19 infection was confirmed by the RT-PCR test. The patients' data were extracted from their records. Venous blood samples were obtained from the patients to investigate the serum levels of apelin-17 and inflammatory mediators. Results: Results: Eighty-six COVID-19 patients were studied. The mean age of the participants was 55.56±14.88, and 43 (50%) were male. Clinical symptoms were dyspnea 77.6%, fever 52.3%, cough 48.8%, gastrointestinal symptoms 15.1%, and chest pain 7%. The overall mortality rate was 7%. No significant relationship was found between serum apelin-17 levels and COVID-19 severity (P= 0.48). However, there was a significant and direct relationship between COVID-19 severity and serum levels of CRP (P= 0.038) and D-dimer (P= 0.029). Conclusion: Serum apelin-17 levels were higher in recovered patients than those who died (4.90 vs. 3.19). Moreover, serum apelin-17 levels were higher in the patients admitted to the general ward than those admitted to the ICU (5.15 vs. 3.98). The difference was not statistically significant. However, there was a significant and direct relationship between serum apelin-17 levels and lymphocyte count (P= 0.022). Moreover, there was a significant and inverse relationship between lymphocyte count and COVID-19 severity (P= 0.004). Therefore, it can be interpreted that COVID-19 severity may decrease with an increase in serum apelin-17 levels. Therefore, to prove this hypothesis, a study with larger sample size is recommended.

Introduction: Bronchial asthma is a chronic disorder with high prevalence among women. Visfatin as a pro-inflammatory adipokine has been linked to inflammatory lung diseases such as asthma and can be used as a forthcoming biomarker target to diagnose and treat asthmatic patients. background: Bronchial asthma is a chronic disorder with high prevalence among women. Visfatin as a pro-inflammatory adipokine has been linked to inflammatory lung diseases such as asthma and can be used as a forthcoming biomarker target to diagnose and treat asthmatic patients. Aim: The aim of this study is to evaluate plasma visfatin level and its correlation with pulmonary function of female asthmatic patients. objective: To evaluate plasma visfatin level and its correlation with pulmonary function of female asthmatic patients. Methods: This cross-sectional study was conducted on all female asthmatic patients referred to the Be'sat Pulmonary Clinic of Kerman from 1 November 2019 to 20 February 2020. Patients with confirmed diagnosis of asthma were included. The data were collected through a checklist and the corresponding author conducted all face-to-face interviews in the physician’s office of the pulmonary clinic. Then, blood samples (5 cc) were taken from the patients to determine the plasma level of visfatin. Data was analyzed by SPSS Software. Results: 113 women with asthma were studied. The mean ± SD age of patients was 46.71 ± 13.91 years (range: 13 to 75). The mean ± SD of visfatin plasma levels was 26.30 ± 6.98 mg/dl (range: 8.50 to 46.88). The forced expiratory volume in the first second (FEV1) had a significant and negative correlation with plasma visfatin concentrations (P-value=0.03). method: This cross-sectional study was conducted on all female asthmatic patients referred to the Be''sat Pulmonary Clinic of Kerman from 1 November 2019 to 20 February 2020. Patients with confirmed diagnosis of asthma were included. The data were collected through a checklist and the corresponding author conducted all face-to-face interviews in the physician’s office of the pulmonary clinic. Then, blood samples (5 cc) were taken from the patients to determine the plasma level of visfatin. Data was analyzed by SPSS Software. Conclusion: The results of this study indicated that plasma visfatin levels were correlated inversely with FEV1 among asthmatic women. Further studies with large samples are recommended to evaluate the role of visfatin in asthma pathogenesis. result: 113 women with asthma were studied. The mean ± SD age of patients was 46.71 ± 13.91 years (range: 13 to 75). The mean ± SD of visfatin plasma levels was 26.30 ± 6.98 mg/dl (range: 8.50 to 46.88). The forced expiratory volume in the first second (FEV1) had a significant and negative correlation with plasma visfatin concentrations (P-value=0.03). conclusion: The results of this study indicated that plasma visfatin levels were correlated inversely with FEV1 among the asthmatic women. Further studies with large samples are recommended to evaluate the role of visfatin in asthma pathogenesis. other: -