It has been reported that IFN-γ, TNF-α, and IL-12 stimulate, and that IL-10, TGF-β, and IL-4 suppress the protective immune response against tuberculosis. We aim to evaluate changes in the serum levels of pro and antiinflammatory cytokines in active pulmonary tuberculosis (APTB) and the possible effects of treatment on these changes. Serum IL-12p40, IL-4, IL-10, TNF-α, IFN-γ, and TGF-β1 levels were determined in 20 APTB cases (group 1) before and 2, 4, and 6 months after therapy. The same parameters were also determined in 9 inactive pulmonary tuberculosis (IPTB) cases (group 2) and 9 healthy controls (HC, group 3). Before treatment, the mean serum IFN-γ, TNF-α, and IL-10 levels in group 1 were statistically higher than those in group 2 (P = .001, P = .024, P = .016, resp) or group 3 (P = .003, P = .002, P = .011, resp). The levels in group 1 decreased significantly after treatment (P = .001 for IFN-γ, P = .004 for TNF-α, P = .000 for IL-10). The serum levels of IL-12p40 were significantly higher in group 1 than in group 3 (P = .012) and decreased insignificantly after treatment. There was no difference in serum IL-4 and TGF-β1 levels among the groups (P > .05). Because the serum IL-12p40, IL-10, TNF-α, and IFN-γ levels were high in APTB, we believe that these cytokines have important roles in the immune response to Mycobacterium tuberculosis (M tuberculosis). These parameters could be used in follow-up as indicators of the success of APTB therapy.
Background: Chronic obstructive pulmonary disease (COPD) is characterized by airflow obstruction caused by emphysema or airway narrowing, or both. Recently airway dimensions have been measured using high-resolution computed tomography (HRCT). To evaluate large and small airway dimensions by HRCT and compare them with pulmonary function tests in patients with COPD and in smokers with or without airflow obstruction. Methods: We used HRCT scanning to measure airway wall thickness at the segmental and sub-segmental levels in COPD patients (group II, stage II, n = 17, and group III, stage III, n = 5), healthy current smokers (group I, n = 10) and healthy non-smokers (group 0, n = 10). Results: FEV1 was lower in patients with severe or moderate COPD than in healthy current smokers and non-smokers. FEV1 was lower in group I than group 0 (p < 0.005). There was no statistically significant difference between patients with moderate COPD and severe COPD in the ratio of airway wall thickness to outer diameter (T/D ratio) or the percentage wall area (WA%). Both groups II and III had higher T/D ratios than group I (p < 0.01), and group I had a higher T/D ratio than group 0 (p < 0.001). Both groups II and III had higher WA% than group I (p < 0.01 and p < 0.05, respectively), and group I had a higher WA% than group 0 (p < 0.001). A negative correlation was found between airway wall thickness and FEV1. Conclusions: Computed tomography measurements of large and small airway dimensions are useful for evaluating lung function in patients with COPD and healthy current smokers. Airway wall thickening is inversely related to the degree of airflow obstruction and positively related to cumulative smoking history.
Airway structural changes that occur in patients with asthma in response to persistent inflammation are termed airway remodeling. The cysteinyl leukotrienes (LTC 4 , D 4 and E 4 ) are known to play important roles in the pathobiology of asthma. To evaluate the effect of low dose montelukast (MK) on the development of airway remodeling using a chronic murine model of allergic airway inflammation with subepithelial fibrosis, BALB/c mice, after intraperitoneal ovalbumin (OVA) sensitization on days 0 and 14, received intranasal OVA periodically on days 14-75. MK treated mice received montelukast sodium intraperitoneally on days 26-75. The OVA sensitized/challenged mice developed an extensive eosinophil cell inflammatory response, goblet cell hyperplasia, mucus occlusion, and smooth muscle hypertrophy of the airways. In addition, in OVA sensitized/challenged mice, dense collagen deposition/fibrosis was seen throughout the lung interstitium surrounding the airways, blood vessels, and alveolar septae. The cysteinyl leukotriene 1 (CysLT1) receptor antagonist, MK significantly reduced the airway eosinophil infiltration, goblet cell hyperplasia, mucus occlusion, and lung fibrosis except airway smooth muscle hypertrophy in the OVA sensitized/challenged mice. The OVA sensitized/challenged mice had significantly increased epithelial desquamation compared with control mice. MK markedly reduced epithelial desquamation of airways in OVA/MK treated animals compared with OVA sensitized/challenged mice. MK treatment did not affect the levels of CysLT in lung tissue. Our results show that the important role of cysteinyl leukotrienes in the pathogenesis of asthma. Lower dose of CysLT1 receptor antagonism has a significant anti-inflammatory effect on allergen-induced lung inflammation and fibrosis but not airway smooth muscle hypertrophy in an animal model of asthma.
The COVID-19-related death rate varies between countries and is affected by various risk factors. This multicenter registry study was designed to evaluate the mortality rate and the related risk factors in Turkey. We retrospectively evaluated 1500 adults with COVID-19 from 26 centers who were hospitalized between March 11 and July 31, 2020. In the study group, 1041 and 459 cases were diagnosed as definite and highly probable cases, respectively. There were 993 PCR-positive cases (66.2%). Among all cases, 1144 (76.3%) were diagnosed with non-severe pneumonia, whereas 212 (14.1%) had severe pneumonia. Death occurred in 67 patients, corresponding to a mortality rate of 4.5% (95% CI:3.5-5.6). The univariate analysis demonstrated that various factors, including male sex, age ≥65 years and the presence of dyspnea or confusion, malignity, chronic obstructive lung disease, interstitial lung disease, immunosuppressive conditions, severe pneumonia, multiorgan dysfunction, and sepsis, were positively associated with mortality. Favipiravir, hydroxychloroquine and azithromycin were not associated with survival. Following multivariate analysis, male sex, severe pneumonia, multiorgan dysfunction, malignancy, sepsis and interstitial lung diseases were found to be independent risk factors for mortality. Among the biomarkers, procalcitonin levels on the 3 rd -5 th days of admission showed the strongest associations with mortality (OR: 6.18; 1.6-23.93). This study demonstrated that the mortality rate in hospitalized patients in the early phase of the COVID-19 pandemic was a serious threat and that those patients with male sex, severe pneumonia, multiorgan dysfunction, malignancy, sepsis and interstitial lung diseases were at increased risk of mortality; therefore, such patients should be closely monitored.
Aim : This study aims to determine the prognostic value of the Glasgow Prognostic Score (GPS) and fibrinogen to albumin ratio (FAR) in patients with COVID-19. Methods : Electronic database records of 400 patients with COVID-19 were retrospectively analyzed and the initial levels of CRP, albumin, fibrinogen values were recorded. The ground-glass opacities (GGO) and consolidations were evaluated on thorax CT. Hospital mortality and the need for intensive care unit (ICU) transfer were determined as adverse outcomes. Results : It was determined that 345 patients (86.25%) were discharged while 31 patients (7.75%) were transferred to ICU in addition to 24 patients who died (6%). The rates of deaths and transfers to ICU were significantly increased in GPS 2 group compared to both GPS 0 and 1 groups. Additionally, increased FAR was observed in patients who died and transferred to ICU compared to the discharged patients. The FAR was significantly increased in patients with diffuse GGO. Logistic regression analysis indicated that FAR ≥144.59 and the presence of GPS 2 were independent predictors of the adverse outcomes in COVID-19 patients. Conclusion : Our results demonstrated that the GPS and FAR could possess a predictive value for adverse outcomes in patients with COVID-19.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.