Obstructive sleep apnea syndrome (OSAS) is an independent risk factor for the development of cardiovascular events and hypertension. Mean platelet volume (MPV), an indicator of platelet activation and aggregation, is closely related with cardiovascular diseases (CVDs). We aimed to show the relationship between OSAS and MPV with CVD. The medical records of 205 patients who were admitted to the sleep study were evaluated. OSAS was diagnosed by polysomnography if the apnea-hypopnea index (AHI) was greater than 5. MPV was calculated from blood samples. According to AHI, individuals in whom AHI was less than 5 were recruited as the control group, those in whom AHI was 5-15 as the mild OSAS group, those in whom AHI was equal to 15-30 as the moderate OSAS group, and those in whom AHI was greater than 30 as the severe OSAS group. Of the patients, 137 (67%) were men and 68 (33%) were women; the mean age was 53.0±14.1 years. There were 35 (17%), 20 (10.2%), 42 (20.4%), and 108 (52.6%) participants in groups 1, 2, 3, and 4, respectively. There were significant differences in terms of coronary artery disease and hypertension between all groups (P<0.05). There was a significant association between the severity of OSAS and MPV in groups 3 and 4, whereas there was not any association in groups 1 and 2 (group 1=9.3±0.7, group 2=9.4±0.8, group 3=9.5±1.1, group 4=10.2±1.2; P for trend 0.03). We showed that MPV was significantly increased in patients with OSAS, which is an independent risk factor for CVD. Therefore, MPV could be used as a marker to predict CVD in OSAS.
Background: Bronchiolitis obliterans organizing pneumonia (BOOP) may be classified as cryptogenic (idiopathic) and secondary. There are no clear clinical and radiological features distinguishing between idiopathic and secondary BOOP. Objectives: To analyze the etiologic factors, clinical and radiological features, diagnostic approach and response to therapy at onset and outcome in subjects with BOOP. Methods: The medical files of Erciyes University Hospital from 1995 to 2003 were retrospectively reviewed. Patients with biopsy-proven BOOP were selected for evaluation. The etiology and initial features of BOOP, treatment, resolution, relapse, and survival were obtained from medical records, and a follow-up patient questionnaire. Results: We have diagnosed 26 cases (13 males /13 females) with BOOP syndrome (mean age 54 ± 15 years, range 14–93). More than half the patients (58%) were classified as idiopathic BOOP. Patients presented with cough (92%), dyspnea (70%), pleuritic chest pain, hemoptysis and fever (50%). The biopsy specimens had been obtained by transbronchial and/or transthoracic lung biopsy in 18 cases (69%). At radiological evaluation, there were bilateral patchy alveolar and/or interstitial infiltrates in 16 patients (62%), and solitary pneumonic involvement in 10 patients (38%). Three patients recovered spontaneously, 5 remained cured after resection of the focal lesion. Corticosteroid therapy was given in 17 patients (65%). Apart from four patients who died (death was attributable to BOOP in only 1 patient) and three patients who relapsed, the prognosis was good in all patients. Conclusions: The etiology of BOOP is usually idiopathic. We observed that hemoptysis and pleuritic chest pain were a relatively frequent symptom in BOOP in the present series, in contrast to previous observations. The diversity of radiological and clinical presentations including hemotysis and pleuritic chest pain should prompt consideration of the diagnosis in patients with persisting pulmonary symptoms and radiological findings.
In the light of the present study, we speculate that OSAS is an independent risk factor for the progression of chronic kidney disease, which is a growing health problem. Further randomized-multicenter prospective studies are warranted to evaluate this relationship.
Background. Proinflammatory cytokines are prime candidates as causative agents of the metabolic changes that eventually result in tuberculosis-associated weight loss. Microbial products and cytokines such as TNF and IL-1 increase leptin expression dose dependently in adipose tissue. Leptin plays an important role in cellular immunity. Objectives. In this study, we investigated serum leptin and TNF-α levels before and after antituberculosis therapy in patients with active pulmonary tuberculosis (TB). Methods. Twenty five in patients with active pulmonary TB and 18 healthy controls participated in the study. Leptin and TNF-α levels were measured before treatment and six months after the treatment and they were compared with the control group. Body mass index (BMI) and chest X-rays before and after the treatment were also evaluated. Results. The leptin levels before and after the treatment were 1.66±1.68 ng/mL and 3.26±3.81 ng/mL, respectively. The leptin levels of tuberculous patients were significant than in healthy patients (P < .05). The BMI was 19.36 ± 2.55 kg/m2 before the treatment and 22.87 ± 3.13 kg/m2 after the treatment. The TNF-α level was 23.19±12.78 pg/mL before the treatment and 15.95±6.58 pg/mL after the treatment. There was no correlation between leptin and TNF-α levels. Leptin levels were low in patients who had sequela lesion on chest radiographs. Conclusion. Leptin levels are suppressed in tuberculous patients and low leptin levels may contribute to increased susceptibility to infection and recovery with sequela lesions.
Among the several different asthma phenotypes, eosinophilic inflammation occurs in more than 50% of patients with either atopic or nonatopic asthma. High eosinophil counts, in both peripheral blood and the airways, are associated with recurrent disease exacerbations and severe airflow limitation [6]. Adultonset eosinophilic asthma is increasingly recognized as one of the most severe asthma phenotypes [7-10]. Another characteristic feature of adult-onset eosinophilic asthma is comorbid chronic rhinosinusitis with nasal polyps (CRSwNP), a feature known for many years and, in some cases, linked with aspirin and other nonsteroidal antiinflammatory drug hypersensitivities [11-13]. Concern regarding nonallergic, severe eosinophilic asthma and its associated comorbidities has increased Background/aim: Oral corticosteroid (OCS)-dependent severe eosinophilic asthma with chronic rhinosinusitis with nasal polyps (SEA-CRSwNP) would be a suitable phenotype for mepolizumab treatment. This study evaluated the short-term efficacy of mepolizumab treatment in OCS-dependent SEA-CRSwNP. Materials and methods: Baseline and 24th week results [daily OCS doses, asthma exacerbation frequency, asthma control test (ACT) scores, blood eosinophil levels, FEV 1 values, and numerical analog scale (NAS) of CRSwNP symptoms] of patients who were treated for at least 24 weeks with mepolizumab were retrospectively evaluated and compared. Results: A total of 16 patients were enrolled in the study. Mepolizumab was discontinued in one patient due to side effects. The daily OCS dosage was reduced from baseline in all patients, and at week 24 OCS was discontinued in 40% of the patients (baseline mean steroid dose: 9.2 ± 5.2 mg, 24th week: 1.3 ± 1.4 mg; P < 0.001). The number of asthma exacerbations within 24 weeks significantly decreased after beginning mepolizumab treatment (2.1 ± 2.7 vs. 0.07 ± 0.26; P = 0.012), and a significant increase in ACT scores (baseline mean ACT: 18 ± 5.7; 24th week mean ACT: 23.3 ± 3; P = 0.006) was observed despite the decrease in daily OCS dosages. There was no significant difference in FEV 1 values between baseline and week 24. Evaluation of the general symptoms of CRSwNP, as per NAS, revealed that the baseline mean NAS was 5.6 ± 4.4, and the 24th week mean NAS was 3.2 ± 3.2 (P = 0.021). Conclusion: This is the first real-life study evaluating the short-term efficacy of mepolizumab treatment on OCS-dependent SEA-CRSwNP. This study demonstrates that mepolizumab is an effective and safe biologic for the treatment of this severe asthma subphenotype.
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