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Background/aim: It is known that the correlation of pulmonary function tests (PFT) with muscle dysfunction is insufficient. Here, we aimed to evaluate the diaphragm functions in individuals with Friedreich's ataxia (FRDA) and to examine its relationship with respiratory parameters and disease severity. Materials and methods: This prospective study, conducted between November and December 2022, at Erciyes University, included 14 individuals with genetically confirmed FRDA and an age- and gender-matched healthy control group of eight individuals. We examined pulmonary functions with spirometric methods and evaluated diaphragm excursion, and diaphragm thickness-expiratory (Tde) and - end of inspiration (Tdi) with ultrasonography during calm breathing. Thickening fraction (TF) calculated. Also, we examined PaCO2 at rest. The neurological status of individuals was assessed using the Scale for the Assessment and Rating of Ataxia (SARA). Results: The mean values of FEV1(lt), FEV1(%), FVC (lt), and FVC (%) were higher in the control group (p; <0.001, 0.013, <0.001, and 0.009, respectively). Also, mean Tdi, Tde, excursion and TF were lower in the FRDA group compared to the control group (p = 0.005, 0.294,0.005, and 0.019, respectively). The mean excursion value was 1.13 ± 0.54cm in the FRDA group and 1.71 ± 0.49cm in the control group. There is a strong, negative, and statistically significant correlation between SARA total score with excursion and TF (r = -0.7432, p = 0.002; r = -0.697, p = 0.008). There is no statistically significant relationship between excursion and BMI, standing-to-supine decrease in FVC, FEV1, and PaCO2. Also, the relationship between maximal inspiratory pressure (PImax) and excursion was moderate. Conclusion: Diaphragm ultrasound may reveal respiratory dysfunction better than PFT. Diaphragm excursion and TF are associated with disease scores in individuals with FDRA. Further studies are needed regarding the detection of alveolar hypoventilation. [ABSTRACT FROM AUTHOR]

Background/aim: Sensitivity and symptoms related to animal proteins have been investigated in various occupational groups. However, data from horse farm workers are limited. We aimed to determine horse allergen sensitivity in the horse farm workers, and to evaluate its relationship with respiratory symptoms and functional parameters. Materials and methods: A total of 110 subjects were enrolled in the study. The study group consisted of 80 horse farm workers. Face-to-face surveys, skin prick tests (SPT), and pulmonary function tests (PFT) were performed in the study group. Control group consisted of 30 healthy subjects. SPT and PFTs were also performed for control group. The SPT test results of the horse farm workers were compared with the SPT results provided from the medical records of 1376 subjects who admitted to the outpatient clinic with respiratory symptoms. Results: Atopy rate was significantly higher in horse farm workers than in healthy subjects (41% and 13%, respectively; P = 0.008). Horse allergen sensitivity was positive 8/80 (10%) in horse farm workers, 0/30 in healthy subjects, and 32/1376 (2%) in medical records of subjects who were admitted to the outpatient clinic with respiratory symptoms. (P = 0.07, P = 0.001, respectively). There was no statistically significant relationship between respiratory symptoms and horse allergen sensitivity in horse farm workers (P = 0.67). However, mean FEV1 ratios were lower in horse farm workers with horse allergen sensitivity than healthy subjects (88.6% ± 17.9, 103.7 ± 10, P = 0.031, respectively). Conclusion: Atopy and animal allergen sensitization were significantly higher in horse farm workers, suggesting the relationship between the intensity of specific allergen exposure and the sensitization to this specific allergen. [ABSTRACT FROM AUTHOR]

Introduction: Why do only some of patients who are prescribed angiotensin converting enzyme inhibitors (ACE‐I) develop cough? The pathogenesis of ACE‐I‐induced cough remains controversial and requires further studies. Objective: We aim to investigate whether asthma is a contributing cause of ACE‐I‐induced cough. Methods: Patients attending a cardiology clinic between March 2016 and March 2017 who were diagnosed with ACE‐I induced cough were included in this study. ACE‐I‐induced cough was defined as cough which developed within 4 weeks after initiation of ACE‐I therapy and which improved within 4 weeks after discontinuation of the ACE‐I. Patients who had received ACE‐I treatment for at least 6 months without side effects were included in the study as a control group. Face‐to‐face questionnaires, pulmonary function tests (PFT) and skin prick tests were applied to all the patients. If there was discordance between asthma history and PFT results, a methacholine bronchial provocation test (BPT) was performed. Results: A total of 43 patients with ACE‐I induce cough were compared with 50 controls. Bronchial hyperreactivity (BHR), rhinitis, atopy and family history of asthma were more frequent in patients with ACE‐I induced cough (P <.001). Patients with ACE‐I‐induced cough had significantly higher incidence of diagnosed asthma [OR = 8.28 (95%CI: 3.26‐21.03) P <.001]. Conclusions: Asthma and an atopic background constitute a substantial risk factor for ACE‐I induced cough. The presence of underlying asthma should be investigated in patients diagnosed with ACE inhibitor induced cough. However, the fact that most asthma patients tolerate ACE‐I therapy, indicates that other cofactors are likely involved. [ABSTRACT FROM AUTHOR]

OBJECTIVES: Eosinophilic granulomatosis with poliangiitis (EGPA) which was previously called Churg-Strauss Syndrome, is classified into eosinophilic and vasculitic phases. To characterize the eosinophilic and vasculitic phases of the disease in terms of clinical findings, serology, and treatment. MATERIALS AND METHODS: We included 15 EGPA patients in the study. The clinical, serological, and therapeutic characteristics and the treatment responses of the patients were recorded. RESULTS: Thirteen patients were classified as being in the eosinophilic phase and two were classified as being in the vasculitic phase of EGPA. Initial symptoms were worsening asthma in all patients (n=15; 100%). All patients had rhinosinusitis, and 66.6% had hypersensitivity to nonsteroidal anti-inflammatory drugs. The two patients in the vasculitic phase did not have nasal polyposis. Pulmonary and nervous system involvement were the most common symptoms. The erythrocyte sedimentation rates (ESRs) of the two patients in the vasculitic phase were 65 mm/h and 55 mm/h, while ESR was normal in eosinophilic-phase patients. Antineutrophil cytoplasmic antibodies (ANCA) was detected in one patient (6.6%) who was in the vasculitic phase (Case 15). The disease was under control with higher doses of methylprednisolone in the vasculitic phase (Case 14: 12 mg/day, Case 15: 10 mg/day) than in the eosinophilic phase. Relapse was detected in the two patients in the vasculitic phase. Oral corticosteroid was not discontinued in any case, and no mortality was reported. CONCLUSION: Patients with eosinophilic phase or vasculitic phase EGPA had similar clinical onset. However, higher ESR, ANCA positivity, and extrapulmonary organ involvement were only found in patients in the vasculitic phase. Corticosteroid responsiveness was very good in all patients in the eosinophilic phase, and the disease could be controlled with a very low maintenance dose of a corticosteroid. [ABSTRACT FROM AUTHOR]

Gemcitabine is a nucleoside analog that has been increasingly used in the chemotherapy of solide tumors, including breast, pancreas ovary and non small cell lung cancer. It is generally well tolerated and has few side effects. Gemcitabine induced pulmonary complications range from mild dyspnea to death from ARDS. A 57- year- old man was treated with six cycles of gem­citabine because of pancreatic carcinoma in July, 2004.The patient had self limiting weakness, lack of appetite, nausea and no dyspnea in treatment period. One year later, he was admitted to a local hospital with exercises induced dyspnea. He had been given levofloxacin for 14 days. On admission to our hospital, his complaint kept on. A few inspiratory crackles were present at right base. CXR demonstrated interstitial infiltrations in the right lung lower zone. HRCT showed grand glass opacity and mild reticular patterns in right lung middle and lower lobes. Bronchoscopy was performed. Transbronchial biopsy revealed nonspecific interstitial pneumonia. Following the administration of oral corticosteroid, he had complete resolution of all signs and symptoms of gemcitabine toxicity. [ABSTRACT FROM AUTHOR]