Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diffuse Interstitial Pneumonia (PID) is probably, although rarely, a complication of Amiodarone therapy. We describe two new cases and review 19 from the recent literature. The first patient was a man treated solely with Amiodarone for three years (total dose 185 g). He presented clinically with a picture of PID with slight dyspnoea, weight loss of 4 kilos and a dry cough. There were pulmonary crackles on auscultation, diffuse reticulo-nodular shadows radiographically and compatible pulmonary function tests. Broncho-alveolar lavage (LBA) was lymphocytic (30%). Stopping Amiodarone without resorting to steroids led to the disappearance of the clinical signs within 15 days and the return to normal of the LBA and pulmonary radiograph within six months though the pulmonary function was unchanged. The second case was a 78 year old man treatment with Amiodarone for six months (total dose 20 g). He presents acutely with grade IV dyspnoea and low grade fever. There were pulmonary crackles on auscultation and a bilateral pulmonary infiltrate on the chest radiograph. The pulmonary function tests were compatible with PID showing a restrictive ventilatory defect, a reduced Carbon Monoxide transfer (single breath) and hypoxia. The diagnosis was confirmed by a transbronchial biopsy showing a parieto-alveolar infiltration with increased cellularity and collagen formation. The LBA was predominantly polymorphonuclear. Stopping the Amiodarone associated with steroid treatment produced a normal chest radiograph within six weeks, whilst moderate dyspnoea and less severe restrictive ventilatory defects persisted. The clinical, radiological, functional and histological features of our patients were comparable to those 19 cases reported in the literature.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Amiodarone: a new etiology of diffuse interstitial pneumopathy? Apropos of 2 personal cases and 10 cases from the literature]. 646 49

Nine young calves given respiratory syncytial virus by a combined intranasal and intratracheal route developed a severe respiratory tract disease in which coughing, tachypnea, and hyperpnea were prominent clinical features. Calves were euthanatized on postinoculation (initial) days (PID) 1 to 13. At necropsy, large areas of consolidation were present in the cranial, middle, accessory, and cranial parts of the caudal lung lobes of calves killed between PID 4 and 13. Histopathologic examination revealed widespread and severe lesions in small bronchi, bronchioli, and alveoli. Multinucleate epithelial syncytia on bronchiolar and alveolar walls, many containing eosinophilic intracytoplasmic inclusion bodies, were present in the lungs of calves killed on PID 4, 5, and 6. Necrosis and epithelial loss, hyperplasia, and metaplasia were also observed in the epithelium of small bronchi and bronchioli. The lumina of these airways were occluded to varying degrees with exudate. Exudate was present within alveoli, and interalveolar septa were markedly thickened. Collapse of the thickened septa produced large areas where alveolar air spaces were totally obliterated. Repair was evident in the lungs of calves killed at PID 10 and 13 with reepithelialization of damaged bronchiolar mucosa, organization of bronchiolar exudate leading to bronchiolitis obliterans, and peribronchial and peribronchiolar fibrosis. Inoculation of 3 calves by an intranasal route alone produced a less severe clinical disease with only minimal lesions present at necropsy.
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PMID:Respiratory syncytial virus pneumonia in young calves: clinical and pathologic findings. 662 18

The purpose of this study was to investigate for the change in cough reflex sensitivity (CRS) caused by parainfluenza virus type 3 (PIV3) infection. Guinea pigs were randomized into a vehicle control, an asthma control, or 1 of 4 PIV3-inoculated groups (referred to as postinfection day [PID] 6, 12, 28, and 42 groups). Evidence of viral protein and nucleic acid within the lung confirmed successful PIV3 infection. Plethysmography was used to assess CRS and airway reaction and airway inflammation was assessed via bronchoalveolar lavage fluid cytology and lung histopathology. Compared with the vehicle control group, CRS was significantly increased in all PID groups (P <.05) in concert with an obvious airway hyperresponsiveness in the PID 6 group. Though a small increase in CRS in the asthma control group was noted, it was not significant compared to the vehicle control group. Total cell counts from the bronchoalveolar lavage fluid of all PIV3-inoculated groups increased markedly and the number of lymphocytes was significantly increased in the PID 6 and PID 12 groups. The lung pathology of PIV3-inoculated animals showed airway inflammation without pneumonia in the acute infectious phase. The temporal and spatial variation of CRS may be the essential mechanism of cough caused by PIV3.
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PMID:Cough reflex sensitivity is increased in guinea pigs with parainfluenza virus infection. 2141 16

Interstitial lung disease (ILD) is becoming one of the main causes of death of patients with systemic sclerosis (SSc). The prevalence of ILD associated with SSc (SSc-ILD) varies from 33% to 100% according to diagnostic methods. Clinical features such as dyspnea on exertion, dry cough, and chest pains are not specific and usually late-appearing, implying more specific tests in the diagnostic, prognosis, and follow-up of ILD in patients with SSc. High resolution thoracic CT scanner (HRCT) is more sensitive than chest X-ray in the detection of SSc-ILD. Pulmonary function tests (PFT) are non-invasive and periodically used to assess the impacts of SSc on respiratory function. Diagnostic values of bronchoalveolar lavage and histological examination on lung biopsy are controversial. However, these techniques are essential for studying cellular and molecular mechanisms underlying the pathophysiology of SSc-ILD. Several biomarkers such as surfactant-A (SP-A), -D (SP-D), mucin-like high molecular weight glycoprotein (KL-6), and chemokine CCL-18 have been implicated in SSc-PID. Serum levels of these proteins are correlated with the severity of SSc-ILD, as assessed by HRCT and/or PFT. Finally, alveolar concentration of exhaled nitric oxide can be used to screen SSc patients with high risk of deterioration of respiratory function, in whom immunosuppressant treatment could be useful in preventing the evolution to irreversible lung fibrosis.
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PMID:[Use of pulmonary function tests and biomarkers studies to diagnose and follow-up interstitial lung disease in systemic sclerosis]. 2545 18