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

The field of application for fibreoptic bronchoscopy (FB) in the intensive care unit has been extended since the generalised introduction of fibroscopes of 4.9 mm in diameter (previously called paediatric fibroscopes). Paediatric and neonatal intensive care units have benefited from the availability in the market of these small endoscopes for 3.5 and 2.2 mm. The protected brush and alveolar lavage (LBA) enables a specific diagnosis to be made in bacterial pneumonia acquired during ventilation. The sensitivity of these techniques however is insufficient to be able to recommend their use as routine. Inversely, the FB with LBA remains a fundamental feature in the diagnosis of opportunistic infections in pneumonia. For the treatment of atelectasis, FB is overall not superior to physiotherapy. Aspiration with a fibroscope can however be recommended straight away in cases of alteration in blood gasses if cough is ineffective or if the atelectasis complicates endobronchial bleeding. The FB enables problems with difficult intubation to be resolved or for the positioning of probes. The conditions under which this is performed are more delicate than in routine anaesthesia (in cases of urgency, hypoxia). In the case of respiratory burns, tracheobronchial fracture and post intubation stenosis, FB enables both the diagnosis to be established and the level at which the lesion occurs. In paediatric intensive care, a fibroscope of 3.5 mm is used for performing LBA (opportunistic pneumonias), difficult intubation (facial dysmorphia), endoscopic diagnoses, in particular where there is a suspicion of an endobronchial foreign body, the assessment of unexplained dyspnoea (tracheal stenosis by vascular ring) and obstructive lesions. In neonatal intensive care, a fibroscope of 2.2 mm is used for difficult intubation and the localisation of lesions induced by ventilation.
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PMID:[Fibroscopic bronchoscopy in intensive care]. 949 16

Temozolomide (TMZ) is a cytotoxic agent of the imidazotetrazine class, chemically related to dacarbazine. Its use poses higher risks of lymphopenia and opportunistic infections. Prophylaxis for Pneumocystis jiroveci must be considered up to 12 months after treatment discontinuation. The due literature (MEDLINE) makes no mention of a possible connection between the use of TMZ and tuberculosis (TB). A female patient, aged 59, featuring glioblastoma multiforme and having undergone solely a brain biopsy, was submitted to TMZ along with radiotherapy. After the first TMZ maintenance cycle, the referred patient was admitted displaying a background of a 40-day afternoon fever and productive coughing. She was thus submitted to a bronchoscopy and LBA, which resulted BAAR 1+/4+. TMZ was then suspended, and rifampicin, isoniazid, and pyrazinamide introduced. Considerations on prophylaxis with isoniazide in cancer patients are long-lived and scarce. Some subgroups are likely to benefit from the prophylactic administration of isoniazide during TMZ treatment, such as those patients under high doses of corticoids, patients with past medical history of TB, the malnourished, patients from endemic regions, and patients with highly reactive tuberculinic tests. That, nevertheless, must not restrict the administration of TMZ, but, rather, stand for a warning about its possible toxicity, and thus mitigate complications.
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PMID:Tuberculosis in a patient on temozolomide: a case report. 1897 31

Amyopathic dermatomyositis (ADM) is a clinical subtype of dermatomyositis, characterized by the absence of motor weakness and the presence of normal muscle enzyme levels. ADM is sometimes accompanied by neoplasm or interstitial pneumonia that shows a rapid progressive course both of them are associated with a poor prognosis. A 56-year-old woman with no medical history was referred to the department of medicine because of arthralgia with a remarkable weight loss. She also complained of rapidly progressive dyspnea, cough and photosensitivity. Physical examination on admission showed scaly erythema on the dorsum of the hands (Gottron sign) and periorbital edema with a purplish appearance (heliotropic rash), arthritis, but no muscle weakness. Auscultation of the chest identified audible fine crackles on the lower aspects of both lungs. Results of laboratory findings on admission revealed a lymphopenia. The serum creatine kinase and serum lactate dehydrogenase concentration were normal. IRM muscle and electromyography were normal. Antinuclear antibody was positive 1:80 and anti-Jo-1 antibody and other autoantibodies to specific antigens were all negative. High resolution computed tomographic chest scans also revealed diffuse ground-glass opacities in both lungs with basilar predominance. Arterial blood gas analysis revealed hypoxia and hypocapnia. LBA was not performed because of the deterioration of respiratory symptoms. There was no neoplasm associated. The diagnosis of ADM complicated with ADM rapidly progressive interstitial pneumonia was made. Despite of IV methylprednisolone pulse therapy (1g*day-1 for 3 days) and cyclophosphamide, she died by respiratory failure.
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PMID:[Interstitial pneumonia complicating amyopathic dermatomyositis: a case report]. 1999 56