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)

The hypersensitivity reactions induced by drugs, some widely used, like central nervous system medication, can have various presentations. The lung is a frequent target for such events. We present the case of 40-year-old male patient, non-smoker, with infant encephalopaty, seizures since age of 6 with polimorphic crisis (mainly absences), with anticonvulsivant treatment since 2011 (carbamazepine, sodium valproate, levetiracetam), with no respiratory medical history. Current symptoms started two weeks before, with chest pain, dry cough. He received no antibiotics. Chest X-ray and thoracic CT scan (27 June 2013) showed a left pleral effusion. Left exploratory thoracocentesis extracted 20 ml reddish pleural fluid: eosinophilic exsudate (60%) with normal adenosin deaminase. He also presents moderate blood eosinophilia (13.7%-1780/mm3). Pulmonary infarction with secondary pleurisy, thoracic trauma, acute pancreatitis with secondary pleurisy were excluded. No Loeffler transient infiltrates were documented, serology for Toxocara is IgG positive (historical) and not significant for current episode, no symptoms suggestive for toxocarosis (characteristic to young children, patient had no liver enlargement etc.), no hidatidosis or trichinelosis were found. As an exclusion diagnosis, a hypersensitivity reaction to anticonvulsivant medication was considered (mentioned in literature) carbamazepine and sodium valproate (even if medication was taken for a longer time), with blood and pleural eosinophilia. Together with the neurologist, the mentioned drugs were stopped and he was started on lamotrigine 2 tb/day and levetiracetam 1 tb/day, well tolerated, no absences were noticed. Total remission of blood eosinophilia and partial remission of pleural effusion were noticed. Subsequent follow-ups confirm favourable evolution, with healing of pleurisy and normal blood cell count, which are stable at 7 months after changing anticonvulsivant treatment.
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PMID:[Drug induced eosinophilic pleural effusion]. 2524 60

We reported a 9-year-old boy with mycoplasma pneumonia who developed pulmonary infarction. The child first had fever and cough, and then had difficult breathing. But, the signs of his lung were not obvious. Mycoplasma antibody IgM was positive. The child was given intravenous azithromycin for anti-infection, and intravenous low molecular weight heparin and oral warfarin for anti-coagulation. Although difficult breathing was relieved, sudden cardiac arrest occurred. His parents requested to give up treatment.
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PMID:Mycoplasma pneumonia combined with pulmonary infarction in a child. 2578 59

Radiological findings of pulmonary infarction have been well characterized mainly in established infarction. However, the early course CT appearance of patients who develop pulmonary infarction has not yet been fully elucidated. A 50-year-old female with a history of postmenopausal hormone replacement therapy (HRT) presented with dry cough and high-resolution computed tomography (HRCT) findings of fan-shaped segmental ground-glass opacity (GGO) in the right lower lobe. As the parenchymal density in the GGO gradually enlarged over a period of 4 weeks in spite of antibiotic treatment, the patient was referred to our hospital on clinical suspicion of bronchioloalveolar cell carcinoma. However, the pathological findings of a transbronchial biopsy of the lesion were compatible with pulmonary infarction. After an endoscopic examination, the typical CT appearance of established pulmonary infarction was observed. Moreover, enhanced CT detected an intraluminal filling defect in the right lower lobe artery suggesting peripheral pulmonary emboli. Our case was a peripheral pulmonary infarction probably induced by HRT, and suggested that fan-shaped GGO may be a premonitory sign of pulmonary infarction.
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PMID:Fan-shaped ground-glass opacity (GGO) as a premonitory sign of pulmonary infarction: a case report. 2960 Jan 5

Cocaine can be responsible for many psychiatric and/or somatic disorders. The aim of this systematic literature review of data was to expose relations between cocaine use and pulmonary complications. Cocaine can be responsible for acute respiratory symptoms (cough, black sputum, hemoptysis, dyspnea, wheezing, chest pain) and for various pulmonary disorders including barotrauma (pneumothorax, pneumomediastinum, subcutaneous emphysema, pneumopericardium), airway damage, asthma, bronchiolitis obliterans with organizing pneumonia, acute pulmonary edema, alveolar hemorrhage, alveolar pneumonia with carbonaceous material, bullous emphysema, acute eosinophilic pneumonia, pulmonary granulomatosis caused by talc or cellulose, interstitial pneumonitis and pulmonary fibrosis, vasculitis, pulmonary hypertension, pulmonary embolism and pulmonary infarction, mycotic pulmonary arterial aneurysms, septic emboli, aspiration pneumonia, community-acquired pneumonia, HIV-related opportunistic infections, latent tuberculosis infection, pulmonary tuberculosis, lung cancer and crack lung. Some of these complications are serious and may have a fatal outcome. Pulmonary function tests, thoracic tomodensitometry, bronchial fibroscopy with bronchoalveolar lavage and lung scintigraphy may be an aid to the diagnosis of these pulmonary compications. Cocaine use must be sought in case of respiratory symptoms in young persons.
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PMID:[Pulmonary complications in cocaine users]. 3188 17

We report on a 51 years old woman patients with pulmonary artery intimal sarcoma, whose first symptoms was paroxysmal cough without obvious cause, and with left chest pain. It is misdiagnosed as Pleural effusion, cryptogenic organizing pneumonia and pulmonary artery embolism with pulmonary infarction successively. After pulmonary artery endarterectomy and tumor biopsy, histopathology revealed right pulmonary artery intimal sarcoma. And then she was treated by radiotherapy and chemotherapy, and died 32 months after operation.
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PMID:Idiopathic intimal sarcoma of the pulmonary artery: report of a case. 3196 39


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