Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019079 (hemoptysis)
 6,129 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infection of the central nervous system with Nocardia sp. usually manifests as supratentorial abscesses. Supratentorial and cerebellar abscesses from infection with Nocardia sp. following immunosuppression with long-term corticosteroids for idiopathic thrombocytopenia (ITP) have not been reported. An 83 years-old, human immunodeficiency virus (HIV)-negative, polymorbid male with ITP for which he required corticosteroids since age 53 years developed tiredness, dyspnoea, hemoptysis, abdominal pain, and progressive gait disturbance. Imaging studies of the lung revealed an enhancing tumour in the right upper lobe with central and peripheral necrosis, multiple irregularly contoured hyperdensities over both lungs, and right-sided pleural effusions. Sputum culture grew Nocardia sp. Neurological diagnostic work-up revealed dysarthria, dysphagia, ptosis, hypoacusis, tremor, dysdiadochokinesia, proximal weakness of the lower limbs, diffuse wasting, and stocking-type sensory disturbances. The neurological deficits were attributed to an abscess in the upper cerebellar vermis, myopathy from corticosteroids, and polyneuropathy. Meropenem for 37 days and trimethoprime-sulfamethoxazole for 3 months resulted in a reduction of the pulmonary, but not the cerebral lesions. Therefore, sultamicillin was begun, but without success. Long-term therapy with corticosteroids for ITP may induce not only steroid myopathy but also immune-incompetence with the development of pulmonary and cerebral nocardiosis. Cerebral nocardiosis may not sufficiently respond to long-term antibiotic therapy why switching to alternative antibiotics or surgery may be necessary.
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PMID:Cerebellar nocardiosis and myopathy from long-term corticosteroids for idiopathic thrombocytopenia. 2004 27

Ischemic stroke involving multiple artery territory with normal vessels gives a clue for an embolic stroke. Paradoxical embolization is a recognized cause of ischemic stroke. We describe a 48-year-old male who presented with acute onset giddiness, mild dysarthria, right hemiparesis, and ataxia. Clinical examinations indicated left cerebellar signs with right hemiparesis. Additionally, the patient had significant clubbing and mild cyanosis. A strong family history of epistaxis and hemoptysis was noted. His Magnetic resonance imaging of the brain showed acute left cerebellar and left frontal cortical infarct with normal vessels. The routine stroke and cardiac workup were normal. Chest X-ray showed bilateral lower zone opacities. Contrast-enhanced computerized tomogram (CT) of the chest showed bilateral pulmonary arteriovenous malformation. Paradoxical embolism due to pulmonary arteriovenous malformation resulted in ischemic stroke in our patient. He fulfilled all of the four criteria for diagnosing definite hereditary hemorrhagic telangiectasia. Our case highlights the importance of a systematic search for paradoxical embolism in a cryptogenic stroke.
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PMID:Paradoxical Embolism in a Case of Hereditary Hemorrhagic Telangiectasia: Case Report with Literature Review. 3264 84