Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

HIV-1-related neurological diseases, excluding opportunistic infections and HIV encephalitis, are considered here. Most occur in severely immunosuppressed patients, with CD4 counts of under 200 x 10(6) l-1. Primary brain lymphoma and metastases from systemic non-Hodgkin's lymphoma, the second commonest cause of cerebral mass lesions in AIDS, are usually aggressive B cell tumours. Their poor median survival after treatment, compared with that of lymphomas in non-AIDS patients, seems related to systemic complications, particularly opportunistic infections. Kaposi's sarcoma produces neurological symptoms exceptionally. Cerebral infarction is often unrecognized clinically but large vessel arteritic occlusions may occur. Intracranial haemorrhages occur mostly in thrombocytopenic patients. Seizures are frequently referred to the neurologist; investigation may lead to a diagnosis of AIDS. Nearly 50% of patients with seizures have cerebral toxoplasmosis or cryptococcal meningitis; HIV-1 encephalitis is presumed to be the cause in 30%. A subacute or chronic vacuolar myelopathy with pyramidal and posterior column signs is the commonest form of spinal cord involvement in AIDS; its cause remains unknown. Peripheral nerve syndromes occur at all stages of HIV-1 infection. Distal symmetrical peripheral neuropathies are the most frequent, particularly a painful form with axonal atrophy, associated with CMV infection, and seen during ARC or AIDS. Mononeuritis multiplex due to vasculitis, CMV, or lymphoma and a serious lumbosacral polyradiculopathy due to CMV are infrequent. The commonest myopathy is due to zidovudine (AZT); it usually responds to drug withdrawal. The nature, prognosis and optimal management of most other myopathies is yet to be determined.
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PMID:Other neurological diseases in HIV-1 infection: clinical aspects. 134 49

A prospective controlled clinical-neurophysiological-pathological study of 71 patients with oat cell carcinoma of the lung revealed no increased incidence of peripheral neuropathy at the initial stages of illness. All patients developed neuropathy by the time they had lost 15% of their body weight, but the neuropathy was less severe than in 20 age-matched alcoholic patients with an equal degree of weight loss. The weight loss and peripheral neuropathy progressed with atrophy of type II (adenosine triphosphatase-positive) muscle fibers out of proportion to the patient's loss of body weight. By 40% body weight loss, all the patients had moderate symmetrical peripheral neuropathy, 6 had proximal brachial or lumbosacral plexus metastases, and 9 had distal pressure palsies. Mononeuritis multiplex developed in only 1 patient, who had diabetes mellitus. Two patients developed Eaton-Lambert syndrome, which resolved in 1 when chemotherapy controlled the systemic tumor, with no protein in the tumor postmortem which could produce the characteristic electromyographic findings of the syndrome.
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PMID:The carcinomatous neuromyopathy of oat cell lung cancer. 624 73