Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The currently recognized toxic effects of quinine in humans are identified and the problems of management of overdosage of quinine are discussed. Quinine, available therapeutically as sulphate or hydrochloride salts, also is widely used in tonic water, and there are several case reports of allergic reactions to the drug when a patient has consumed the drug in this way. Another unintentional source of poisoning is its use as an adulterant in heroin for "street" use. This appears to be a problem in the US. Quinine, termed a "general protoplasmic poison" is toxic to many bacteria, yeasts, and trypanosomes, as well as to malarial plasmodia. Quinine has local anesthetic action but also is an irritant. The irritant effects may be responsible in part for the nausea associated with its clinical use. In addition it has a mild antipyretic effect. Several features are common to both an acute single overdose in self-poisoning and accumulation of quinine during therapy for malaria: together they are termed cinchonism. Auditory symptoms, gastrointestinal disturbances, vasodilatation, sweating, and headache occur with moderately elevated plasma quinine concentration. As these rise, increasingly severe visual disturbances and then cardiac and neurologic features occur. Mild nausea may be the only symptom, but with large overdoses profuse vomiting, abdominal pain, and diarrhea may occur. These result from a combination of the local irritant effect of quinine on the gut and the central effects of quinine on the chemoreceptor trigger zone. Vasodilatation and sweating are well recognized, and tinnitus is common. Visual symptoms usually are delayed, and blindness may not be discovered for a day or more. Aspirin-sensitive patients, and others, may develop angioedema by nonimmunological mechanisms in response to drugs, and quinine has been reported to produce pseudo-allergic reactions in aspirin-sensitive patients. Quinine also can cause drug-induced thrombocytopenia and purpura. In patients suffering with malaria due to "Plasmodium falciparum," anemia and acute intravascular hemolysis with renal failure are recognized complications. There appears to be little evidence in the literature in support of the folk tradition of quinine as an inducer of abortion. Quinine is known to cause deterioration in patients with myasthenia gravis and erythema multiforme, to stimulate insulin release in patients receiving treatment for falicparum malaria, and to be responsible at times for ataxia following moderate overdosage. Clinically, quinine poisoning is observed in 3 situations: self-poisoning; accidentally; and following use of quinine in excessive doses in the hope of achieving abortion. Treatment courses are reviewed.
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PMID:Quinine toxicity. 354 70

We evaluated clinical presentation, cerebrospinal fluid (CSF), and magnetic resonance imaging (MRI) in patients with late-onset multiple sclerosis (LOMS). Fifty-two patients with definitive multiple sclerosis (MS) diagnosed after the age of 50 years were identified between 1991 and 2002. Data pertaining to clinical characteristics, CSF analysis, and cerebral and spinal MRI were compared with those of 52 young-onset MS (YOMS) patients matched for sex and disease duration. Mean age at the time of diagnosis was 57 years in the LOMS group - the oldest patient was 82 - and 29 years in the YOMS group. Motor symptoms were significantly more often present in the LOMS than in patients with YOMS (90 % vs. 67 %, p = 0.014). Visual symptoms, residual signs of optic neuritis, and dysarthria were less frequent for LOMS. Sensory symptoms, ataxia, oculomotor symptoms, cognitive disorder, or fatigue did not differ between both groups. The majority of LOMS patients (83 %) had a primary progressive disease course, whereas 94 % of the YOMS group had a relapsing-remitting course. MRI showed typical multifocal supratentorial (LOMS vs. YOMS: 96 % vs. 98 %) and infratentorial (44 % vs. 62 %) lesions without significant group differences. Of particular interest, spinal lesions were more common (81 %) in LOMS compared to YOMS (48 %, p = 0.024), and cerebellar lesions were less frequent in the LOMS group (11 % vs. 44 %, p = 0.001). Gadolinium-enhanced lesions were initially present in less LOMS patients (15 %) than in YOMS (63 %, p < 0.001). CSF analysis revealed pleocytosis less frequently in LOMS (34 %) compared to YOMS (67 %, p = 0.006) but oligoclonal banding occurred without in both groups without differences. YOMS patients responded to corticosteroids (93 %) to a significantly greater degree than LOMS patients (73 %; p = 0.004). For individuals who develop LOMS, a primary progressive course is frequent, with motor symptoms as the prominent feature. Vigilance is necessary to recognise MS in this population because of its unusual presentation.
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PMID:Clinical characteristics of patients with late-onset multiple sclerosis. 1828 94