17 Agosto 2001
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Ann Pharmacother 2001 Apr;35(4):435-7
South Dakota State University College of Pharmacy, South Dakota Human Services Center, Yankton 57078-0076, USA. dfarver@usd.edu
OBJECTIVE: To report a case of antipsychotic-induced parkinsonism that was managed with zolpidem. CASE SUMMARY: A 34-year-old white man who had had antipsychotic-induced parkinsonism with symptoms of repetitive persistent gross tremors of the hands for numerous years was unresponsive to traditional antiparkinsonian medications. With the initiation of zolpidem 10 mg four times daily, the tremors decreased significantly. DISCUSSION: The use of zolpidem for antipsychotic-induced parkinsonian hand tremors in this patient was based on the severity of the symptoms and the lack of response to several trials of traditional medications. When zolpidem was started at 10 mg four times a day, the motor examination score on the Unified Parkinson's Disease Rating Scale decreased from 29 at baseline to a score of 9 after one month of use. After four months of zolpidem use, the patient's mental status decompensated, and clozapine was initiated. As the patient experienced excessive sedation, zolpidem was discontinued while clozapine was maintained to help with the psychosis and, potentially, the tremors. The tremors reemerged with a motor examination score of 30. Zolpidem was reinitiated at 5 mg four times daily, and the patient's tremors have been stable for two years. CONCLUSIONS: Further investigation is needed to study the use of nontraditional medications in patients requiring antipsychotic medications who have refractory parkinsonian symptoms.
PMID: 11302407, UI: 21196759
BMJ 2001 Jul 7;323(7303):23
Digestive Disease Centre, Royal Sussex County Hospital, Brighton BN2 5BE.
PMID: 11440939, UI: 21334108
Lancet 2001 Aug 4;358(9279):387-8
[Medline record in process]
We investigated the hypothesis that sporadic food poisoning is a result of the consumption of food cooked or prepared outside the home. We did a case-control study, set in an urban emergency department, to find out the odds ratios for the risk of food poisoning associated with various patterns of consumption. We found that recent eating out (exposure on the day of or day before presentation) was associated with an odds ratio of 2.41 (95% CI 1.29-4.50) for presenting with food poisoning.
PMID: 11502323, UI: 21394220
Med J Aust 2001 Jul 2;175(1):33-4
Department of Cardiothoracic Surgery, Prince of Wales Hospital, Sydney, NSW. weissbx@usa.net
Injuries to the extremities from stingray barbs are not uncommon along the Australian seaboard. Cardiac injuries from stingray barbs are rare, even worldwide, and all but one have been fatal. We report a survivor of a cardiac injury caused by a stingray barb. Penetration of a body cavity by a stingray barb requires early surgical referral and management.
PMID: 11476200, UI: 21368440
Postgrad Med 2001 Jul;110(1):24-6, 29-30, 35-6 passim
Department of Family Practice, Hennepin County Medical Center, 5 W Lake St, Minneapolis, MN 55408, USA. gmdoc2000@hotmail.com
As much as we hate to admit it, even the gentlest of our friendly pets can harbor harmful pathogens, and although the fact is not widely known, pet-associated infections can significantly affect the health of humans. In this article, Dr Morrison focuses on pets and their accompanying potential zoonoses, outlining how these diseases can be transmitted to humans and how the infections are treated. Special attention is paid to rabies and toxoplasmosis, which have attained particular notoriety over time.
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PMID: 11467041, UI: 21360676
Toxicol Sci 2001 Jun;61(2):234-40
Department of Environmental Health, University of Washington, 4225 Roosevelt Way NE, Suite 100, Seattle, Washington 98105, USA.
Changes in urinary porphyrin excretion patterns (porphyrin profiles) during prolonged mercury exposure are attributable to mercury accumulation in the kidney and to consequent effects of Hg2+ on renal porphyrin metabolism. In the present study, we evaluated the quantitative relationship of urinary porphyrin concentrations to mobilizable renal mercury content, using the metal chelator 2,3-dimercapto-1-propanesulfonic acid (DMPS) to modulate kidney mercury levels. Rats exposed to methylmercury hydroxide (MMH) at 10 ppm in drinking water for 6 weeks were treated with up to 3 consecutive doses of DMPS (100mg/kg, ip) at 72-h intervals. Consistent with previous findings, the concentrations of pentacarboxyl- (5-) and copro- (4-) porphyrins and of an atypical porphyrin specific to mercury exposure, precoproporphyrin, were significantly elevated in urine of MMH-exposed rats, compared with that of rats exposed to distilled water (dH2O) for the same period. Consecutive DMPS treatments of MMH-exposed rats significantly decreased kidney concentrations of total, as well as Hg2+ and CH3Hg+ species, and promoted increased urinary mercury excretion. Concomitantly, DMPS treatment decreased both kidney and urinary porphyrin concentrations, consistent with depletion of renal mercury levels. Regression analyses demonstrated a high correlation (r approximately 0.9) between prechelation urinary porphyrins and postchelation urinary mercury levels and also between prechelation urinary porphyrins and prechelation kidney mercury concentrations. These findings demonstrate that urinary porphyrin concentrations relate quantitatively to DMPS-mobilizable mercury in the kidney and, therefore, serve as a biochemical measure of renal mercury content.
PMID: 11353132, UI: 21251347
Toxicol Sci 2001 Jun;61(2):224-33
Methylmercury, a potent neurotoxicant, accumulates in the brain as well as the kidney during chronic exposure. We evaluated the capacity of 2,3-dimercapto-1-propanesulfonic acid (DMPS), a tissue-permeable metal chelator, to reduce brain, kidney, and blood Hg levels and to promote Hg elimination in urine following exposure of F-344 rats to methylmercury hydroxide (MMH) (10 ppm) in drinking water for up to 9 weeks. Inorganic (Hg2+) and organic (CH3Hg+) mercury species in urine and tissues were assayed by cold vapor atomic fluorescence spectroscopy (CVAFS). Following MMH treatment for 9 weeks, Hg2+ and CH3Hg+ concentrations were 0.28 and 4.80 microg/g in the brain and 51.5 and 42.2 microg/g in the kidney, respectively. Twenty-four hours after ip administration of a single DMPS injection (100 mg/kg), kidney Hg2+ and CH3Hg+ declined 38% and 59%, whereas brain mercury levels were slightly increased, attributable entirely to the CH3Hg+ fraction. Concomitantly, Hg2+ and CH3Hg+ in urine increased by 7.2- and 28.3-fold, respectively, compared with prechelation values. A higher dose of DMPS (200 mg/kg) was no more effective than 100 mg/kg in promoting mercury excretion. In contrast, consecutive DMPS injections (100 mg/kg) given at 72-h intervals significantly decreased total mercury concentrations in kidney, brain, and blood. However, the decrease in brain and blood mercury content was restricted entirely to the CH3Hg+ fraction, consistent with the slow dealkylation rate of MMH in these tissues. Mass balance calculations showed that the total amount of mercury excreted in the urine following successive DMPS injections corresponds quantitatively to the total amount of mercury removed from the kidney, brain, and blood of MMH-exposed rats. These findings confirm the efficacy of consecutive DMPS treatments in decreasing mercury concentrations in target tissue and in reducing overall mercury body burden. They demonstrate further that the capacity of DMPS to deplete tissue Hg2+ is highly tissue-specific and reflects the relative capacity of the tissue for methylmercury dealkylation. In light of this observation, the inability of DMPS to reduce Hg2+ levels in brain or blood may explain the inefficacy of DMPS and similar chelating agents in the remediation of neurotoxicity associated with prolonged MMH exposure.
PMID: 11353131, UI: 21251346
Toxicol Sci 2001 Jun;61(2):197-8
University of Maryland, Toxicology Program, 1450 South Rolling Road, Baltimore, Maryland 21227, USA.
PMID: 11353126, UI: 21251341
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