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Biomedical subjects

R Garnier

Publications and source records attributed to R Garnier.

At least 91 records · Page 5Linked to original sources
PubMed1981

[Acute mercury vapour poisoning (author's transl)].

Two persons, exposed to high concentration of mercury vapour in their home developed a few hours later febrile illness with interstitial pneumonitis and mercurial stomatitis. Symptomatic treatment was associated with dimercaprol (BAL) and steroïds; an alveolar washing was performed to remove non-absorbed mercury in the respiratory three which seems to be responsible for the observed inflammatory reaction and, sometimes, the delayed development of fibrosis. A review of the literature revealed that such intoxications had been previously described in about 20 cases. Prognosis depends on the severity of the pulmonary lesions. Fatalities have been described in 9 cases (10%); in 8 cases the victims were young children or old people. An acute gingivo-stomatitis is generally observed. The onset of mercurial encephalopathy is an uncommon feature. Renal disturbances are exceptionally described and always mild. There is no correlation between the clinical condition of the patient and the levels of mercury in the urine.

Adult↗
PubMed1980

Thioproline.

Explore the source record for details and available documents.

Adult↗
PubMed1978

[Acute poisoning by Gyromitra esculenta (author's transl)].

This kind of poisoning is scarce in France, on the contrary it is most frequent in Eastern Europe. Clinical picture associating cytolytic hepatitis, seizures, and hemolysis reminds us intoxication by hydrazine. In fact there is some evidence that the toxin of this mushroom--called gyromitrin--is transformed in the stomach in methylhydrazine. The mechanism of hepatotoxicity of the later can be compared with that of the metabolites of isoniazid.

Chemical Phenomena↗
PubMedDate not supplied

2,3-Dimercaptosuccinic acid treatment of heavy metal poisoning in humans.

14 patients with heavy metal poisoning received 2,3-dimercaptosuccinic acid (DMSA). 12 subjects were given 30 mg/kg/day for 5 days; 1 subject was started on a lower dose because of a history of atopy; another subject was treated for 15 days because of very high initial blood lead concentrations. In the 9 subjects who had lead poisoning, DMSA decreased blood lead concentrations by 35 to 81%, and induced a 4.5- to 16.9-fold increase in mean daily urinary excretion of the metal. In the acutely arsenic-poisoned case, the plasma arsenic concentration on day 7 was half the pretreatment value, while no clear decrease was observed in a chronically exposed subject. In 3 mercury cases, DMSA increased daily mercury urinary excretion 1.5-, 2.8- and 8.4-fold, respectively, while blood mercury concentrations remained below detection limits. No serious side effects were observed and 3 weeks after administration of the drug the clinical condition of all subjects was either stable or improved. These results indicate the efficacy of DMSA for lead poisoning in humans and provide a rationale for further investigating its usefulness in mercury and arsenic poisoning cases.

Adolescent↗
PubMedDate not supplied

Acute fluvoxamine poisoning.

A total of 221 cases of deliberate acute overdose with fluvoxamine reported to the Paris Poison Centre, and 78 cases collected by the International Drug Safety Department of Duphar BV were analysed. Other agents, mainly benzodiazepines, neuroleptics, other antidepressants and alcohol, were also taken in 77% of the cases. The acute toxicity that could be attributed to fluvoxamine alone was rarely severe. The symptoms observed were always benign when the dose of fluvoxamine was below 1000 mg and included drowsiness, tremor, nausea, vomiting, abdominal pain, bradycardia and/or anticholinergic effects (dry mouth, mydriasis, sinus tachycardia, urinary retention). Seizures occurred in a few cases after high doses (generally > 1500 mg). Cardiotoxicity was not a serious problem; sinus bradycardia was noted with doses of less than 1000 mg, but was always moderate and required no treatment. Conduction abnormalities were rare.

Adolescent↗
PubMedDate not supplied

Paraquat poisoning. An overview of the current status.

Paraquat is a bipyridyl compound with no known chronic toxicity or teratogenicity. It is poorly absorbed when inhaled, but causes severe illness when ingested orally, death usually occurring within 2 days of ingestion of 50 mg/kg. At lower doses death may be delayed for several weeks. The toxic compound accumulates in lung tissue where free radicals are formed, lipid peroxidation is induced and nicotinamide adenine dinucleotide phosphate (NADPH) is depleted. This produces diffuse alveolitis followed by extensive pulmonary fibrosis. The most important prognostic indicator is the quantity of paraquat absorbed, as shown by the plasma paraquat concentration. While renal failure will develop in the majority of those patients who eventually die, it may not, if present alone, indicate a fatal outcome. The absence of caustic burns in the upper digestive tract indicates a good prognosis. Treatment of paraquat poisoning remains ineffective, but Fuller's earth, activated charcoal and resins may prevent some absorption of the toxin. When tubular necrosis occurs, renal excretion of the compound decreases rapidly. A 3-compartment pharmacokinetic model has been described following ingestion of tracer doses including a 'deep' compartment for active pulmonary accumulation. Haemodialysis, haemoperfusion and forced dialysis have been attempted, with no clear improvement in survival rates. Superoxide dismutase, glutathione peroxidase, N-acetylcysteine and other 'free radical scavengers' have failed to alter the outcome in poisoned patients. Other theoretical treatments, such as deferoxamine, immunotherapy, NADPH repletion and lung transplantation still require clinical validation.

Charcoal↗
PubMedDate not supplied

4-Methylpyrazole may be an alternative to ethanol therapy for ethylene glycol intoxication in man.

4-Methylpyrazole (4 MP) is a strong inhibitor of alcohol dehydrogenase. Its use in acute ethylene glycol (EG) or methanol intoxication has been suggested in experimental studies about its efficacy and safety. We report three cases of accidental intoxication with ethylene glycol in man treated orally with 20 mg/kg/day of 4 MP. The treatment was maintained until plasma EG concentrations became unmeasurable. The patients were admitted early during the course of the poisoning. Their neurological status was good. A slight metabolic acidosis observed in two cases was easily corrected and did not recur. Renal function remained normal in all cases. No patient underwent hemodialysis. On admission plasma EG concentrations were 24.2 mmol/l, 13 mmol/l and 9.7 mmol/l respectively. Plasma EG half-lives were 14.5, 11.5 and 14.75 hours respectively. Plasma oxalate concentrations and the rate of urine oxalate elimination, determined in two patients, were high on admission but quickly returned to normal. Concerning possible side effects of 4 MP, a skin rash was observed in one patient and a possible eosinophilia in the others. These three cases suggest that 4 MP may decrease the metabolic consequences of EG poisoning in man and may be of therapeutic value when administered early during the course of the intoxication before coma, seizures and organic renal failure have occurred.

Adult↗