Adult Schönlein-Henoch purpura after lisinopril.
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Biomedical subjects
Publications and source records attributed to J Jouglard.
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Buprenorphine, a synthetic central analgesic, marketed since 1987, was rapidly suspected to be subject to abuse. We tried to confirm this abuse in the context of our analytical activity at the Drug Dependence Evaluation and Information Centre. The study was based on 50 drug addicts admitted to Marseille Hospital between June and October 1992. Buprenorphine and its N-dealkylated metabolite were identified in the urine by high performance liquid chromatography equipped with a diode array detector. Nine (18%) of the 50 samples analysed were positive for buprenorphine and/or norbuprenorphine, with a confidence interval of 8 to 28%, which confirms the existence of abuse of this analgesic.
We report a case of an axonal sensorimotor neuropathy involving salazosulphapyridine in a slow-acetylator patient with ulcerative colitis. Rather than hypersensitivity the mechanism of the neuropathy can be assumed to be toxicity. The role played by the respective different metabolites in the occurrence of this uncommon side effect is uncertain.
Bismuth encephalopathies appeared in the mid-seventies in France and concerned about 1,000 people and led to a fatal outcome in 70 cases. Responsibility of Bi was clearly confirmed by the disappearance of the intoxication after prescription of drugs containing Bi had been more tightly regulated. Since the implication of a substance increasing the intestinal absorption of Bi has been suspected, we studied the concentrations of Bi in the tissues of rats who had been treated with bismuth nitrate basic 400 mg/kg per d for one month with and without an intake of a chelating agent added to the drinking water at a concentration of 10 mmol/l. The chelating agents tested were ethylenediaminetetraacetic acid (EDTA), nitriloacetic acid (NTA) and tripolyphosphate (TPP), cysteine and diethyldithiocarbamate (DEDTC). Cysteine and DEDTC gave the highest increase of Bi in tissues but with a wide dispersion of levels. However, even in the rats with the highest levels of Bi, there were no behavioral problems. EDTA induced an increase of Bi in kidney, brain and bone and NTA in kidney but there was no obvious sign of toxicity. We did not succeed in reproducing in rats the Bi toxicity observed in patients some years ago.
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A case of peripheral neuropathy following cimetidine treatment is reported. Four days after beginning cimetidine (200 mg four times a day), the patient developed muscle pain and a symmetric motor neuropathy in all 4 limbs, predominant distally and in the lower limbs. Cimetidine was discontinued. Within seven days motor function began to return and within five months recovery was complete. Electrophysiological studies showed an axonal neuropathy. Morphometric studies revealed loss of large myelinated fibers in some fascicles while other fascicles were normal. Teasing studies showed predominant axonal lesions. Microvasculitis was present in the epineurium. Such findings suggest a role for small-vessel immune-complex vasculitis in the pathogenesis of this cimetidine-induced peripheral neuropathy.
The authors report a case of methemoglobinemia following a suicidal attempts with a popper containing isobutyl nitrite. The toxic effects of this substances, either by ingestion or inhalation, are described as well as risks of use in "everyday life". Regulations, still incomplete has been suggested in USA. In France, preventive measures should be taken.
The system used in the Marseilles Poison Control Center is discussed. Input of data on a daily basis and uses of these data for emergency (evaluation of a toxic situation) or for non-emergency (statistics, toxicity files) work is reviewed.
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Among the calls for information recently received by the French Poison Control Centers, 78 concerned a liver protecting agent, thiazolidine carboxylic acid. In almost every case, doses well above the therapeutic range have provided a status epilepticus. Thus confirming the neurotoxicity of the drug which had been known to the Poison control Centers for the past 10 years. Several patients had also metabolic acidosis, severe hypoglycaemia, or, more scarcely, hyperglycaemia. Seizures convulsions occurred specially in young children whose immature blood-brain barrier allowed penetration into the CSF of thiazolidine carboxylic acid, later metabolized locally into the strongly irritant compound formaldehyde. In view of its toxicity, the drug should never be administered to young children. The usual measures to prevent intoxication should be applied and in case of overdosage the patients should be admitted to hospital for observation. Long-lasting anti-epileptic treatments should be avoided.
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The therapeutic approach to the management of corrosive burns of the upper gastrointestinal tract leaves a considerable morbidity and a heavy mortality rate. This work evaluates the effectiveness of a new therapeutic approach given to 94 consecutive patients. The management has been based on three major points: (1) the definition of extent of upper gastrointestinal lesions by immediate fibroendoscopy; (2) immediate protection of the upper gastrointestinal tract by total parenteral nutrition in cases with serious burns (41 cases), normal oral nutrition being allowed for minor burns (35 cases); (3) reparative surgical procedures for any of the sequelae of such burns during the fibrosing phase. The results were as follows: (a) healing, depending upon the degree of burn, occurred between eight to 90 days; (b) the frequency of subsequent local complications was small with total parenteral nutrition started a few hours after ingestion of the corrosive product; (c) after reconstructive surgery no serious complications occurred; (d) the overall morbidity stayed at a very low level (four patients). We conclude that the general prognosis of a severe burn of the upper gastrointestinal tract, without other trauma, is appreciably improved by the very early institution of total parenteral nutrition.
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