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Biomedical subjects

C Cottin

Publications and source records attributed to C Cottin.

9 recordsLinked to original sources
PubMed1996

[A wine pitcher, cause of lead poisoning].

A 35-year-old male nurse hospitalized for recurrent episodes of intolerable abdominal pain was found to have non-hemolytic anemia and saturnism with blood lead level reaching 500 micrograms/l. Search for the source of the lead led to the discovery of an earthenware jug purchased in a Corsica craftsware shop. This jug had been used to hold the patient's daily consumption of wine (estimated at one-half to three-quarters liters per day) in the refrigerator. On the basis of lead release measurements using the method described in the EEC directive 84/500 (maximum tolerated limit for crockery = 4 mg lead/litter contents), it was found that the jug released 216 mg/l and estimated that the patient had ingested 0.8 to 1 mg of soluble lead daily for the past 8 years. The patient was successfully treated with chelator agents. This case of lead poisoning caused by a single earthenware wine jug confirms the need for rigourous governmental directives to control the production and distribution of varnished earthenware.

Adult↗
PubMed1994

Regulation of acetylcholine receptor alpha subunit variants in human myasthenia gravis. Quantification of steady-state levels of messenger RNA in muscle biopsy using the polymerase chain reaction.

Myasthenia gravis (MG) is an autoimmune disease mediated by auto-antibodies that attack the nicotinic acetylcholine receptor (AChR). To elucidate the molecular mechanisms underlying the decrease in AChR levels at the neuromuscular junction, we investigated the regulation of AChR expression by analyzing mRNA of the two AChR alpha subunit isoforms (P3A+ and P3A-) in muscle samples from myasthenic patients relative to controls. We applied a quantitative method based on reverse transcription of total RNA followed by polymerase chain reaction (PCR), using an internal standard we constructed by site-directed mutagenesis. An increased expression of mRNA coding for the alpha subunit of the AChR isoforms was observed in severely affected patients (P < 0.003 versus controls) but not in moderately affected patients, independently of the anti-AChR antibody titer. Study of mRNA precursor levels indicates a higher expression in severely affected patients compared to controls, suggesting an enhanced rate of transcription of the message coding for the alpha subunit isoforms in these patients. We have also reported that mRNA encoding both isoforms are expressed at an approximate 1:1 ratio in controls and in patients. We have thus identified a new biological parameter correlated with disease severity, and provide evidence of a compensatory mechanism to balance the loss of AChR in human myasthenia gravis, which is probably triggered only above a certain degree of AChR loss.

Adolescent↗
PubMed1993

Retraction.

Explore the source record for details and available documents.

Retraction Notice↗
PubMed1993

[Iatrogenic axonal neuropathy and erythroderma induced by piroxicam. Manifestations of hypersensitivity?].

A case of peripheral neuropathy following treatment with piroxicam is reported. The patient developed muscle pain and asymmetrical sensory distal neuropathy of the lower limbs a few months after the onset of the treatment. Piroxicam was withdrawn and full recovery was achieved within one year. The simultaneous appearance in the same patient of erythroderma with microvasculitis on nerve and skin biopsies suggests a common type III hypersensitivity mechanism in the pathogenesis of these two side-effects of piroxicam.

Aged↗
PubMed1992

Combined effects of a thymic peptide, thymopoietin and myasthenic patient sera in rat myotube culture.

We investigated in a rat myotube assay the combined effect of 26 myasthenic (MG) patient sera and a thymic peptide, thymopoietin (Tpo) which had previously been shown to bind Torpedo and human AChR and to compete with alpha-bungarotoxin (alpha-Bgt) binding. Cultures were first exposed to Tpo alone for 3 h (0.3, 7.5, 15 nM), then MG sera (5% final dilution) were added for an additional 18 h. Reduction in the amount of 125I-alpha-Bgt binding sites in the presence of various concentrations of Tpo were similar with control sera and in all the patients with low or undetectable anti-AChR Ab (11 cases). In cultures exposed to Tpo and sera with high anti-AChR Ab titre (15 cases), Tpo and anti-AChR Ab have an additive capacity to reduce the number of alpha-Bgt binding sites. The results are compatible with the hypothesis that anti-AChR Ab and Tpo could impair neuromuscular transmission by complementary mechanisms.

Acetylcholinesterase↗
PubMed1992

[Axonal neuropathy and salazosulfapyridine: slow-acetylator phenotype].

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.

Acetylation↗
PubMedDate not supplied

[Transdermal scopolamine and mydriasis].

The authors report five cases of mydriasis induced by the use of transdermal scopolamine delivery systems. Anisocoria and narrow angle glaucoma were involved in four cases; in one case, the use of a strong dosage resulted in a bilateral mydriasis in a child.

Administration, Cutaneous↗