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PubMed1996

Adverse events in patients treated with 5-aminosalicyclic acid: 1993-1994 pharmacovigilance report for Pentasa in France.

BACKGROUND: The incidence of the side-effects of 5-aminosalicylic acid (5-ASA) in clinical practice is not known. AIM: To present the safety reports on the use of Pentasa in France. METHODS: Pentasa-related adverse events were recorded from 1 January 1993 to 31 December 1994. Spontaneous reports to Ferring S.A. came from physicians or pharmacovigilance regional centres. RESULTS: In 1993 and 1994, 51 and 79 adverse events were reported; the estimated gross incidence was 6.6 and 9.0 per million days of therapy. Detailed information was obtained 64% of cases in 1993 and 53% in 1994. Adverse events with a high likelihood of causalty included five cases of diarrhoea, 14 cases of pancreatitis, seven cases of liver abnormalities, seven of blood dyscrasias, two cases of renal insufficiency (one of which was in a fetus), and eight of cardiac disorders including three myocarditis. CONCLUSIONS: Pentasa seldom has adverse effects. The majority of the adverse events do not seem to be dose-related. Clinicians should be aware of exceptional but severe adverse events including pancreatitis, cardiac disorders, blood dyscrasias and renal insufficiency.

Aminosalicylic Acids↗
PubMedDate not supplied

Specificity data of the salicylate assay by fluorescent polarization immunoassay.

We studied the recently developed Abbott Laboratories fluorescent polarization immunoassay (FPIA) for salicylates in serum. The cross-reactivity test of the assay was performed with 20 substances that showed a similar chemical structure as salicylic acid. A chemical substitution on the 5- position of the salicylate formula enhanced the cross-reactivity. 5-Methylsalicylic acid, diflunisal, salazosulfapyridin, and 5-aminosalicylic acid (5-ASA) showed a significant cross-reactivity with 1200%, 222%, 153% and 122%, respectively. Diflunisal and salazosulfapyridin at a similar therapeutic serum level as salicylic acid can produce false positive salicylate results, in case of unknown medication of these compounds.

Evaluation Studies as Topic↗
PubMedDate not supplied

Extrahepatic expression of N-acetylator genotype in the inbred hamster.

The genetic control of S-acetylcoenzyme A (AcCoA)-dependent N-acetyltransferase activity (EC 2.3.1.5) was investigated in liver, intestine, kidney, and lung cytosols derived from homozygous rapid acetylator (Bio. 87.20), heterozygous acetylator (Bio. 87.20 X 82.73/H F1), and homozygous slow acetylator (Bio. 82.73/H) Syrian inbred hamsters. AcCoA-dependent N-acetyltransferase activity was highest in hepatic cytosol, followed by intestine, kidney, and lung cytosol. In each of these tissues, cytosolic N-acetyltransferase exhibited an acetylator genotype-dependent activity with highest levels in homozygous rapid, intermediate levels in heterozygous F1 progeny, and lowest levels in homozygous slow acetylators. The ratio of N-acetyltransferase activity between acetylator genotypes was in general substrate dependent but not tissue dependent. Acetylator genotype-dependent N-acetyltransferase activity differences were highest for p-aminobenzoic acid, followed by p-aminosalicylic acid, 2-aminofluorene, and beta-naphthylamine. Expression of isoniazid N-acetyltransferase activity in each tissue was acetylator genotype independent. Determination of Michaelis-Menten kinetic constants in each tissue suggested that p-aminobenzoic acid N-acetyltransferase activity was acetylator genotype-dependent because of catalysis by an isozyme(s) that is both an apparent Km and a Vmax variant. In contrast, the acetylator genotype-independent expression of isoniazid N-acetyltransferase activity in each tissue appeared to result from a common isozyme(s) present in each tissue with equivalent kinetic constants in the two phenotypes. These data suggest that acetylator genotype-dependent expression of AcCoA-dependent N-acetyltransferase activity in extrahepatic tissues may play an important role in hereditary predisposition to toxicity and/or carcinogenesis in extrahepatic organs following exposure to arylamine drugs and foreign chemicals.

Acetylation↗