Paracetamol
goes bad with
Gilbert's Syndrome
Paracetamol
goes bad with
Gilbert's Syndrome
4.8
ValidityScore
Valid or Invalid?
Paracetamol, with its well-known hepatotoxicity in overdose, has been studied in this area. A subgroup of those with GS have been found to shift metabolism to an oxidative pathway over a glucuronidation pathway, thereby increasing the toxic metabolites of paracetamol, namely cysteine and mercapturic acid conjugates. There have, however, been no reported cases of liver injury in this setting in the literature. Therefore, there is no good quality evidence that those with GS should avoid paracetamol use or alter the recommended dosage.
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2019
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King D and Armstrong MJ
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The, mainly theoretical, concern is that glucuronidation
in the metabolism of drugs may not be optimal and therefore lead
to toxic metabolite build-up. Paracetamol, with its well-known
hepatotoxicity in overdose, has been studied in this area. A subgroup of those with GS have been found to shift metabolism to an oxidative pathway over a glucuronidation pathway, thereby increasing the toxic metabolites of paracetamol, namely cysteine and mercapturic acid conjugatese. Therefore, there is no good quality evidence that those with GS should avoid paracetamol use or alter the recommended dosage. -
- From this research we know that
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-0.4Perhaps, Sulfasalazine goes bad with Gilbert's Syndrome(BioMindmap Proof Quality is Negative.)
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2015Case Report
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Flores-Villalba E, et al.
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Once diagnosis is made, the most important aspect is to notify the patients on the benign course of the disease and instruct them on the circumstances that may precipitate an elevation of bilirubin and appearance of jaundice. Also is very important to inform the patient on side effects or unexpected toxicity due to some drugs which metabolism is due to hepatic glucoronidation:
Tolbutamide Aminopyrine Menthol Estradiol Lamotrigine Irinotecan NSAID (included acetaminophen) HIV protease inhibitors - Organism: Humans
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2013Case Report
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Raza A, et al.
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He was homozygous for A(TA)7TAA promoter mutation consistent with GS. Two months prior to evaluation, he began ingesting six Excedrin caplets (acetaminophen 250 mg, aspirin 250 mg, and caffeine 65 mg) daily for migraine headache. Abnormal levels of aminotransferases had been noted previously while using simvastatin and gemfi brozil. Discontinuation of these medications in the past led to normalization of aminotransferase levels. On the basis of these observations, a diagnosis of drug-induced liver injury was made. Th e patient discontinued Excedrin, and aminotransferase levels normalized in 1 month.
- Organism: Humans
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1999
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Esteban A and Pérez-Mateo M
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«Gilbert's syndrome (GS) is an inherited bilirubin UDP-glucuronosyl transferase deficiency. The object of this study was to investigate the possible effects of this disorder on the metabolism of a drug, such as paracetamol, which is basically eliminated by hepatic glucuronidation. We studied 32 healthy volunteers and 18 people with GS, all of whom were given 1.5 g of paracetamol orally. In the 24 h urine collected, we determined the elimination of free paracetamol, the conjugates (glucuronide, sulphate) and the oxidation products (cysteine, mercapturic acid) by high pressure liquid chromatography (HPLC). The results are given as a percentage of the total quantity of paracetamol eliminated. The patients with GS were divided into 2 subgroups (GS-I and GS-II) according to whether glucuronidation was more or less than 50%. The overall results of the GS group showed no significant difference in the urinary elimination of metabolites as compared to the control group. However, in subgroup GS-I, a reduction in glucuronidation (P = 0.0012) and an increase in oxidation (P = 0.0051) was seen, as compared with the other 2 groups. There was inverse correlation between the glucuronide produced by conjugation and the oxidation products (r = -0.8718; P<0.005). People with GS are a heterogeneous group with respect to the metabolism of paracetamol. In one subgroup this was normal. In the other subgroup there was a marked reduction in glucuronidation and an increase in oxidation. These changes could mean that people in this subgroup are more liable to liver damage after an overdose of paracetamol.»
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1 year ago
on Apr 8, 2019
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