Feprazone: Absence of Hemolytic Effects in Glucose‐6‐Phosphate Dehydrogenase‐Deficient Subjects

Meloni, T; Fórteleoni, G; Serra, M.V.; Daniotti, S.; Negri, Luigi; Giuntini, Patrizia; Canepa, Letizia; Gaetani, Gian Franco

doi:10.1002/j.1552-4604.1982.tb02695.x

Cited by 4 publications

(1 citation statement)

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“…A case report after use of ciprofloxacin was reported in an adult patient with Mediterranean mutation (Sansone et al, 2010). Use of feprazone against fever in children did not cause AHA (Meloni et al, 1982). In cases where Mediterranean variant was presumed (no test result reported), subsequent case reports of AHA have been described with chlorproguanil-dapsone (Leslie et al, 2007), dapsone alone (Murphy and Grossman, 2016), normal or excessive doses of paracetamol (Bartsocas et al, 1982;Phillpotts et al, 2014) and other uncommonly used drugs ( Supplementary Table S1).…”

Section: Other Drugsmentioning

confidence: 99%

G6PD Variants and Haemolytic Sensitivity to Primaquine and Other Drugs

Bancone

Chu

2021

Front. Pharmacol.

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Restrictions on the cultivation and ingestion of fava beans were first reported as early as the fifth century BC. Not until the late 19th century were clinical descriptions of fava-induced disease reported and soon after characterised as “favism” in the early 20th century. It is now well known that favism as well as drug-induced haemolysis is caused by a deficiency of the glucose-6-phosphate dehydrogenase (G6PD) enzyme, one of the most common enzyme deficiency in humans. Interest about the interaction between G6PD deficiency and therapeutics has increased recently because mass treatment with oxidative 8-aminoquinolines is necessary for malaria elimination. Historically, assessments of haemolytic risk have focused on the clinical outcomes (e.g., haemolysis) associated with either a simplified phenotypic G6PD characterisation (deficient or normal) or an ill-fitting classification of G6PD genetic variants. It is increasingly apparent that detailed knowledge of both aspects is required for a complete understanding of haemolytic risk. While more attention has been devoted recently to better phenotypic characterisation of G6PD activity (including the development of new point-of care tests), the classification of G6PD variants should be revised to be clinically useful in malaria eliminating countries and in populations with prevalent G6PD deficiency. The scope of this work is to summarize available literature on drug-induced haemolysis among individuals with different G6PD variants and to highlight knowledge gaps that could be filled with further clinical and laboratory research.

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Section: Other Drugsmentioning

confidence: 99%

G6PD Variants and Haemolytic Sensitivity to Primaquine and Other Drugs

Bancone

Chu

2021

Front. Pharmacol.

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Adverse effects of drugs on the blood

Meulenhoff

1984

Pharmaceutisch Weekblad Scientific Edition

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Amongst adverse drug reactions blood dyscrasias are not frequent, but they may have serious consequences. Compared with Sweden, data from The Netherlands are scarce. It is to be expected that regular reports about the incidence of drug-induced blood dyscrasias may play an important role in general prevention. Blood dyscrasias may be caused by a variety of drugs, from many pharmacotherapeutic groups with diverse chemical structures and with all application forms. Metabolism and distribution may influence the activity of drugs. Drug-induced anaemias, including aplastic anaemia, are briefly discussed. Toxic and immune mechanisms may occur. The same holds with regard to the leucopenias. Drug-induced thrombocytopenia is mainly immune-mediated (cytostatics being excluded as causative agents). In immune-mediated drug-induced blood dyscrasias often haptens must be formed. They can be formed in vivo in the liver or in the lymphocytes. In some cases they appear to be formed even in vitro. Tracing the causative agent of a dyscrasia, be it a drug or some other substance, requires a series of investigations, comprising usage of the drug, serology and cell culture. Provocation tests are seldom justified. Distinct preventive measures can be taken to minimize the risk of blood dyscrasias: avoidance of risky drugs, awareness of the patient about early clinical signs and haematological control.

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