RESUMEN
INTRODUCTION: Multivisceral, neurological, hepatic, and renal damage has been witnessed following the use of artemisinin-based combination therapy (ACT) and herbal medicine. These multiple organ damages make us think of muscle damage. The objective was to study the myotoxicity of the combination of ACTs with medicinal plants. MATERIALS AND METHODS: Muscle cells (RD cells) were brought into contact with preparations of antimalarial drugs and/or antimalarial herbs. The following drugs were used: artesunate 100 mg/amodiaquine 270 mg (ASAQ) and artemether 80 mg/lumefantrine 480 mg (AL); plant Sida acuta (PSA) and plant Enantia polycarpa (PEP) at 10 µg/ml. After 5 days of incubation, the cells were counted by using a hemocytometer with trypan blue solution. RESULTS: Artesunate/amodiaquine caused a significant drop in the number of muscle cells, compared to the control, between D2 and D4 (p < 0.001). There was also a significant difference between the control and artemether/lumefantrine between D2 (p < 0.01) and D4 (p < 0.001) and between the control and the Sida acuta plant, on D2 (p < 0.001), D4 (p < 0.001), and D5 (p < 0.05). In tubes treated with ASAQ and Sida acuta, cell mortality was over 30%. Finally, statistically significant cell destruction in the tubes treated with the combination of antimalarial drugs and traditional plants compared to those of the control was observed from D2 (p < 0.001). CONCLUSION: Artemisinin-based combination therapy remains effective and well tolerated. But its combination with medicinal plants induced myotoxic effects. This toxicity would appear to be of the additive type. Further studies should be able to better elucidate the mechanism of this toxicity.
RESUMEN
INTRODUCTION: Prior studies have shown an association between the onset of hepatonephritis and the use of arteminisin-based combination therapy (ACT) during the treatment of uncomplicated malaria. The objective of this study was to identify the risk factors of hepatonephritis occurrence because of the uncertainty regarding the appearance and the aggravation of this syndrome. METHODS: A case-non case study was carried out on 428 notifications of pharmacovigilance extracted from the database of the clinical pharmacology department of the teaching hospital of Cocody from 2008 to 2012. Twenty-two cases of hepatonephritis were identified. Univariate analysis and multivariate logistic regression were performed to identify the risk factors and an adjusted odds ratio (AOR) was calculated for each factor. The cut-off for significant association was set at 0.05. RESULTS: The average age of cases was comparable with that of non-cases (34.04±3.68 years versus 33.94±3.92 years) with a median duration of therapy of 5 days and 6 days respectively. Male (AOR: 6.71; P<0.0001), toxic antecedents, traditherapy (AOR: 6.25; P<0.0001), consumption of CTA (AOR: 1.25; P<0.0001), betalactam (AOR: 0.46; P<0.0001), fluoroquinolone and self-medication (AOR: 2.89; P<0.0001) would be the majors risk factors associated with hepatonephritis onset. The risk increased with the number of antimalarial drugs taken. The evolution towards the offset was less frequent (AOR: 0.078; P<0.02). CONCLUSION: The risk factors of hepatonephritis were the consumption of malarial drugs and connected molecules, self-medication and misuse. The outcome was generally unfavourable. Both the general population and health professionals should be trained on the good use of the antimalarial drugs.
