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Scientific Reports Mar 2021The aim of this systematic review was to perform qualitative and quantitative analysis on the toxic effects of chloroquine (CQ) and hydroxychloroquine (HCQ) on skeletal... (Meta-Analysis)
Meta-Analysis
The aim of this systematic review was to perform qualitative and quantitative analysis on the toxic effects of chloroquine (CQ) and hydroxychloroquine (HCQ) on skeletal muscles. We designed the study according to PRISMA guidelines. Studies for qualitative and quantitative analyses were selected according to the following inclusion criteria: English language; size of sample (> 5 patients), adult (> age of 18) patients, treated with CQ/HCQ for inflammatory diseases, and presenting and not presenting with toxic effects on skeletal muscles. We collected data published from 1990 to April 2020 using PubMed, Cochrane Library, EMBASE, and SciELO. Risk of bias for observational studies was assessed regarding the ROBIN-I scale. Studies with less than five patients (case reports) were selected for an additional qualitative analysis. We used the software Comprehensive Meta-Analysis at the confidence level of 0.05. We identified 23 studies for qualitative analysis (17 case-reports), and five studies were eligible for quantitative analysis. From case reports, 21 patients presented muscle weakness and confirmatory biopsy for CQ/HCQ induced myopathy. From observational studies, 37 patients out of 1,367 patients from five studies presented muscle weakness related to the use of CQ/HCQ, and 252 patients presented elevated levels of muscle enzymes (aldolase, creatine phosphokinase, and lactate dehydrogenase). Four studies presented data on 34 patients with confirmatory biopsy for drug-induced myopathy. No study presented randomized samples. The chronic use of CQ/HCQ may be a risk for drug-induced myopathy. There is substantiated need for proper randomized trials and controlled prospective studies needed to assess the clinical and subclinical stages of CQ/HCQ -induced muscle myopathy.
Topics: Adult; Aged; Creatine Kinase; Fructose-Bisphosphate Aldolase; Humans; Hydroxychloroquine; L-Lactate Dehydrogenase; Middle Aged; Muscle Weakness; Muscle, Skeletal; Observational Studies as Topic
PubMed: 33758324
DOI: 10.1038/s41598-021-86079-4 -
Frontiers in Bioscience (Landmark... Jan 2018Elevated levels of low density lipoproteins (LDLs) cause atherosclerotic disease, and proteomic analyses have found that these lipoproteins are endowed with... (Review)
Review
Elevated levels of low density lipoproteins (LDLs) cause atherosclerotic disease, and proteomic analyses have found that these lipoproteins are endowed with prenylcysteine lyase. This systematic review summarizes current understanding of this enzyme, now known as prenylcysteine oxidase 1 (PCYOX1), which hydrolyzes the thioether bond of prenylcysteines in the final step in the degradation of prenylated proteins, releasing hydrogen peroxide, cysteine and the isoprenoid aldehyde. Despite the high variability of the gene, no polymorphism has yet been associated with any disease. The liver, which is responsible for vehiculization of the enzyme in lipoproteins, is one of the main organs responsible for its expression, together with the gastrointestinal tract, kidney, male reproductive tissue and muscle. Moreover, although hepatic mRNA expression is sensitive to diet and hormones, the repercussion of these changes in LDLs containing PCYOX1 has not been addressed. One consequence of its elevated activity could be an increase in hydrogen peroxide, which might help to propagate the oxidative burden of LDLs, thus making PCYOX1 a potential pharmacological target and a new biomarker in cardiovascular disease.
Topics: Animals; Carbon-Sulfur Lyases; Cardiovascular Diseases; Gene Expression Profiling; Humans; Lipoproteins, LDL; Liver; Neoplasms; Neurodegenerative Diseases; Polymorphism, Single Nucleotide
PubMed: 28930587
DOI: 10.2741/4631