Nonalcoholic fatty liver disease and nonalcoholic steatohepatitis in HIV infection: a metabolic approach of an infectious disease

Coronel-Castillo, Carlos E.; Qi, Xingshun; Contreras-Carmona, Jocelyn; Ramírez-Pérez, Oscar; Méndez-Sánchez, Nahúm

doi:10.1080/17474124.2019.1599284

Cited by 18 publications

(19 citation statements)

References 71 publications

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“…Hepatocellular carcinoma is the leading cause of death in patients with chronic liver disease. HCC is usually developed in an orderly progression from hepatitis to cirrhosis to early stage of cancer [33,34]. Serum marker detection shows many advantages over histopathological examination and there is a true need for sensitive and specific biomarkers.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of alpha-l-fucosidase for the diagnosis of hepatocellular carcinoma based on meta-analysis

Liu

Yang

2020

Journal of Laboratory Medicine

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ObjectivesThe main aim of the present study was to assess the diagnostic value of alpha-l-fucosidase (AFU) for hepatocellular carcinoma (HCC).MethodsStudies that explored the diagnostic value of AFU in HCC were searched in EMBASE, SCI, and PUBMED. The sensitivity, specificity, and DOR about the accuracy of serum AFU in the diagnosis of HCC were pooled. The methodological quality of each article was evaluated with QUADAS-2 (quality assessment for studies of diagnostic accuracy 2). Receiver operating characteristic curves (ROC) analysis was performed. Statistical analysis was conducted by using Review Manager 5 and Open Meta-analyst.ResultsEighteen studies were selected in this study. The pooled estimates for AFU vs. α-fetoprotein (AFP) in the diagnosis of HCC in 18 studies were as follows: sensitivity of 0.7352 (0.6827, 0.7818) vs. 0.7501 (0.6725, 0.8144), and specificity of 0.7681 (0.6946, 0.8283) vs. 0.8208 (0.7586, 0.8697), diagnostic odds ratio (DOR) of 7.974(5.302, 11.993) vs. 13.401 (8.359, 21.483), area under the curve (AUC) of 0.7968 vs. 0.8451, respectively.ConclusionsAFU is comparable to AFP for the diagnosis of HCC.

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Section: Discussionmentioning

confidence: 99%

Evaluation of alpha-l-fucosidase for the diagnosis of hepatocellular carcinoma based on meta-analysis

Liu

Yang

2020

Journal of Laboratory Medicine

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“…This occurrence causes mitochondrial dysfunction, ROS accumulation and augmented apoptosis, accompanied by increased lipid deposition within the cells, contributing to NAFLD in HIV-infected patients [ 233 ]. Finally, it has been reported that, in a clinical picture of HIV/HCV coinfection, the combined therapy with didanosine and ribavirin caused mitochondrial toxicity and consequent lipid deposition, due to reduced didanosine phosphorylation and its cytosolic accumulation [ 234 ]. Didanosine itself also leads to a dose-dependent inhibition of oxygen consumption and complex I and III activity, causing mitotoxicity and reduced ATP production.…”

Section: Drugs Inducing Hepatic Steatosismentioning

confidence: 99%

Detailed Molecular Mechanisms Involved in Drug-Induced Non-Alcoholic Fatty Liver Disease and Non-Alcoholic Steatohepatitis: An Update

et al. 2022

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Non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) are some of the biggest public health challenges due to their spread and increasing incidence around the world. NAFLD is characterized by intrahepatic lipid deposition, accompanied by dyslipidemia, hypertension, and insulin resistance, leading to more serious complications. Among the various causes, drug administration for the treatment of numerous kinds of diseases, such as antiarrhythmic and antihypertensive drugs, promotes the onset and progression of steatosis, causing drug-induced hepatic steatosis (DIHS). Here, we reviewed in detail the major classes of drugs that cause DIHS and the specific molecular mechanisms involved in these processes. Eight classes of drugs, among the most used for the treatment of common pathologies, were considered. The most diffused mechanism whereby drugs can induce NAFLD/NASH is interfering with mitochondrial activity, inhibiting fatty acid oxidation, but other pathways involved in lipid homeostasis are also affected. PubMed research was performed to obtain significant papers published up to November 2021. The key words included the class of drugs, or the specific compound, combined with steatosis, nonalcoholic steatohepatitis, fibrosis, fatty liver and hepatic lipid deposition. Additional information was found in the citations listed in other papers, when they were not displayed in the original search.

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“…The patient contracted the human immunodeficiency virus (HIV) and developed secondary TMAU after antiretroviral pharmacological therapy. It is well known that antiretroviral treatment induces liver damage 12 . He was tested for FMO3 genetic variants.…”

Section: What Is Known and Objectivesmentioning

confidence: 99%

Antiretroviral treatment leading to secondary trimethylaminuria: Genetic associations and successful management with riboflavin

et al. 2020

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What is known and objective Trimethylaminuria is a metabolic disorder characterized by excessive excretion of trimethylamine in body fluids following FMO3 gene mutations. Secondary forms of the disease may be due to consumption of trimethylamine precursor‐rich foods or metabolism of some xenobiotics. Case summary A HIV patient developed secondary trimethylaminuria following antiretroviral treatment. Riboflavin supplementation ameliorated his phenotype. 1H‐NMR confirmed increased urine level of TMA. Several genes involved in choline catabolism harboured missense mutations. Riboflavin supplement improved enzymatic activity of mutated enzymes promoting TMA clearance. What is new and conclusion Antiretrovirals may increase the concentration of TMA precursors. The present study reports antiretroviral treatment as risk factor for such secondary trimethylaminuria. Riboflavin is an effective treatment.

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Nonalcoholic fatty liver disease and nonalcoholic steatohepatitis in HIV infection: a metabolic approach of an infectious disease

Cited by 18 publications

References 71 publications

Evaluation of alpha-l-fucosidase for the diagnosis of hepatocellular carcinoma based on meta-analysis

Evaluation of alpha-l-fucosidase for the diagnosis of hepatocellular carcinoma based on meta-analysis

Detailed Molecular Mechanisms Involved in Drug-Induced Non-Alcoholic Fatty Liver Disease and Non-Alcoholic Steatohepatitis: An Update

Antiretroviral treatment leading to secondary trimethylaminuria: Genetic associations and successful management with riboflavin

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