World Journal of Hepatology最新文献

{"title":"Coinfection with hepatic cystic and alveolar echinococcosis with abdominal wall abscess and sinus tract formation: A case report.","authors":"Miao-Miao Wang, Xiu-Qing An, Jin-Ping Chai, Jin-Yu Yang, Ji-De A, Xiang-Ren A","doi":"10.4254/wjh.v16.i2.279","DOIUrl":"10.4254/wjh.v16.i2.279","url":null,"abstract":"<p><strong>Background: </strong>Hepatic cystic and alveolar echinococcosis coinfections, particularly with concurrent abscesses and sinus tract formation, are extremely rare. This article presents a case of a patient diagnosed with this unique presentation, discussing the typical imaging manifestations of both echinococcosis types and detailing the diagnosis and surgical treatment experience thereof.</p><p><strong>Case summary: </strong>A 39-year-old Tibetan woman presented with concurrent hepatic cystic and alveolar echinococcosis, accompanied by abdominal wall abscesses and sinus tract formation. Initial conventional imaging examinations suggested only hepatic cystic echinococcosis, but intraoperative and postoperative pathological examination revealed the coinfection. Following radical resection of the lesions, the patient's condition improved, and she was discharged soon thereafter. Subsequent outpatient follow-ups confirmed no recurrence of the hydatid lesion and normal surgical wound healing. Though mixed hepatic cystic and alveolar echinococcosis with abdominal wall abscesses and sinus tract formations are rare, the general treatment approach remains consistent with that of simpler infections of alveolar echinococcosis.</p><p><strong>Conclusion: </strong>Lesions involving the abdominal wall and sinus tract formation, may require radical resection. Long-term prognosis includes albendazole and follow-up examinations.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2024-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10941752/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140144193","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Insights into skullcap herb-induced liver injury.","authors":"Jonathan Soldera","doi":"10.4254/wjh.v16.i2.120","DOIUrl":"10.4254/wjh.v16.i2.120","url":null,"abstract":"<p><p>This editorial addresses the growing concern of herb-induced liver injury (HILI), focusing on a unique case of Skullcap-induced HILI report. This editorial underscore the significant mortality rate linked to Skullcap-induced HILI, emphasizing the importance of vigilant monitoring and intervention. As herbal supplement usage rises, collaboration among clinicians and researchers is crucial to comprehend and address the complexities of HILI, particularly those involving Skullcap.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2024-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10941739/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140144199","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Yinhuang granule alleviates carbon tetrachloride-induced liver fibrosis in mice and its mechanism.","authors":"Hao Ouyang, Hui Miao, Zhen Li, Duan Wu, Si-Cheng Gao, Yao-Yao Dai, Xiao-Di Gao, Hai-Sheng Chai, Wei-Ye Hu, Jun-Feng Zhu","doi":"10.4254/wjh.v16.i2.264","DOIUrl":"10.4254/wjh.v16.i2.264","url":null,"abstract":"<p><strong>Background: </strong>Liver fibrosis is a formidable global medical challenge, with no effective clinical treatment currently available. Yinhuang granule (YHG) is a proprietary Chinese medicine comprising <i>Scutellariae</i> Radix and <i>Lonicerae Japonicae</i> Flos. It is frequently used for upper respiratory tract infections, pharyngitis, as well as acute and chronic tonsillitis.</p><p><strong>Aim: </strong>To investigate the potential of YHG in alleviating carbon tetrachloride (CCl₄)-induced liver fibrosis in mice.</p><p><strong>Methods: </strong>To induce a hepatic fibrosis model in mice, this study involved intraperitoneal injections of 2 mL/kg of CCl₄ twice a week for 4 wk. Meanwhile, liver fibrosis mice in the low dose of YHG (0.4 g/kg) and high dose of YHG (0.8 g/kg) groups were orally administered YHG once a day for 4 wk. Serum alanine/aspartate aminotransferase (ALT/AST) activity and liver hydroxyproline content were detected. Sirius red and Masson's trichrome staining assay were conducted. Real-time polymerase chain reaction, western-blot and enzyme-linked immunosorbent assay were conducted. Liver glutathione content, superoxide dismutase activity level, reactive oxygen species and protein carbonylation amount were detected.</p><p><strong>Results: </strong>The administration of YHG ameliorated hepatocellular injury in CCl₄-treated mice, as reflected by decreased serum ALT/AST activity and improved liver histological evaluation. YHG also attenuated liver fibrosis, evident through reduced liver hydroxyproline content, improvements in Sirius red and Masson's trichrome staining, and lowered serum hyaluronic acid levels. Furthermore, YHG hindered the activation of hepatic stellate cells (HSCs) and ameliorated oxidative stress injury and inflammation in liver from CCl₄-treated mice. YHG prompted the nuclear accumulation of nuclear factor erythroid 2-related factor 2 (Nrf2) and upregulated the expression of Nrf2-dependent downstream antioxidant genes. In addition, YHG promoted mitochondrial biogenesis in liver from CCl₄-treated mice, as demonstrated by increased liver adenosine triphosphate content, mitochondrial DNA levels, and the expression of peroxisome proliferator-activated receptor gamma coactivator 1 alpha and nuclear respiratory factor 1.</p><p><strong>Conclusion: </strong>YHG effectively attenuates CCl₄-induced liver fibrosis in mice by inhibiting the activation of HSCs, reducing inflammation, alleviating liver oxidative stress damage through Nrf2 activation, and promoting liver mitochondrial biogenesis.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2024-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10941736/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140144207","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of G3BP1 in the prognosis of acute and acute-on-chronic liver failure after the treatment of artificial liver support system.","authors":"Wen-Yuan Li, Lu-Wen Wang, Jin Dong, Yao Wang","doi":"10.4254/wjh.v16.i2.251","DOIUrl":"10.4254/wjh.v16.i2.251","url":null,"abstract":"<p><strong>Background: </strong>The increased expression of G3BP1 was positively correlated with the prognosis of liver failure.</p><p><strong>Aim: </strong>To investigate the effect of G3BP1 on the prognosis of acute liver failure (ALF) and acute-on-chronic liver failure (ACLF) after the treatment of artificial liver support system (ALSS).</p><p><strong>Methods: </strong>A total of 244 patients with ALF and ACLF were enrolled in this study. The levels of G3BP1 on admission and at discharge were detected. The validation set of 514 patients was collected to verify the predicted effect of G3BP1 and the viability of prognosis.</p><p><strong>Results: </strong>This study was shown that lactate dehydrogenase (LDH), alpha-fetoprotein (AFP) and prothrombin time were closely related to the prognosis of patients. After the ALSS treatment, the patient' amount of decreased G3BP1 index in difference of G3BP1 between the value of discharge and admission (difG3BP1) < 0 group had a nearly 10-fold increased risk of progression compared with the amount of increased G3BP1 index. The subgroup analysis showed that the difG3BP1 < 0 group had a higher risk of progression, regardless of model for end-stage liver disease high-risk or low-risk group. At the same time, compared with the inflammatory marks [tumor necrosis factor-α, interleukin (IL)-1β and IL-18], G3BP1 had higher discrimination and was more stable in the model analysis and validation set. When combined with AFP and LDH, concordance index was respectively 0.84 and 0.8 in training and validation cohorts.</p><p><strong>Conclusion: </strong>This study indicated that G3BP1 could predict the prognosis of ALF or ACLF patients treated with ALSS. The combination of G3BP1, AFP and LDH could accurately evaluate the disease condition and predict the clinical endpoint of patients.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2024-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10941744/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140144198","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-oxidative stress treatment and current clinical trials.","authors":"Chun-Ye Zhang, Ming Yang","doi":"10.4254/wjh.v16.i2.294","DOIUrl":"10.4254/wjh.v16.i2.294","url":null,"abstract":"<p><p>Oxidative stress disturbs the balance between the production of reactive oxygen species (ROS) and the detoxification biological process. It plays an important role in the development and progression of many chronic diseases. Upon exposure to oxidative stress or the inducers of ROS, the cellular nucleus undergoes some biological processes <i>via</i> different signaling pathways, such as stress adaption through the forkhead box O signaling pathway, inflammatory response through the IκB kinase/nuclear factor-κB signaling pathway, hypoxic response <i>via</i> the hypoxia-inducible factor/prolyl hydroxylase domain proteins pathway, DNA repair or apoptosis through the p53 signaling pathway, and antioxidant response through the Kelch-like ECH-associated protein 1/nuclear factor E2-related factor 2 signaling pathway. These processes are involved in many diseases. Therefore, oxidative stress has gained more attraction as a targeting process for disease treatment. Meanwhile, anti-oxidative stress agents have been widely explored in pre-clinical trials. However, only limited clinical trials are performed to evaluate the efficacy of anti-oxidative stress agents or antioxidants in diseases. In this letter, we further discuss the current clinical trials related to anti-oxidative stress treatment in different diseases. More pre-clinical studies and clinical trials are expected to use anti-oxidative stress strategies as disease treatment or dietary supplementation to improve disease treatment outcomes.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2024-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10941751/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140144189","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Autoimmune hepatitis and primary sclerosing cholangitis after direct-acting antiviral treatment for hepatitis C virus: A case report.","authors":"Yoshiki Morihisa, Hobyung Chung, Shuichiro Towatari, Daisuke Yamashita, Tetsuro Inokuma","doi":"10.4254/wjh.v16.i2.286","DOIUrl":"10.4254/wjh.v16.i2.286","url":null,"abstract":"<p><strong>Background: </strong>Chronic hepatitis C virus (HCV) infection is a major global health concern that leads to liver fibrosis, cirrhosis, and cancer. Regimens containing direct-acting antivirals (DAAs) have become the mainstay of HCV treatment, achieving a high sustained virological response (SVR) with minimal adverse events.</p><p><strong>Case summary: </strong>A 74-year-old woman with chronic HCV infection was treated with the DAAs ledipasvir, and sofosbuvir for 12 wk and achieved SVR. Twenty-four weeks after treatment completion, the liver enzyme and serum IgG levels increased, and antinuclear antibody became positive without HCV viremia, suggesting the development of autoimmune hepatitis (AIH). After liver biopsy indicated AIH, a definite AIH diagnosis was made and prednisolone was initiated. The treatment was effective, and the liver enzyme and serum IgG levels normalized. However, multiple strictures of the intrahepatic and extrahepatic bile ducts with dilatation of the peripheral bile ducts appeared on magnetic resonance cholangiopancreatography after 3 years of achieving SVR, which were consistent with primary sclerosing cholangitis.</p><p><strong>Conclusion: </strong>The potential risk of developing autoimmune liver diseases after DAA treatment should be considered.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2024-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10941733/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140144190","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Contemporary concepts of prevention and management of gastroesophageal variceal bleeding in liver cirrhosis patients.","authors":"Dmitry Victorovich Garbuzenko","doi":"10.4254/wjh.v16.i2.126","DOIUrl":"10.4254/wjh.v16.i2.126","url":null,"abstract":"<p><p>This editorial describes the contemporary concepts of prevention and management of gastroesophageal variceal bleeding in liver cirrhosis (LC) patients according to the current guidelines. Gastroesophageal variceal bleeding is the most dangerous complication of portal hypertension in LC patients. Risk stratification and determination of an individual approach to the choice of therapeutic measures aimed at their prevention and management has emerged as one of the top concerns in modern hepatology. According to the current guidelines, in the absence of clinically significant portal hypertension, etiological and non-etiological therapies of LC is advisable for the primary preventing gastroesophageal variceal bleeding, whereas its presence serves as an indication for the administration of non-selective β-blockers, among which carvedilol is the drug of choice. Non-selective β-blockers, as well as endoscopic variceal ligation and transjugular intrahepatic portosystemic shunt can be used to prevent recurrence of gastroesophageal variceal bleeding. Pharmacotherapy with vasoactive drugs (terlipressin, somatostatin, octreotide), endoscopic variceal ligation, endovascular techniques and transjugular intrahepatic portosystemic shunt are recommended for the treatment of acute gastroesophageal variceal bleeding. Objective and accurate risk stratification of gastroesophageal variceal bleeding will allow developing individual strategies for their prevention and management, avoiding the first and further decompensation in LC, which will improve the prognosis and survival of patients suffering from it.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2024-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10941750/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140144194","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of SARS-CoV-2 infection on incidence and treatment strategies of hepatocellular carcinoma in people with chronic liver disease.","authors":"Lung-Yi Mak, Matthew Shing Hin Chung, Xue Li, Francisco Tsz Tsun Lai, Eric Yuk Fai Wan, Celine Sze Ling Chui, Franco Wing Tak Cheng, Esther Wai Yin Chan, Ching Lung Cheung, Ivan Chi Ho Au, Xi Xiong, Wai-Kay Seto, Man-Fung Yuen, Carlos King Ho Wong, Ian Chi Kei Wong","doi":"10.4254/wjh.v16.i2.211","DOIUrl":"10.4254/wjh.v16.i2.211","url":null,"abstract":"<p><strong>Background: </strong>Chronic liver disease (CLD) was associated with adverse clinical outcomes among people with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection.</p><p><strong>Aim: </strong>To determine the effects of SARS-CoV-2 infection on the incidence and treatment strategy of hepatocellular carcinoma (HCC) among patients with CLD.</p><p><strong>Methods: </strong>A retrospective, territory-wide cohort of CLD patients was identified from an electronic health database in Hong Kong. Patients with confirmed SARS-CoV-2 infection [coronavirus disease 2019 (COVID-19)+CLD] between January 1, 2020 and October 25, 2022 were identified and matched 1:1 by propensity-score with those without (COVID-19-CLD). Each patient was followed up until death, outcome event, or November 15, 2022. Primary outcome was incidence of HCC. Secondary outcomes included all-cause mortality, adverse hepatic outcomes, and different treatment strategies to HCC (curative, non-curative treatment, and palliative care). Analyses were further stratified by acute (within 20 d) and post-acute (21 d or beyond) phases of SARS-CoV-2 infection. Incidence rate ratios (IRRs) were estimated by Poisson regression models.</p><p><strong>Results: </strong>Of 193589 CLD patients (> 95% non-cirrhotic) in the cohort, 55163 patients with COVID-19+CLD and 55163 patients with COVID-19-CLD were included after 1:1 propensity-score matching. Upon 249-d median follow-up, COVID-19+CLD was not associated with increased risk of incident HCC (IRR: 1.19, 95%CI: 0.99-1.42, <i>P</i> = 0.06), but higher risks of receiving palliative care for HCC (IRR: 1.60, 95%CI: 1.46-1.75, <i>P</i> < 0.001), compared to COVID-19-CLD. In both acute and post-acute phases of infection, COVID-19+CLD were associated with increased risks of all-cause mortality (acute: IRR: 7.06, 95%CI: 5.78-8.63, <i>P</i> < 0.001; post-acute: IRR: 1.24, 95%CI: 1.14-1.36, <i>P</i> < 0.001) and adverse hepatic outcomes (acute: IRR: 1.98, 95%CI: 1.79-2.18, <i>P</i> < 0.001; post-acute: IRR: 1.24, 95%CI: 1.13-1.35, <i>P</i> < 0.001), compared to COVID-19-CLD.</p><p><strong>Conclusion: </strong>Although CLD patients with SARS-CoV-2 infection were not associated with increased risk of HCC, they were more likely to receive palliative treatment than those without. The detrimental effects of SARS-CoV-2 infection persisted in post-acute phase.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2024-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10941734/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140144196","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Predictors of portal vein thrombosis after splenectomy in patients with cirrhosis.","authors":"Ting Li, Li-Li Wang, Ya-Ping Li, Jian Gan, Xi-Sheng Wei, Xiao-Rong Mao, Jun-Feng Li","doi":"10.4254/wjh.v16.i2.241","DOIUrl":"10.4254/wjh.v16.i2.241","url":null,"abstract":"<p><strong>Background: </strong>Portal vein thrombosis (PVT) is a commonthsn complication after splenectomy in patients with cirrhosis. However, the predictors of postoperative PVT are not known.</p><p><strong>Aim: </strong>To investigate the predictors of PVT after splenectomy in patient with cirrhosis.</p><p><strong>Methods: </strong>A total of 45 patients with cirrhosis who underwent splenectomy were consecutively enrolled from January 2017 to December 2018. The incidence of PVT at 1 months, 3 months, and 12 months after splenectomy in patients with cirrhosis was observed. The hematological indicators, biochemical and coagulation parameters, and imaging features were recorded at baseline and at each observation point. The univariable, multivariable, receiver operating characteristic curve and time-dependent curve analyses were performed.</p><p><strong>Results: </strong>The cumulative incidence of PVT was 40.0%, 46.6%, and 48.9% at 1 months, 3 months, and 12 months after splenectomy. Multivariable analysis showed that portal vein diameter (PVD) ≥ 14.5 mm and monthsdel‎ end-stage liver disease (MELD) score > 10 were independent predictors of PVT at 1 months, 3 months, and 12 months after splenectomy (<i>P</i> < 0.05). Time-dependent curve showed that the cumulative incidence of PVT was significantly different between patients with MELD score ≤ 10 and > 10 (<i>P</i> < 0.05). In addition, the cumulative incidence of PVT in the PVD ≥ 14.5 mm group was significantly higher than that in the PVD < 14.5 mm group (<i>P</i> < 0.05).</p><p><strong>Conclusion: </strong>Wider PVD and MELD score > 10 were independent predictors of PVT at 1 months, 3 months, and 12 months after splenectomy in patient with cirrhosis.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2024-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10941749/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140144205","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic-associated fatty liver disease and sarcopenia: A double whammy.","authors":"Aditya Viswanath, Sherouk Fouda, Cornelius James Fernandez, Joseph M Pappachan","doi":"10.4254/wjh.v16.i2.152","DOIUrl":"10.4254/wjh.v16.i2.152","url":null,"abstract":"<p><p>The prevalence of metabolic-associated fatty liver disease (MAFLD) has increased substantially in recent years because of the global obesity pandemic. MAFLD, now recognized as the number one cause of chronic liver disease in the world, not only increases liver-related morbidity and mortality among sufferers but also worsens the complications associated with other comorbid conditions such as cardiovascular disease, type 2 diabetes mellitus, obstructive sleep apnoea, lipid disorders and sarcopenia. Understanding the interplay between MAFLD and these comorbidities is important to design optimal therapeutic strategies. Sarcopenia can be either part of the disease process that results in MAFLD (<i>e.g.</i>, obesity or adiposity) or a consequence of MAFLD, especially in the advanced stages such as fibrosis and cirrhosis. Sarcopenia can also worsen MAFLD by reducing exercise capacity and by the production of various muscle-related chemical factors. Therefore, it is crucial to thoroughly understand how we deal with these diseases, especially when they coexist. We explore the pathobiological interlinks between MAFLD and sarcopenia in this comprehensive clinical update review article and propose evidence-based therapeutic strategies to enhance patient care.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2024-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10941748/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140145036","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}