Liver Disease In Persons Research Articles

Metabolic dysfunction associated steatotic liver disease in persons with HIV: understanding the serious implications and renaming of 'fatty liver disease'.

Metabolic dysfunction associated steatotic liver disease in persons with HIV: understanding the serious implications and renaming of 'fatty liver disease'.

Non-alcoholic fatty liver disease is not associated with impairment in health-related quality of life in virally suppressed persons with human immune deficiency virus.

Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease in persons with HIV (PWH) (HIV-NAFLD). It is unknown if HIV-NAFLD is associated with impairment in health-related quality of life (HRQOL). We examined HRQOL in PWH with and without NAFLD, compared HRQOL in HIV- versus primary NAFLD, and determined factors associated with HRQOL in these groups. Prospectively enrolled 200 PWH and 474 participants with primary NAFLD completed the Rand SF-36 assessment which measures 8 domains of HRQOL. Individual domain scores were used to create composite physical and mental component summary scores. Univariate and multivariate analyses determined variables associated with HRQOL in PWH and in HIV- and primary NAFLD. In PWH, 48% had HIV-NAFLD, 10.2% had clinically significant fibrosis, 99.5% were on antiretroviral therapy, and 96.5% had HIV RNA <200 copies/ml. There was no difference in HRQOL in PWH with or without NAFLD. Diabetes, non-Hispanic ethnicity, and nadir CD4 counts were independently associated with impaired HRQOL in PWH. In HIV-NAFLD, HRQOL did not differ between participants with or without clinically significant fibrosis. Participants with HIV-NAFLD compared to those with primary NAFLD were less frequently cisgender females, White, more frequently Hispanic, had lower BMI and lower frequency of obesity and diabetes. HRQOL of individuals with HIV-NAFLD was not significantly different from those with primary NAFLD. In conclusion, in virally suppressed PWH, HRQOL is not different between participants with or without HIV-NAFLD. HRQOL is not different between HIV-NAFLD and primary NAFLD.

Synergistic Associations of PNPLA3 I148M Variant, Alcohol Intake, and Obesity With Risk of Cirrhosis, Hepatocellular Carcinoma, and Mortality

Alcohol drinking and obesity are associated with an increased risk of cirrhosis and hepatocellular carcinoma (HCC), but the risk is not uniform among people with these risk factors. Genetic variants, such as I148M in the patatin-like phospholipase domain-containing protein 3 (PNPLA3) gene, may play an important role in modulating cirrhosis and HCC risk. To investigate the joint associations of the PNPLA3 I148M variant, alcohol intake, and obesity with the risk of cirrhosis, HCC, and liver disease-related mortality. This prospective cohort study analyzed 414 209 participants enrolled in the UK Biobank study from March 2006 to December 2010. Participants had no previous diagnosis of cirrhosis and HCC and were followed up through March 2021. Self-reported alcohol intake (nonexcessive vs excessive), obesity (body mass index ≥30 [calculated as weight in kilograms divided by height in meters squared]), and PNPLA3 I148M variant status (noncarrier, heterozygous carrier, or homozygous carrier) from initial assessment. The primary outcomes were incident cirrhosis and HCC cases and liver disease-related death ascertained from inpatient hospitalization records and death registry. The risks were calculated by Cox proportional hazards regression models. A total of 414 209 participants (mean [SD] age, 56.3 [8.09] years; 218 567 women [52.8%]; 389 452 White race and ethnicity [94.0%]) were included. Of these participants, 2398 participants (0.6%) developed cirrhosis (5.07 [95% CI, 4.87-5.28] cases per 100 person-years), 323 (0.1%) developed HCC (0.68 [95% CI, 0.61-0.76] cases per 100 person-years), and 878 (0.2%) died from a liver disease-related cause (1.76 [95% CI, 1.64-1.88] cases per 100 person-years) during a median follow-up of 10.9 years. Synergistic interactions between the PNPLA3 I148M variant, obesity, and alcohol intake were associated with the risk of cirrhosis, HCC, and liver disease-related mortality. The risk of cirrhosis increased supramultiplicatively (adjusted hazard ratio [aHR], 17.52; 95% CI, 12.84-23.90) in individuals with obesity, with excessive drinking, and who were homozygous carriers compared with those with no obesity, with nonexcessive drinking, and who were noncarriers. Supramultiplicative associations between the 3 factors and risks of HCC were found in individuals with 3 risk factors (aHR, 30.13; 95% CI, 16.51-54.98) and liver disease-related mortality (aHR, 21.82; 95% CI, 13.78-34.56). The PNPLA3 I148M variant status significantly differentiated the risk of cirrhosis, HCC, and liver disease-related mortality in persons with excessive drinking and obesity. This study found synergistic associations of the PNPLA3 I148M variant, excessive alcohol intake, and obesity with increased risk of cirrhosis, HCC, and liver disease-related death in the general population. The PNPLA3 I148M variant status may help refine the risk stratification for liver disease in persons with excessive drinking and obesity who may need early preventive measures.

Long-term trends of alanine aminotransferase levels among persons living with human immunodeficiency virus/hepatitis B virus with and without hepatitis delta coinfection

BackgroundHepatitis delta virus (HDV) infection accelerates the progression of liver disease in persons living with HIV and hepatitis B virus (HBV) coinfection. We explored the association between HDV infection and alanine aminotransferase (ALT) elevation during tenofovir-containing antiretroviral treatment among persons living with HIV/HBV.Materials and methodsWe included persons living with HIV/HBV with and without HDV starting tenofovir-containing antiretroviral therapy (ART) in three European cohorts with at least 18 months of follow-up. We defined HDV infection as a positive anti-HDV antibody test. We assessed risk factors for ALT elevation ≥ 1.25x upper limit of normal after 5 years of tenofovir-treatment using multivariate logistic regression models. The difference in ALT trends between individuals with and without HDV was evaluated using linear mixed effects models.Results61/518 (11.8%) participants had an HDV infection. Among individuals with HDV, 63.9% had ALT elevation after 2 years and 55.6% after 5 years of tenofovir, whereas the estimates were 34.1% after two and 27.0% after 5 years in those without HDV. HDV coinfection (adjusted odds ratio 2.8, 95% confidence interval 1.4–5.8) and obesity at baseline (adjusted odds ratio 3.2, 95% confidence interval 1.2–8.0) were associated with ALT elevation after 5 years of tenofovir therapy. Mean ALT levels were consistently higher during follow-up in participants with HDV compared to those without HDV.ConclusionPersistent ALT elevation is common in persons living with HIV/HBV in Europe despite adequate HBV therapy. HDV coinfection and obesity are independent risk factors for persistent ALT elevation during long-term tenofovir treatment.

Study of prevalence of non- alcoholic fatty liver disease in type 2 diabetes and its correlation with liver function tests and fasting lipid profile

Introduction: NAFLD is the third leading indication for liver transplantation. The prevalence of NAFLD has been documented to be 15%-30% in general population and 70%-75% in type 2 diabetes population. Indian population has a higher body fat content and abdominal adiposity: the more upper body fat content is associated with insulin resistance causing more NAFLD. There is evidence that Type 2 DM patients with NAFLD are at higher risk of developing cirrhosis compared to non-diabetic patients. The present study was conducted in a tertiary care hospital from south India to know the Prevalence of Non -Alcoholic Fatty Liver Disease in persons with Type 2 Diabetes Mellitus and to correlate the results of Liver Function Tests and fasting Lipid Profile with NAFLD. Materials and Methods: This is an observational study done in patients attending OPDs in department of General Medicine during 1st January 2018 to 30th June 2019 in Maharajah’s Institute of Medical Sciences, Vizianagaram and Andhra Pradesh. Results: The prevalence of NAFLD, as assessed by ultrasound examination, was 67%, mean age of subjects in the NAFLD group was 53.06 ± 6.20 years. Prevalence in males was 45.2%. High BMI is associated with NAFLD (P&lt; 0.001).

End-stage liver disease in persons with hemophilia and transfusion-associated infections

Many persons with hemophilia were infected with hepatitis C and B viruses (HCV, HBV) and HIV, but the consequences of these transfusion-acquired infections are poorly defined. We estimated the risk of HCV-related end-stage liver disease (ESLD) and the associations of age, HBV, and HIV with that risk. All 1816 HCV-seropositive hemophilic patients at 16 centers were followed for up to 16 years. Of these, 624 were HIV(-) and 1192 were HIV-coinfected; 135 had persistent HBV surface antigenemia, 1374 had resolved HBV infection, and 287 were HBV-uninfected. ESLD was defined as bleeding esophageal varices, hepatic encephalopathy, persistent ascites, or death excluding nonhepatic causes of these conditions. Competing risk models were used to estimate the annual hazard rate and cumulative incidence of ESLD. Proportional hazards models were used to estimate relative hazards of ESLD with covariates. ESLD developed in 127 of the HCV/HIV-coinfected participants, with an estimated 16-year cumulative incidence of 14.0% (95% confidence interval [CI], 11.6%-16.4%). Without HIV, 10 HCV-infected participants developed ESLD, for a significantly lower cumulative incidence of 2.6% (95% CI, 1.0%-4.3%, P <.0001). ESLD risk increased steeply with age in both groups. With HIV, ESLD risk was increased 8.1-fold (95% CI, 1.9-35.2) with HBV surface antigenemia, 2.1-fold (95% CI, 1.3-3.3) with fewer than 0.2 x 10(9)/L (200/microL) CD4(+) lymphocytes, and 1.04-fold (95% CI, 1.03-1.06) per year of age. Thus, HIV is associated with a markedly increased risk of HCV-related ESLD for persons with hemophilia, particularly with HBV infection, low CD4(+) lymphocytes, or older age.

Screening for Nonalcoholic Fatty Liver Disease in Persons with Type 2 Diabetes in the United States Is Cost-effective: A Comprehensive Cost-Utility Analysis

Screening for Nonalcoholic Fatty Liver Disease in Persons with Type 2 Diabetes in the United States Is Cost-effective: A Comprehensive Cost-Utility Analysis

LBP22 - Screening for non-alcoholic fatty liver disease in persons with type 2 diabetes in the U.S. is cost effective: A comprehensive economical analysis

LBP22 - Screening for non-alcoholic fatty liver disease in persons with type 2 diabetes in the U.S. is cost effective: A comprehensive economical analysis

Features of therapy of alcoholic liver disease in persons of young age

The aim of this study was to study the eff ects of using the infusion drug Remaxol in young patients with alcoholic liver disease.Materials and methods: the clinical and laboratory data of 80 young patients with alcoholic liver disease were analyzed, divided depending on the treatment regimen into 2 groups: the main (n = 44) who received Remaxol according to the scheme: 400 ml iv, drip, at a rate 40–60 drops per minute daily, course No. 5–10, and control (n = 36) — received basic therapy. In all patients, the dynamics in blood serum was studied: lipid peroxidation indices (malondialdehyde, diene conjugates), antioxidant protection enzymes (catalase, SOD, glutathione peroxidase), markers of cytolysis, cholestasis and lipid metabolism.Results: initially there was a significant increase in lipid peroxidation processes, accompanied by slight stimulation of the antioxidant system of the liver and pronounced signs of cytolysis and cholestasis. The inclusion of Remaxol in treatment regimens leads to a significant decrease in the level of malondialdehyde and diene conjugates, and the restoration of the antioxidant system (increase in catalase, SOD, and glutathione peroxidase). At the same time, a marked decrease in the syndromes of cytolysis and cholestasis was noted, which was accompanied by an improvement in the condition of the patients: cessation of nausea, restoration of appetite and sleep, and improvement of well-being.

Risk Factors for Severe Liver Disease in Patients With Type 2 Diabetes

Type 2 diabetes is a risk factor for development of cirrhosis and hepatocellular carcinoma. However, risk factors that identify persons with the highest risk for these outcomes are missing from unselected, population-based cohorts. The National Diabetes Register contains data on about 90% of persons in Sweden with type 2 diabetes. In this cohort study, persons with type 2 diabetes listed in the National Diabetes Register were compared with 5 individuals from the general population (controls), matched for age, sex, and county. In total, 406 770 persons with type 2 diabetes and 2 033 850 controls were included and followed for 21 596 934 person-years. We used population-based registers to determine the incidence of severe liver disease, defined as a diagnosis of hepatocellular carcinoma, cirrhosis, decompensation, liver failure and/or death due to liver disease during follow up. Cox regression was performed to estimate the risk of severe liver disease and to examine risk factors in persons with type 2 diabetes. Risk for severe liver disease was increased in patients with type 2 diabetes compared to controls (hazard ratio, 2.28; 95% CI, 2.21-2.36). Risk factors associated with severe liver disease in persons with type 2 diabetes were higher age, male sex, hypertension, higher body mass index, lower glomerular filtration rate, microalbuminuria, and smoking. Statins were associated with a decreased risk of severe liver disease. Persons with type 2 diabetes have an increased risk for severe liver disease. Knowledge of risk factors can be helpful in identifying persons with type 2 diabetes who have a high risk for severe liver disease.

Impact of Birth Cohort Screening for Hepatitis C

Hepatitis C (HCV) is a leading cause of liver-related complications, and the burden of liver disease is expected to increase. Given the over-representation of HCV-related liver disease in persons born between 1945 and 1965, and the failure of risk-based screening to identify many infected persons, birth cohort screening has been advocated and endorsed by both the Centers for Disease Control and United States Preventive Services Task Force, regardless of the presence of risk factors. Birth cohort testing is more cost-effective than risk-based screening especially when those with more advanced disease are given priority for treatment. Several barriers exist at the patient and provider level that need to be overcome to fully realize the potential benefit of birth cohort screening in reducing HCV-related morbidity and mortality.

A Novel SERPINA1 Mutation Causing Serum Alpha1-Antitrypsin Deficiency

Mutations in the SERPINA1 gene can cause deficiency in the circulating serine protease inhibitor α1-Antitrypsin (α1AT). α1AT deficiency is the major contributor to pulmonary emphysema and liver disease in persons of European ancestry, with a prevalence of 1 in 2500 in the USA. We present the discovery and characterization of a novel SERPINA1 mutant from an asymptomatic Middle Eastern male with circulating α1AT deficiency. This 49 base pair deletion mutation (T379Δ), originally mistyped by IEF, causes a frame-shift replacement of the last sixteen α1AT residues and adds an extra twenty-four residues. Functional analysis showed that the mutant protein is not secreted and prone to intracellular aggregation.

Human Immunodeficiency Virus-Related Microbial Translocation and Progression of Hepatitis C

Human immunodeficiency virus (HIV)-1 infection has been associated with enhanced microbial translocation, and microbial translocation is a mechanism through which alcohol and some enteric conditions cause liver disease. We hypothesized that HIV promotes liver disease by enhancing microbial translocation. We studied human cohorts in which hepatitis C virus (HCV) and HIV outcomes were carefully characterized. HIV-related CD4(+) lymphocyte depletion was strongly associated with microbial translocation as indicated by elevated levels of circulating lipopolysaccharide (LPS), LPS-binding protein, soluble CD14, and fucose-binding lectin (AAL) reactive to immunoglobulin G specific for the alpha-galactose epitope and suppressed levels of endotoxin core antibodies (EndoCAb IgM) in HIV-infected subjects compared with the same persons before they had HIV infection and compared with HIV-uninfected subjects. The same measures of microbial translocation were strongly associated with HCV-related liver disease progression (cirrhosis), eg, LPS, odds ratio, 19.0 (P = .002); AAL, odds ratio, 27.8 (P < .0001); in addition, levels of LPS were elevated prior to recognition of cirrhosis. Microbial translocation may be a fundamental mechanism through which HIV accelerates progression of chronic liver disease.

Psychiatric behavioral aspects of comanagement of hepatitis C virus and HIV

Coinfection with HIV hastens the progression of liver disease in persons with hepatitis C virus (HCV) infection. As mortality directly due to HIV continues to decrease among persons who are HIV-positive, coinfection with HCV has emerged as a leading cause of death. There is increasing attention to the need to actively treat HCV infection in HIV/HCV coinfected patients. Current HCV treatment with pegylated interferon and ribavirin achieves sustained viral response in up to 40% of coinfected patients but has numerous neuropsychiatric side effects. Providers are hesitant to begin HCV treatment in the coinfected population given the high prevalence of existing psychiatric illness, cognitive impairment, and substance use disorders. There is an urgent need for research into the psychiatric and behavioral predictors of HCV treatment adherence and virologic outcome, as well as into the optimal psychiatric management of the neuropsychiatric sequelae of HCV therapy.

HAART and the HCV-infected liver: friend or foe?

HAART and the HCV-infected liver: friend or foe?

Slowing the progression of chronic hepatitis B

PREVIEWAbout 350 million people worldwide have chronic hepatitis B virus (HBV) infection. Up to 40% of persons infected with the virus may go on to have complications related to cirrhosis or hepatocellular carcinoma. Antiviral therapy can suppress viral replication and halt the progression of liver disease in persons with chronic infection. In this article, the authors explore the modes of HBV transmission, describe the characteristics of chronic infection, and review the drugs available to treat it.

End-stage liver disease in persons with hemophilia and transfusion-associated infections : J. Goedert, E. Eyster, M. Lederman, et al. Blood 100:1584–1589, 2002

End-stage liver disease in persons with hemophilia and transfusion-associated infections : J. Goedert, E. Eyster, M. Lederman, et al. Blood 100:1584–1589, 2002

Insights into SEN virus prevalence, transmission, and treatment in community-based persons and patients with liver disease referred to a liver disease unit.

To document the prevalence and routes of transmission of SEN virus (SEN-V) in community-based individuals and patients referred to a liver disease unit, stored serum samples obtained from 160 Canadian Inuit and 140 patients with liver disease were tested for SEN-V DNA by polymerase chain reaction. In the community-based population, SEN-V was present in 57 (36%) of 160 persons. SEN-V-positive individuals tended to be younger and were more often male. Liver enzyme levels and serologic markers for hepatitis A and B viruses were similar in SEN-V-positive and SEN-V-negative individuals. SEN-V was present in 30 (21%) of the 140 patients with liver disease. Age, sex, risk factors for viral acquisition, prevalence of symptoms, and liver biochemical and histological findings were similar in SEN-V-positive and SEN-V-negative patients. These results indicate that SEN-V infection is a common viral infection in both healthy individuals and patients with chronic liver disease, that transmission likely occurs via nonparenteral routes, and that SEN-V infection is not associated with higher rates of or more-severe liver disease in persons with preexisting liver disease.

Influence of Human Immunodeficiency Virus Infection on the Course of Hepatitis C Virus Infection: A Meta‐Analysis

Studies have shown that rates of liver disease are higher in persons who are coinfected with human immunodeficiency virus (HIV) and hepatitis C virus (HCV) than they are in persons with HCV alone, but estimates of risk vary widely and are based on data for dissimilar patient populations. We performed a meta-analysis to quantify the effect of HIV coinfection on progressive liver disease in persons with HCV. Eight studies were identified that included outcomes of histological cirrhosis or decompensated liver disease. These studies yielded a combined adjusted relative risk (RR) of 2.92 (95% confidence interval [CI], 1.70-5.01). Of note, studies that examined decompensated liver disease had a combined RR of 6.14 (95% CI, 2.86-13.20), whereas studies that examined histological cirrhosis had a pooled RR of 2.07 (95% CI, 1.40-3.07). There is a significantly elevated RR of severe liver disease in persons who are coinfected with HIV and HCV. This has important implications for timely diagnosis and consideration of treatment in coinfected persons.

THE MANAGEMENT OF INFECTIOUS HEPATITIS

Article1 March 1947THE MANAGEMENT OF INFECTIOUS HEPATITISRICHARD B. CAPPS, M.D., F.A.C.P., M. HERBERT BARKER, M.D., F.A.C.P.RICHARD B. CAPPS, M.D., F.A.C.P.Search for more papers by this author, M. HERBERT BARKER, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-26-3-405 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptINTRODUCTIONDuring the last five years the incidence of infectious hepatitis has approached epidemic proportions among both civilians and military personnel in various parts of the world.1, 2The opportunity thus offered for intensive study has led to a better understanding of the nature of the disease and to certain radical changes in our point of view towards it.2, 3It has become apparent that infectious hepatitis may have more serious consequences than was thought in the past. Thus proper treatment assumes increased importance which is further enhanced by the demonstration that it can significantly influence the course of the...Bibliography1. HAVENS WP: Infectious hepatitis in the Middle East, Jr. Am. Med. Assoc., 1944, cxxvi, 17. CrossrefGoogle Scholar2. BARKERCAPPSALLEN MHRBFW: Acute infectious hepatitis in the Mediterranean Theater, Jr. Am. Med. Assoc., 1945, cxxviii, 997. CrossrefGoogle Scholar3. BARKERCAPPSALLEN MHRBFW: Chronic hepatitis in the Mediterranean Theater, Jr. Am. Med. Assoc., 1945, cxxix, 653. CrossrefGoogle Scholar4. SNELLWOODMEIENBERG AMDALJ: Infectious hepatitis with especial reference to its occurrence in wounded men, Gastroenterol., 1945, v, 241. Google Scholar5. LUCKÉ B: The structure of the liver after recovery from epidemic hepatitis, Am. Jr. Path., 1944, xx, 595. Google Scholar6. 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PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byIS EARLY AMBULATION SAFE IN VIRAL HEPATITIS?Acute Viral Hepatitis TreatmentDie „persistierende Hepatitis“ im Vergleich mit den anderen chronischen Verlaufsformen nach epidemischer VirushepatitisRestrictive Practices in PaediatricsThe Management of Hepatic ComaWhy Put Him to Bed?The natural history of postnecrotic cirrhosisAN EVALUATION OF DIETARY PROTEIN IN THE TREATMENT OF LIVER DISEASE*THOMAS C. CHALMERS, M.D.Zur Therapie diffuser hepatocellulärer Erkrankungen (Hepatitis, Cirrhose usw.)Management of the Patient with Acute (Virus A) HepatitisTreatment of Infective HepatitisChloramphenicol (Chloromycetin) in the Treatment of Viral HepatitisNutrition and Disease of the LiverClinical course of viral hepatitis and the effect of exercise during convalescenceHazards in the Therapeutic Use of MorphineRed Blood Cell Diameter in Acute HepatitisHepatic InsufficiencyViral HepatitisInfectious Hepatitis 1 March 1947Volume 26, Issue 3Page: 405-416KeywordsArmed forcesInfectious diseasesInfectious hepatitis ePublished: 1 December 2008 Issue Published: 1 March 1947 PDF downloadLoading ...