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1.
Praxis (Bern 1994) ; 109(9): 677-686, 2020 Jul.
Artigo em Alemão | MEDLINE | ID: mdl-32635847

RESUMO

Ethyl-Toxic Steatohepatitis, the "Quiet Killer" - from Inflamed Fat to Multi-Organ Failure Abstract. The spectrum of the alcohol-associated liver disease (ALD) includes the potentially reversible simple fatty degeneration of the liver (AFLD), ethyl-toxic steatohepatitis (ASH), and the ethyl-toxic liver cirrhosis. Despite an interdisciplinary andn intensive care approach, alcohol-associated steatohepatitis (ASH), clinically characterized by jaundice and SIRS, may, in case of a fulminant course and due to the limited therapeutic options, have a mortality rate of up to 40 % . In highly selected cases, if the basic medical care of corticosteroids combined with N-acetylcysteine fails, a liver transplantation might be discussed, which occasionally shows a satisfactory long-term course. With the presented case we would like to raise awareness about the underlying disease, emphasize prevention, and summarize the most important facts for the clinical practice.


Assuntos
Fígado Gorduroso Alcoólico , Fígado Gorduroso , Hepatopatias Alcoólicas , Transplante de Fígado , Humanos
2.
Toxicol Lett ; 331: 65-74, 2020 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-32492475

RESUMO

Although disturbance of the methionine cycle and sequent decrease in hepatic methylation capacity are known to be important factors in the development of alcoholic liver injury, the underlying mechanisms are not fully understood. Here, we investigated the importance of the methylation of protein phosphatase 2A (PP2A) in alcoholic liver disease (ALD). We found that the severity of ethanol-induced liver injury and the extent of demethylation of PP2A catalytic C subunit (PP2Ac) were reduced after treatment with betaine, a methyl donor involved in the methionine-homocysteine cycle. These results suggest that PP2Ac methylation is decreased due to a broad decrease in hepatic methylation capacity after exposure to ethanol. Moreover, we found that the reduction in PP2Ac methylation led to increased degradation of the regulatory Bα subunit, thus promoting the phosphorylation and nuclear exclusion of Forkhead box O1 (FOXO1) and reducing FOXO1 transcriptional activity. Ultimately, the reduced activity of FOXO1 led to increased expression of TXNIP, which caused hepatic lipid accumulation. Our findings suggest that the reduction of PP2A methylation, a result of decrease hepatic methylation capacity, played an important role in ethanol-induced lipid accumulation via down-regulation of PP2A/Bα and FOXO1 phosphorylation.


Assuntos
Etanol/toxicidade , Proteína Forkhead Box O1/metabolismo , Hepatócitos/efeitos dos fármacos , Hepatopatias Alcoólicas/metabolismo , Fígado/efeitos dos fármacos , Proteína Fosfatase 2/metabolismo , Animais , Linhagem Celular , Hepatócitos/metabolismo , Fígado/metabolismo , Fígado/patologia , Hepatopatias Alcoólicas/patologia , Masculino , Metilação , Camundongos , Camundongos Endogâmicos C57BL , Fosforilação
3.
Lancet Gastroenterol Hepatol ; 5(5): 485-493, 2020 05.
Artigo em Inglês | MEDLINE | ID: mdl-32277901

RESUMO

Alcohol-related liver disease has become the leading indication for liver transplantation in the USA, partly due to an increase in the prevalence of high-risk drinking behaviour and alcohol use disorder, particularly among young women. Achieving sustained alcohol abstinence might not only prevent the development and progression of alcohol-related liver disease, but could also lead to clinically significant improvements, even in the advanced stages of disease. In this Series paper, we discuss the diagnosis and outpatient management of alcohol-related liver disease, with an emphasis on treatment options for alcohol use disorder and the assessment of nutritional status.


Assuntos
Assistência Ambulatorial/métodos , Hepatopatias Alcoólicas/diagnóstico , Hepatopatias Alcoólicas/terapia , Abstinência de Álcool , Comorbidade , Diagnóstico Diferencial , Humanos , Hepatopatias Alcoólicas/complicações , Hepatopatias Alcoólicas/patologia , Desnutrição/etiologia , Desnutrição/terapia , Programas de Rastreamento , Avaliação Nutricional , Estado Nutricional , Apoio Nutricional
4.
Lancet Gastroenterol Hepatol ; 5(5): 507-514, 2020 05.
Artigo em Inglês | MEDLINE | ID: mdl-32277903

RESUMO

The survival of patients with alcohol-related liver disease who receive a liver transplant has steadily improved to reach 80-85% at 1 year post-transplantation. The standard requirement for liver transplant-abstinence from alcohol for 6 months before transplantation-has been applied widely, but few data support the use of this rule as the sole criterion for selecting candidates for liver transplantation. When determining the suitability of a patient for transplantation, many liver transplant programmes now try to balance the period of abstinence against the risk of death associated with the severity of liver damage. Data accumulated since 2011 suggest that early liver transplantation (ie, transplantation without a specific period of abstinence) in patients with severe alcoholic hepatitis who do not respond to medical therapy is an effective therapeutic strategy. Further studies are needed to help refine the selection of patients with alcohol-related liver disease who have been abstinent for less than 6 months as suitable liver transplant candidates, and to improve the treatment of alcohol use disorder in those patients who have received a liver transplant.


Assuntos
Hepatopatias Alcoólicas/cirurgia , Transplante de Fígado , Seleção de Pacientes , Abstinência de Álcool , Consumo de Bebidas Alcoólicas/psicologia , Alcoolismo/complicações , Alcoolismo/terapia , Aloenxertos/patologia , Hepatite Alcoólica/cirurgia , Humanos , Hepatopatias Alcoólicas/etiologia , Hepatopatias Alcoólicas/psicologia , Período Pós-Operatório
5.
Chem Biol Interact ; 321: 109044, 2020 Apr 25.
Artigo em Inglês | MEDLINE | ID: mdl-32151596

RESUMO

Overconsumption of alcohol could lead to severe liver injury that connects with oxidative stress, apoptosis, and inflammatory response. Previously, we proved that p-coumaric acid prevents ethanol induced reproductive toxicity; however, p-coumaric acid (PCA) on ethanol mediated hepatotoxicity has not been examined yet. In our work, we sought to study the potential of PCA in contradiction of ethanol induced hepatoxicity which linking with MAPKs, apoptosis, oxidative stress, and Nrf2 signaling. Foremost, we found that PCA could protect ethanol induced both L-02 and HepG2 hepatic cells by inhibiting cytotoxicity, ROS production, mitochondrial depolarization, and nuclear fragmentation. Also, in vivo experiments showed that the ethanol increasing the lipid markers (TBARS, CD) and depletes the antioxidants thereby increased phosphorylation of JNK, ERK, and p38 in rat liver tissues. Interestingly, PCA treatments inhibit ethanol exposed lipid markers and depletion of antioxidants, which directs the inhibition of MAPKs activation in rat liver tissues. We also noticed that the PCA protected ethanol induced apoptosis and liver markers by inhibiting the expression of Bax, caspases; AST, ALT, ALS, and LDH in liver tissue. Overall, the ameliorative consequence of PCA on ethanol induced oxidative stress and apoptosis was achieved by suppressing the expression of CYP2E1 and overexpressing Nrf2 and its target protein HO-1 in rat liver tissue. As a result, PCA was marked to be an effective antioxidant with notable hepatoprotection by inhibiting MAPKs and apoptosis signaling via enhancing Nrf2 signaling.


Assuntos
Hepatopatias Alcoólicas/metabolismo , Hepatopatias Alcoólicas/prevenção & controle , Propionatos/farmacologia , Animais , Antioxidantes/farmacologia , Apoptose/efeitos dos fármacos , Linhagem Celular , Modelos Animais de Doenças , Etanol/toxicidade , Células Hep G2 , Humanos , Peroxidação de Lipídeos/efeitos dos fármacos , Fígado/efeitos dos fármacos , Fígado/lesões , Fígado/metabolismo , Hepatopatias Alcoólicas/patologia , Sistema de Sinalização das MAP Quinases/efeitos dos fármacos , Masculino , Potencial da Membrana Mitocondrial/efeitos dos fármacos , Fator 2 Relacionado a NF-E2/metabolismo , Substâncias Protetoras/farmacologia , Ratos , Ratos Wistar , Espécies Reativas de Oxigênio/metabolismo , Transdução de Sinais/efeitos dos fármacos
9.
Lancet Gastroenterol Hepatol ; 5(3): 245-266, 2020 03.
Artigo em Inglês | MEDLINE | ID: mdl-31981519

RESUMO

BACKGROUND: Cirrhosis and other chronic liver diseases (collectively referred to as cirrhosis in this paper) are a major cause of morbidity and mortality globally, although the burden and underlying causes differ across locations and demographic groups. We report on results from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2017 on the burden of cirrhosis and its trends since 1990, by cause, sex, and age, for 195 countries and territories. METHODS: We used data from vital registrations, vital registration samples, and verbal autopsies to estimate mortality. We modelled prevalence of total, compensated, and decompensated cirrhosis on the basis of hospital and claims data. Disability-adjusted life-years (DALYs) were calculated as the sum of years of life lost due to premature death and years lived with disability. Estimates are presented as numbers and age-standardised or age-specific rates per 100 000 population, with 95% uncertainty intervals (UIs). All estimates are presented for five causes of cirrhosis: hepatitis B, hepatitis C, alcohol-related liver disease, non-alcoholic steatohepatitis (NASH), and other causes. We compared mortality, prevalence, and DALY estimates with those expected according to the Socio-demographic Index (SDI) as a proxy for the development status of regions and countries. FINDINGS: In 2017, cirrhosis caused more than 1·32 million (95% UI 1·27-1·45) deaths (440 000 [416 000-518 000; 33·3%] in females and 883 000 [838 000-967 000; 66·7%] in males) globally, compared with less than 899 000 (829 000-948 000) deaths in 1990. Deaths due to cirrhosis constituted 2·4% (2·3-2·6) of total deaths globally in 2017 compared with 1·9% (1·8-2·0) in 1990. Despite an increase in the number of deaths, the age-standardised death rate decreased from 21·0 (19·2-22·3) per 100 000 population in 1990 to 16·5 (15·8-18·1) per 100 000 population in 2017. Sub-Saharan Africa had the highest age-standardised death rate among GBD super-regions for all years of the study period (32·2 [25·8-38·6] deaths per 100 000 population in 2017), and the high-income super-region had the lowest (10·1 [9·8-10·5] deaths per 100 000 population in 2017). The age-standardised death rate decreased or remained constant from 1990 to 2017 in all GBD regions except eastern Europe and central Asia, where the age-standardised death rate increased, primarily due to increases in alcohol-related liver disease prevalence. At the national level, the age-standardised death rate of cirrhosis was lowest in Singapore in 2017 (3·7 [3·3-4·0] per 100 000 in 2017) and highest in Egypt in all years since 1990 (103·3 [64·4-133·4] per 100 000 in 2017). There were 10·6 million (10·3-10·9) prevalent cases of decompensated cirrhosis and 112 million (107-119) prevalent cases of compensated cirrhosis globally in 2017. There was a significant increase in age-standardised prevalence rate of decompensated cirrhosis between 1990 and 2017. Cirrhosis caused by NASH had a steady age-standardised death rate throughout the study period, whereas the other four causes showed declines in age-standardised death rate. The age-standardised prevalence of compensated and decompensated cirrhosis due to NASH increased more than for any other cause of cirrhosis (by 33·2% for compensated cirrhosis and 54·8% for decompensated cirrhosis) over the study period. From 1990 to 2017, the number of prevalent cases more than doubled for compensated cirrhosis due to NASH and more than tripled for decompensated cirrhosis due to NASH. In 2017, age-standardised death and DALY rates were lower among countries and territories with higher SDI. INTERPRETATION: Cirrhosis imposes a substantial health burden on many countries and this burden has increased at the global level since 1990, partly due to population growth and ageing. Although the age-standardised death and DALY rates of cirrhosis decreased from 1990 to 2017, numbers of deaths and DALYs and the proportion of all global deaths due to cirrhosis increased. Despite the availability of effective interventions for the prevention and treatment of hepatitis B and C, they were still the main causes of cirrhosis burden worldwide, particularly in low-income countries. The impact of hepatitis B and C is expected to be attenuated and overtaken by that of NASH in the near future. Cost-effective interventions are required to continue the prevention and treatment of viral hepatitis, and to achieve early diagnosis and prevention of cirrhosis due to alcohol-related liver disease and NASH. FUNDING: Bill & Melinda Gates Foundation.


Assuntos
Carga Global da Doença/tendências , Hepatite B/complicações , Hepatite C/complicações , Cirrose Hepática/epidemiologia , Cirrose Hepática/etiologia , Adulto , África ao Sul do Saara/epidemiologia , Idoso , Idoso de 80 Anos ou mais , Ásia Central/epidemiologia , Análise Custo-Benefício/métodos , Avaliação da Deficiência , Diagnóstico Precoce , Egito/epidemiologia , Europa Oriental/epidemiologia , Feminino , Hepatite B/epidemiologia , Hepatite B/prevenção & controle , Hepatite C/epidemiologia , Hepatite C/prevenção & controle , Humanos , Cirrose Hepática/mortalidade , Cirrose Hepática/prevenção & controle , Hepatopatias Alcoólicas/complicações , Hepatopatias Alcoólicas/epidemiologia , Masculino , Pessoa de Meia-Idade , Hepatopatia Gordurosa não Alcoólica/complicações , Hepatopatia Gordurosa não Alcoólica/epidemiologia , Prevalência , Anos de Vida Ajustados por Qualidade de Vida , Fatores de Risco , Singapura/epidemiologia , Fatores Socioeconômicos
10.
Cell ; 180(2): 218-220, 2020 01 23.
Artigo em Inglês | MEDLINE | ID: mdl-31978341

RESUMO

Alcoholic hepatitis is a severe alcohol-associated liver disease with minimal treatment options. A recent study by Duan et al. uncovers that the exotoxin-secreting gut bacterium Enterococcus faecalis is a critical contributor to alcoholic hepatitis. This bacterium can now be eliminated with a bacteriophage, suggesting a new way to treat this life-threatening disease.


Assuntos
Bacteriófagos , Microbioma Gastrointestinal , Hepatite Alcoólica , Hepatopatias Alcoólicas , Enterococcus faecalis , Humanos
11.
12.
Ultraschall Med ; 41(1): 60-68, 2020 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-30616265

RESUMO

BACKGROUND: Transient elastography-based liver stiffness value (TE-LSV) has been studied for the diagnosis of portal hypertension. Liver stiffness is influenced by the disease etiology. We aimed to perform a meta-analysis to determine the performance of TE-LSV for diagnosing portal hypertension in patients with alcoholic liver disease (ALD). METHODS: We searched PubMed, Web of Science, Ovid and Cochrane library. A bivariate model was used to compute sensitivity and specificity. A random effects model was used to pool diagnostic odds ratios. RESULTS: 9 studies with 679 patients were included. The pooled sensitivity and specificity based on a cut-off value around 21.8 kPa for clinically significant portal hypertension (CSPH) were 0.89 (95 % confidence interval (CI), 0.83-0.93) and 0.71(95 % CI, 0.64-0.78), respectively. For severe portal hypertension (SPH), the pooled sensitivity and specificity for a cut-off value around 29.1 kPa were 0.88 (95 % CI, 0.83-0.92) and 0.74 (95 % CI, 0.67-0.81), respectively. CONCLUSION: TE-LSV showed good performance for diagnosing portal hypertension in patients with ALD. The optimal cut-off value for CSPH and SPH was around 21.8 kPa and 29.1 kPa, respectively, and these two cut-off values showed good sensitivity and modest specificity. The etiology should be clear before using TE-LSV for portal hypertension.


Assuntos
Técnicas de Imagem por Elasticidade , Hipertensão Portal , Hepatopatias Alcoólicas , Humanos , Hipertensão Portal/diagnóstico por imagem , Fígado , Cirrose Hepática/diagnóstico por imagem , Hepatopatias Alcoólicas/diagnóstico por imagem , Reprodutibilidade dos Testes
13.
Am J Gastroenterol ; 115(1): 96-104, 2020 01.
Artigo em Inglês | MEDLINE | ID: mdl-31517639

RESUMO

OBJECTIVES: Alcoholic liver disease (ALD) prevalence, particularly the subset with advanced liver disease, is not well defined. Herein, we aim to provide a comprehensive assessment of ALD epidemiology across the spectrum of disease severity and across different settings using 3 unique US databases. METHODS: We performed a retrospective, observational study of US adults with ALD using 2001-2016 National Health and Nutrition Examination Survey (NHANES), 2007-2014 Nationwide Inpatient Sample (NIS), and 2007-2017 United Network for Organ Sharing (UNOS) registry. ALD in the NHANES was defined using clinical laboratory data and self-reported alcohol use, among which fibrosis-4 score of >2.67 defined stage ≥3 fibrosis. Alcoholic cirrhosis (AC) in the NIS was identified using International Classification of Diseases, Ninth Revision codes. ALD in the UNOS was identified using UNOS coding. RESULTS: From 2001-2002 to 2015-2016, the overall weighted ALD prevalence was stable from 8.8% to 8.1% (P = 0.102), whereas the proportion of ALD with stage ≥3 fibrosis increased from 2.2% (95% CI: 0.4-4.0) to 6.6% (95% CI: 2.0-9.9; P = 0.007) (NHANES). From 2007 to 2014, the number of hospitalizations among patients with AC per 1,000 increased by 32.8%, and the proportion of hospitalizations among the patients with AC with ≥3 cirrhosis complications increased from 11.6% in 2007 to 25.8% in 2014 (Ptrend < 0.0001) (NIS). From 2007 to 2017, the total number of adults with ALD listed for liver transplant increased by 63.4% and the proportion with concurrent hepatocellular carcinoma increased by 178% (UNOS). DISCUSSION: Among these 3 US databases, consistent observations of increasing ALD severity emphasize the urgent need for greater awareness about the consequences of unhealthy alcohol use and interventions aimed specifically at addressing alcohol use disorders.


Assuntos
Pacientes Internados/estatística & dados numéricos , Hepatopatias Alcoólicas/epidemiologia , Inquéritos Nutricionais/métodos , Adulto , Bases de Dados Factuais , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Prevalência , Prognóstico , Estudos Retrospectivos
14.
Toxicol Lett ; 319: 11-21, 2020 Feb 01.
Artigo em Inglês | MEDLINE | ID: mdl-31711802

RESUMO

Alcoholic liver injury (ALI) is a part of alcohol-related liver diseases. These diseases include steatohepatitis, alcoholic fibrosis, cirrhosis and hepatocellular carcinoma (HCC). Accumulating data indicates that alcohol metabolism and circulating endotoxin/lipopolysaccharide (LPS) contribute to macrophage activation, which leads to the development of ALI. Protein tyrosine phosphatase 1B (PTP1B) has been shown to be involved in many tissue inflammations as well as liver fibrosis; however, the role of PTP1B in ALI is still unclear. In this study, PTP1B expression was elevated in liver tissues and primary macrophages isolated from EtOH-fed mice. Moreover, PTP1B expression was elevated in RAW264.7 cells stimulated with alcohol and LPS. Additional studies showed that silencing of PTP1B reduced the inflammatory response and expression of inflammatory cytokines such as IL-1ß, IL-6 and TNF-α, while overexpression of PTP1B induced inflammation in RAW264.7 cells. In addition, we found that NF-κB pathway was activated in RAW264.7 cells stimulated with alcohol and LPS, and PTP1B silencing or overexpression could regulate NF-κB signaling. In conclusion, this study revealed the function of PTP1B in ALI via its regulation of the NF-κB signaling pathway and may provide theoretical support for further research on ALI.


Assuntos
Hepatopatias Alcoólicas/genética , Ativação de Macrófagos , NF-kappa B/genética , Proteína Tirosina Fosfatase não Receptora Tipo 1/genética , Transdução de Sinais/genética , Animais , Depressores do Sistema Nervoso Central/farmacologia , Citocinas/biossíntese , Etanol/farmacologia , Lipopolissacarídeos/farmacologia , Fígado/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Proteína Tirosina Fosfatase não Receptora Tipo 1/biossíntese , Células RAW 264.7 , Regulação para Cima
16.
Am J Gastroenterol ; 115(1): 79-87, 2020 01.
Artigo em Inglês | MEDLINE | ID: mdl-31688021

RESUMO

OBJECTIVES: In contrast with other developed nations, life expectancy is decreasing in the United States, in part due to increasing mortality from alcohol-associated liver disease (ALD). Up-to-date estimates of ALD mortality are necessary for setting public health priorities to reverse this concerning trend. We therefore aimed to assess current (2017) estimates of ALD mortality and temporal trends from 1999 to 2017. METHODS: Using national data from the Centers for Disease Control and Prevention, we analyzed stratified ALD mortality rates between 1999 and 2017. We determined the age-adjusted death rates, stratified by sex and categorized by age, race/ethnicity, urbanization, and census region. We also identified statistically significant changes in the annual rate difference (ARD), annual percentage change (APC), and average APC in ALD mortality. RESULTS: In 2017, mortality from ALD was higher than any other year since 1999 with age-adjusted rates of 13.1 per 100,000 (95% confidence interval [CI] 12.9-13.3) in men and 5.6 per 100,000 (95% CI 5.4-5.7) in women. Mortality was highest among men and women who were middle aged, Native American, and from rural areas. Since 2006, ALD mortality has increased in almost every age group and race with the exception of non-Hispanic black men. Absolute increases in mortality rates have been particularly pronounced in Native American women (2005-2017 ARD 0.8, 95% CI 0.6-0.9), non-Hispanic/white men (2006-2017 ARD 0.4, 95% CI 0.3-0.4), and non-Hispanic/white women (2013-2017 ARD 0.4, 95% CI 0.3-0.5). DISCUSSION: Mortality from ALD is increasing over time in most demographic groups. Increased effort is needed to develop targeted public health strategies to address high and increasing ALD mortality.


Assuntos
Grupos Étnicos , Hepatopatias Alcoólicas/mortalidade , Saúde Pública , Adulto , Distribuição por Idade , Idoso , Idoso de 80 Anos ou mais , Causas de Morte/tendências , Centers for Disease Control and Prevention, U.S./estatística & dados numéricos , Feminino , Seguimentos , Humanos , Masculino , Pessoa de Meia-Idade , Estudos Retrospectivos , Distribuição por Sexo , Taxa de Sobrevida/tendências , Estados Unidos/epidemiologia
18.
Exp Anim ; 69(1): 110-118, 2020 Jan 29.
Artigo em Inglês | MEDLINE | ID: mdl-31554748

RESUMO

There has been a lack of suitable fatty liver models and characterization techniques for histopathological evaluation of alcoholic fatty liver (AFL). This work aimed to exploit an magnetic resonance imaging (MRI) technique for characterizing an alcohol-induced fatty liver model established in tree shrews (Tupaia belangeri chinese). The animals were treated with 15% alcohol for two weeks instead of drinking water to induce AFL. Blood alanine aminotransferase (ALT), aspartate aminotransferase (AST), alcohol, and liver malondialdehyde (MDA) concentrations were determined, and the histopathology of the liver was checked by hematoxylin & eosin (HE) and Oil red O staining on day 0 and on the 4th, 7th and 14th days after alcohol feeding. MRI was used to trace the histopathological changes in the liver of tree shrews in real time. Compared with the control group, the levels of ALT, AST, and MDA significantly increased in the alcohol-induced group and were positively correlated with the induction time. HE and Oil red O staining revealed that a moderate fatty lesion occurred in the liver on the 4th day and that a serious AFL was successfully induced on the 14th day. MRI further confirmed the formation of AFL. MRI, as noninvasive examination technique, provides an alternative tool for accurate characterization of AFL in live subjects. It is comparable to HE or Oil red O staining for histopathological examination, but is more suitable by virtue of its high flexibility and compliance. The AFL model of tree shrews combined with MRI characterization can work as a platform for studying fatty liver diseases and medications for their treatment.


Assuntos
Alanina Transaminase/sangue , Aspartato Aminotransferases/sangue , Modelos Animais de Doenças , Hepatopatias Alcoólicas/diagnóstico por imagem , Fígado , Malondialdeído/metabolismo , Tupaia , Animais , Etanol/sangue , Feminino , Fígado/patologia , Fígado/fisiopatologia , Hepatopatias Alcoólicas/patologia , Hepatopatias Alcoólicas/fisiopatologia , Imagem por Ressonância Magnética , Masculino
19.
Gut ; 69(3): 564-568, 2020 03.
Artigo em Inglês | MEDLINE | ID: mdl-31366455

RESUMO

OBJECTIVE: Given significant advances in treatment of viral hepatitis and the growing epidemic of obesity, the burden of the different types of liver diseases in the USA may be changing. Our aim was to assess the shift in the prevalence of different liver disease aetiologies in the USA over the past three decades. DESIGN: National Health and Nutrition Examination Surveys (NHANES; cross-sectional 1988-1994 and 1999-2016) were used. RESULTS: A total of 58 731 adults from NHANES (1988-2016) were included. Over the study period, the prevalence of chronic hepatitis B and alcoholic liver disease remained stable: 0.3%-0.4% and 0.8%-1.0%, respectively (p>0.05). The prevalence of chronic hepatitis C decreased nearly twofold: 1.6% in 1988-1994 to 0.9% in 2013-2016 (p=0.03). In contrast, the prevalence of non-alcoholic fatty liver disease (NAFLD; by US-Fatty Liver Index) increased from 20.0% (1988-1994) to 28.3% (1999-2004) to 33.2% (2009-2012) and 31.9% (2013-2016) (p<0.0001). Furthermore, steady increases were observed in the rates of obesity (22.2% in 1988-1994 to 31.0% in 1999-2004 to 38.9% in 2013-2016), type 2 diabetes mellitus (T2DM) (from 7.2% to 8.2% to 13.5% same years), insulin resistance and hypertension (all p<0.0001). Yearly trend analyses showed that the only LD with consistently increasing prevalence was NAFLD (trend p=0.01). Multivariable regression analysis showed that obesity (OR 10.4; 95% CI 9.5 to 11.3) and T2DM (OR 3.7; 95% CI 3.2 to 4.2) were the major independent predictors of NAFLD. CONCLUSIONS: Over the past 30 years in the USA, NAFLD is the only liver disease with growing prevalence, synchronous with the increasing rates of obesity and T2DM.


Assuntos
Diabetes Mellitus Tipo 2/epidemiologia , Hepatopatias/epidemiologia , Obesidade/epidemiologia , Adulto , Idoso , Idoso de 80 Anos ou mais , Doença Crônica , Feminino , Hepatite B Crônica/epidemiologia , Hepatite C Crônica/epidemiologia , Humanos , Hipertensão/epidemiologia , Resistência à Insulina , Hepatopatias Alcoólicas/epidemiologia , Masculino , Pessoa de Meia-Idade , Hepatopatia Gordurosa não Alcoólica/epidemiologia , Inquéritos Nutricionais , Prevalência , Fatores de Risco , Estados Unidos/epidemiologia , Adulto Jovem
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