Disparities among ethnic groups in mortality and outcomes among adults with MASLD: A multicenter study.

BACKGROUND: Metabolic dysfunction-associated steatotic liver disease (MASLD) is the leading cause of chronic liver disease and 10%-20% occurs in lean individuals. There is little data in the literature regarding outcomes in an ethnically-diverse patient populations with MASLD. Thus, we aim to investigate the natural history and ethnic disparities of MASLD patients in a diverse population, and stratified by body mass index categories. METHODS: We conducted a retrospective multicenter study on patients with MASLD at the Banner Health System from 2012 to 2022. Main outcomes included mortality and incidence of cirrhosis, cardiovascular disease, diabetes mellitus (DM), liver-related events (LREs), and cancer. We used competing risk and Cox proportional hazard regression analysis for outcome modelling. RESULTS: A total of 51 452 (cross-sectional cohort) and 37 027 (longitudinal cohort) patients were identified with 9.6% lean. The cohort was 63.33% European ancestry, 27.96% Hispanic ancestry, 3.45% African ancestry, and 2.31% Native American/Alaskan ancestry. Median follow-up was 45.8 months. After adjusting for confounders, compared to European individuals, Hispanic and Native American/Alaskan patients had higher prevalence of cirrhosis and DM, and individuals of Hispanic, African, and Native American/Alaskan ancestry had higher mortality and incidence of LREs and DM. Lean patients had higher mortality and incidence of LREs compared with non-lean patients. CONCLUSION: Native American/Alaskan, Hispanic, and African patients had higher mortality and incidence of LREs and DM compared with European patients. Further studies to explore the underlying disparities and intervention to prevent LREs in lean patients, particularly several ethnic groups, may improve clinical outcomes.

Service Requirements of Liver Transplant Anesthesia Teams: Society for the Advancement of Transplant Anesthesia Recommendations.

There are disparities in liver transplant anesthesia team (LTAT) care across the United States. However, no policies address essential resources for liver transplant anesthesia services similar to other specialists. In response, the Society for the Advancement of Transplant Anesthesia appointed a task force to develop national recommendations. The Conditions of Transplant Center Participation were adapted to anesthesia team care and used to develop Delphi statements. A Delphi panel was put together by enlisting 21 experts from the fields of liver transplant anesthesiology and surgery, hepatology, critical care, and transplant nursing. Each panelist rated their agreement with and the importance of 17 statements. Strong support for the necessity and importance of 13 final items were as follows: resources, including preprocedure anesthesia assessment, advanced monitoring, immediate availability of consultants, and the presence of a documented expert in liver transplant anesthesia credentialed at the site of practice; call coverage, including schedules to assure uninterrupted coverage and methods to communicate availability; and characteristics of the team, including membership criteria, credentials at the site of practice, and identification of who supervises patient care. Unstructured comments identified competing time obligations for anesthesia and transplant services as the principle reason that the remaining recommendations to attend integrative patient selection and quality review committees were reduced to a suggestion rather than being a requirement. This has important consequences because deficits in team integration cause higher failure rates in service quality, timeliness, and efficiency. Solutions are needed that remove the time-related financial constraints of competing service requirements for anesthesiologists. In conclusion, using a modified Delphi technique, 13 recommendations for the structure of LTATs were agreed upon by a multidisciplinary group of experts.

Knockout of l-Histidine Decarboxylase Prevents Cholangiocyte Damage and Hepatic Fibrosis in Mice Subjected to High-Fat Diet Feeding via Disrupted Histamine/Leptin Signaling.

Feeding a high-fat diet (HFD) coupled with sugar, mimicking a Western diet, causes fatty liver disease in mice. Histamine induces biliary proliferation and fibrosis and regulates leptin signaling. Wild-type (WT) and l-histidine decarboxylase (Hdc-/-) mice were fed a control diet or an HFD coupled with a high fructose corn syrup equivalent. Hematoxylin and eosin and Oil Red O staining were performed to determine steatosis. Biliary mass and cholangiocyte proliferation were evaluated by immunohistochemistry. Senescence and fibrosis were measured by quantitative PCR and immunohistochemistry. Hepatic stellate cell activation was detected by immunofluorescence. Histamine and leptin levels were measured by enzyme immunoassay. Leptin receptor (Ob-R) was evaluated by quantitative PCR. The HDC/histamine/histamine receptor axis, ductular reaction, and biliary senescence were evaluated in patients with nonalcoholic fatty liver disease, nonalcoholic steatohepatitis, or end-stage liver disease. Hdc-/- HFD mice had increased steatosis compared with WT HFD mice. WT HFD mice had increased biliary mass, biliary proliferation, senescence, fibrosis, and hepatic stellate cell activation, which were reduced in Hdc-/- HFD mice. In Hdc-/- HFD mice, serum leptin levels increased, whereas biliary Ob-R expression decreased. Nonalcoholic steatohepatitis patients had increased HDC/histamine/histamine receptor signaling. Hdc-/- HFD mice are susceptible to obesity via dysregulated leptin/Ob-R signaling, whereas the lack of HDC protects from HFD-induced fibrosis and cholangiocyte damage. HDC/histamine/leptin signaling may be important in managing obesity-induced biliary damage.

Pulmonary complications of cirrhosis.

Pulmonary vascular complications of liver disease comprise two distinct clinical entities: hepatopulmonary syndrome (HPS-microvascular dilatation and angiogenesis) and portopulmonary hypertension (POPH-vasoconstriction and remodeling in resistance vessels). These complications occur in similar pathophysiologic environments and may share pathogenic mechanisms. HPS is found in 15% to 30% of patients with cirrhosis and its presence increases mortality and the risks of liver transplantation, particularly when hypoxemia is present. Contrast echocardiography and arterial blood gas analysis are required to establish the diagnosis. No medical therapies are available, although liver transplantation is effective in reversing the syndrome. POPH is found in 4% to 8% of patients undergoing liver transplantation evaluation, and the presence of moderate to severe disease significantly increases perioperative transplant mortality. Transthoracic echocardiography is recommended for screening and right-heart catheterization is required to establish the diagnosis. Medical therapies are increasingly effective in improving pulmonary vascular hemodynamics in POPH and may result in better perioperative outcomes.

Postinfectious Autoimmune Hepatitis-Induced Liver Failure: A Consequence of Hepatitis A Virus Infection.

Autoimmune hepatitis (AIH) is a chronic inflammatory immune-mediated hepatic pathology of unclear etiology. The mechanisms initiating and driving autoimmune inflammation of the liver and the loss of hepatic tolerance are still elusive. Several studies have documented the involvement of genetic factors and triggering agents such as toxic injury, treatment with immune-modifying drugs, or previous viral infections with perhaps strongest evidence for the hepatitis C virus. Rarely, AIH has been reported to develop after hepatitis A virus infection. We describe a case of de novo AIH in a patient with a history of recent hepatitis A virus infection.

Posttransplant Lymphoproliferative Disorder in a Patient with Worsening Ascites after Liver Transplantation.

Posttransplant lymphoproliferative disorder (PTLD) is a spectrum of diseases that involves abnormal lymphoid and/or plasmacytic proliferation in patients with solid organ or hematopoietic cell transplantation. It is a condition with a low incidence of 3.5-4.3% in liver transplant (LT) recipients. This case involves a 63-year-old male with history of LT for chronic HCV induced cirrhosis who presented with abdominal distension related to worsening ascites. Cytological ascitic fluid analysis revealed EBV (+) malignant cells without a malignant focal point on imaging. Diagnosis of monomorphic PTLD with primary effusion lymphoma-like morphology and immunophenotype was established. This case highlights the complexity in diagnosis, different diagnostic modalities, and rare clinical presentations of PTLD.

Severe esophageal injury after radiofrequency ablation - a deadly complication.

Various degrees of esophageal injury have been described after radiofrequency ablation performed for treatment of atrial fibrillation. The main mechanism of injury is thermal and may lead to a range of esophageal mucosal changes, some clinically insignificant, however when deep ulceration occurs, this may be further complicated by perforation and mediastinitis, a rare but life threatening sequelae. We present a case of a severe esophageal injury leading to mediastinitis, with interesting endoscopic findings.