A Comprehensive Analysis of Liver Transplantation Outcomes Among Ethnic Minorities in the United States.

GOALS: The aim of this study was to perform a comprehensive assessment of liver transplant (LT) outcomes among US adults with a specific focus on understanding race/ethnicity-specific disparities. BACKGROUND: Despite improvements in the liver allocation and LT-related care, disparities in LT outcomes persist. STUDY: Using data from the 2005 to 2016 United Networks for Organ Sharing LT registry, we evaluated waitlist survival, probability of receiving LT, and post-LT survival among US adults stratified by race/ethnicity and liver disease etiology. Kaplan-Meier methods evaluated unadjusted waitlist and post-LT outcomes, and multivariate regression models evaluated adjusted waitlist and post-LT outcomes. RESULTS: Among 88,542 listed for LT patients (41.3% hepatitis C virus, 25.3% alcoholic liver disease, 22.3% nonalcoholic steatohepatitis, 11.1% hepatitis C virus/alcoholic liver disease), significant race/ethnicity-specific disparities were observed. Compared with non-Hispanic whites, Hispanics had a significantly lower risk of waitlist death [hazard ratio (HR)=0.84, 95% confidence interval (CI): 0.79-0.90, P<0.001]. Compared with non-Hispanic whites, significantly lower likelihood of receiving LT was observed in African Americans (HR=0.94, 95% CI: 0.91-0.98, P<0.001), Hispanics (HR=0.70, 95% CI: 0.68-0.73, P<0.001) and Asians (HR=0.74, 95% CI: 0.69-0.80, P<0.001). Compared with non-Hispanic whites, African Americans had a significantly higher risk of 5-year post-LT death (HR=1.31, 95% CI: 1.23-1.39, P<0.001). CONCLUSION: Among US adults awaiting LT, significant race/ethnicity-specific disparities in LT outcomes were observed. Despite evaluating an era after implementation of the Model for End-Stage Liver Disease, ethnic minorities continue to demonstrate a lower probability of receiving LT, and significantly higher risk of death post-LT in African Americans.

Fibrosis Assessment in Nonalcoholic Fatty Liver Disease (NAFLD) in 2016.

Nonalcoholic fatty liver disease (NAFLD) is a spectrum of liver pathologies characterized by hepatic steatosis with a history of little to no alcohol consumption or secondary causes of hepatic steatosis. The prevalence of NAFLD is 20-25 % of the general population in the Western countries and is associated with metabolic risk factors such as obesity, diabetes mellitus, and dyslipidemia. The spectrum of disease ranges from simple steatosis to nonalcoholic steatohepatitis, fibrosis, and cirrhosis. Advanced fibrosis is the most significant predictor of mortality in NAFLD. It is crucial to assess for the presence and degree of hepatic fibrosis in order to make therapeutic decisions and predict clinical outcomes. Liver biopsy, the current gold standard to assess the liver fibrosis, has a number of drawbacks such as invasiveness, sampling error, cost, and inter-/intra-observer variability. There are currently available a number of noninvasive tests as an alternative to liver biopsy for fibrosis staging. These noninvasive fibrosis tests are increasingly used to rule out advanced fibrosis and help guide disease management. While these noninvasive tests perform relatively well for ruling out advanced fibrosis, they also have limitations. Understanding the strengths and limitations of liver biopsy and the noninvasive tests is necessary for deciding when to use the appropriate tests in the evaluation of patients with NAFLD.

An unusual initial presentation of hepatocellular carcinoma as a sellar mass.

Sellar masses are frequently adenomatous pituitary tumors. Metastatic disease is unusual, often mimicking the presentations of adenomas. Hepatocellular carcinoma (HCC) is the most common primary hepatic malignancy but unusual to have a pituitary metastasis (PM). A 65-year-old man presented with headache, diplopia, ptosis, decreased vision in the right eye and unintentional weight loss of 32lbs. Preliminary out-patient work-up revealed a mass in the pituitary region. Cranial imaging showed 3.1 cm × 3.2 cm × 4.4 cm lesion. Abdominal imaging (computed tomography and magnetic resonance imaging) demonstrated a lobulated, nodular and heterogeneous right lobe of the liver. Trans-sphenoidal resection of the sellar mass favored metastatic HCC on histology. Liver biopsy confirmed HCC. We recommend maintaining an increased clinical suspicion upon evaluation of nonclassical clinical and radiological presentations of suspected PM/malignancy; as well as pursuing additional investigations in all early cases.

Development of hyperplastic polyps following argon plasma coagulation of gastric antral vascular ectasia.

The etiology of gastric antral vascular ectasia (GAVE) syndrome or gastric hyperplastic polyps (HPs) is not fully understood. We report a case of gastric HP arising in a patient treated with argon plasma coagulation (APC) for GAVE syndrome. Despite unclear etiologic progression, this and previously reported cases suggest a temporal relationship between the treatment of GAVE and HP. A 68-year-old male with a history of coronary artery disease, congestive heart failure and diabetes type II who initially presented with symptomatic anemia 2 weeks after starting aspirin and clopidogrel therapy. Diagnostic esophagogastroduodenoscopy (EGD) demonstrated diffuse GAVE. He was treated with 5 APC treatments, at 6-week intervals, over a 30 weeks period. 16 months after the initial APC treatment, an EGD performed secondary to persistent anemia demonstrated innumerable, large, bleeding polyps in the gastric antrum. Biopsy performed at that time confirmed hyperplastic gastric polyps. It has been proposed that HPs are regenerative lesions that arise at sites of severe mucosal injury. Our patient's treatment of GAVE with APC created significant mucosal injury, resulting in HP. Technique and genetic factors may have promoted hyperplastic changes during the regeneration of mucosa, at sites previously treated with APC. This case highlights the potential progression of GAVE to HP in a patient with persistent anemia after APC therapy.

Celiac disease 2015 update: new therapies.

Celiac disease (CD) is a chronic, small intestinal, immune-mediated enteropathy triggered by exposure to dietary gluten in genetically susceptible individuals. Currently, lifelong adherence to a gluten-free diet (GFD) is the only available treatment. However, GFD alone is not sufficient to relieve symptoms, control small intestinal inflammation and prevent long-term complications in many patients. The GFD has its challenges including issues related to adherence, lifestyle restrictions and cost. As a result, there is growing interest in and a need for non-dietary therapies to manage this condition. In recent years, different targets in the immune-mediated cascade of CD have been identified in clinical and pre-clinical trials for potential therapies. This review will discuss the latest non-dietary therapies in CD, including endopeptidases, modulators of enterocyte tight junctions and agents involved in gluten tolerization and immunomodulation. We will also discuss the potential implications of approved therapeutics on CD clinical practice.

Celiac Disease: Diagnostic Standards and Dilemmas.

Celiac Disease (CD) affects at least 1% of the population and evidence suggests that prevalence is increasing. The diagnosis of CD depends on providers being alert to both typical and atypical presentations and those situations in which patients are at high risk for the disease. Because of variable presentation, physicians need to have a low threshold for celiac testing. Robust knowledge of the pathogenesis of this autoimmune disease has served as a catalyst for the development of novel diagnostic tools. Highly sensitive and specific serological assays including Endomysial Antibody (EMA), tissue transglutaminase (tTG), and Deamidated Gliadin Peptide (DGP) have greatly simplified testing for CD and serve as the foundation for celiac diagnosis. In addition, genetic testing for HLA DQ2 and DQ8 has become more widely available and there has been refinement of the gluten challenge for use in diagnostic algorithms. While diagnosis is usually straightforward, in special conditions including IgA deficiency, very young children, discrepant histology and serology, and adoption of a gluten free diet prior to testing, CD can be difficult to diagnose. In this review, we provide an overview of the history and current state of celiac disease diagnosis and provide guidance for evaluation of CD in difficult diagnostic circumstances.

Metastatic prostate cancer to the duodenum: a rare case.

Prostate cancer is the third most common cancer in man. About 1 in 6 males developed prostate cancer and 1 in 35 males die of this disease. Prostate cancer behavior ranges from microscopic tumors to aggressive cancer with metastatic potential. While metastasis to bone is relatively common, prostate cancer rarely metastasizes to the cecum, pituitary gland, small bowel, maxillary sinus and skin. Our case report presents a rare presentation of metastatic prostate cancer to the duodenum. Our search of the literature found only 2 cases of prostate metastases to duodenum published from 1966 to the present. To our knowledge this is the third case of metastatic prostate cancer presenting with duodenal metastasis. Although it is rare but in symptomatic patients small intestine metastasis should not be ignored with advanced prostate cancer. The case demonstrates a novel presentation of a common malignancy, and should raise awareness in clinicians and radiologists that prostate cancer can present with distant metastases in absence of any local lymphadenopathy.

Drug Rash with Eosinophilia and Systemic Symptoms Syndrome Due to Anti-TB Medication.

Drug rash with eosinophilia and systemic symptoms (DRESS) syndrome is a severe, idiosyncratic, multi-system reaction characterized by the clinical triad of fever, rash, and internal organ involvement. The mortality rate is estimated to be 8%, especially among patients with liver involvement, so early recognition is imperative. Drugs commonly associated with the development of DRESS syndrome include anticonvulsants, long-acting sulfonamides, and anti-inflammatory medications; however, there are no reported cases implicating anti-tuberculosis (anti-TB) medications. We report a case of DRESS syndrome from anti-TB therapy. A 68-year-old male with pulmonary TB presented with pruritic skin eruption and sore throat, 8 weeks after starting Rifampin, Isoniazid, Pyrazinamide, and Ethambutol (RIPE) therapy. He takes metformin and glyburide for diabetes. Physical exam was significant for diffuse, exfoliative erythematous macules with target lesions involving the entire skin surface, without mucosal involvement. Laboratory data was significant for mild transaminitis and new onset eosinophilia. Given suspicion of drug eruption, RIPE therapy was discontinued. Skin biopsy confirmed erythema multiforme. Despite discontinuation of the implicated medications, eosinophilia and transaminitis continued to worsen, and so systemic corticosteroids were started. After 4 weeks of discontinuation of RIPE therapy, the cutaneous eruption resolved and laboratory data returned to normal. The patient is finishing course of anti-TB with cycloserine and moxifloxacin. Upon follow up as outpatient, the rash was resolving and disappeared in 1 month. DRESS syndrome is always considered when there is high eosinophil counts and multisystem involvement with skin eruptions. It can be potentially life threatening with certain drugs and infectious agents in predisposed individuals. It is imperative to discontinue the causative medication and avoid re-exposure.