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PurposeTo investigate the magnitude of racial/ethnic differences in hospital mortality after transjugular intrahepatic portosystemic shunt (TIPS) creation for acute variceal bleeding and whether hospital care processes contribute to them.MethodsPatients aged ≥18 years undergoing TIPS creation for acute variceal bleeding in the United States (n = 10,331) were identified from 10 years (2007–2016) available in the National Inpatient Sample. Hierarchical logistic regression was used to examine the relationship between patient race and inpatient mortality, controlling for disease severity, treatment utilization, and hospital characteristics.ResultsA total of 6,350 (62%) patients were White, 1,780 (17%) were Hispanic, and 482 (5%) were Black. A greater proportion of Black patients were admitted to urban teaching hospitals (Black, n = 409 (85%); Hispanic, n = 1,310 (74%); and White, n = 4,802 (76%); P < .001) and liver transplant centers (Black, n = 215 (45%); Hispanic, n = 401 (23%); and White, n = 2,267 (36%); P < .001). Being Black was strongly associated with mortality (Black, 32% vs non-Black, 15%; odds ratio, 3.0 [95% confidence interval, 1.6–5.8]; P = .001), as assessed using the risk-adjusted regression model. This racial disparity disappeared in a sensitivity analysis including only patients with a maximum Child-Pugh score of 13 (odds ratio 1.2 [95% confidence interval, 0.4–3.6]; P = .68), performed to compensate for the absence of Model for End-stage Liver Disease scores. Ethnoracial differences in access to teaching hospitals, liver transplant centers, first-line endoscopy, and transfusion did not significantly contribute (P > .05) to risk-adjusted mortality.ConclusionsBlack patients have a 2-fold higher inpatient mortality than non-Black patients following TIPS creation for acute variceal bleeding, possibly related to greater disease severity before the procedure.  相似文献   
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Nonalcoholic fatty liver disease (NAFLD) is the leading cause of liver disease worldwide, with rising rates in parallel to those of obesity, type 2 diabetes, and metabolic syndrome. NAFLD encompasses a wide spectrum of pathology from simple steatosis to nonalcoholic steatohepatitis (NASH) and cirrhosis, which are linked to poor outcomes. Studies confirm a significant amount of undiagnosed NAFLD and related fibrosis within the community, increasing the overall burden of the disease. NAFLD appears to be more prevalent in certain populations, such as those with type 2 diabetes and metabolic syndrome. Early detection and lifestyle modifications, including weight loss and regular exercise, have been shown to improve outcomes. Adverse cardiovascular events are a key contributor to NAFLD-associated morbidity and mortality, and efforts to minimize their occurrence are essential. A targeted and algorithmic approach using noninvasive diagnostic techniques is promptly required to identify and risk-stratify patients with NAFLD. Patients at low risk of progression to NASH and advanced fibrosis can be managed in the primary care setting, while those at high risk of disease progression should be referred to hepatology specialists for surveillance and treatment. This review summarizes the key data of NAFLD's impact within primary care populations and proposes a potential algorithmic approach to identifying and managing such patients.  相似文献   
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The nondystrophic myotonias are rare muscle hyperexcitability disorders caused by gain-of-function mutations in the SCN4A gene or loss-of-function mutations in the CLCN1 gene. Clinically, they are characterized by myotonia, defined as delayed muscle relaxation after voluntary contraction, which leads to symptoms of muscle stiffness, pain, fatigue, and weakness. Diagnosis is based on history and examination findings, the presence of electrical myotonia on electromyography, and genetic confirmation. In the absence of genetic confirmation, the diagnosis is supported by detailed electrophysiological testing, exclusion of other related disorders, and analysis of a variant of uncertain significance if present. Symptomatic treatment with a sodium channel blocker, such as mexiletine, is usually the first step in management, as well as educating patients about potential anesthetic complications.  相似文献   
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ABSTRACT

Introduction

Osteoarthritis is a chronic disease that leads to the destruction of articular cartilage and joints. As the most common joint disorder, osteoarthritis poses a great burden to the healthcare system. Most importantly, osteoarthritis is a heterogeneous disease characterized by a wide range of clinical features, phenotypes, and treatments. The burden of osteoarthritis is not equally distributed between men and women. Women have an increased risk of developing osteoarthritis, with worse symptoms, and poorer outcomes.  相似文献   
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Pharmacogenetics influences oral tacrolimus exposure; however, little data exist regarding i.v. tacrolimus. We investigated the impact of genetic polymorphisms in CYP3A4, CYP3A5, and ABCB1 on i.v. tacrolimus exposure and toxicity in adult patients receiving an allogeneic hematopoietic stem cell transplant for hematologic malignancies. Germline DNA was extracted from buccal swabs and genotyped for CYP3A4, CYP3A5, and ABCB1 polymorphisms. Continuous i.v. infusion of tacrolimus .03 mg/kg/day was initiated on day +5 post-transplant, and steady-state blood concentrations were measured 4days later. We evaluated the association between phenotypes and prevalence of nontherapeutic target concentrations (below or above 5 to 15 ng/mL) as well as tacrolimus-related toxicities. Of 63 patients, 28.6% achieved the target concentration; 71.4% were >15ng/mL, which was more common in CYP3A4 intermediate/normal metabolizers (compared with rapid) and those with at least 1 ABCB1 C2677T loss-of-function allele (P < .05). ABCB1 C2677T was significantly associated with concentrations >15ng/mL (odds ratio, 6.2; 95% confidence interval, 1.8 to 23.6; P = .004) and tacrolimus-related toxicities (odds ratio, 7.5; 95% confidence interval, 1.6 to 55.2; P = .02). ABCB1 C2677T and CYP3A4 are important determinants of i.v. tacrolimus exposure, whereas ABCB1 C2677T also impacts tacrolimus-related toxicities in stem cell transplants.  相似文献   
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