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This implicit bias in the evaluation process may impact appropriate timing of referral for advanced heart failure therapies.

Though significant racial and sex disparities exist in the management and treatment of patients with decompensated heart failure, these disparities are minimized when therapies are properly utilized and patients are treated according to guidelines.

Though significant racial and sex disparities exist in the management and treatment of patients with decompensated heart failure, these disparities are minimized when therapies are properly utilized and patients are treated according to guidelines.

Dilated cardiomyopathy (DCM), which include genetic and nongenetic forms, is the most common form of cardiomyopathy. DCM is characterized by left ventricular or biventricular dilation with impaired contraction. In the United States, DCM is a burden to healthcare that accounts for approximately 10,000 deaths and 46,000 hospitalizations annually. In this review, we will focus on the genetic forms of DCM and on recent advances in the understanding of cytoskeletal, sarcomeric, desmosomal, nuclear membrane, and RNA binding genes that contribute to the complexity and genetic heterogeneity of DCM.

Although mutations in TTN remain the most common identifiable cause of genetic DCM, there is a growing appreciation for arrhythmogenic-prone DCM due to mutations in LMNA, desmosomal genes, and the recently described FLNC gene encoding the structural filamin C protein. Mutations in RBM20 highlight the relevance of RNA splicing regulation in the pathogenesis of DCM. GS-0976 supplier Although expanded genetic testing has improved access to genetic diagnostic studies for many patients, the molecular mechanisms in the pathogenesis of the disease remained largely unknown.

The identification of the molecular causes and subsequent insight into the molecular mechanisms of DCM is expanding our understanding of DCM pathogenesis and highlights the complexity of DCM and the need to develop multifaceted strategies to treat the various causes of DCM.

The identification of the molecular causes and subsequent insight into the molecular mechanisms of DCM is expanding our understanding of DCM pathogenesis and highlights the complexity of DCM and the need to develop multifaceted strategies to treat the various causes of DCM.

Small bowel diseases pose a unique diagnostic and management challenge and often requires tertiary specialist referral. The use of biomarkers may provide a cheap, noninvasive tool to assess the small bowel in terms of diagnosis, offering a better way to triage referrals and select patients for early management. This review looks at the most recent evidence behind the use of several faecal and urine biomarkers for small bowel diseases.

Faecal calprotectin shows the most promise, with evidence to support its role in predicting relapse postsurgery and monitoring treatment response in patients with Crohn’s disease. A faecal calprotectin less than 50 μg/g may also be used as a cut-off to triage further investigation. Faecal lactoferrin also appears promising as a marker of small bowel inflammation. A positive faecal immunohistochemistry test precapsule may help to prioritize referrals for obscure bleeding.

The use of biomarkers in the diagnosis and management of small bowel disease is still controversial and remains unclear. More studies are required to further develop their potential and before societal guidelines can be developed to direct their appropriate use in clinical practice.

The use of biomarkers in the diagnosis and management of small bowel disease is still controversial and remains unclear. More studies are required to further develop their potential and before societal guidelines can be developed to direct their appropriate use in clinical practice.

Small bowel fibrosis is a significant burden on Crohn’s disease patients with limited effective medical treatments that then requires surgery. A better understanding of the molecular mechanisms causing fibrosis and the evidence of benefit of available biologics will potentially lighten this burden and avoid the need for surgery.

Transforming growth factor-beta and it’s associated pathways remain the central cog in the wheel of fibrosis formation. Various new enzymes, cellular pathways, interleukins and molecules have been associated with beneficial modification of the fibrotic process. Licensed biologics such as antitumour necrosis factors continue to show evidence of efficacy in the treatment of fibrostenotic small bowel disease as well as the newer biologics ustekinumab and vedolizumab.

Fibrostenotic disease of the small bowel is a significant and common debilitating complication in Crohn’s disease patients. Multiple new molecular targets have been identified that may prove to become effective therapies in future. Antitumour necrosis factors remain the treatment with the best available evidence to date in fibrostenotic Crohn’s disease.

Fibrostenotic disease of the small bowel is a significant and common debilitating complication in Crohn’s disease patients. Multiple new molecular targets have been identified that may prove to become effective therapies in future. Antitumour necrosis factors remain the treatment with the best available evidence to date in fibrostenotic Crohn’s disease.

This review summarizes infectious diseases involving the small bowel (SB) with a focus on recent literature related to diagnosis and pathophysiology.

Typical symptom for SB infections is diarrhea, mostly self-limiting. Pathogens include bacteria, viruses, fungi, protozoan parasites, and helminths. Host-pathogen interaction is of special interest in infections with potentially severe or prolonged course. Research uses increasingly enterocyte cell culture systems. SARS-CoV2 can also infect enterocytes via angiotensin converting enzyme 2 (ACE2) receptor and causes gastrointestinal complaints in some patients. Chronic SB infections as tuberculosis, Cytomegalovirus, or Epstein-Barr virus have to be differentiated from Crohn’s and other diseases. Severe rare fungal and protozoan parasitic infections can cause relevant morbidity in immunocompromised patients. Soil-transmitted helminthic infections are a special issue in endemic areas.

Many infections involve the SB, typically causing mild and self-limiting diarrhea.