Antithrombotics and Gastrointestinal Prophylaxis: A Systematic Review.

Antithrombotic medications include both antiplatelet and anticoagulants and are used for a wide variety of cardiovascular conditions. A common complication of antithrombotic use is gastrointestinal bleeding. As a result, gastrointestinal prophylaxis is a common consideration for patients on a single or combination antithrombotic regimen.

Infective Endocarditis: A Rare and Dangerous Cause of Endocarditis.

Infective endocarditis is an uncommon heart infection, typically involving heart valves. is a rare cause of endocarditis, typically found within the GI tract, and is usually difficult to isolate and requires specialized media. We report a case of endocarditis following a root canal.

ESTROGEN REPLACEMENT THERAPY FOR STROKE.

Stroke is the third most common cause of death and severe disability among Western populations. Overall, the incidence of stroke is uniformly higher in men than in women. Stroke is rare in women during the reproductive years, and rapidly increases after menopause, strongly suggesting that estrogen (E2) plays an important role in the prevention of stroke.

The battle of the sexes for stroke therapy: female- versus male-derived stem cells.

Cell therapy is a major discipline of regenerative medicine that has been continually growing over the last two decades. The aging of the population necessitates discovery of therapeutic innovations to combat debilitating disorders, such as stroke. Menstrual blood and Sertoli cells are two gender-specific sources of viable transplantable cells for stroke therapy.

Anti-Yersinia antibodies are not associated with microscopic colitis in an American case-control study.

Background: Microscopic colitis (MC), which consists of lymphocytic colitis and collagenous colitis, may be triggered by gastrointestinal infections. Studies have suggested a relationship between MC and Yersinia enterocolitica infection. We tested this hypothesis in a case-control study of American patients with MC.

Current and future role of biomarkers in Crohn's disease risk assessment and treatment.

Background: Crohn's disease (CD), a chronic inflammatory bowel disease (IBD), occurs in genetically susceptible individuals who develop aberrant immune responses to endoluminal bacteria. Recurrent inflammation increases the risk of several complications. Despite use of a traditional "step-up" therapy with corticosteroids and immunomodulators, most CD patients eventually require surgery at some time in their disease course.

Advances in epidemiology and diagnosis of inflammatory bowel diseases.

The etiology of chronic inflammatory bowel diseases (IBD) remains unknown. Understanding IBD epidemiology helps to identify at-risk individuals, to appreciate the changing demographic profile of IBD, and to interpret theories of IBD pathogenesis. This article reviews recent advances in epidemiology and diagnostics.

Testing concordance of clinical characteristics in familial studies with application to inflammatory bowel diseases.

The etiology of chronic Inflammatory Bowel Diseases (IBD) remains unknown, with both genetic and environmental risk factors having been implicated. A recent collaborative study of IBD provides clinical data from families with three or more affected first-degree relatives. The scientific question is whether specific clinical characteristics aggregate among affected individuals within families.

Current medical therapy for chronic inflammatory bowel diseases.

Chronic idiopathic inflammatory bowel diseases (IBD) include Crohn's disease (CD), ulcerative colitis (UC), and colonic IBD type unclassified (IBDU). This article focuses upon current medical therapies for adult CD and UC, and is organized according to therapy for the corresponding disease type, stage, and severity.

No evidence for an involvement of the p38 and JNK mitogen-activated protein in inflammatory bowel diseases.

Involvement of mitogen-activated protein (MAPK) in inflammatory bowel disease (IBD) remains enigmatic. We sought to evaluate the expression and activity of p38 and JNK MAPK in IBD and 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis; and the effects of a p38 inhibitor, SB203580, in TNBS colitis. P38 and JNK were quantified in colonic mucosa of 28 IBD patients and 19 controls and in 77 TNBS or control mice treated or not with SB203580.

Polycystic liver disease: experience at a teaching hospital.

Objectives: This study describes the natural history of patients with polycystic liver disease, a rare disorder characterized by multiple hepatic cysts.

Methods: Cases were identified through review of charts from a hepatology practice, a hepatobiliary surgery practice and a retrospective chart review of inpatient charts from 1990 to 2002. All patients had greater than four simple liver cysts without infectious etiology.

Clinical relevance of advances in genetics and pharmacogenetics of IBD.

Crohn's disease and ulcerative colitis result from an inappropriate response of the mucosal immune system to the normal enteric flora in a genetically susceptible individual. During the past decade, exciting progress has been made in our understanding of the contribution of genetics to inflammatory bowel disease susceptibility and phenotype. This article reviews recent advances in the genetics of inflammatory bowel disease and explores how they might impact on clinical practice.

Probiotics in inflammatory bowel disease: a critical review.

Intestinal bacteria play a key role in inflammatory bowel disease. Probiotics attempt to modify disease by favourably altering bacterial composition, immune status, and inflammation. Until recently, probiotic therapy was considered 'folk' medicine, but there now is emerging interest on the part of the general public and scientific communities in the use of probiotics in human disease.

What are the major arguments in favour of the genetic susceptibility for inflammatory bowel disease?

Epidemiological data, notably concordance rates in twin pairs and familial aggregation, have provided strong evidence for the importance of the genetic contribution in inflammatory bowel diseases. Genome wide scanning has been remarkably successful in identifying a number of susceptibility loci. The identification of the IBD1 gene on chromosome 16 as NOD2/CARD15 definitely establishes that a significant proportion of Crohn's disease has an underlying genetic cause.