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Gastrointestinal Inflammation (gastrointestinal + inflammation)

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Medical Sciences100%

Selected Abstracts

Endoscopic, Biopsy, and Histopathologic Guidelines for the Evaluation of Gastrointestinal Inflammation in Companion Animals

JOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 1 2010
The WSAVA International Gastrointestinal Standardization Group
First page of article [source]

Ion channel remodeling in gastrointestinal inflammation

NEUROGASTROENTEROLOGY & MOTILITY, Issue 10 2010
H. I. Akbarali
Abstract Background,Gastrointestinal inflammation significantly affects the electrical excitability of smooth muscle cells. Considerable progress over the last few years have been made to establish the mechanisms by which ion channel function is altered in the setting of gastrointestinal inflammation. Details have begun to emerge on the molecular basis by which ion channel function may be regulated in smooth muscle following inflammation. These include changes in protein and gene expression of the smooth muscle isoform of L-type Ca2+ channels and ATP-sensitive K+ channels. Recent attention has also focused on post-translational modifications as a primary means of altering ion channel function in the absence of changes in protein/gene expression. Protein phosphorylation of serine/theronine or tyrosine residues, cysteine thiol modifications, and tyrosine nitration are potential mechanisms affected by oxidative/nitrosative stress that alter the gating kinetics of ion channels. Collectively, these findings suggest that inflammation results in electrical remodeling of smooth muscle cells in addition to structural remodeling. Purpose,The purpose of this review is to synthesize our current understanding regarding molecular mechanisms that result in altered ion channel function during gastrointestinal inflammation and to address potential areas that can lead to targeted new therapies. [source]

Aicardi,Goutičres syndrome presenting with haematemesis in infancy

ACTA PAEDIATRICA, Issue 12 2009
D Hall
Abstract Aicardi,Goutičres syndrome is a genetic childhood encephalopathy characterized by basal ganglia calcification, chronic cerebrospinal lymphocytosis and elevated cerebrospinal fluid interferon-alpha, mimicking acquired congenital viral infections. As more is discovered about the pathogenesis of Aicardi,Goutičres, it is becoming evident that a dysfunction of the immune system is likely to be responsible for the disease phenotype. We describe a previously healthy 2-month-old female infant who presented with haematemesis and seizures and was subsequently diagnosed with Aicardi,Goutičres syndrome. To our knowledge, this is the first documented case of Aicardi,Goutičres syndrome presenting with haematemesis. The gastrointestinal tract is an area of high cell loss, revealing early signs of systemic inflammation and we postulate that a systemic proinflammatory milieu occurs in Aicardi,Goutičres syndrome. Conclusion: Aicardi,Goutičres syndrome can present with haematemesis, adding to the growing evidence that the Aicardi,Goutičres syndrome spectrum encompasses an immune-mediated multisystem involvement. Gastrointestinal inflammation should also be considered in these patients and treated appropriately. [source]

Fecal S100A12 and fecal calprotectin as noninvasive markers for inflammatory bowel disease in children

INFLAMMATORY BOWEL DISEASES, Issue 3 2008
Marc A. Sidler MD
Abstract Background: Fecal calprotectin is a sensitive marker for gut inflammation. Recently, we have established that a related protein, S100A12, is elevated in the feces of children with inflammatory bowel disease (IBD). This may represent a specific and sensitive disease marker. The objective was to investigate the utility of fecal S100A12, in comparison to fecal calprotectin and standard inflammatory markers, as a screening marker for IBD in children with gastrointestinal symptoms. Methods: Stool samples were obtained from 61 children presenting with gastrointestinal symptoms requiring endoscopy. Fecal S100A12, calprotectin, and serum S100A12 levels were measured and correlated to final diagnosis and standard tests (ESR, CRP, platelet count, and albumin). Results: Children diagnosed with IBD (n = 31) had elevated fecal S100A12 (median 55.2 mg/kg) and calprotectin (median 1265 mg/kg) levels compared with the children without IBD (n = 30; S100A12: median 1.1 mg/kg, P < 0.0001; calprotectin: median 30.5 mg/kg; P < 0.0001). The sensitivity and specificity of fecal S100A12 (cutoff 10 mg/kg) for the detection of IBD were both 97%, whereas fecal calprotectin (cutoff 50 mg/kg) gave a sensitivity of 100% and a specificity of 67%. Conclusions: Both fecal markers were superior to the sensitivities and specificities of any standard inflammatory test. Both fecal S100A12 and calprotectin are sensitive markers of gastrointestinal inflammation, but fecal S100A12 provided exceptional specificity in distinguishing children with IBD from children without IBD. Fecal S100A12 is a simple, noninvasive test that can be used to screen and select children warranting further invasive and laborious procedures such as endoscopy for the investigation of their gastrointestinal symptoms. (Inflamm Bowel Dis 2007) [source]

Infliximab regulates lamina propria T lymphocytes in patients with Crohn's disease

ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 2006
O. WATANABE
Summary Background and Aims The immune system is a major determinant of the pathophysiological inflammation, which may lead to gastrointestinal mucosal injury in patients with Crohn's disease. Cytokines such as tumour necrosis factor-alpha are well-known mediators of the immune system, and treatment with a chimeric anti-tumour necrosis factor-alpha antibody (infliximab) has been shown to be highly effective in patients with Crohn's disease. Recent evidence indicates that infliximab induces apoptosis in lamina propria T lymphocytes in these patients. To better understand the mechanisms of infliximab's effect on gastrointestinal inflammation, we investigated changes in the serum level of cytokines after treatment in these patients, and the effect of infliximab in inducing the apoptosis of T lymphocytes. Methods Thirteen patients with Crohn's disease were treated with infliximab at a dosage of 5-mg/kg body weight. Clinical response was evaluated using the Crohn's Disease Activity Index, and serum soluble interleukin-2 receptor, interleukin-6, tumour necrosis factor-alpha levels were analysed by enzyme-linked immunosorbent assay at 0 and 2 weeks after treatment. Apoptosis of peripheral and lamina propria T lymphocytes after culture with infliximab was detected by flow cytometry. Results Crohn's Disease Activity Index decreased in 12 of 13 patients, and serum soluble interleukin-2 receptor, interleukin-6 and tumour necrosis factor-alpha levels decreased in most patients after treatment with infliximab. Tumour necrosis factor-alpha level before treatment in the six patients in whom Crohn's Disease Activity Index decreased by more than 70 was <5 ng/mL. Infliximab induced the apoptosis of lamina propria but not of peripheral T lymphocytes. Conclusion These findings suggest that a low level of serum tumour necrosis factor-alpha is an indicator for infliximab treatment. The induction of apoptosis of lamina propria T lymphocytes by infliximab may be an important mechanism of its anti-inflammatory effect in patients with Crohn's disease. [source]

The effects of supraphysiological doses of corticosteroids in hypotensive liver failure

LIVER INTERNATIONAL, Issue 2 2003
Rachael Harry
Abstract: Background: In septic shock, supraphysiological doses of corticosteroids reduce norepinephrine requirements. We reviewed our experience of this treatment in hypotensive liver failure. Methods: We retrospectively analysed 20 patients with liver failure who were treated with supraphysiological doses of hydrocortisone because of norepinephrine dependence. We compared their norepinephrine requirements, outcome, microbiology and incidence of gastrointestinal bleeding to an historical control group treated with norepinephrine but not corticosteroids. Results: After 48 h of steroid treatment, the median norepinephrine dose was reduced (0.14 µg/kg/min to 0.08 µg/kg/min; P < 0.05) while the blood pressure over the same period of time did not change significantly (67.3 mm Hg to 70 mm Hg). Duration of ITU stay was longer in the steroid treated group (13.5 days vs 3 days; P < 0.05) but survival was similar in both groups. There were 23 episodes of positive bacterial cultures after norepinephrine was started in the steroid treated group, compared with 18 episodes in the control group. More of the positive cultures were due to resistant organisms in the steroid treated group (65% vs 17% in the control group; P < 0.002). There was no significant bleeding due to gastrointestinal inflammation in either group. Conclusions: Supraphysiological doses of corticosteroids reduce norepinephrine requirements in hypotensive liver failure. They do not improve survival but may extend time to find a suitable donor in those awaiting urgent liver transplantation. [source]

Ion channel remodeling in gastrointestinal inflammation

NEUROGASTROENTEROLOGY & MOTILITY, Issue 10 2010
H. I. Akbarali
Abstract Background,Gastrointestinal inflammation significantly affects the electrical excitability of smooth muscle cells. Considerable progress over the last few years have been made to establish the mechanisms by which ion channel function is altered in the setting of gastrointestinal inflammation. Details have begun to emerge on the molecular basis by which ion channel function may be regulated in smooth muscle following inflammation. These include changes in protein and gene expression of the smooth muscle isoform of L-type Ca2+ channels and ATP-sensitive K+ channels. Recent attention has also focused on post-translational modifications as a primary means of altering ion channel function in the absence of changes in protein/gene expression. Protein phosphorylation of serine/theronine or tyrosine residues, cysteine thiol modifications, and tyrosine nitration are potential mechanisms affected by oxidative/nitrosative stress that alter the gating kinetics of ion channels. Collectively, these findings suggest that inflammation results in electrical remodeling of smooth muscle cells in addition to structural remodeling. Purpose,The purpose of this review is to synthesize our current understanding regarding molecular mechanisms that result in altered ion channel function during gastrointestinal inflammation and to address potential areas that can lead to targeted new therapies. [source]

Cannabinoid CB2 receptors in the gastrointestinal tract: a regulatory system in states of inflammation

BRITISH JOURNAL OF PHARMACOLOGY, Issue 2 2008
K L Wright
The emerging potential for the cannabinoid (CB) system in modulating gastrointestinal inflammation has gained momentum over the last few years. Traditional and anecdotal use of marijuana for gastrointestinal disorders, such as diarrhoea and abdominal cramps is recognized, but the therapeutic benefit of cannabinoids in the 21st century is overshadowed by the psychoactive problems associated with CB1 receptor activation. However, the presence and function of the CB2 receptor in the GI tract, whilst not yet well characterized, holds great promise due to its immunomodulatory roles in inflammatory systems and its lack of psychotropic effects. This review of our current knowledge of CB2 receptors in the gastrointestinal tract highlights its role in regulating abnormal motility, modulating intestinal inflammation and limiting visceral sensitivity and pain. CB2 receptors represent a braking system and a pathophysiological mechanism for the resolution of inflammation and many of its symptoms. CB2 receptor activation therefore represents a very promising therapeutic target in gastrointestinal inflammatory states where there is immune activation and motility dysfunction. British Journal of Pharmacology (2008) 153, 263,270; doi:10.1038/sj.bjp.0707486; published online 1 October 2007 [source]