Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021390 (inflammatory bowel disease)
 23,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 7-year-old, male, castrated, Labrador Retriever with a history of pancreatitis and inflammatory bowel disease presented for vomiting and anorexia. Serum biochemistry findings were indicative of cholestasis, hepatocellular insult, and decreased hepatic function. Ultrasound examination showed sediment and gas within the gallbladder, and a diagnosis of emphysematous cholecystitis was made. Emergency gallbladder resection was performed. Cytologic examination of bile fluid collected at surgery showed a mixed population of bacteria (bactibilia) together with fungal organisms consistent with Cyniclomyces guttulatus (previously known as Saccharomycopsis guttulatus). Similar fungal organisms were seen on a fecal smear. Bacteria cultured were normal gastrointestinal flora, supporting ascending infection; the fungal organisms were interpreted as incidental. Histopathology of the gallbladder indicated active (suppurative) and chronic (lymphocytic) cholecystitis and sections of liver tissue had evidence of chronic liver disease. A positive liver culture indicated concurrent bacterial hepatitis or cholangiohepatitis. Despite supportive care, the dog continued to decline and was euthanized 30 days later. Necropsy results confirmed end stage liver disease, but an initiating cause was not found. This case highlights the role of bactibilia in the development of acute cholecystitis and the unique cytologic appearance of C guttulatus as an incidental finding in bile fluid.
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PMID:Gallbladder aspirate from a dog. 1712 57

Undernutrition with weight loss, protein deficiency and specific deficiencies in vitamins, and trace elements are common in the acute phase of IBD. Anorexia, increased intestinal losses and systemic inflammation are the main causes of undernutrition. The relevance and extent of these deficiencies vary according to the site and extent of diseased intestine as well as disease activity. Mechanisms of EN efficacy as a primary treatment of IBD are not revealed yet. However, most physicians start to be earnest about enteral feeding because this treatment method does not cause any serious or prolonged complications. There are no significant differences in the effect of free amino acid, peptide-based and whole protein formulae for EN in IBD. Nutritional support with normal food is considered the treatment of choice. This article gives recommendations for the indication, application and type of formula of EN (oral nutritional supplements (ONS) or tube feeding (TF)) in patients with IBD. These are based on all relevant publications since 1995 and own authors experience. ONS and/or TF in addition to normal food is indicated in undernourished patients with IBD to improve nutritional status and quality of life. In active IBD EN should be used as sole therapy in adults mainly when treatment with corticosteroids is not feasible, e.g. due to intolerance or refusal. Combined therapy (EN and drugs) is indicated in undernourished patients as well as in those with inflammatory stenosis of the intestine. With ONS, a supplementary intake of up to 600 kcal/day can be achieved in addition to normal food. If a higher intake is required, TF is necessary. TF can be safely delivered by the nasogastric tube (NGT). Continuous administration of TF rather than bolus delivery is preferred because of the lower complication. In remission of IBD ONS and/or TF are recommended.
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PMID:[Clinical efficacy of enteral nutrition in inflammatory bowel diseases]. 1761 3

The researchers' view regarding the role of white adipose tissue (WAT) in inflammation has been greatly transformed over the last 10 years. WAT is now considered as an active organ producing many crucial molecules called adipokines. Resistin is a recently discovered cysteine-rich adipokine that has emerged during this decade as a promising inflammatory marker in various diseases. It is synthesized either from adipocytes or from immune cells, and exerts a pro-inflammatory profile in a variety of different experimental settings. Inflammatory bowel disease (IBD) is characterized by anorexia, malnutrition, altered body composition and the development of mesenteric WAT hypertrophy. The study by Konrad-Zerna et al. in this issue of the journal demonstrates an increased serum resistin in IBD patients, this being in agreement with previous IBD studies in mesenteric WAT and serum. Interesting aspects like the true validity of resistin as a marker of disease activity, the role of its different molecular isoforms, the cells that predominantly produce this molecule, and the possible use of resistin as a guide for therapeutic interventions, arise.
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PMID:Resistin: another rising biomarker in inflammatory bowel disease? 1799 23

A 15-year-old girl was admitted in April 2004 owing to fatigue and loss of appetite. Her paediatrician had found elevated serum levels for alkaline phosphatase. The endoscopic retrograde cholangiography documented typical signs of primary sclerosing cholangitis with involvement of the small and large ducts. The liver biopsy revealed extensive septal and portal fibrosis. No evidence of inflammatory bowel disease was present. She was started on ursodeoxycholic acid therapy and improved clinically. After 22 months she presented again with rising transaminase levels up to 600 U/l. The second liver biopsy was strongly suggestive for autoimmune hepatitis besides the already known features of primary sclerosing cholangitis. Elevated levels of IgG, and elevated titres for ANA and antismooth muscle antibodies (ASMA) were also found. The duct irregularities seen on re-endoscopic retrograde cholangiography were slightly regredient as compared with the first investigation. We added prednisolone and azathioprine to the ursodeoxycholic acid and the transaminase levels dropped together with clinical improvement.
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PMID:Autoimmune hepatitis 2 years after the diagnosis of primary sclerosing cholangitis: an unusual overlap syndrome in a 17-year-old adolescent. 1830 6

Inflammatory bowel disease (IBD) is characterized by anorexia, malnutrition, altered body composition, and development of mesenteric white adipose tissue (WAT) hypertrophy. Increasing evidence suggests that adipokines synthesized either in WAT or in immune cells, are involved in these manifestations of IBD. Among adipokines leptin, adiponectin and resistin hold a fundamental role while the role of ghrelin in inflammation is not well established. Preliminary studies have shown overexpression of leptin, adiponectin, and resistin in mesenteric WAT of patients with Crohn's disease (CD) and significant alterations of circulating serum levels of these adipokines in IBD. It has also been demonstrated that intestinal inflammation causes an increase in endogenous ghrelin production. In animal models of intestinal inflammation, existing data suggest that leptin, adiponectin, and resistin are pivotal mediators of inflammation. Interesting therapeutic interventions based on these data have been suggested. A specific role for hypertrophic WAT has also been implicated in CD. Further efforts with experimental and clinical studies are needed to better understand the role of adipokines in IBD.
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PMID:Leptin, adiponectin, resistin, and ghrelin--implications for inflammatory bowel disease. 1838 34

CRH, the hypothalamic component of the hypothalamic-pituitary adrenal axis, attenuates inflammation through stimulation of glucocorticoid release, whereas peripherally expressed CRH acts as a proinflammatory mediator. CRH is expressed in the intestine and up-regulated in patients with ulcerative colitis. However, its pathophysiological significance in intestinal inflammatory diseases has just started to emerge. In a mouse model of acute, trinitrobenzene sulfonic acid-induced experimental colitis, we demonstrate that, despite low glucocorticoid levels, CRH-deficient mice develop substantially reduced local inflammatory responses. These effects were shown by histological scoring of tissue damage and neutrophil infiltration. At the same time, CRH deficiency was found to be associated with higher serum leptin and IL-6 levels along with sustained anorexia and weight loss, although central CRH has been reported to be a strong appetite suppressor. Taken together, our results support an important proinflammatory role for CRH during mouse experimental colitis and possibly in inflammatory bowel disease in humans. Moreover, the results suggest that CRH is involved in homeostatic pathways that link inflammation and metabolism.
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PMID:Corticotropin-releasing hormone deficiency is associated with reduced local inflammation in a mouse model of experimental colitis. 1840 81

The melanocortins (alpha, beta and gamma-melanocyte-stimulating hormones: MSHs; adrenocorticotrophic hormone: ACTH), a family of pro-opiomelanocortin (POMC)-derived peptides having in common the tetrapeptide sequence His-Phe-Arg-Trp, have progressively revealed an incredibly wide range of extra-hormonal effects, so to become one of the most promising source of innovative drugs for many, important and widespread pathological conditions. The discovery of their effects on some brain functions, independently made by William Ferrari and David De Wied about half a century ago, led to the formulation of the term "neuropeptide" at a time when no demonstration of the actual production of peptide molecules by neurons, in the brain, was still available, and there were no receptors characterized for these molecules. In the course of the subsequent decades it came out that melanocortins, besides inducing one of the most complex and bizarre behavioural syndromes (excessive grooming, crises of stretchings and yawnings, repeated episodes of spontaneous penile erection and ejaculation, increased sexual receptivity), play a key role in functions of fundamental physiological importance as well as impressive therapeutic effects in different pathological conditions. If serendipity had been an important determinant in the discovery of the above-mentioned first-noticed extra-hormonal effects of melanocortins, many of the subsequent discoveries in the pharmacology of these peptides (feeding inhibition, shock reversal, role in opiate tolerance/withdrawal, etc.) have been the result of a planned research, aimed at testing the "pro-nociceptive/anti-nociceptive homeostatic system" hypothesis. The discovery of melanocortin receptors, and the ensuing synthesis of selective ligands with agonist or antagonist activity, is generating completely innovative drugs for the treatment of a potentially very long list of important and widespread pathological conditions: sexual impotence, frigidity, overweight/obesity, anorexia, cachexia, haemorrhagic shock, other forms of shock, myocardial infarction, ischemia/reperfusion-induced brain damage, neuropathic pain, rheumathoid arthritis, inflammatory bowel disease, nerve injury, toxic neuropathies, diabetic neuropathy, etc. This review recalls the history of these researches and outlines the pharmacology of the extra-hormonal effects of melanocortins which are produced by an action at the brain level (or mainly at the brain level). In our opinion the picture is still incomplete, in spite of being already so incredibly vast and complex. So, for example, several of their effects and preliminary animal data suggest that melanocortins might be of concrete effectiveness in one of the areas of most increasing concern, i.e., that of neurodegenerative diseases.
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PMID:Brain effects of melanocortins. 1899 99

Off-label use of uncoated sulfasalazine tablets (TAB) by rheumatoid arthritis (RA) patients in the United States has resulted in poor gastrointestinal (GI) tolerance and compliance. Two studies have shown that treatment of inflammatory bowel disease with enteric-coated sulfasalazine ([EN] Azulfidine ENtabs) resulted in significantly less frequent and severe GI symptoms, compared with treatment with TAB. The current study was conducted to compare GI tolerance of EN and TAB in rheumatoid arthritis (RA) patients. Fifty adult sulfasalazine-naive patients, who displayed stable RA and no significant GI toxicity with nonsteroidal anti-inflammatory drugs and disease-modifying anti-rheumatic drugs at baseline, were randomized to receive 2 g EN or TAB, in a prospective, 10-week, investigator-blinded, crossover study. After an initial 3-week dosing period with either EN or TAB and a 2-week washout, patients were crossed over to the alternative sulfasalazine formulation for a 2nd 3-week dosing period and 2-week follow-up. GI tolerance of EN and TAB in patients who completed both arms of the crossover was assessed bv frequency and intensity of reported adverse events (primary endpoints) and responses to health questionnaires (secondary endpoints).Twelve patients dropped out early because of adverse events and the discontinuation rate was similar in E\ and TAB-treated patients. Patients taking EN who completed the study reported significantly fewer (p < 0.001) GI adverse events (abdominal pain, anorexia, flatulence, diarrhea, heartburn, nausea, and vomiting), compared with those patients taking TAB. The intensity of adverse events was predominantly mild in patients treated with either EN or TAB. Responses to questionnaires were similar in patients taking either formulation of sulfasalazine. However, when asked which treatment period was preferred at the end of the study, 849 of patients completing the study (p < 0.001) chose EN. This study suggests that enteric-coating of sulfasalazine improved GI tolerance and RA patient preference.
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PMID:Improved gastrointestinal tolerance and patient preference of enteric-coated sulfasalazine versus uncoated sulfasalazine tablets in patients with rheumatoid arthritis. 1907 85

Diseases of the gastrointestinal (GI) tract are a common problem in cats, and the clinical signs associated with these diseases, vomiting, diarrhea, anorexia, or weight loss, are some of the most common presenting complaints for cats taken to veterinary clinics in the United States. There are many causes for GI disease in cats, and an equally diverse number of pharmacologic approaches for management of GI disease; however, management of any GI disease is not complete without the concurrent addition of appropriate dietary therapy. This therapy may be completely curative in some instances (eg, dietary allergy), but even in cases where diet is not the cause of the GI problem, appropriate dietary therapy is essential to the long-term management of GI disease. Whether that is a highly digestible diet to improve digestion of foods by a diseased GI tract (eg, inflammatory bowel disease or lymphoma) or a high-fiber diet to improve colonic function in cats with colitis, the role of diet in management of disorders of the GI tract cannot be ignored. This article will review the current state of understanding of the role of diet in the management of GI diseases in cats and will offer the reader an overview of diet management strategies in cats.
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PMID:Nutritional management of feline gastrointestinal diseases. 1908 54

Ciclosporin is an immunosuppressive drug that has been used to treat allergies and other immune-mediated diseases in cats, dogs and humans. Information about the adverse effects of ciclosporin in cats has been limited to smaller studies and case reports. Adverse effects in dogs are mainly gastrointestinal in nature, but humans can also experience hypertension and altered renal function. The aim of this retrospective case series study was to document the occurrence and clinical appearance of adverse events in cats receiving ciclosporin to treat allergic skin disease. The medical records of 50 cats with allergic dermatitis treated with oral ciclosporin (1.9-7.3 mg/kg/day) were reviewed. Adverse events occurred in 66% (33 cats). Adverse events likely to be associated with ciclosporin included the following: vomiting or diarrhoea within 1-8 weeks of receiving ciclosporin (24%), weight loss (16%), anorexia and subsequent hepatic lipidosis (2%) and gingival hyperplasia (2%). Other adverse events less likely to be associated with ciclosporin therapy included the following: weight gain (14%), dental tartar and gingivitis (10%), otitis (4%), chronic diarrhoea (4%), inflammatory bowel disease with indolent gastrointestinal lymphoma (2%), urinary tract infection (2%), cataract (2%), elevated liver enzymes (2%), hyperthyroidism and renal failure (2%) and transient inappropriate urination (2%). Some cats experienced multiple adverse events. Case-control studies are needed to prove cause and effect of ciclosporin with regard to these adverse events.
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PMID:Adverse events in 50 cats with allergic dermatitis receiving ciclosporin. 2154 60


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