Colitis: Inflammation of the COLON section of the large intestine (INTESTINE, LARGE), usually with symptoms such as DIARRHEA (often with blood and mucus), ABDOMINAL PAIN, and FEVER.Colitis, Ulcerative: Inflammation of the COLON that is predominantly confined to the MUCOSA. Its major symptoms include DIARRHEA, rectal BLEEDING, the passage of MUCUS, and ABDOMINAL PAIN.Colitis, Ischemic: Inflammation of the COLON due to colonic ISCHEMIA resulting from alterations in systemic circulation or local vasculature.Colitis, Microscopic: A condition characterized by chronic watery DIARRHEA of unknown origin, a normal COLONOSCOPY but abnormal histopathology on BIOPSY. This syndrome was first described in 1980 by Read and associates. Subtypes include COLLAGENOUS COLITIS and LYMPHOCYTIC COLITIS. Both have similar clinical symptoms and are distinguishable only by histology.Dextran Sulfate: Long-chain polymer of glucose containing 17-20% sulfur. It has been used as an anticoagulant and also has been shown to inhibit the binding of HIV-1 to CD4-POSITIVE T-LYMPHOCYTES. It is commonly used as both an experimental and clinical laboratory reagent and has been investigated for use as an antiviral agent, in the treatment of hypolipidemia, and for the prevention of free radical damage, among other applications.Colitis, Collagenous: A subtype of MICROSCOPIC COLITIS, characterized by chronic watery DIARRHEA of unknown origin, a normal COLONOSCOPY but abnormal histopathology on BIOPSY. Microscopic examination of biopsy samples taken from the COLON show larger-than-normal band of subepithelial COLLAGEN.Colon: The segment of LARGE INTESTINE between the CECUM and the RECTUM. It includes the ASCENDING COLON; the TRANSVERSE COLON; the DESCENDING COLON; and the SIGMOID COLON.Trinitrobenzenesulfonic Acid: A reagent that is used to neutralize peptide terminal amino groups.Colitis, Lymphocytic: A subtype of MICROSCOPIC COLITIS, characterized by chronic watery DIARRHEA of unknown origin, a normal COLONOSCOPY but abnormal histopathology on BIOPSY. Microscopic examination of biopsy samples taken from the COLON show infiltration of LYMPHOCYTES in the superficial EPITHELIUM and the underlying connective tissue (lamina propria).Crohn Disease: A chronic transmural inflammation that may involve any part of the DIGESTIVE TRACT from MOUTH to ANUS, mostly found in the ILEUM, the CECUM, and the COLON. In Crohn disease, the inflammation, extending through the intestinal wall from the MUCOSA to the serosa, is characteristically asymmetric and segmental. Epithelioid GRANULOMAS may be seen in some patients.Intestinal Mucosa: Lining of the INTESTINES, consisting of an inner EPITHELIUM, a middle LAMINA PROPRIA, and an outer MUSCULARIS MUCOSAE. In the SMALL INTESTINE, the mucosa is characterized by a series of folds and abundance of absorptive cells (ENTEROCYTES) with MICROVILLI.Inflammatory Bowel Diseases: Chronic, non-specific inflammation of the GASTROINTESTINAL TRACT. Etiology may be genetic or environmental. This term includes CROHN DISEASE and ULCERATIVE COLITIS.Mesalamine: An anti-inflammatory agent, structurally related to the SALICYLATES, which is active in INFLAMMATORY BOWEL DISEASE. It is considered to be the active moiety of SULPHASALAZINE. (From Martindale, The Extra Pharmacopoeia, 30th ed)Rectum: The distal segment of the LARGE INTESTINE, between the SIGMOID COLON and the ANAL CANAL.Sulfasalazine: A drug that is used in the management of inflammatory bowel diseases. Its activity is generally considered to lie in its metabolic breakdown product, 5-aminosalicylic acid (see MESALAMINE) released in the colon. (From Martindale, The Extra Pharmacopoeia, 30th ed, p907)Peroxidase: A hemeprotein from leukocytes. Deficiency of this enzyme leads to a hereditary disorder coupled with disseminated moniliasis. It catalyzes the conversion of a donor and peroxide to an oxidized donor and water. EC Agents: Drugs used for their effects on the gastrointestinal system, as to control gastric acidity, regulate gastrointestinal motility and water flow, and improve digestion.Colectomy: Excision of a portion of the colon or of the whole colon. (Dorland, 28th ed)Proctocolectomy, Restorative: A surgical procedure involving the excision of the COLON and RECTUM and the formation of an ILEOANAL RESERVOIR (pouch). In patients with intestinal diseases, such as ulcerative colitis, this procedure avoids the need for an OSTOMY by allowing for transanal defecation.Disease Models, Animal: Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.Colonoscopy: Endoscopic examination, therapy or surgery of the luminal surface of the colon.Dysentery, Amebic: DYSENTERY caused by intestinal amebic infection, chiefly with ENTAMOEBA HISTOLYTICA. This condition may be associated with amebic infection of the LIVER and other distant sites.Ileostomy: Surgical creation of an external opening into the ILEUM for fecal diversion or drainage. This replacement for the RECTUM is usually created in patients with severe INFLAMMATORY BOWEL DISEASES. Loop (continent) or tube (incontinent) procedures are most often employed.Administration, Rectal: The insertion of drugs into the rectum, usually for confused or incompetent patients, like children, infants, and the very old or comatose.Enterocolitis, Pseudomembranous: An acute inflammation of the INTESTINAL MUCOSA that is characterized by the presence of pseudomembranes or plaques in the SMALL INTESTINE (pseudomembranous enteritis) and the LARGE INTESTINE (pseudomembranous colitis). It is commonly associated with antibiotic therapy and CLOSTRIDIUM DIFFICILE colonization.Pouchitis: Acute INFLAMMATION in the INTESTINAL MUCOSA of the continent ileal reservoir (or pouch) in patients who have undergone ILEOSTOMY and restorative proctocolectomy (PROCTOCOLECTOMY, RESTORATIVE).Mice, Inbred C57BLEnterocolitis: Inflammation of the MUCOSA of both the SMALL INTESTINE and the LARGE INTESTINE. Etiology includes ISCHEMIA, infections, allergic, and immune responses.Mice, Knockout: Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.Diarrhea: An increased liquidity or decreased consistency of FECES, such as running stool. Fecal consistency is related to the ratio of water-holding capacity of insoluble solids to total water, rather than the amount of water present. Diarrhea is not hyperdefecation or increased fecal weight.Colonic Pouches: Sacs or reservoirs created to function in place of the COLON and/or RECTUM in patients who have undergone restorative proctocolectomy (PROCTOCOLECTOMY, RESTORATIVE).Acetic Acid: Product of the oxidation of ethanol and of the destructive distillation of wood. It is used locally, occasionally internally, as a counterirritant and also as a reagent. (Stedman, 26th ed)Intestines: The section of the alimentary canal from the STOMACH to the ANAL CANAL. It includes the LARGE INTESTINE and SMALL INTESTINE.Probiotics: Live microbial DIETARY SUPPLEMENTS which beneficially affect the host animal by improving its intestinal microbial balance. Antibiotics and other related compounds are not included in this definition. In humans, lactobacilli are commonly used as probiotics, either as single species or in mixed culture with other bacteria. Other genera that have been used are bifidobacteria and streptococci. (J. Nutr. 1995;125:1401-12)Interleukin-10: A cytokine produced by a variety of cell types, including T-LYMPHOCYTES; MONOCYTES; DENDRITIC CELLS; and EPITHELIAL CELLS that exerts a variety of effects on immunoregulation and INFLAMMATION. Interleukin-10 combines with itself to form a homodimeric molecule that is the biologically active form of the protein.Cytokines: Non-antibody proteins secreted by inflammatory leukocytes and some non-leukocytic cells, that act as intercellular mediators. They differ from classical hormones in that they are produced by a number of tissue or cell types rather than by specialized glands. They generally act locally in a paracrine or autocrine rather than endocrine manner.Cecum: The blind sac or outpouching area of the LARGE INTESTINE that is below the entrance of the SMALL INTESTINE. It has a worm-like extension, the vermiform APPENDIX.Citrobacter rodentium: A species of gram-negative bacteria in the genus CITROBACTER, family ENTEROBACTERIACEAE. As an important pathogen of laboratory mice, it serves as a model for investigating epithelial hyperproliferation and tumor promotion. It was previously considered a strain of CITROBACTER FREUNDII.Ileitis: Inflammation of any segment of the ILEUM and the ILEOCECAL VALVE.Feces: Excrement from the INTESTINES, containing unabsorbed solids, waste products, secretions, and BACTERIA of the DIGESTIVE SYSTEM.Helicobacter hepaticus: A species of HELICOBACTER that colonizes the CECUM and COLON of several strains of MICE, and is associated with HEPATITIS and carcinogenesis.Mice, Inbred BALB CAnti-Inflammatory Agents, Non-Steroidal: Anti-inflammatory agents that are non-steroidal in nature. In addition to anti-inflammatory actions, they have analgesic, antipyretic, and platelet-inhibitory actions.They act by blocking the synthesis of prostaglandins by inhibiting cyclooxygenase, which converts arachidonic acid to cyclic endoperoxides, precursors of prostaglandins. Inhibition of prostaglandin synthesis accounts for their analgesic, antipyretic, and platelet-inhibitory actions; other mechanisms may contribute to their anti-inflammatory effects.Megacolon, Toxic: An acute form of MEGACOLON, severe pathological dilatation of the COLON. It is associated with clinical conditions such as ULCERATIVE COLITIS; CROHN DISEASE; AMEBIC DYSENTERY; or CLOSTRIDIUM ENTEROCOLITIS.Ileum: The distal and narrowest portion of the SMALL INTESTINE, between the JEJUNUM and the ILEOCECAL VALVE of the LARGE INTESTINE.Oxazolone: Immunologic adjuvant and sensitizing agent.Biopsy: Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body.Clostridium difficile: A common inhabitant of the colon flora in human infants and sometimes in adults. It produces a toxin that causes pseudomembranous enterocolitis (ENTEROCOLITIS, PSEUDOMEMBRANOUS) in patients receiving antibiotic therapy.Inflammation: A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function.Colon, Sigmoid: A segment of the COLON between the RECTUM and the descending colon.Chronic Disease: Diseases which have one or more of the following characteristics: they are permanent, leave residual disability, are caused by nonreversible pathological alteration, require special training of the patient for rehabilitation, or may be expected to require a long period of supervision, observation, or care. (Dictionary of Health Services Management, 2d ed)Sigmoidoscopy: Endoscopic examination, therapy or surgery of the sigmoid flexure.Colonic Diseases: Pathological processes in the COLON region of the large intestine (INTESTINE, LARGE).Proctitis: INFLAMMATION of the MUCOUS MEMBRANE of the RECTUM, the distal end of the large intestine (INTESTINE, LARGE).Intestine, Large: A segment of the LOWER GASTROINTESTINAL TRACT that includes the CECUM; the COLON; and the RECTUM.Cholangitis, Sclerosing: Chronic inflammatory disease of the BILIARY TRACT. It is characterized by fibrosis and hardening of the intrahepatic and extrahepatic biliary ductal systems leading to bile duct strictures, CHOLESTASIS, and eventual BILIARY CIRRHOSIS.Mucous Membrane: An EPITHELIUM with MUCUS-secreting cells, such as GOBLET CELLS. It forms the lining of many body cavities, such as the DIGESTIVE TRACT, the RESPIRATORY TRACT, and the reproductive tract. Mucosa, rich in blood and lymph vessels, comprises an inner epithelium, a middle layer (lamina propria) of loose CONNECTIVE TISSUE, and an outer layer (muscularis mucosae) of SMOOTH MUSCLE CELLS that separates the mucosa from submucosa.Azathioprine: An immunosuppressive agent used in combination with cyclophosphamide and hydroxychloroquine in the treatment of rheumatoid arthritis. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), this substance has been listed as a known carcinogen. (Merck Index, 11th ed)Colonic Neoplasms: Tumors or cancer of the COLON.Proctocolitis: Inflammation of the RECTUM and the distal portion of the COLON.Acute Disease: Disease having a short and relatively severe course.Prednisolone: A glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states.Tumor Necrosis Factor-alpha: Serum glycoprotein produced by activated MACROPHAGES and other mammalian MONONUCLEAR LEUKOCYTES. It has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. Also known as TNF-alpha, it is only 30% homologous to TNF-beta (LYMPHOTOXIN), but they share TNF RECEPTORS.Dinitrofluorobenzene: Irritants and reagents for labeling terminal amino acid groups.Gastrointestinal Hemorrhage: Bleeding in any segment of the GASTROINTESTINAL TRACT from ESOPHAGUS to RECTUM.Bacterial Translocation: The passage of viable bacteria from the GASTROINTESTINAL TRACT to extra-intestinal sites, such as the mesenteric lymph node complex, liver, spleen, kidney, and blood. Factors that promote bacterial translocation include overgrowth with gram-negative enteric bacilli, impaired host immune defenses, and injury to the INTESTINAL MUCOSA resulting in increased intestinal permeability. Bacterial translocation from the lung to the circulation is also possible and sometimes accompanies MECHANICAL VENTILATION.Mesentery: A layer of the peritoneum which attaches the abdominal viscera to the ABDOMINAL WALL and conveys their blood vessels and nerves.Clostridium Infections: Infections with bacteria of the genus CLOSTRIDIUM.Collagen Diseases: Historically, a heterogeneous group of acute and chronic diseases, including rheumatoid arthritis, systemic lupus erythematosus, progressive systemic sclerosis, dermatomyositis, etc. This classification was based on the notion that "collagen" was equivalent to "connective tissue", but with the present recognition of the different types of collagen and the aggregates derived from them as distinct entities, the term "collagen diseases" now pertains exclusively to those inherited conditions in which the primary defect is at the gene level and affects collagen biosynthesis, post-translational modification, or extracellular processing directly. (From Cecil Textbook of Medicine, 19th ed, p1494)CD4-Positive T-Lymphocytes: A critical subpopulation of T-lymphocytes involved in the induction of most immunological functions. The HIV virus has selective tropism for the T4 cell which expresses the CD4 phenotypic marker, a receptor for HIV. In fact, the key element in the profound immunosuppression seen in HIV infection is the depletion of this subset of T-lymphocytes.Severity of Illness Index: Levels within a diagnostic group which are established by various measurement criteria applied to the seriousness of a patient's disorder.Ulcer: A lesion on the surface of the skin or a mucous surface, produced by the sloughing of inflammatory necrotic tissue.Mucin-2: A gel-forming mucin found predominantly in SMALL INTESTINE and variety of mucous membrane-containing organs. It provides a protective, lubricating barrier against particles and infectious agents.Administration, Oral: The giving of drugs, chemicals, or other substances by mouth.

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Ulcerative Colitis and Your Family. Raquel Feldberg is a mother of two who developed ulcerative colitis shortly after the birth ... Growing Up with Ulcerative Colitis. Orly Borovitch was diagnosed with Ulcerative Colitis as a teen. In 'Growing Up with ... Living with Ulcerative Colitis. James Mireau from Alberta candidly talks about his journey with ulcerative colitis from the ... Conquering Ulcerative Colitis. Professional triathlete Jonathan Caron from Quebec is not letting the ulcerative colitis he has ...

Colitis: - K52Microscopic colitisLymphocytic colitis: Lymphocytic colitis, a subtype of microscopic colitis, is a rare condition characterized by chronic non-bloody watery diarrhea. The colonoscopy is normal but the mucosal biopsy reveals an accumulation of lymphocytes in the colonic epithelium and connective tissue (lamina propria).Crohn's Disease Activity Index: The Crohn's Disease Activity Index or CDAI is a research tool used to quantify the symptoms of patients with Crohn's disease. This is of useful importance in research studies done on medications used to treat Crohn's disease; most major studies on newer medications use the CDAI in order to define response or remission of disease.Transverse folds of rectum: The transverse folds of rectum (or Houston's valves) are semi-lunar transverse folds of the rectal wall that protrude into the rectum, not the anal canal as that lies below the rectum. Their use seems to be to support the weight of fecal matter, and prevent its urging toward the anus, which would produce a strong urge to defecate.SulfasalazineMyeloperoxidase deficiency: Myeloperoxidase deficiency is an autosomal recessive genetic disorder featuring deficiency, either in quantity or of function, of myeloperoxidase, an enzyme found in certain phagocytic immune cells, especially polymorphonuclear leukocytes.FontolizumabColectomyProctocolectomy: Proctocolectomy is the surgical removal of the rectum and all or part of the colon. It is a most widely accepted surgical method for ulcerative colitis and Familial adenomatous polyposis (FAP) .Gross pathology: Gross pathology refers to macroscopic manifestations of disease in organs, tissues, and body cavities. The term is commonly used by anatomical pathologists to refer to diagnostically useful findings made during the gross examination portion of surgical specimen processing or an autopsy.Virtual colonoscopy: Virtual colonoscopy (VC, also called CT Colonography or CT Pneumocolon) is a medical imaging procedure which uses x-rays and computers to produce two- and three-dimensional images of the colon (large intestine) from the lowest part, the rectum, all the way to the lower end of the small intestine and display them on a screen. The procedure is used to diagnose colon and bowel disease, including polyps, diverticulosis and cancer.IleostomyIferanserin: Iferanserin (INN; VEN-309) is a drug which acts as a selective 5-HT2A receptor antagonist. It is under development as an intra-rectal formulation for the treatment of hemorrhoid disease, and as of February 2012, is in phase IIb clinical trials.Colitis-X: Colitis X, equine colitis X or peracute toxemic colitis is a catchall term for various fatal forms of acute or peracute colitis found in horses, but particularly a fulminant colitis where clinical signs include sudden onset of severe diarrhea, abdominal pain, shock, and dehydration. Death is common, with 90% to 100% mortality, usually in less than 24 hours.Food protein-induced enterocolitis syndrome: Food Protein-Induced Enterocolitis Syndrome (FPIES) is a severe systemic response to food protein that typically occurs 1 to 4 hours after the ingestion of the causative food and frequently develops in the first few years of life.Powell GK.Congenital chloride diarrhea: Congenital chloride diarrhea (CCD, also congenital chloridorrhea or Darrow Gamble syndrome) is a genetic disorder due to an autosomal recessive mutation on chromosome 7. The mutation is in downregulated-in-adenoma (DRA), a gene that encodes a membrane protein of intestinal cells.Acetic acid bacteria: Acetic acid bacteria (AAB) derive their energy from the oxidation of ethanol to acetic acid during fermentation. They are gram-negative, aerobic, rod-shaped bacteria.Mutaflor: Mutaflor is a probiotic consisting of a viable non-pathogenic bacteria strain named Escherichia coli Nissle 1917.Mutaflor Information page "The Escherichia coli strain Nissle 1917-designated DSM 6601 in the German Collection for Microorganisms in Braunschweig is one of the best-examined and therapeutically relevant bacterial strains worldwide" as claimed by the manufacturerManufacturers WebsiteProinflammatory cytokine: A proinflammatory cytokine is a cytokine which promotes systemic inflammation.CecectomyIntimin: Intimin is a virulence factor (adhesin) of EPEC (e.g.IleitisFetor hepaticusCelecoxibToxic megacolonC3H3NO2Brain biopsyFidaxomicinInflammation: Inflammation (Latin, [is part of the complex biological response of body tissues to harmful stimuli, such as pathogen]s, damaged cells, or irritants.Sigmoidocele: Sigmoidocele (also known as Pouch of Douglas descent) refers to a condition where the sigmoid colon descends (prolapses) into the lower pelvic cavity. This can obstruct the rectum and cause symptoms of obstructed defecation.Non-communicable disease: Non-communicable disease (NCD) is a medical condition or disease that is non-infectious or non-transmissible. NCDs can refer to chronic diseases which last for long periods of time and progress slowly.ProctitisHaustrum (anatomy): The haustra (singular haustrum) of the colon are the small pouches caused by sacculation (sac formation), which give the colon its segmented appearance. The teniae coli run the length of the large intestine.Secondary sclerosing cholangitis: Secondary sclerosing cholangitis abbreviated as (SSC) is a disease that is morphologically similar to primary sclerosing cholangitis (PSC) but that originates from a known pathological process. Its clinical and cholangiographic features may mimic PSC, yet its natural history may be more favorable if recognition is prompt and appropriate therapy is introduced.AzathioprineOncotype DX Colon Cancer AssayPrednisoloneG-CSF factor stem-loop destabilising elementFluorobenzeneGlasgow-Blatchford score: The Glasgow-Blatchford bleeding score (GBS) is a screening tool to assess the likelihood that a patient with an acute upper gastrointestinal bleeding (UGIB) will need to have medical intervention such as a blood transfusion or endoscopic intervention. The tool may be able to identify patients who do not need to be admitted to hospital after a UGIB.Otospondylomegaepiphyseal dysplasia: Otospondylomegaepiphyseal dysplasia (OSMED) is an autosomal recessive disorder of bone growth that results in skeletal abnormalities, severe hearing loss, and distinctive facial features. The name of the condition indicates that it affects hearing (oto-) and the bones of the spine (spondylo-), and enlarges the ends of bones (megaepiphyses).Penetrating atherosclerotic ulcer: A penetrating atherosclerotic ulcer (PAU) is an atherosclerotic lesion that ulcerates, leading to a hematoma forming within the walls of the aorta.Osmotic controlled-release oral delivery system: OROS (Osmotic [Controlled] Release Oral [Delivery] System) is a controlled release oral drug delivery system in the form of a tablet. The tablet has a rigid water-permeable jacket with one or more laser drilled small holes.

(1/3046) Histocompatibility antigens in inflammatory bowel disease. Their clinical significance and their association with arthropathy with special reference to HLA-B27 (W27).

Histocompatibility (HLA) antigen phenotypes have been studied in 100 patients with ulcerative colitis, 100 with Crohn's disease, and 283 normal controls. In addition the incidence of ankylosing spondylitis, sacroiliitis, and "enteropathic" peripheral arthropathy was determined in the patients with inflammatory bowel disease (IBD). There was no significant difference in antigen frequency between patients and controls. However, the incidence of HLA-B27 was increased in the patients complicated by ankylosing spondylitis and/or sacroiliitis in both ulcerative colitis and Crohn's disease. In contrast, none of the 29 IBD patients with "enteropathic" peripheral arthropathy had B27 antigen. Furthermore, ankylosing spondylitis was found more frequently in ulcerative colitis bearing HLA-B27 compared with non-B27 patients (P less than 0-01). The same was found in Crohn's disease, although this difference was not statistically significant. In addition, 12 of 14 ulcerative colitis patients and five out of six Crohn's patients with HLA-B27 had total colitis, compared with the frequency of total colitis in non-B27 patients (P less than 0-024 and less than 0-03 respectively). The data suggest that B27 histocompatibility antigen could be a pathogenetic discriminator between the arthropathies in IBD and may be of prognostic significance with respect to extension and severity of the disease.  (+info)

(2/3046) Expression of nitric oxide synthase in inflammatory bowel disease is not affected by corticosteroid treatment.

AIM: To examine the effect of corticosteroid treatment on the expression of inducible nitric oxide synthase (iNOS) in the colon of patients with inflammatory bowel disease. METHODS: Four groups of patients were studied: (1) ulcerative colitis treated with high dose corticosteroids (six patients, 10 blocks); (2) ulcerative colitis patients who had never received corticosteroids (10 patients, 16 blocks); (3) Crohn's disease treated with high dose corticosteroids (12 patients, 24 blocks); (4) Non-inflammatory, non-neoplastic controls (four patients, six blocks). Full thickness paraffin sections of colons removed at surgery were immunostained with an antibody raised against the C terminal end of iNOS. Sections were assessed semiquantitatively for the presence and degree of inflammation and immunoreactivity for nitric oxide synthase. RESULTS: Cases of ulcerative colitis and Crohn's disease with active inflammation showed strong staining for nitric oxide synthase. The staining was diffuse in ulcerative colitis and patchy in Crohn's disease, in accordance with the distribution of active inflammation. Staining was seen in epithelial cells and was most intense near areas of inflammation such as crypt abscesses. Non-inflamed epithelium showed no immunoreactivity. Treatment with corticosteroids made no difference to the amount of nitric oxide synthase. CONCLUSIONS: Expression of nitric oxide synthase is increased in both ulcerative colitis and Crohn's disease and appears to be unaffected by treatment with corticosteroids. Disease severity necessitated surgery in all the cases included in this study, regardless of whether or not the patients had received long term corticosteroid treatment. It seems therefore that a high level of iNOS expression and, presumably, production of nitric oxide characterise cases which are refractory to clinical treatment; this suggests that specific inhibition of the enzyme may be a useful therapeutic adjunct.  (+info)

(3/3046) Perioperative growth hormone treatment and functional outcome after major abdominal surgery: a randomized, double-blind, controlled study.

OBJECTIVE: To evaluate short- and long-term effects of perioperative human growth hormone (hGH) treatment on physical performance and fatigue in younger patients undergoing a major abdominal operation in a normal postoperative regimen with oral nutrition. SUMMARY BACKGROUND DATA: Muscle wasting and functional impairment follow major abdominal surgery. METHODS: Twenty-four patients with ulcerative colitis undergoing ileoanal J-pouch surgery were randomized to hGH (12 IU/day) or placebo treatment from 2 days before to 7 days after surgery. Measurements were performed 2 days before and 10, 30, and 90 days after surgery. RESULTS: The total muscle strength of four limb muscle groups was reduced by 7.6% in the hGH group and by 17.1% in the placebo group at postoperative day 10 compared with baseline values. There was also a significant difference between treatment groups in total muscle strength at day 30, and at the 90-day follow-up total muscle strength was equal to baseline values in the hGH group, but still significantly 5.9% below in the placebo group. The work capacity decreased by approximately 20% at day 10 after surgery, with no significant difference between treatment groups. Both groups were equally fatigued at day 10 after surgery, but at day 30 and 90 the hGH patients were less fatigued than the placebo patients. During the treatment period, patients receiving hGH had reduced loss of limb lean tissue mass, and 3 months after surgery the hGH patients had regained more lean tissue mass than placebo patients. CONCLUSIONS: Perioperative hGH treatment of younger patients undergoing major abdominal surgery preserved limb lean tissue mass, increased postoperative muscular strength, and reduced long-term postoperative fatigue.  (+info)

(4/3046) Biased JH usage in plasma cell immunoglobulin gene sequences from colonic mucosa in ulcerative colitis but not in Crohn's disease.

BACKGROUND: Ulcerative colitis is an inflammatory disease of the colonic and rectal mucosa. Autoantibodies have been observed in ulcerative colitis which may have a role in the pathogenesis of the disease. Evidence also suggests that there is an hereditary predisposition towards the disease, although no individual genes have been identified. AIMS: This is a pilot study of immunoglobulin heavy chain genes (IgH) in ulcerative colitis to determine whether they have any particular genetic characteristics which may lead to a better understanding of the disease aetiology. SUBJECTS: Colonic or rectal tissue was obtained from five children with ulcerative colitis. Tissue was also obtained from five children with Crohn's disease and five children who did not have inflammatory bowel disease as controls. METHODS: B cells and IgD+ B cells were identified by immunohistochemistry on frozen sections. Areas of lamina propria containing plasma cells, and areas of IgD+ B cells were microdissected. The immunoglobulin genes were PCR amplified, cloned, and sequenced. Sequences were analysed for content of somatic mutations and composition of heavy chain. RESULTS: An increase in the use of JH6 and DXP'1, and a decrease in the use of JH4, gene segments in immunoglobulin genes from lamina propria plasma cells, and from virgin IgD+ B cells, was found in patients with ulcerative colitis. These biases were not present in the control groups. CONCLUSIONS: There is a fundamental difference in the immunoglobulin genes from patients with ulcerative colitis. Whether this is caused by a difference in content of immunoglobulin gene segments in the germline or a difference in the recombination mechanism is not known.  (+info)

(5/3046) Sulphation and secretion of the predominant secretory human colonic mucin MUC2 in ulcerative colitis.

BACKGROUND: Decreased synthesis of the predominant secretory human colonic mucin (MUC2) occurs during active ulcerative colitis. AIMS: To study possible alterations in mucin sulphation and mucin secretion, which could be the cause of decreased mucosal protection in ulcerative colitis. METHODS: Colonic biopsy specimens from patients with active ulcerative colitis, ulcerative colitis in remission, and controls were metabolically labelled with [35S]-amino acids or [35S]-sulphate, chase incubated and analysed by SDS-PAGE, followed by quantitation of mature [35S]-labelled MUC2. For quantitation of total MUC2, which includes non-radiolabelled and radiolabelled MUC2, dot blotting was performed, using a MUC2 monoclonal antibody. RESULTS: Between patient groups, no significant differences were found in [35S]-sulphate content of secreted MUC2 or in the secreted percentage of either [35S]-amino acid labelled MUC2 or total MUC2. During active ulcerative colitis, secretion of [35S]-sulphate labelled MUC2 was significantly increased twofold, whereas [35S]-sulphate incorporation into MUC2 was significantly reduced to half. CONCLUSIONS: During active ulcerative colitis, less MUC2 is secreted, because MUC2 synthesis is decreased while the secreted percentage of MUC2 is unaltered. Furthermore, sulphate content of secreted MUC2 is unaltered by a specific compensatory mechanism, because sulphated MUC2 is preferentially secreted while sulphate incorporation into MUC2 is reduced.  (+info)

(6/3046) A genomewide analysis provides evidence for novel linkages in inflammatory bowel disease in a large European cohort.

Inflammatory bowel disease (IBD) is characterized by a chronic relapsing intestinal inflammation, typically starting in early adulthood. IBD is subdivided into two subtypes, on the basis of clinical and histologic features: Crohn disease and ulcerative colitis (UC). Previous genomewide searches identified regions harboring susceptibility loci on chromosomes 1, 3, 4, 7, 12, and 16. To expand our understanding of the genetic risk profile, we performed a 9-cM genomewide search for susceptibility loci in 268 families containing 353 affected sibling pairs. Previous linkages on chromosomes 12 and 16 were replicated, and the chromosome 4 linkage was extended in this sample. New suggestive evidence for autosomal linkages was observed on chromosomes 1, 6, 10, and 22, with LOD scores of 2.08, 2.07, 2.30, and 1.52, respectively. A maximum LOD score of 1.76 was observed on the X chromosome, for UC, which is consistent with the clinical association of IBD with Ullrich-Turner syndrome. The linkage finding on chromosome 6p is of interest, given the possible contribution of human leukocyte antigen and tumor necrosis-factor genes in IBD. This genomewide linkage scan, done with a large family cohort, has confirmed three previous IBD linkages and has provided evidence for five additional regions that may harbor IBD predisposition genes.  (+info)

(7/3046) The systemic load and efficient delivery of active 5-aminosalicylic acid in patients with ulcerative colitis on treatment with olsalazine or mesalazine.

BACKGROUND: There have been reports of nephrotoxic reactions in patients with ulcerative colitis treated with 5-aminosalicylic acid (5-ASA) preparations. AIM: To compare the efficacy in delivery of active 5-ASA to the colon and the systemic load as the basis for potential long-term toxicity during treatment with olsalazine or mesalazine in patients with ulcerative colitis in remission. PATIENTS AND METHODS: Fifteen patients with ulcerative colitis were treated with olsalazine or mesalazine, each for 7 days in an open, randomized, crossover design study. 5-ASA and acetyl-5-ASA (Ac-5-ASA) in plasma and urine were measured by high performance liquid chromatography. RESULTS: The plasma concentration of 5-ASA was 1.2 +/- 0.1 micromol/L (mean +/- S.E.M.) for olsalazine and 8.0 +/- 1.9 micromol/L for mesalazine, while the plasma concentration of Ac-5-ASA was 2.8 +/- 0.2 micromol/L for olsalazine and 10.8 +/- 1.6 micromol/L for mesalazine. The amount of 5-ASA excreted in the urine was 68 +/- 30 micromol/24 h for olsalazine and 593 +/- 164 micromol/24 h for mesalazine. The amount of Ac-5-ASA in the urine was 1260 +/- 102 micromol/24 h for olsalazine and 3223 +/- 229 micromol/24 h for mesalazine. The urinary recovery of total 5-ASA plus Ac-5-ASA (as a percentage of the given dose) was 23 +/- 2.1% for olsalazine and 39 +/- 3.6% for mesalazine. The ratio between the plasma concentrations of mesalazine and olsalazine differed significantly both for 5-ASA (5.1) and Ac-5-ASA (3.6); for 5-ASA (9. 9) and Ac-5-ASA (2.6) in urine, and for the urinary recovery of total 5-ASA plus Ac-5-ASA (1.7). Moreover, in the mesalazine group there was a large variation in the individual plasma concentrations of 5-ASA and Ac-5-ASA, with maximal values 5-6-fold higher than that in the olsalazine group. CONCLUSION: The systemic load of active 5-ASA is significantly higher for mesalazine than for olsalazine, when based on the dosages given and when calculated on an equimolar basis. Some of the patients in the mesalazine group showed unexpected high levels of plasma and urinary 5-ASA concentrations, a finding which may have long-term safety implications.  (+info)

(8/3046) Is maintenance therapy always necessary for patients with ulcerative colitis in remission?

BACKGROUND: The efficacy of sulphasalazine and mesalazine in preventing relapse in patients with ulcerative colitis is well known. It is less clear how long such maintenance should be continued, and if the duration of disease remission is a factor that affects the risk of recurrence. AIM: To determine whether the duration of disease remission affects the relapse rate, by comparing the efficacy of a delayed-release mesalazine (Asacol, Bracco S.p.A., Milan, Italy) against placebo in patients with ulcerative colitis with short- and long-duration of disease remission. METHODS: 112 patients (66 male, 46 female, mean age 35 years), with intermittent chronic ulcerative colitis in clinical, endoscopic and histological remission with sulphasalazine or mesalazine for at least 1 year, were included in the study. Assuming that a lower duration of remission might be associated with a higher relapse rate, the patients were stratified according to the length of their disease remission, prior to randomization into Group A (Asacol 26, placebo 35) in remission from 1 to 2 years, or Group B (Asacol 28, placebo 23) in remission for over 2 years, median 4 years. Patients were treated daily with oral Asacol 1.2 g vs. placebo, for a follow-up period of 1 year. RESULTS: We employed an intention-to-treat analysis. In Group A, whilst no difference was found between the two treatments after 6 months, mesalazine was significantly more effective than placebo in preventing relapse at 12 months [Asacol 6/26 (23%), placebo 17/35 (49%), P = 0.035, 95% Cl: 48-2.3%]. In contrast, in Group B no statistically significant difference was observed between the two treatments, either at 6 or 12 months [Asacol 5/28 (18%), placebo 6/23 (26%), P = 0.35, 95% Cl: 31-14%] of follow-up. Patients in group B were older, and had the disease and remission duration for longer, than those in Group A. CONCLUSIONS: Mesalazine prophylaxis is necessary for the prevention of relapse by patients with ulcerative colitis in remission for less than 2 years, but this study casts doubt over whether continuous maintenance treatment is necessary in patients with prolonged clinical, endoscopic and histological remission, who are at very low risk of relapse.  (+info)

inflammatory bowel d

  • Ulcerative colitis is a chronic inflammatory disease of the gastrointestinal (GI) tract, called inflammatory bowel disease (IBD). (
  • Ulcerative colitis is an idiopathic inflammatory bowel disease (IBD), which affects the colon in a diffuse, continuous, and superficial pattern. (
  • Ulcerative colitis is a type of inflammatory bowel disease that is an autoimmune disease affecting the colon -- it can devastate people's lives. (
  • There has been another consistent observation, though, and that is that most people with inflammatory bowel disease (either Crohn's or ulcerative colitis) seem to respond favorably to the probiotic Primal Defense . (
  • Millions of people around the world have ulcerative colitis - an inflammatory bowel disease (IBD) where there is chronic or recurring immune response and inflammation of the colon or large intestine. (
  • Ulcerative colitis (UC) is a chronic inflammatory bowel disease (IBD) associated with multiple colonic and extraintestinal complications, the most severe being the development of colorectal cancer (CRC). (
  • Ulcerative Colitis (UC) is one of two types of inflammatory bowel disease (IBD) with disease limited to the colonic mucosa. (

Crohn's Disease

  • Crohn's disease and microscopic colitis are the other common IBDs. (
  • More information is provided in the NIDDK health topics, Crohn's Disease and Microscopic Colitis: Collagenous Colitis and Lymphocytic Colitis . (


  • Ulcerative colitis is a chronic, or long lasting, disease that causes inflammation-irritation or swelling-and sores called ulcers on the inner lining of the large intestine. (
  • A mouse study suggests vinegar - or its main ingredient acetic acid - may alleviate ulcerative colitis, a condition that causes ulcers, abdominal pain and other symptoms. (


  • During a flare-up, some people with ulcerative colitis also experience symptoms elsewhere in their body. (
  • You should see your GP as soon as possible if you have symptoms of ulcerative colitis and you haven't been diagnosed with the condition. (
  • Treatment for ulcerative colitis aims to relieve symptoms during a flare-up and prevent symptoms from returning (known as maintaining remission). (
  • What are the signs and symptoms of ulcerative colitis? (
  • The most common signs and symptoms of ulcerative colitis are diarrhea with blood or pus and abdominal discomfort. (
  • You may need additional medications to manage specific symptoms of ulcerative colitis. (
  • For their study, the researchers gave vinegar and its main ingredient acetic acid to mice chemically induced to develop symptoms of ulcerative colitis. (
  • The results showed that either substance significantly reduced symptoms of ulcerative colitis in the mice. (
  • The authors note that other studies have shown these strains of bacteria are beneficial to mice with symptoms of colitis. (
  • Common symptoms of ulcerative colitis include rectal bleeding, abdominal pain, and diarrhea, but there is a wide range of symptoms among patients with this disease. (
  • Symptoms of left-sided colitis include bloody diarrhea, abdominal cramps, weight loss , and left-sided abdominal pain . (


  • A high-fat diet may also slightly increase the chance of getting ulcerative colitis. (

autoimmune condition

  • Ulcerative colitis is thought to be an autoimmune condition. (
  • Many experts believe ulcerative colitis is an autoimmune condition (when the immune system mistakenly attacks healthy tissue). (

immune system

  • Researchers have identified several genes that seem to make people more likely to develop ulcerative colitis, and it's believed that many of these genes play a role in the immune system. (
  • Ulcerative colitis likely involves abnormal activation of the immune system in the intestines. (
  • In patients with ulcerative colitis, however, the immune system is abnormally and chronically activated in the absence of any known invader. (


  • What causes ulcerative colitis? (
  • Read more about the causes of ulcerative colitis . (
  • Although the causes of ulcerative colitis are not well understood, research suggests gut bacteria may play an important role. (


  • Various environmental factors that may be linked to ulcerative colitis have been studied, including air pollution, medication and certain diets. (
  • This medication was recently approved for treatment of ulcerative colitis for people who don't respond to or can't tolerate other treatments. (
  • Fairview Specialty Pharmacy's Ulcerative Colitis Program is designed to help you safely and successfully take your medication. (
  • Our pharmacists and nurses are committed to helping patients take ulcerative colitis medications correctly to achieve the best outcomes and prevent potential medication problems. (
  • We will monitor your ulcerative colitis medication supply so you don't have to worry about running out. (


  • Research studies have shown that certain abnormal genes may appear in people with ulcerative colitis. (
  • However, researchers have not been able to show a clear link between the abnormal genes and ulcerative colitis. (
  • It also seems inherited genes are a factor in the development of ulcerative colitis. (
  • These studies have found there to be approximately 30 genes that might increase susceptibility to ulcerative colitis including immunoglobulin receptor gene FCGR2A, 5p15, 2p16, ORMDL3, ECM1, as well as regions on chromosomes 1p36, 12q15, 7q22, 22q13, and IL23R. (


  • These drugs, which include prednisone and hydrocortisone, are generally reserved for moderate to severe ulcerative colitis that doesn't respond to other treatments. (
  • In this clinical trial, 77 percent of those treated with a probiotic bacteria mixture experienced relief of their mild to moderate ulcerative colitis. (


  • In many patients with ulcerative proctitis, mild intermittent rectal bleeding may be the only symptom. (


  • Vinegar - the centuries-old culinary ingredient and traditional remedy - could help fight ulcerative colitis, say researchers, after testing its effects on mice with the disease. (
  • Generally, however, patients with pancolitis suffer more severe disease and are more difficult to treat than those with more limited forms of ulcerative colitis. (


  • Scientists believe one cause of ulcerative colitis may be an abnormal immune reaction in the intestine. (


  • Researchers from the University of Bologna in Italy and the University of North Carolina found that ulcerative colitis was improved in the majority of patients taking a probiotic mixture of eight bacteria for six weeks. (
  • The researchers carried out their investigation after learning of a previous study that had suggested vinegar - used in traditional medicine - might be a remedy for ulcerative colitis. (
  • Also, from an examination of the animals' stools, the researchers found that mice treated with vinegar for a month before chemically inducing colitis had higher levels of friendly bacteria in their gut, such as Lactobacillus and Bifidobacteria . (

abdominal pain

  • Patients with fulminant colitis are extremely ill with dehydration , severe abdominal pain, protracted diarrhea with bleeding, and even shock . (


  • Vinegar treatment prevents the development of murine experimental colitis via inhibition of inflammation and apoptosis, Fengge Shen et al. (
  • Ulcerative proctitis refers to inflammation that is limited to the rectum. (
  • Left-sided colitis involves inflammation that starts at the rectum and extends up the left colon (sigmoid colon and descending colon). (
  • Pancolitis or universal colitis refers to inflammation affecting the entire colon (right colon, left colon, transverse colon and the rectum). (
  • While the exact pathogenesis behind the development of colitis related CRC has not been identified, studies have shown it is most likely a result of chronic inflammation that leads to progressive dysplasia and eventually adenocarcinoma. (


  • If you've been diagnosed with ulcerative colitis and think you may be having a severe flare-up, contact your GP or care team for advice. (
  • They are for people with severe ulcerative colitis who don't respond to or can't tolerate other treatments. (
  • Fulminant colitis is a rare but severe form of pancolitis. (


  • Most people with ulcerative colitis receive care from a gastroenterologist, a doctor who specializes in digestive diseases. (
  • Some people believe eating certain foods, stress, or emotional distress can cause ulcerative colitis. (
  • Ulcerative colitis can occur in people of any age. (
  • Studies have found that more than one in four people with ulcerative colitis has a family history of the condition. (
  • People with ulcerative colitis who run fevers will likely take antibiotics to help prevent or control infection. (


  • The good bacteria will help normalize your gut flora and help to address potential infections in the colon that might actually be causing the colitis. (


  • Ulcerative colitis treatment usually involves either drug therapy or surgery. (
  • Anti-inflammatory drugs are often the first step in the treatment of ulcerative colitis. (
  • Our therapy management program provides regular telephone calls from nurses and pharmacists who have special training in ulcerative colitis treatment. (


  • Where and how you live also seems to affect your chances of developing ulcerative colitis, which suggests environmental factors are important. (


  • Ulcerative colitis is an inflammatory disorder of the gastrointestinal tract that affects the colorectum. (
  • Ulcerative colitis affects more than half a million Americans. (


  • Some studies suggest that certain things in the environment may increase the chance of a person getting ulcerative colitis, although the overall chance is low. (
  • A few studies suggest that stress may increase a person's chance of having a flare-up of ulcerative colitis. (
  • There have been multiple studies using genome wide association scans investigating genetic susceptibility in ulcerative colitis. (


  • The ulcerative colitis patients I have seen frequently come in on dangerous immune-suppressing drugs like prednisone. (
  • Patients with fulminant colitis and toxic megacolon are treated in the hospital with potent intravenous medications. (


  • Billing ulcerative colitis medications can be complicated, but we utilize our expertise to help you get the most benefit from your insurance and health care dollar. (
  • We ship your ulcerative colitis medications at no extra charge to the address of your choice, whether it be your home, place of employment, or travel destination. (



  • Nonsteroidal anti-inflammatory drugs, 1 antibiotics, 1 and oral contraceptives 2 may slightly increase the chance of developing ulcerative colitis. (


  • Who is more likely to develop ulcerative colitis? (


  • Ulcerative colitis most often begins gradually and can become worse over time. (


  • Levels of ulcerative colitis are also a lot higher in certain ethnic groups, further suggesting that genetics are a factor. (


  • The exact cause of ulcerative colitis is unknown. (


  • Several categories of drugs may be effective in treating ulcerative colitis. (


  • There are no known methods of preventing ulcerative colitis. (
  • The cause of ulcerative colitis is not known. (


  • Read more about living with ulcerative colitis . (
  • Read more about diagnosing ulcerative colitis . (