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Ulcerative cohtis

GI diseases ulcerative coHtis and anorectal disorders Bacterial meningitis... [Pg.94]

Summers RW, Elliott DE, Urban JF Jr, Thompson RA, Weinstock JV Trichuris suis therapy for active ulcerative cohtis a randomized controlled trial. Gastroenterology 2005 128 825-832. [Pg.121]

Inflammatory Bowel Disease (IBD) comprises several diseases, including ulcerative colitis and Crohn s disease. Ulcerative cohtis is a disease of the colon, originating in the rectum and extending proximally to a variable extent. It frequently affects the entire colon but never... [Pg.174]

Sutherland L, MacDonald JK. Oral 5-aminosahcylic acid for induction of remission in ulcerative cohtis. Cochrane Database Syst Rev 2006. [Pg.386]

Severe ulcerative cohtis or toxic megacolon Unstable cardiovascular status in acute hemorrhage... [Pg.19]

Steroids do not have a role in the maintenance of remission with ulcerative cohtis because they are ineffective. Steroids should he gradually withdrawn after remission is induced (over 3 to 4 weeks). If they are continued, the patient will he exposed to steroid side effects without likelihood of benefits. Azathioprine is effective in preventing relapse of ulcerative colitis for periods exceeding 4 years. However, 3 to 6 months may be required for beneficial effect. For patients who initially respond to infliximab, continued administration of 5 mg/kg every 8 weeks as maintenance therapy is an alternative for steroid dependent patients. [Pg.289]

Thomas, P. Richards, D. Richards, A. Rojers, L. Evans, B.K. Drew, M.J. Rhodes, J. Absorption of delayed-release prednisolone in ulcerative cohtis and crohn s disease. Int. J. Pharm. 1985, 37, 757. [Pg.1239]

Short-chain fatty acids, especially butyrate, are a preferred source of energy for the colonic epithelium. There is evidence to suggest that butyrate enemas are effective in the treatment of ulcerative cohtis. The seeds of Plantago ovata (a source of fermentable dietary fiber) increase fecal concentrations of butyrate and acetate. In a randomized, open, parallel-group, multicenter study in 105 patients with ulcerative cohtis, P. ovata seeds 10 mg bd were as effective as mesalazine 500 mg tds in maintaining remission over 12 months (10). Adverse effects were similar in the two groups, and included constipation, flatulence, nausea, and diarrhea. [Pg.138]

The role of mesalazine in the acute and long-term treatment of ulcerative cohtis has been reviewed (17). Mesalazine is equivalent to or better than sulfasalazine... [Pg.139]

A 29-year-old woman with ulcerative cohtis taking mesalazine 1 g tds developed respiratory distress (40). Her respiratory symptoms (chest pain and respiratory distress, especially exertional dyspnea) occurred 48 hours after she started to take mesalazine and disappeared immediately on withdrawal. Similar sjmptoms recurred on rechallenge 3 weeks later in a lower dose of 500 mg bd. Chest X-ray and white cell count a day later were normal. [Pg.141]

Bronchiolitis obliterans has been reported in an 18-year-old female non-smoker with ulcerative cohtis, 3 months after reintroduction of mesalazine 1.6 g/day orally (41). She recovered after mesalazine withdrawal and treatment with glucocorticoids. [Pg.141]

Two patients with long-standing ulcerative colitis developed what seemed to be a drug-induced chronic interstitial nephritis after taking sulfasalazine for several years, with no other detectable cause (73) the same problem has arisen with mesalazine. However, in a long-term stndy (mean treatment time 10 years) in 36 patients taking sulfasalazine for ulcerative cohtis, there was no nephrotoxicity (74). [Pg.142]

In patients with ulcerative cohtis, Boswellia serrata 350 mg tds for 6 weeks produced improvements in stool properties, histopathology of rectal biopsies, hemoglobin, serum iron, calcium, phosphorus, proteins, and total leukocyte and eosinophil counts, with remission in 82% of patients (3). The corresponding figure with sulfasalazine 1 g tds was 75%. [Pg.1563]

In contrast, the second study (140) showed that the use of NSAIDs was not associated with a higher incidence of active inflammatory bowel disease. The authors retrospectively examined the records of 192 outpatients with inflammatory bowel disease 112 with Crohn s disease (mean age 53 years) and 80 with ulcerative colitis (mean age 61 years). The use of NSAIDs was more common in patients with inactive inflammatory bowel disease than in those with active disease. Of 40 patients with active Crohn s disease, three were using NSAIDs compared with 14 of 72 with inactive disease. Of 58 patients with active ulcerative cohtis, eight were using NSAIDs compared with five of 21 patients with ulcerative colitis in remission. [Pg.2566]

Rampton DS, McNeil NI, Sarner M. Analgesic ingestion and other factors preceding relapse in ulcerative cohtis. Gut 1983 24(3) 187-9. [Pg.2579]

Thyroid disorders (hypothyroidism or hyperthyroidism) Cardiovascular disease (arrhythmias, congestive heart failure) Gastrointestinal disease or disorder (sprue or other malabsorption syndromes, peptic ulcer, cohtis)... [Pg.1244]

The immunologic basis of IBD is supported by a number of observations. First is the pathology of the lesions. With Crohn s disease, the bowel waU is infiltrated with lymphocytes, plasma cells, mast cells, macrophages, and neutrophils. Similar infiltration has been observed in the mucosal layer of the colon in patients with ulcerative cohtis. Inflammation in IBDs is maintained by an influx of leukocytes from the vascular system into sites of active disease. This influx is promoted by expression of adhesion molecules (such as alpha-4 in-tegrins) on the surface of endothefial cells in the microvasculature in the area of inflammation. Second, many of the systemic manifestations of IBD have an immunologic etiology (e.g., arthritis or uveitis). Finally, IBD is responsive to immunosuppressive drugs (e.g., corticosteroids and azathioprine). [Pg.650]

Parenteral nutrition is an important component of the treatment of severe Crohn s disease or ulcerative colitis. The use of parenteral nutrition allows complete bowel rest in patients with severe ulcerative cohtis, which may alter the need for proctocolectomy. Parenteral nutrition has also been valuable in Crohn s disease, because remission may be achieved with parenteral nutrition in about 50% of patients. In some patients, the disease may worsen when parenteral nutrition is stopped. Patients with enterocutaneous fistulas of various etiologies benefit from parenteral nutrition. Parenteral nutrition may also be valuable in children or adolescents with growth retardation associated with Crohn s disease, but surgery is often necessary with severe disease. Finally, when possible, home parenteral nutrition should be used for patients requiring long-term therapy, particularly those with short gut as a consequence of surgical resection. [Pg.654]

There is a growing interest in using probiotic approaches for IBD. Probiotics involves the reestablishment of normal bacterial flora within the gut by oral administration of live bacteria such as non-pathogenic Escherichia coli, bifidobacteria, lactobacflli, or Streptococcus thermophilus. Probiotic formulations have been effective in maintaining remission in ulcerative cohtis. ... [Pg.654]

Surgical procedures have an established place in the treatment of IBD. Although surgery (proctocolectomy) is curative for ulcerative cohtis, this is not the case for Crohn s disease. Surgical procedures involve resection of segments of intestine that are affected, as well as correction of complications (e.g., fismlas) or drainage of abscesses. [Pg.655]

Corticosteroids and adrenocorticotropic hormone have been widely used for the treatment of ulcerative cohtis and Crohn s disease, given parenterally, orally, or rectally. Corticosteroids are believed to modulate the immune system and inhibit production of cytokines and mediators. It is not clear whether the most important steroid effects are systemic or local (mucosal). Budesonide is a corticosteroid that is administered orally in a controlled-release formulation. The drug undergoes extensive first-pass metabolism, so systemic exposure is thought to be minimized. Immunosuppressive agents such as azathioprine, mercaptopurine (a metabolite of azathioprine), methotrexate, or cyclosporine are sometimes used for the treatment of IBD. ... [Pg.655]

Monocytosis (>800/mm of blood) occurs with some infections (e.g., tuberculosis, histoplasmosis, toxoplasmosis, bacterial endocarditis, and salmonellosis), collagen vascular diseases (rheumatoid arthritis and systematic lupus erythematosus), gastrointestinal disorders (ulcerative cohtis and alcoholic liver disease), leukemias, and up to 60% of nonhematologic malignancies, whereas abnormally low monocyte concentrations occur in patients with hairy cell leukemia or aplastic anemia." ... [Pg.1800]

A genetic model has been proposed for colorectal tumorigenesis that describes a process of transformation from adenoma to carcinoma. However, at least three separate additional molecular pathways to developing colorectal cancer have been identifled. These include a pathway for HNPCC, an ulcerative cohtis-dysplasia-carcinoma sequence, and a pathway involving loss of function of the estrogen receptor gene through hypermethylation. Some of the molecular processes are common to more than one pathway. [Pg.2388]

The incidence and severity of Salmonellosis is increased in the following conditions or comorbidities. Achlorhydria, pernicious anemia, impaired immune response, HIV infection, malnutrition, chronic steroid administration, frequent administration of antibiotics which affects intestinal flora and lowers resistance of colonization, lymphoproliferative diseases, malignant tumors, schistosomiasis, chronic hemolytic syndromes (sickle cell disease), malaria and inflammatory bowel disease, mainly ulcerative cohtis. [Pg.132]

The fact that most intestinal nematodes elicit a Th2 response in chronic infection has suggested the possibility to use experimental infections with such parasites for the treatment of Thl-mediated diseases, such as the inflammatory bowel diseases. Patients affected with Crohn s disease or ulcerative cohtis were treated with the ova of a porcine whipworm Trichuris suis, which resulted in clinical amehoration of both diseases. [Pg.357]

The targeting of molecular markers associated with inflammation could, in principle, be useful for the imaging and therapy of several other inflammatory diseases. Besides rheumatoid arthritis, these include inflammatory bowel diseases (Crohn s disease and ulcerative cohtis), psoriasis, atherosclerosis, and diseases of the central nervous system (Alzheimeris disease, multiple sclerosis, etc.). [Pg.1285]

Streptokinase is contraindicated in patients with nlcerative wounds, active internal bleeding, recent trauma with possible internal injuries, visceral or intracranial malignancy, ulcerative cohtis, diverticulitis, severe hypertension, acute or chronic hepatic or renal insufficiency, uncontrolled hypoco-agnlation, chronic pulmonary disease with cavitation, sub-acnte bacterial endocarditis or rheumatic valvular disease, recent cerebral embolism, thrombosis, or hemorrhage, and diabetic hemorrhagic retinopathy, becanse excessive bleeding may occur. [Pg.652]

The effects of glucocorticoids on the inflammatory response are numerous and weU documented (see Chapter 59). Although glucocorticoids are universally recognized as effective in acute exacerbations, their use in either ulcerative colitis or Crohn s disease involves considerable challenges and pitfalls, and they are indicated only for moderate-to-severe IBD. Because the same issues impact steroid use in both ulcerative cohtis and Crohn s disease, they are discussed together. [Pg.657]

Ulcerative cohtis involves the rectum and extends proximally to all or different portions of the colon (ulcerative proctitis, sigmoiditis, left-sided cohtis or pancolitis). Rectosigmoid involvement is present in almost all patients at endoscopy, with approximately 40-50%ofpatientshavingdiseaselimitedtotherectum... [Pg.73]

Fig.8.3a-d. Ultrasonographic features of bowel wall in a patient with ulcerative cohtis. Transverse (a) and longitudinal (b) sections of descending colon in patient with left-sided active ulcerative colitis. Thickened bowel walls characterised by stratified echo pattern and absence of haustra coli (c) in the left colon. The presence of haustra coli (arrows) in the transverse colon (d) clearly define the extension of the disease... [Pg.75]


See other pages where Ulcerative cohtis is mentioned: [Pg.203]    [Pg.561]    [Pg.69]    [Pg.225]    [Pg.314]    [Pg.62]    [Pg.44]    [Pg.452]    [Pg.1813]    [Pg.1822]    [Pg.610]    [Pg.650]    [Pg.654]    [Pg.655]    [Pg.655]    [Pg.276]    [Pg.416]    [Pg.85]    [Pg.187]   
See also in sourсe #XX -- [ Pg.119 ]




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