Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021831 (enteropathy)
4,403 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Skin disease is common in patients with inflammatory bowel disease. Described herein is a child with ulcerative colitis and cutaneous polyarteritis nodosa. Review of the literature suggests cutaneous polyarteritis must be considered as another skin lesion associated with inflammatory bowel disease. Cutaneous polyarteritis tends to run a chronic relapsing course independent of bowel disease, however.
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PMID:Cutaneous polyarteritis nodosa in a patient with ulcerative colitis. 287 86

A 24-year-old man with agammaglobulinemia developed a form of chronic inflammatory bowel disease over the past 18 years characterized by recurrent diarrhea, malabsorption, and protein-losing enteropathy. In the most recent admission he presented with abdominal cramps and active intestinal bleeding. Radiologic studies showed distal ileal irregularities and strictures that led to two distal intestinal and ileocecal resections. The gross pathologic appearance of these specimens was consistent with regional enteritis. Microscopically, healing ulcers, mucosal irregularities, and a prominent lymphocytic infiltrate without plasma cells or granulomas were observed. Immunocytochemical studies revealed a prominent T-helper cell and a modest T-suppressor/cytotoxic lymphocyte population in the lamina propria. Early and late B-cell differentiation markers were not detected in any of the cells. The immunocytologic findings suggest that T-helper lymphocytes proliferated without inhibition to stimulate non-existent B cells. The study confirms the occurrence of a regional enteropathy-like lesion in the total absence of B-cell function.
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PMID:Regional enteritis-like enteropathy in a patient with agammaglobulinemia: histologic and immunocytologic studies. 296 59

Six children with inflammatory bowel disease and nephrolithiasis are reported. Their mean age at the passage of the first stone was 12.5 years and the mean duration of active inflammatory bowel disease was 34.5 months. Four had ulcerative colitis and two had Crohn's disease. In three patients, the onset of stone disease was associated with a flare in the bowel disease. Stone passage in four patients was accompanied by an increase in abdominal pain; three experienced gross hematuria. Stones from four of the patients were composed primarily of calcium phosphate; stones from the remaining patients contained uric acid and/or calcium oxalate. The pathogenesis of nephrolithiasis as it relates to inflammatory bowel disease is considered and an approach to therapy offered.
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PMID:Nephrolithiasis in childhood inflammatory bowel disease. 299 32

The clinical picture and course of inflammatory bowel disease are influenced by nutritional abnormalities and malnutrition. Interest at present concentrates on high-fibre low-refined sugar diets, elimination diets with identification of specific food intolerance and low-residue diets. All three failed to show significant positive effects on the course of the disease, need for hospitalisation, surgical procedures required or post-operative recurrence. Only a low lactose diet seems to be justified, since we found lactose intolerance in 25-35% of patients with inflammatory bowel disease, as compared with 5-10% in the normal population. In 25 patients with Crohn's disease (CD) a reduction in inflammatory activity and improvement of nutritional status was obtained with parenteral nutrition (PN). Nevertheless, longer follow up periods revealed no additional benefit in comparison with conventional therapies. Furthermore, the combination of PN and total bowel rest resulted in the same improvement as with PN alone. 25 patients with CD manifesting an acute phase of the condition were treated with tube feeding (TF) as primary therapy. TF reduced CD activity and improved nutritional status in 15 patients with small bowel disease, whereas the patients with colonic disease and extraintestinal manifestations did not react. A comparison of the effect of PN and TF in 10 patients with CD showed no significant difference with regard to clinical course and objective parameters. In view of the high costs and risks of complications of PN, TF is recommended as primary therapy for the acute phase of CD. The importance of substitution therapy, especially of vitamin D, is documented.
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PMID:[Role of nutrition in acute and long-term therapy of chronic inflammatory bowel diseases]. 302 94

Clinical differences between the two human intestinal mucosal folate conjugases were assessed by measurement of their activities in normal individuals and in patients with chronic diarrhea of differing causes. Intracellular folate conjugase (ICFC) was 15-fold more active than brush border folate conjugase (BBFC) in jejunal mucosa from seven obese patients undergoing elective gastric bypass surgery. The activity of ICFC was similar among normal volunteers and patients with diarrhea of unknown origin (DUO), gluten-sensitive enteropathy (GSE), inflammatory bowel disease (IBD), and the short bowel syndrome (IBD-SBS). By contrast, BBFC, sucrase, and lactase were decreased significantly in GSE, and BBFC was increased in IBD-SBS. The activity of BBFC correlated with lactase and with sucrase in the normal subjects and in patients with DUO, whereas no correlations were found with the activity of ICFC in any group. Our clinical studies confirm that ICFC and BBFC are different enzymes. ICFC is not affected by intestinal disease, whereas the activity of jejunal BBFC, like that of other brush border enzymes, is decreased by mucosal injury and is also capable of adapting to distal small intestinal disease or surgical resection.
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PMID:Clinical studies of intestinal folate conjugases. 308 71

51Cr-EDTA was administered both orally and per rectum via a catheter to controls and to patients with inflammatory bowel disease. The patients were divided into two groups, either with active inflammation of the small bowel or with active inflammation of the colon. Fifteen patients with Crohn's disease of the small bowel and 19 patients with either Crohn's disease of the colon or ulcerative colitis were investigated. After oral administration of the probe, controls showed a median excretion of 1.17%/24 h of the dose compared to 3.47%/24 h by patients with small bowel disease and 6.07%/24 h by patients with colonic disease. After rectal administration, controls showed a median excretion of 0.74%/24 h of the dose compared to 0.93%/24 h by patients with small bowel disease and 5.73%/24 h by patients with colonic disease. The rectal test differentiated small bowel disease from colonic disease with an accuracy of 85%. The results confirmed the inflamed colon as a site of increased intestinal permeation.
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PMID:Small bowel and colonic permeability to 51Cr-EDTA in patients with active inflammatory bowel disease. 313 36

A random sample of 170 patients (88 men) with chronic inflammatory bowel disease (75 ulcerative colitis) were first interviewed in 1978 about their employment status, problems at work, and influence of surgery. Surgery had been carried out on 120 and 53 had an ileostomy. After six years 144 (92%) of the 156 survivors replied to a follow up postal questionnaire. Of the initial sample, 122 (72%) were working and there were only three (1%) registered unemployed. After six years a similar proportion were working and only seven (5%) were unemployed. Continuity of employment was good with 57% in the same job. Changes in work because of health had been made by 72 patients mainly caused by bowel disease. After surgery 10% completely changed and 22% modified their work while a few had to retrain or retire. Panproctocolectomy and ileostomy resulted in more changes and longer time off work after surgery than colectomy and ileorectal anastomosis, with 35% and 17% respectively off work after one year. Problems at work, in particular general malaise and arthritis were experienced by 34 (28%) patients. Fewer problems were experienced by patients with a stoma who also had less sickness absence than those without a stoma. Colleagues and employers were usually supportive although some patients encountered discrimination especially those with a stoma or working in the food industry. Few patients had been counselled on their work. In general employment prospects and time off work were good and employers should be encouraged to take an optimistic and supportive role. Doctors should consider that convalescence after surgery may be longer than they perceive and must provide better counselling for patients.
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PMID:Employment problems and prospects for patients with inflammatory bowel disease. 319 97

The clinical features of primary sclerosing cholangitis were studied in 46 consecutive patients. Jaundice was the most common symptom (57%), followed by pruritus (28%), pain (24%), and fever (15%). Thirty-three per cent of the patients had no symptoms, merely laboratory changes. No significant relationship was observed between a numerical score of radiological bile duct changes at diagnosis and the clinical picture, or the clinical course during follow-up. If clinical deterioration occurred, this seemed to happen within the first eight years after the clinical presentation. Patients with only intra-hepatic bile duct changes (n = 10) did not differ clinically from those with extrahepatic changes as well. Forty-three out of 44 patients examined had inflammatory bowel disease, usually ulcerative colitis, with total colitis in 84%. Radiological bile duct changes had a significantly higher score in patients who had to be treated with a combination of sulfasalazine and steroids, suggesting a weak relationship between severity of bowel disease and bile duct disease.
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PMID:Forty-six patients with primary sclerosing cholangitis: radiological bile duct changes in relationship to clinical course and concomitant inflammatory bowel disease. 321 25

This review focuses on the behavior and pathogenesis of selected dermatologic and rheumatologic manifestations of inflammatory bowel disease. Erythema nodosum, the most common skin lesion, correlates with activity of the bowel disease but not with its duration or extent. Resolution occurs with therapy of inflammatory bowel disease. Pyoderma gangrenosum, the most severe skin lesion, bears little relationship to the activity or extent of the colitis. Therapy is usually supportive, but dapsone and steroids appear promising. Immune and vasculitic mechanisms have been postulated for both skin lesions. Peripheral arthritis usually has its onset with or after the development of colitic symptoms. It worsens with exacerbation of bowel inflammation and responds to treatment of the bowel disease. Immune mechanisms are likely. Spondyloarthropathy usually occurs before the onset of overt intestinal disease. Its course is unrelated to the bowel inflammation, it does not respond to treatment of bowel disease, and it is associated with HLA B27.
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PMID:Selected rheumatologic and dermatologic manifestations of inflammatory bowel disease. 327 91

The intestinal mucosal immune defense mechanisms involve both humoral and cellular immunity. The prominence of suppressor/cytotoxic T lymphocytes in the epithelial layer suggests that these interepithelial lymphocytes play a role in defense against infections within this layer. Secretory IgA is overwhelmingly the major humoral immune response along the gastrointestinal tract and along other mucosal surfaces (respiratory tract, mammary glands, salivary glands, and lacrimal glands). While the functions of secretory IgA are incompletely understood, it is clear that it prevents attachment of microorganisms and toxins (cholera toxin, shiga toxin, etc.) to the surface epithelial cells. Furthermore, secretory IgA may collaborate with eosinophils or killer lymphocytes to mediate cytotoxic reactions against enteropathogens. By learning more about the mucosal immune response, we should be able to understand the relationship between the lamina propria plasmacytosis in inflammatory bowel disease and the increased number of interepithelial lymphocytes that we see in gluten-sensitive enteropathy and the underlying pathogenic mechanisms.
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PMID:Intestinal mucosal immune defense mechanisms. 328 83


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