Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0010346 (Crohn's disease)
21,615 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several investigators have reported the presence of circulating immune complexes in serum from patients with Crohn's disease and chronic ulcerative colitis. Because previous assays employed conditions which might have caused immunoglobulin aggregates to form in vitro, thus falsely suggesting the presence of immune complexes in vivo, we tested inflammatory bowel disease sera for immune complexes using four assays designed to minimize in vitro immunoglobulin aggregation. In three assays immune complexes were not detectable, while in a fourth, the Clq precipitin test, positive reactions occurred. These precipitin reactions did not have characteristics of immune complexes. Our data suggest that circulating immune complexes are either not present in patients with inflammatory bowel disease or that they occur infrequently or in low concentration.
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PMID:Evidence against the presence of circulating immune complexes in chronic inflammatory bowel disease. 15 47

We have developed an enzymatic technique for isolating human intestinal mucosal lymphoid cells. This method was found to be superior to mechanical methods in regard to cell yield and survival. It is based on treating mucosa with serum-free solutions containing collagenase and deoxyribonuclease, followed by isolating the lymphoid cells through centrifugation steps involving fetal calf serum and ficoll-hypaque. Exposure of peripheral blood lymphocytes to the components of the enzymatic solution did not appreciably alter their uptake of tritiated thymidine in the presence or absence of mitogens. Application of the method to derive lymphoid cells from Crohn's disease, ulcerative colitis, and normal intestinal mucosa has shown that gut mucosal lymphocytes from inflammatory bowel disease (1) exceed the number of those from normal mucosa by a factor of 3 to 5; (2) show different degrees of tritiated thymidine uptake, spontaneously and in response to mitogens, depending upon the time they are harvested during the dissociation process; (3) are better stimulators than responders in the allogeneic mixed lymphocyte reaction; (4) generate suppressor cell activity comparable to that of peripheral blood lymphocytes; (5) cannot, in contrast to peripheral blood lymphocytes, generate antibody-dependent cell mediated cytotoxicity; and (6) produce an average of 5 times more IgM than equal numbers of peripheral blood lymphocytes.
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PMID:Gut mucosal lymphocytes in inflammatory bowel disease: isolation and preliminary functional characterization. 15 97

Althouth serological studies have revealed a high incidence and mean titer of antibody to cytomegalovirus (CMV) in some patients with inflammatory bowel disease, electron microscopy has not confirmed the presence of mature virus in diseased tissue. Sensitive biochemical techniques for detection of viral nucleic acid were applied therefore to test the proposed disease-virus association. Membrane cRNA-DNA hybridization showed that CMV DNA was not detectable in 3 cases of Crohn's disease, nor was it present in 3 or 4 cases of ulcerative colitis examined. Five tissue specimens taken 5 cm away from a colonic tumor were also negative. An in situ hybridization study of diseased tissue, including specimens from 6 inflammatory bowel disease patients in addition to those above, showed a few grains distributed over cells superficial to the muscularis mucosa, but was not regarded as significantly different from controls. The association of CMV with Crohn's disease (0 positives in 4 patients by either test) is not supported by this study; the association with ulcerative colitis (1 positive in 9 patients by either test) requires further study before a definitive conclusion can be made.
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PMID:Viral DNA in inflammatory bowel disease. CMV-bearing cells as a target for immune-mediated enterocytolysis. 18 23

Prolyl hydroxylase activity in rectal mucosa was found to be significantly greater in 11 patients with Crohn's disease than in 11 control subjects with the irritable bowel syndrome and 16 patients with ulcerative colitis (P less than 0.005). Seven of the patients with Crohn's disease had a histologically normal rectum. This abnormality in apparently normal mucosa supports the concept that Crohn's disease is a 'continuous' disease of the gastrointestinal tract. Although there was no significant difference in prolyl hydroxylase activity between control subjects and patients with ulcerative colitis, those patients with quiescent disease tended to have lower values than those with active mucosal inflammation. Prolyl hydroxylase activity could not, however, be detected in the sera of either healthy control subjects or patients with inflammatory bowel disease.
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PMID:Prolyl hydroxylase activity in serum and rectal mucosa in inflammatory bowel disease. 21 89

In order to investigate the prevalence of iodine depletion in chronic inflammatory bowel disease two separate studies have been performed. One was devoted to the 24-hour urinary iodine excretion and 50 patients with ulcerative colitis or Crohn's disease were examined and compared with 102 controls. In the other study the thyroid 131I uptake was compared in 38 patients and 36 controls. Ten of the 50 patients with chronic inflammatory bowel disease had a 24-hour urinary iodine excretion less than 40 mug, compared with 5 of the 102 controls (p greater than 0.01). Sixteen of the 38 patients had a 24-hour thyroid 131I uptake of 50% or more of the administered test does, compared with 4 of the 36 controls (p smaller than 0.01). These results are compatible with an increased occurrence of iodine deficiency in patients with chronic inflammatory bowel disease. Treatment with corticosteroids or Salazopyrin or a milk-free diet did not influence these findings. No evidence was found of an impaired absorption of inorganic iodide from the gut.?31
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PMID:The thyroid in ulcerative colitis and Crohn's disease. I. Thyroid radioiodide uptake and urinary iodine excretion. 23 26

Sulfapyridine (SP) is one of the main metabolites of salicylazosulfapyridine (sulfasalazine) that is used extensively in the management of inflammatory bowel disease. One hundred and twenty-two patients with ulcerative colitis or Crohn's disease were studied, including 21 new, untreated patients and 101 previously treated patients. Patients were studied for at least one year during active disease and remission. It was shown that sulfapyridine shares the same acetylation polymorphism as sulfadimidine. The acetylation capability of each patient as determined in serum and urine was constant irrespective of dose (2 to 8 gm/day) and state of disease. A single study of serum can determine acetylator phenotype in patients on sulfasalazine therapy without using any other drug for this purpose and may help ascertain dosage and assess side effects.
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PMID:Acetylation polymorphism of sulfapyridine in patients with ulcerative colitis and Crohn's disease. 24 31

Thymus-derived (T) rosette-forming cells were enumerated in patients with alcoholic liver disease and in patients with inflammatory bowel disease using variable sheep red blood cell (SRBC)/lymphocyte ratios. SRBC/lymphocyte ratios of 60:1 and 32:1 did not reveal significant differences from controls in Crohn's disease. The percentage, but not absolute count, of T cells was significantly reduced in alcoholic hepatitis at the 60:1 ratio. Both the percentage and absolute count of T cells were reduced in alcoholic hepatitis and Crohn's disease with the 8:1 ratio. No significant reduction in T cells was seen at any ratio in patients with compensated alcoholic cirrhosis or ulcerative colitis. Use of a SRBC/lymphocyte ratio of 8:1 indentifies T cells which demonstrate an avidity for SRBC. This avidity may be related to the density of SRBC receptors on the surface of T cells and/or the affinity of these receptor sites for SRBC. Use of the 8:1 ratio may provide a more sensitive means by which to monitor changes in T-cell rosettes in patients suspected of having an altered cellular immune state.
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PMID:Influence of SRBC/lymphocyte ratio on T-cell rosettes in alcoholic liver disease and inflammatory bowel disease. 30 83

In the peripheral blood of patients with Crohn's disease (CD) the numerical distribution of the three major B lymphocyte subsets was determined by the identification of surface immunoglobulins using F(ab)(2)-antibody fragments. T cell counts were also obtained and the number of null cells was calculated. Twenty-eight patients with Crohn's disease including 14 patients with previously untreated and very short-standing disease (group CD 1) and 14 patients with long-standing and/or previous drug treated disease (group CD 2) were compared with 28 sex and age-matched normals as well as with 13 patients with acute inflammatory bowel disease (group D). Patients in group D and inactive patients of group CD 1 showed a significant absolute lymphocytosis due to an increase in both the three B cell subsets and the T cells, without changes in the null cells. While the proportion of T cells was normal, there was a significant relative B lymphocytosis and a relative null cytopenia in these patients. Active CD 1 patients, however, showed significantly lower absolute lymphocyte and T cell numbers. In group CD 2, there was a significant absolute lymphopenia caused by an equal decrease in B and T cells. Highly active CD 2 patients showed higher absolute null cell counts than inactive patients. With increasing disease duration there was a significant decrease of the relative and absolute B cell concentrations. The data obtained suggest that T and B cell populations in the peripheral blood are reduced in certain patients with Crohn's disease and that this occurs secondarily to activity of disease, chronicity of disease, and the effects of therapy.
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PMID:Immune status in Crohn's disease. 3. Peripheral blood B lymphocytes, enumerated by means of F(ab)2-antibody fragments, Null and T lymphocytes. 31 53

Abnormalities in the numbers and function of thymus and function of thymus-derived and bone marrow-derived lymphocytes (T and B cells) and K cells were determined in sixty-nine consecutive patients with Crohn's disease or ulcerative colitis. Rosetting techniques to identify subpopulations of lymphocytes showed a significant decrease in E-rosettes (T cells) and significant increase in EA- and EAC-rosettes (B cells) in patients with inflammatory bowel disease when compared to normals. In vitro lymphocyte transformation responses to mitogens and antigens were depressed to a variable degree. Mean levels of K cell activity were not significantly different from normal controls. A considerable degree of individual variation was noted in all groups. When the results of each groups were considered, none of the laboratory variables correlated with the site, duration or activity of disease, therapy, presence of iron deficiency anemia, weight loss or hypoalbuminaemia. Thus, in vitro evidence of abnormal immune responses in patients with inflammatory bowel disease cannot be directly related to clinical or laboratory variables and probably reflects a multi-factorial aetiology.
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PMID:In vitro testing of immunoresponsiveness in patients with inflammatory bowel disease: prevalence and relationship to disease activity immunoresponsiveness in IBD. 31 71

There is conflicting evidence regarding the adequacy of hypothalamic-pituitary function in children and adolescents with chronic inflammatory bowel disease complicated by growth retardation and delayed sexual maturation. A child with Crohn's disease, who has never received corticosteroid therapy, had delay of both growth and sexual maturation and has been investigated over the course of his disease. In addition to a skull X-ray (normal) and thyroid function tests (normal), a standard insulin tolerance test (insulin 0.15 u/kg) and a standard gonadotropin-releasing hormone (Gn-RH) test (100 microgram Gn-RH i/v) were performed when the bowel disease was in relapse and again during a remission of the bowel disease, achieved by surgery. When the bowel disease was in relapse (coincident with growth arrest) results showed an inadequate release of gonadotrophins and of growth hormone (even after pre-treatment with stilboestrol) but normal release of cortisol and prolactin. During a remission of the bowel disease coinciding with a period of rapid "catch-up" growth, release of growth hormone was normal and that of gonadotrophins supranormal. The demonstration of a reversible apparent partial hypopituitarism in this boy not only re-questions the adequacy of hypothalamic-pituitary function in inflammatory bowel disease but also indicates a potential diagnostic pitfall in the routine investigation of growth retardation if gastrointestinal symptoms are not prominent at presentation.
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PMID:A case of apparent hypopituitarism complicating chronic inflammatory bowel disease in childhood and adolescence. 33 54


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