Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: HUMANGGP:036187 (gut)
 73,132 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sulphasalazine consists of 5-aminosalicylic acid and sulphapyridine both linked together by an azo bond. Sulphasalazine is clearly useful in long-term management of ulcerative colitis and may be useful in Crohn's disease. The absorption, metabolism and excretion of sulphasalazine is similar in volunteers and patients with ulcerative colitis or Crohn's disease. Sulphasalazine serves as a vehicle to deliver its possible active components, 5-aminosalicylic acid and sulphapyridine, to the colon in higher concentrations than could be achieved by oral administration of either one alone. Sulphasalazine reaches the colon mostly unchanged and is split by gut bacteria at the azo linkage, releasing 5-aminosalicylic acid and sulphapyridine. 5-Aminosalicylic acid may act locally and is not absorbed to any great extent. On the contrary, sulphapyridine is mostly absorpbed from the colon and may act both locally, during mucosal absorption, and systemically. A positive correlation exists between serum total sulphapyridine concentration and both therapeutic efficacy and toxicity. Sulphapyridine metabolism is largely determined by inherited acetylator phenotype, either slow or fast. Slow acetylators have higher levels of free sulphapyridine and lower levels of acetylated sulphapyridine than fast acetylators, and are likely to have more toxic symptoms on equivalent doses of sulphasalazine. Therapeutic effects of sulphasalazine in ulcerative colitis and Crohn's disease correlate with serum concentrations of total sulphapyridine (20 to 50 microng/ml), and toxicity with total sulphapyridine concentration greater than 50 microng/ml. Side-effects are mostly observed among slow acetylators. In long-term therapy of ulcerative colitis doses of 2 to 3g/day of sulphasalazine are most likely to sustain remissions and avoid toxicity. During therapy with sulphasalazine, determination of acetylator phenotype and total sulphapyridine concentration can guide effective dosage and avoid side-effects. A single serum sample for free and acetylated sulphapyridine concentrations is sufficient for this purpose.
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PMID:Clinical pharmacokinetics of sulphasalazine. 1 52

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

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

Lymphocytotoxins (LCT) have been recently reported in the serum of patients with inflammatory disease of the bowel, but up to now these antibodies have shown no specificity for B or T lymphocyte subpopulations. A 32-year-old patient with chronic ulcerative colitis, primary hypogammaglobulinemia and a very low number (0.5 to 1.5%) of B lymphocytes in peripheral blood is described. The presence in the serum of a LCT reacting specifically with B cells was demonstrated by cytotoxicity and direct immunofluorescence experiments. Intestinal immunofluorescence studies indicated a dichotomy between blood and gut immunoglobulins, and showed a heterogeneous distribution of plasma cells of the three major classes from the jejunum to the rectum. The significance of the association of hypogammaglobulinemia, chronic ulcerative colitis, and anti-B LCT is discussed. To explain the dissociation between blood and gut immunoglobulins, it is suggested that the intestine was, in this patient, a privileged site for differentiation of B cells.
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PMID:Ulcerative colitis in a patient with anti-B lymphocytotoxin and hypogammaglobulinemia. 33 Mar 4

Finger clubbing, measured objectively by using the hyponychial angle, was present in 75 out of 200 (38%) patients with Crohn's disease, 15 out of 103 (15%) with ulcerative colitis, and two out of 24 (8%) with proctitis. In Crohn's disease and ulcerative colitis the hyponychial angle was significantly correlated with both disease activity and the extent of fibrosis in the resected specimens from 47 surgically treated patients. The prevalence of finger clubbing in patients with macroscopic disease within the area of the gut innervated by the vagus nerve was significantly higher than that in patients in whom the disease was confined to the distal colon and rectum. Finger clubbing in patients with Crohn's disease tended to regress after resection of macroscopic disease. It is concluded that finger clubbing is significantly commoner in Crohn's disease than ulcerative colitis. The focal stimuli for finger clubbing include mucosal inflammatory change and fibrosis mediated by the vagus and possibly other autonomic pathways acting as the afferent arc of a finger-clubbing reflex.
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PMID:Finger clubbing in inflammatory bowel disease: its prevalence and pathogenesis. 50 14

Homogenates of gut and mesenteric lymph node tissue from patients with Crohn's disease, ulcerative colitis, and control patients were tested for cytopathic effect (CPE) production in a series of cell lines including rabbit ileal and W138 cells. A CPE was produced in W138 cells by tissue homogenates from patients with Crohn's disease, ulcerative colitis, and control patients. Evidence was obtained to suggest that this effect, although superficially similar to a viral CPE, was due to toxic protein constituents of inflamed tissue homogenate.
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PMID:Virus isolation studies in Crohn's disease: a negative report. 52 78

In patients with Crohn's disease and ulcerative colitis, alterations in serum storage temperature produced significant changes in serum lysozyme activity (SLA) as measured by the lysoplate method. This was not the case in healthy controls or in a group with other gastrointestinal disorders. Electrophoretic separation of serum revealed two components of lysozyme-type lytic activity but only one in extracts of gut mucosa, leucocytes, and egg white. The major lytic component of serum migrated towards the cathode and reacted with specific antilysozyme serum, but the minor component which migrated towards the anode did not. Although the cause of this anionic lytic activity is uncertain, it contributes to total serum activity as estimated by any method utilising the lysis of Micrococcus lysodeikticus, and may possibly be related to the observed thermolability.
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PMID:Complex nature of serum lysozyme activity: evidence of thermolability in inflammatory bowel disease. 62 14

Blood lymphocytes and rectal plasma cells have been studied in patients with ulcerative colitis taking part in a double-blind trial of treatment with azathioprine. Treatment for 1 year resulted in a modest fall in blood lymphocyte count, with little change in neutrophils or platelets. There was no major change in the proportions of circulating T and B lymphocytes, suggesting that the number of such cells per millilitre of blood fell in proportion to the change in lymphocyte count. The number of plasma cells in the rectal lamina propria was reduced to a mean less than half that of the control patient group. Blood K-cell cytotoxic activity fell at least 25-fold after 1 year's treatment. PHA-induced cytotoxicity was also reduced, but less consistently. Reduced K-cell activity is interpreted as reflecting depletion of effector cells from the circulation. The fall in lymphocyte count, K-cell activity and gut plasma cells was slow, indicating continuous inhibition of lymphopoiesis or differentiation throughout the trial period. Thus, azathioprine has some immunosuppressive effects which develop only after prolonged treatment. The clinical results of the trial did not show a major beneficial effect of azathioprine in the treatment of ulcerative colitis, nor were there clear correlations between the results of lymphocyte assays and clinical response in individual patients.
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PMID:Immunosuppression in the treatment of inflammatory bowel disease. II. The effects of azathioprine on lymphoid cell populations in a double blind trial in ulcerative colitis. 77 64

In this review I have described the pathophysiology of allergic disorders of the gastrointestinal tract. Situations where the intestine cannot be a complete barrier to foreign allergens and antigens were discussed and etiological factors of gastrointestinal allergy were detailed. Clinical features of gastrointestinal allergy include diarrhea, vomiting, abdominal pain and colic, intestinal hemorrhage and malabsorption as well as symptoms and signs outside the gastrointestinal tract such as chronic rhinitis and asthma in the respiratory system, urticaria, angioedema and eczema as dermatological signs, headache, insomnia, hyperkinesis as central nervous system manifestations, failure to thrive and anaphylaxis as constitutional reactions. Milk allergy was discussed as an example of food allergy. Immunology of the gastrointestinal tract was presented, with examples of four types of hypersensitivity reactions, and gastrointestinal disturbances of immunodeficiency disorders and syndromes were named. Lastly, the autoimmune mechanism and the gut were described, with particular discussion of ulcerative colitis as an example of an autoimmune disease.
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PMID:The intestine in allergic diseases. 78 84

Lympho-plasmacytic infiltrates in cryostat sections (resected small intestine or colon specimens and rectal biopsies) from 29 patients with Crohn's disease (CD) were studied with the immunoperoxidase and immunofluorescence technique, by means of specific anti-human lymphocyte globulin (ALG) and specific anti-human T-lymphocyte globulin (ATG). Control specimens were obtained from 16 patients with ulcerative colitis (UC) and 12 subjects without inflammatory bowel disease. Characteristic transmural inflammatory infiltrates in CD consisted mainly of lymphocytes. A wide variation of the relative T-cell proportion was observed. However, in contrast with UC, abundant numbers of T-lymphocytes in CD were often detected, particularly in the deeper layers of the bowel wall. Furthermore, in serial sections immunoglobulin-containing plasma cells were counted, using specific anti-IgA, -IgM, and -IgG antisera. A significant reduction of the IgA/IgM plasma cell-ratio was found in CD in comparison with UC and controls. Our results indicate that in CD a chronic cellular immune reaction is going on within the diseases gut, involving increased numbers of lymphocytes and particularly T-cells. It remains to be established whether a deficient IgA barrier has to be considered of primary pathogenetic importance.
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PMID:Analysis of the lympho-plasmacytic infiltrate in Crohn's disease with special reference to identification of lymphocyte-subpopulations. 79 55


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