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)

Serum cold-reactive lymphocytotoxin (LCT) was detected in twenty-two of fifty-six (40%) patients with inflammatory bowel disease (IBD). The frequency of LCT detection was similar in Crohn's disease and ulcerative colitis. Cytotoxicity testing against T or B cell-enriched peripheral blood lymphocytes from normal donors, together with absorption experiments, indicated that LCT in IBD was reactive against determinants on both cell subpopulations. Reactivity against T cells from patients with common variable immunodeficiency was significantly less than with normal donor T cells. LCT in IBD could not be related to prior allogeneic sensitization and its presence appeared to be unrelated to disease activity or drug therapy. No correlation was found between LCT and peripheral blood T- or B-cell numbers. The present findings suggest the need for further investigation of the role of infectious agents in the pathogenesis of IBD.
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PMID:Serum lymphocytotoxins in inflammatory bowel disease. Studies of frequency and specificity for lymphocyte subpopulations. 108 34

The local response pattern of immunoglobulin-containing cells was compared in Crohn's disease and ulcerative colitis by paired immunohistochemistry on specimens of the large bowel wall. In the "Crohn mucosa" with persisting glands the total cell count was on the average raised more than three times compared with controls. The numbers of IgA, IgM and IgG immunocytes were increased 2.0, 4.8 and 28.6 times, respectively. Only 0-2 IgD- and IgE-containing cells were generally found per section. No consistent differences in the mucosal response pattern were revealed when Crohn's disease was compared with ulcerative colitis. The deeper layers of the bowel wall were in both diseases more or less densely infiltrated by immunocytes-IgG cells compromising about 80%. Immunoglobulin-containing cells in the muscularis propria and subserosa were characteristically found in Crohn's disease. There was no indication of a primary defect in the secretory immunoglobulin system which appeared to be normal in areas with intact glands. The pronounced local humoral immune response, particularly that involving IgG, might be of pathogenetic importance by aggravating and perpetuating in the inflammatory bowel disease.
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PMID:Comparative mapping of the local distribution of immunoglobulin-containing cells in ulcerative colitis and Crohn's disease of the colon. 108 98

Peripheral blood mononuclear cells from patients with either Crohn's disease or ulcerative colitis (collectively referred to as inflammatory bowel disease) are cytotoxic in vitro for isologous or allogeneic colonic epithelial cells. Utilizing the ability of thymus-derived (T) lymphocytes to bind sheep red blood cells to their surface and the property of bone marrow-derived (B) lymphocytes to display easily detectable surface immunoglobulin determinants, the cytoxicity of these lymphocyte subpopulations was tested. The results indicate that the mononuclear cell required for the lysis of colonic epithelium was not included within the bulk of T or B lymphocytes. Indeed, enrichment for cytotoxicity correlated best with enrichment for a mononuclear cell population lacking classical T or B markers. Additionally, mononuclear cells specifically adhering to plastic petri dishes coated with heat-aggregated immunoglobulin, and thus presumably bearing a surface Fc receptor, were enriched in their cytotoxicity. Alternatively, cells not adhering to aggregated Ig-coated petri dishes were relatively depleted of cytotoxicity. The implications of these findings as they relate to possible interactions between cellular and humoral immune mechanisms as a pathogenic mechanism for the colonic inflammatory process noted in patients with inflammatory bowel disease are discussed.
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PMID:In vitro studies of inflammatory bowel disease. Surface receptors of the mononuclear cell required to lyse allogeneic colonic epithelial cells. 108 23

A detailed analysis of the species of lymphocytes was carried out in 58 patients with inflammatory bowel disease (IBD). These individuals were further divided into 31 with Crohn's disease (CD) and 27 with ulcerative colitis (UC). There were 13 CD patients with only small bowel involvement called "regional enteritis" and 18 who had some degree of colonic involvement called "ileocolitis". Similarly, the UC group was subdivided into 9 patients with disease confined to the rectosigmoid area called "proctosigmoiditis" and 18 with more extensive involvement called "universal colitis". We also studied 13 patients who had undergone previous colectomy and ileostomy and 78 healthy age- and sex-matched controls. Although there was no increase in the absolute number of lymphocytes in patients with ileocolitis and universal colitis, the percentage of these cells was decreased because of an increase in both polymorphonuclear leukocytes and monocytes. In IBD and its subgroups, mean T lymphocytes, determined by the sheep red blood cell rosette technique, were not significantly different from the controls either in percentage or absolute number. Furthermore, no difference was noted between UC and CD. However, there seems to be a subpopulation of patients with UC or CD whose T cells are reduced below 1 SD of the mean. There was also no difference in the number of immunoglobulin-bearing B cells in both diseases; however, when the B cells were enumerated by their ability to rosette with antibody-complement-coated sheep cells (EAC), we found a marked decrease in percentage (P less than 0.001) and absolute number (P less than 0.0005) relative to the control population. The decrease bore a direct relation to the severity of the disease process and, although more marked in patients with UC, was present in CD also.
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PMID:The subpopulations of circulating white blood cells in inflammatory bowel disease. 108 44

Skin reactivity to dinitrochlorobenzene (DNCB) and levels of circulating T-lymphocytes were measured in 15 patients with ulcerative colitis, 15 patients with Crohn's disease, and 12 normal control subjects. Diminished reactivity to DNCB was demonstrated in 87% of patients with Crohn's disease (P less than 0-001) and in 53% with ulcerative colitis (P less than 0-02), as compared with only 8-5% of controls; anergy was more frequent in Crohn's disease than in ulcerative colitis (P less than 0-05). Levels of circulating T-lymphoctes were also depressed in both Crohn's disease and ulcerative colitis (P less than 0-001) as compared with controls, with the values lower in Crohn's disease than in ulcerative colitis (P less than 0-02). There were no correlations of DNCB response with extent, duration, or severity of disease nor with T-cell levels within any patient group. These data provide further support for the concept that there is impairment of cell-mediated immunity among many patients with chronic inflammatory bowel disease, including both Crohn's disease and ulcerative colitis.
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PMID:Anergy to dinitrochlorobenzene and depression of T-lymphocytes in Crohn's disease and ulcerative colitis. 108 63

Ulcerative colitis and granulomatous colitis are distinct entities, but up to 10 per cent of colectomy specimens remain unclassified. Ulcerative colitis is primarily a mucosal disease, and other changes appear to be secondary to this process. By contrast, Crohn's disease, or granulomatous colitis, involves the whole thickness of the bowel wall. About 20 per cent of the cases of Crohn's disease involve the small and large bowel, while another 20 per cent are restricted to the large bowel. Since granulomatous colitis is a patchy disease, and many of the changes are deep within the bowel wall, rectal biopsy may not be as helpful as in ulcerative colitis. Fully developed granulomas are present in only a small minority of cases, and a diagnostic report of granulomatous colitis may be given in the absence of granulomas. In biopsy material, the differentiation of inflammatory bowel disease from ischemic colitis and pseudomembranous colitis may be difficult. In the absence of specific demonstration of an organism it may also be impossible on rectal biopsy to distinguish amebic or bacillary dysentery from ulcerative colitis. Even by colectomy, 29 of 300 specimens were sufficiently atypical so as not to warrant a label of Crohn's disease, or ulcerative colitis. Cancer of the colon, which is common in ulcerative colitis, is rare in Crohn's disease, but may also represent a definite complication in the latter. Immunologic studies are still confusing, but it is suggested that patients with ulcerative colitis and Crohn's disease may have a state of altered immunologic reactivity.
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PMID:Inflammatory bowel disease: the surgical pathology of Crohn's disease and ulcerative colitis. 108 84

Serum lysozyme (muramidase) concentrations were determined in patients with different types of inflammatory bowel disease and in normal subjects. The mean (plus or minus S.E.M.) lysozyme concentration for each group was as follows: controls, 8.8 plus or minus 0.3, ulcerative colitis, 9.3 plus or minus 0.6, Crohn's disease, 26.3 plus or minus 1.4. a and bacterial and nonbacterial enteritis, 8.9 plus or minus 0.7 mug per milliliter. Thus, mean enzyme levels were significantly greater in Crohn's disease than in ulcerative colitis (p smaller than 0.001), bacterial and nonbacterial enteritis (p smaller than 0.001) and healthy volunteers (p smaller than 0.001). The elevation of serum lysozyme in Crohn's disease may be related to tissue macrophages because no correlation was found between either the serum lysozyme concentration and the white-cell counts or the absolute numbers of circulating granulocytes or monocytes. Our findings suggest that serum lysozyme may be useful in the differential diagnosis of Crohn's disease from other types of bowel inflammation.
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PMID:Serum lysozyme in Crohn's disease and ulcerative colitis. 111 Jul 25

Simultaneous studies with 131-I-albumin and 125-I-immunoglobulin G (IgG) were made in 48 cases of chronic inflammatory bowel disease. Twenty-one had ulcerative colitis and 27 had Crohn's disease which was confirmed at laparotomy in every case. Intestinal protein loss was measured simultaneously by means of 59-Fe-iron dextran in 44 patients. All patients had abnormal intestinal protein loss. A high correlation was shown between fecal 59-Fe clearance and fractional catabolic rate of albumin, confirming the validity of 59-Fe-iron dextran as a test substance to measure intestinal protein loss. Fecal radioiodide excretion of 131-I from 131-I-albumin (A) and 125-I from 125-I-IgG (G) was significantly different in ulcerative colitis and Crohn's disease. The ratio G/A was close to unity (smaller than 1.60) in ulcerative colitis and Crohn's disease with exclusive or predominant involvement of the colon, whereas it was high in Crohn's disease of the small intestine and highest in cases with jejunal involvement. Thus, the ratio may be valuable in topographic diagnosis of chronic inflammatory bowel disease. A high ratio was found in 2 patients with Crohn's disease of the small intestine and normal radiography of the small intestine, and a low ratio was present in 7 cases of ulcerative colitis with normal radiographic findings. In all 9 patients with normal radiography, fecal 59-Fe clearance was elevated as evidence of abnormal intestinal protein loss. No correlation was present between the size of protein loss and the pathoanatomic extent of the lesions on subsequent laparotomy in 25 patients with Crohn's disease. Fecal radioiodide excretion (131-I from 131-I-albumin and 125-I from 125-I-IgG) was positively correlated with diarrhea (daily stool mass) in both ulcerative colitis and Crohn's disease. Intestinal protein loss was not.
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PMID:Fecal radioiodide excretion following intravenous injection of 131-I-albumin and 125-I-immunoglobulin G in chronic inflammatory bowel disease. An aid to topographic diagnosis. 113 26

A twenty-two-year-old woman and a fourteen-year-old boy with Crohn's disease presented with progressive monarticular arthritis with radiologic evidence of altered articular cartilage and subchondral bone. In one individual, granulomatous inflammation of the synovium was demonstrated. Intestinal symptoms were not prominent. In both individuals, the development of the monarthritis led to the discovery of the underlying inflammatory bowel disease.
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PMID:Destructive monarthritis and granulomatous synovitis as the presenting manifestations of Crohn's disease. 118 10

The cellular immune system was studied in patients with Crohn's disease (CD), not receiving corticosteroids, or azathioprine, by means of in vitro and in vivo methods. It was found, that the in vitro lymphocyte reactivity of 54 CD patients after stimulation with a cocktail of antigens (varidase, trichophyton, candida, mumps, and PPD) was significantly depressed when compared with the response of 20 simultaneously cultured healthy controls (p less than 0-001) or a group of 54 separately cultured healthy controls, matched for age and sex (p less than 0-001). The lymphocyte response of a control group of 18 patients with malnutrition or malabsorption without any evidence of inflammatory bowel disease, was higher than the response of an equal number of CD cases, although the difference failed to reach significance. Intradermally injection of the same five antigens, as used in the antigen cocktail, showed a failure to react to any antigen in 13 out of 48 CD patients, in comparison with three of 48 matched healthy controls (p less than 0-01). In both CD patients, as well as in healthy controls a significant correlation could be demonstrated between the number of positive skin tests, the area of skin induration, and the in vitro lymphocyte responsiveness after stimulation with the antigen cocktail. In the CD group no correlation was found between in vitro responsiveness and disease activity, as defined by a score of clinical and biochemical parameters. The depressed skin reactivity and the hyporesponsiveness in the lymphocyte transformation test after stimulation by an antigen cocktail suggest that depression of the anamnestic cellular immune response is a basic feature in patients with Crohn's disease.
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PMID:Impaired anamnestic cellular immune response in patients with Crohn's disease. 119 15


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