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Biomedical subjects

K M Das

Publications and source records attributed to K M Das.

At least 109 records · Page 6Linked to original sources
PubMed1981

An antibody against revertant forms of cell-wall deficient bacterial variant in sera from patients with Crohn's disease.

Sera from patients with Crohn's disease or ulcerative colitis, and from controls were examined by indirect immunofluorescence for antibody against two strains of pseudomonas-like cell-wall-defective bacterial variants. Serum samples from 22 of 25 patients with Crohn's disease produced fluorescence of both revertant cell-wall-defective bacterial strains. Intensity of fluorescence correlated positively with the degree of disease activity. Sera from 23 patients with ulcerative colitis and from 15 control subjects did not produce any significant staining of either of the two revertant cell-wall-defective bacterial strains. Absorption of sera with Escherichia coli, Bacteroides thetaiotaomicron, and Pseudomonas aeruginosa did not alter the intensity of fluorescence in patients with Crohn's disease, whereas similar absorption of sera from patients with ulcerative colitis and controls abolished the slight staining of cell-wall-defective strains produced by 29% of unabsorbed serum samples.

Antibodies, Bacterial↗
PubMed1981

Detection of colonic antigen(s) in tissues from ulcerative colitis using purified colitis colon tissue-bound IgG (CCA-IgG).

In our report of a disease-specific colonic tissue-bound antibody (CCA) from patients with ulcerative colitis (Proc Natl Acad Sci USA 1978;75:4528), crude CCA was largely fragmented, and the yield was small. We have modified the extraction procedure to increase the yield of intact IgG present in CCA by sequential elution, storage of tissues in presence of a protease inhibitor, 2 mM Phenylmethylsulfonyl Fluoride, and use of Phenylmethylsulfonyl Fluoride in extraction buffers. Intact CCA-IgG was purified using protein A-Sepharose 4B affinity chromatography. 125I-CCA-IgG formed immune complexes in vitro with the aqueous extracts of colonic mucosa from 5 patients with ulcerative colitis but not from 6 patients with Crohn's disease and 6 normal colons from patients with carcinoma (p less than 0.01). We also performed reverse experiments by iodination of the colonic mucosal extracts with Bolton-Hunter reagent and incubating them with several preparations of CCA-IgG. Mucosal extracts of colon from 3 patients with ulcerative colitis bound significantly with CCA-IgG when compared with the identical extracts from 3 patients with Crohn's disease, 3 with a normal colon (p less than 0.005), and with the control human IgG (p less than 0.025). These studies demonstrate a better method of extraction and purification of intact CCA-IgG. Intact CCA-IgG binds to a specific protein(s) present in the homogenates of colonic mucosa from patients with ulcerative colitis but not from patients with Crohn's disease and normal colon.

Antigen-Antibody Complex↗
PubMed1980

Crohn disease lymph node homogenates produce murine lymphoma in athymic mice.

To study the putative agent(s) related to Crohn disease, we intraperitoneally in injected mesenteric lymph node homogenates from four patients with active Crohn disease into 10-week-old athymic (nu/nu) mice. Control mice (nu/nu) were injected with homogenates of mesenteric lymph nodes from two patients with ulcerative colitis and four patients undergoing elective cholecystectomy, and with a homogenate of a cervical lymph node containing sarcoid granuloma. Thirty-four mice received filtered or unfiltered homogenates from Crohn disease lymph nodes. Thirty-two mice received homogenates or filtrates from lymph nodes of control patients. Four mice from the group injected with Crohn disease homogenates from four different patients developed generalized lymphadenopathy due to lymphoma 10-28 weeks after th injection. Two additional mice developed lymphadenopathy due to plasma cell hyperplasia. None of the control mice developed lymphomas or lymphadenopathy. Two lymphomas were homogenized, filtered, and injected intraperitoneally into a second group of nu/nu mice, which also developed lymphoma within 8 weeks of injection. Two lymphomas were cultured in vitro and B cell sur?ACE MARKERS WERE IDENTIFIED. Indirect immunofluorescence studies in two lymphomas showed cytoplasmic staining of lymphoma cells with sera from 10 patients with active Crohn disease but not with sera from 13 control subjects, including 6 with ulcerative colitis and 7 with other gastrointestinal disorders. These results suggest that a transmissible factor present in Crohn disease lymph nodes produces lymphoma in nu/nu mice. Furthermore, sera of Crohn disease patients contain an antibody that recognizes an "antigen(s)" in the murine lymphoma.

Animals↗
PubMed1980

Cronkhite-Canada syndrome: report of a case with bacteriologic, immunologic, and electron microscopic studies.

A case of Cronkhite-Canada syndrome is presented. The patient developed protein-losing enteropathy, generalized gastrointestional polyposis, skin pigmentation, onychodystrophy, and alopecia. This patient also exhibited certain unusual features such as: fluctuating dermal manifestations, sclerodermalike skin changes, elevated levels of carcinoembryonic antigen, retinal detachment, cataracts, and cerebellar atrophy. Bacteriologic studies of small intestinal fluid, chromosomal analysis, immunologic investigations, and morphologic studies failed to provide any etiologic clues.

Adult↗
PubMed1979

Small bowel absorption of sulfasalazine and its hepatic metabolism in human beings, cats, and rats.

To elucidate the role of the small bowel and liver in sulfasalazine (SASP) metabolism, we performed studies in patients, cats, and rats. The role of the small bowel in absorption and metabolism of SASP was determined by the amount of administered SASP excreted in ileostomy effluents, and the concentration of serum and urinary SASP and its metabolites, sulfapyridine and 5-amino salicylic acid. Seventy-five to ninety percent of the drug was excreted in ileostomy effluents of 6 patients as SASP, and only 5% of the dose was sulfapyridine. In cats, ileostomy and portal venous cannulations revealed that 20--30% of administered SASP is absorbed from the small bowel without being metabolized. The role of the liver in SASP metabolism was established in vivo and in vitro. SASP metabolites were measured in bile, serum, and urine of 2 patients with a choledochal T-tube and in serum and bile in six cats and four rats. Twenty to fifty percent of the absorbed drug was excreted in bile as SASP and no detectable sulfapyridine appeared in the bile. SASP concentration in peripheral blood and urine ranged between 3 and 12 microgram/ml, and no significant amount of sulfapyridine metabolites were detected in the bile, serum, or urine of animals with an ileostomy. In vitro experiments with liver from cats and rats showed nearly complete reduction of SASP into metabolites. These studies reveal that SASP is not metabolized by the liver in vivo, and after absorption from the small bowel, 25--50% of the SASP is excreted unchanged in the bile, and the rest enters the circulation. Implications of these results in the treatment of patients with Crohn's disease of the small intestine are discussed.

Animals↗
PubMed1978

Isolation and characterization of colonic tissue-bound antibodies from patients with idiopathic ulcerative colitis.

To determine if specific anticolon antibodies bound to colonic mucosa occur in ulcerative colitis, we obtained surgical specimens of colon from five patients with ulcerative colitis, one patient with diverticulitis, and three control subjects with carcinoma. Two specimens of ileum and cecum were also obtained from patients with Crohn ileocolitis. Tissue was homogenized and washed and bound Ig was eluted by citrate buffer, pH 3.2. Concentrated eluates of all specimens from patients with ulcerative colitis reacted with antisera to kappa and gamma and not with antisera to alpha and mu chains. Corresponding eluates from all other specimens did not react with these antisera, but did react with antialbumin. The presence of IgG in ulcerative colitis eluates was also determined by immunoelectrophoresis, immunocoprecipitation, and affinity chromatography with antisera against human IgG. Indirect immunofluorescence and uptake of radiolabeled antibody demonstrated antigenic sites in diseased colonic epithelium of biopsy specimens obtained from six additional patients with ulcerative colitis and three patients with idiopathic proctitis, but not in patients with Crohn disease, nonspecific diarrhea, and bacillary dysentery and control subjects. Although the role of colitis colon-bound antibody in the pathogenesis of ulcerative colitis is unclear, local antibody-antigen complexes may initiate colonic epithelial cytolysis by various immunologically mediated mechanisms.

Autoantibodies↗
PubMed1978

Comparative analysis of systemic immunological parameters in ulcerative colitis and idiopathic proctitis: effects of sulfasalazine in vivo and in vitro.

Comparative analysis of the systemic immunity revealed similarities between ulcerative colitis and idiopathic proctitis. In the active stage of both diseases, circulating complement receptor positive cells were increased whereas T-cell percentages and lymphocyte functions were decreased. In severe forms of ulcerative colitis and idiopathic proctitis circulating EAC-phagocytosing esterase positive cells, indicative of activated monocytes, were demonstrated. Successful treatment with salicylazosulfapyridine (SASP) reversed these immunological changes. Incubation of SASP and its metabolites with leucocytes from patients and control subjects, in concentrations similar to those demonstrated in sera from patients treated with SASP, did not alter the immunological changes.

Adult↗
PubMed1977

Further studies of sulphasalazine metabolism in the treatment of ulcerative colitis.

Sixty-four outpatients with ulcerative colitis receiving maintenance treatment with sulphasalazine were studied to relate disease activity to serum concentrations of sulphapyridine. Of 43 patients in remission, 32 had serum sulphapyridine levels over 20 microgram/ml. Ten of the 21 patients with active disease were for various reasons taking inadequate doses of sulphasalazine, as indicated by low serum sulphapyridine levels, and of the remaining 11 patients, who had serum levels over 20 microgram/ml, nine had faecal stasis proximal to active distal colitis and went into remission when treated with hydrophilic colloid or bran and an unchanged sulphasalazine dosage. This suggests that to be effective the metabolites of sulphasalazine must be delivered in the faeces to the lumen of the diseased distal segment of the colon. High serum concentrations of sulphapyridine produce side effects; therefore slow acetylators of sulphapyridine need lower doses of sulphasalazine. Estimations of serum sulphapyridine concentrations, as well as identifying the patient's acetylation phenotype, can also be useful in assessing his compliance with treatment.

Adolescent↗
PubMed1977

Idiopathic proctitis. I. The morphology of proximal colonic mucosa and its clinical significance.

A group of 31 patients with idiopathic proctitis were colonoscoped while they were symptomatic. Multiple mucosal biopsies were taken from the transverse, descending, and sigmoid colon and from the rectum. While visualization by colonoscopy revealed abnormalities limited to the most distal 18-20 cm of the colon, microscopic abnormalities were frequently seen in more proximal locations. Analysis of clinicopathological data indicates that there is good correlation between the extent of microscopic mucosal abnormalities and the clinical course. Patients with abnormalities limited to the rectum generally responded well to conventional treatment while patients with more proximal involvement were refractory to such therapy.

Adult↗
PubMed1977

Immunohistochemical changes in morphologically involved and uninvolved colonic mucosa of patients with idiopathic proctitis.

Alterations in secretory component, IgA, IgG, and IgM were studied by immunofluorescent techniques in mucosal biopsy specimens obtained at colonoscopy from inflamed and grossly uninvolved colonic mucosa from 12 patients with idiopathic proctitis. Parotid-salivary secretory component and IgA and serum immunoglobulins were also investigated. Decreased secretory IgA was observed in the epithelium of all grossly involved rectal mucosa and in 40% of proximal normal mucosa. Salivary secretory IgA was not diminished. These observations suggest that a local immune defect may be pathogenetically related to idiopathic proctitis.

Adult↗
PubMed1975

Acetylation polymorphism of sulfapyridine in patients with ulcerative colitis and Crohn's disease.

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.

Acetylation↗