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Biomedical subjects

K M Das

Publications and source records attributed to K M Das.

126 records · Page 7Linked to original sources
PubMed1973

The metabolism of salicylazosulphapyridine in ulcerative colitis. I. The relationship between metabolites and the response to treatment in inpatients.

The metabolism of salicylazosulphapyridine was studied in 16 patients with ulcerative colitis admitted to hospital. The acetylator phenotype was determined on admission. The mean serum concentration (mug/ml) (at steady state eight +/- two days in patients responding to treatment) of SASP, total SP, and 5-ASA were 18.7 +/- 12.8; 53.7 +/- 23.1; and 1 +/- 0.9 for slow acetylators and 17.6 +/- 7.1; 31 +/- 9.0 and 1 +/- 0.9 for fast acetylators respectively. Twenty-four hour urinary excretion of SASP, total SP, and 5-ASA were 4.6% +/- 3.1; 52% +/- 9.6 and 22.3 +/- 6.7% of the administered dose respectively. Serum total SP concentration of 20 to 50 mug/ml appeared to coincide with clinical improvement in the absence of any side effects related to salicylazosulphapyridine. No such relationship could be shown with serum SASP, individual metabolites, or 5-aminosalicyclic acid.

Acetylation↗
PubMedDate not supplied

Role of ultrasonography in blunt abdominal trauma.

Patients with blunt abdominal trauma (BAT) often have equivocal signs of intra-abdominal injury. Diagnostic peritoneal lavage (DPL) has been the 'gold standard' for evaluating these patients, the use of ultrasound (US) being a recent phenomenon. Seventy-three patients with BAT and equivocal physical signs were subjected to both DPL and US for detection of intra-abdominal injury. Based on clinical status, DPL and US findings, the patients underwent laparotomy or non-operative management. DPL was positive in 35 patients. There was one false positive and one false negative result (sensitivity 97.1%, specificity 97.4%, accuracy 97.3%). US was positive in 31 patients. There were 5 false positive and 4 false negative results (sensitivity 86.7%, specificity 88.4%, accuracy 87.7%). Solid viscus injury was documented at laparotomy in 24 patients. DPL failed to detect one pancreatic injury, while US failed to detect 4 splenic and 2 liver injuries. US additionally detected a single case of haemopericardium. Although DPL outperformed US in this study, US can complement DPL in defining the organs injured and in follow up of patients undergoing non-operative management for BAT.

Abdominal Injuries↗
PubMedDate not supplied

Hepatic-pericardio-phrenic collateral (natural shunt) in a patient with Budd-Chiari syndrome.

Hepatic venous outflow tract obstruction, Budd-Chiari syndrome (BCS), leads to portal hypertension and to the development of collaterals that bypass the obstruction. Described here is a BCS patient with an unusually large transdiaphragmatic collateral between the left hepatic and left innominate veins, which decompressed the oesophageal varices. This has not been reported earlier in the literature.

Adult↗
PubMedDate not supplied

An antigen reacting with das-1 monoclonal antibody is ontogenically regulated in diverse organs including liver and indicates sharing of developmental mechanisms among cell lineages.

The monoclonal antibody designated mAb Das-1, which was generated against a colon epithelial protein, reacts with the normal biliary epithelium and keratinocytes, which are among targets of tissue injury in ulcerative colitis. Moreover, mAb Das-1 reacts with abnormal cells in Barrett's esophagus and chronic cystitis profunda, as well as so-called 'oval cells' in the adult liver, which are considered oncogenic progenitor cells. To establish ontogenic regulation of mAb Das-1 reactivity, we studied 7- to 24-week-old human fetuses by immunohistochemistry. In liver, mAb Das-1 reactivity was further correlated with glycogen, dipeptidyl peptidase IV, glucose-6-phosphatase and gamma-glutamyl transpeptidase expression. mAb Das-1 reacted with cells in organs arising from the pharyngeal cleft (thymus), primitive gut (oral cavity, pharynx, lung, esophagus, stomach, biliary tree, pancreas, liver, colon), ureteric bud (renal tubules, collecting duct), mesonephros (kidney, testis), mesoderm (muscle) and elsewhere (skin, adrenal cortex). In distinction from the adult liver, mAb Das-1 staining was more pronounced in hepatoblasts compared with biliary cells. In adult tissues, however, mAb Das-1 reactivity was restricted to the colon, biliary epithelium, keratinocytes, and ciliary body. These data indicated that the mAb Das-1 recognized epitopes in fetal cells of diverse ectodermal, mesodermal and endodermal origin, compatible with sharing of lineage mechanisms in tissues. Reactivation of mAb Das-1 staining in epithelial precancerous conditions, including carcinomas arising in these organs, is compatible with oncofetal regulation of the antigen, which will facilitate analysis of cell subpopulations during organ development, regeneration and oncogenesis.

Adult↗
PubMedDate not supplied

Clinical pharmacokinetics of sulphasalazine.

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.

Acetylation↗
PubMedDate not supplied

Ulcerative colitis: specific antibodies against a colonic epithelial Mr 40,000 protein.

A colon tissue-bound disease specific IgG (CCA-IgG) antibody can be eluted from the colonic tissue of patients with ulcerative colitis (UC). CCA-IgG recognizes an Mr 40,000 protein present in both normal and diseased colon. Using an anti-Mr 40,000 murine monoclonal antibody this protein has been localized exclusively in colonic epithelial cells mainly along the baso-lateral domains of plasma membrane. Non-colonic epithelial tissues from 12 different organs including small intestine did not react with the anti-Mr 40,000 monoclonal antibody. The Mr 40,000 protein is present in the RPMI-4788 colon cancer cells but not in HeLa. The antibody dependent cell-mediated cytolysis by UC sera against RPMI-4788 cells was inhibited by anti-Mr 40,000 polyclonal antibody. These findings suggest that CCA-IgG and the Mr 40,000 colonic epithelial protein are involved in an autoimmune reaction and may be important in the pathogenesis of UC.

Antibodies, Monoclonal↗