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Biomedical subjects

P J Kumar

Publications and source records attributed to P J Kumar.

At least 37 records · Page 2Linked to original sources
PubMed1988

The teenage coeliac: follow up study of 102 patients.

Over a 10 year period a total of 102 teenage patients with coeliac disease were assessed on transfer from paediatric hospitals to an adult clinic. Fifty seven patients said they were on a strict gluten free diet; 36 were semistrict, and nine admitted to eating a normal diet. Jejunal mucosal abnormalities, however, suggested that many patients on the 'strict' diet were actually consuming gluten. All patients were well with biochemical parameters within the normal range. Height percentiles were not significantly different from the normal population but patients, as a group, were significantly lighter.

Adolescent↗
PubMed1988

Low gluten diet in the treatment of adult coeliac disease: effect on jejunal morphology and serum anti-gluten antibodies.

Treatment of patients with coeliac disease with a low gluten containing diet (LGD) remains controversial. We have studied jejunal morphology and antigluten (AG) antibody titres by ELISA in patients on a LGD of 2.5-5 g/day for three to 14 months (median six months) and compared results with patients on a strict gluten free diet (GFD) for six to 27 months (median 13 months). We found no significant difference in villous height or crypt depth (eight LGD v 10 GFD patients) or serum AG-IgA, -IgG, and IgM titres (13 LGD v 12 GFD patients). there was however, a significant increase (p less than 0.05) in intra-epithelial lymphocytes in those patients on a LGD. We conclude that adult coeliac patients can tolerate a LGD without gross morphological change and without initiating significant AG antibody responses.

Adolescent↗
PubMed1987

Gliadin binding to rat and human enterocytes.

Binding of 125I-crude gluten digest (Frazer's fraction III. FF-III) and 125I-concanavalin A (Con A) to isolated rat enterocytes and of 125I-FF-III to human enterocytes was investigated. Specific binding of 125I-FF-III to rat enterocytes was observed but binding was not inhibited by any of a range of simple and complex saccharides. although casein and bovine serum albumin displaced FF-III at high concentrations. Con A also bound to enterocytes in a specific manner and was inhibited by alpha-methyl-D-mannoside, confirming a lectin-mediated interaction. 125I-FF-III exhibited quantitatively similar specific binding to both normal human and coeliac enterocytes. The primary interaction of gliadin peptides with the enterocyte surface membrane is not lectin-mediated and unlikely to be of fundamental importance in the pathogenesis of coeliac disease.

Animals↗
PubMed1987

Evidence for the role of a human intestinal adenovirus in the pathogenesis of coeliac disease.

We previously noted a region of amino acid sequence homology between A-gliadin, a major alpha-gliadin component known to activate coeliac disease, and the early region E1b protein of human adenovirus serotype 12 (Ad12), an adenovirus isolated from the human intestinal tract. In the present study sera from coeliac disease patients from the United Kingdom and the United States were assayed for neutralising antibody to Ad12 as evidence of past exposure to that virus and for antibody to synthetic peptides of A-gliadin from the region of shared sequence with the Ad12 E1b protein. Eighty nine per cent of untreated coeliac disease patients had evidence of previous Ad12 infection. There was also a significant increase in the prevalence of neutralising antibody to Ad12 among treated adults (33.3%) and children (30.8%) with coeliac disease compared with controls (0-12.8%) in the western USA and in London. There was no evidence for an increased prevalence of infection with a closely related adenovirus, adenovirus 18, or another enteric virus, Echovirus 11, among coeliac disease subjects. Additional studies documented that a region of A-gliadin that shares amino acid sequence homology with the adenovirus 12 E1b protein could be recognised as an antigenic determinant in active coeliac disease patients. Taken together, these data are compatible with the hypothesis that a viral protein may play a role in the pathogenesis of coeliac disease, perhaps by virtue of immunological cross reactivity between antigenic determinants shared by the viral protein and alpha-gliadins.

Adenoviridae Infections↗
PubMed1986

Reappraisal of the 'lectin hypothesis' in the aetiopathogenesis of coeliac disease.

The agglutinating properties of a crude gluten digest, purified gliadin fractions and established plant lectins were investigated using mammalian erythrocytes, rat enterocytes and normal and coeliac human enterocytes as the target systems. Gliadin preparations failed to cause agglutination of any of the cells tested, whereas established pure plant lectins were active cell agglutinins. These studies indicate that gliadin peptides do not interact with intestinal cells in a polyvalent, lectin-like manner and as such cannot be regarded as true lectins. Mucosal damage in coeliac disease is unlikely therefore to be related to lectin-like activity of gliadin.

Agglutination↗
PubMed1984

The microvillus in adult jejunal mucosa--an electron microscopic study.

The increase in surface area contributed by microvilli per square unit mucosal surface area in the jejunal villus, i.e. amplification factor, has been studied in four normal adults and three adults with treated coeliac disease. Villi were split into three regions, photomicrographs of microvilli were taken from each region and the microvillus amplification factor calculated. The mid-villus region contributed a significantly greater microvillus amplification factor than either the low or upper regions in all patients studied. In addition surface cell heights were greatest in the low- and mid-villus regions. This suggests that the enterocytes in the mid-villus region are best adapted for absorption, and that the enterocytes in the upper-villus regions are undergoing an ageing process.

Adolescent↗
PubMed1983

Treatment of advanced malignant melanoma with high-dose melphalan and autologous bone marrow transplantation.

Twenty-eight patients with advanced life-threatening metastatic malignant melanoma were treated with high dose (140-260 mgm-2) intravenous melphalan and autologous bone marrow. Cyclophosphamide "priming" 300 mgm-2 i.v. was given to 19 patients one week previously and this resulted in clinical but not histological evidence of amelioration of gastrointestinal toxicity. In 11 patients (43%) there was evidence of tumour response to treatment and in 2 patients complete remissions were observed. However in most patients, responses were short-lived and no patient lived longer than 17 months from start of treatment or 24 months from first recorded evidence of distant metastatic disease.

Adult↗
PubMed1981

Radiologic features of the jejunum in hypoalbuminemia.

Although hypoalbuminemia is a recognized cause of jejunal dilatation, the level of serum albumin at which this occurs and its relation to the extent of jejunal dilatation in celiac disease have not been clearly established. Barium follow-through examination was performed in 12 patients with hypoalbuminemia, in 21 patients with celiac disease, some of whom had a reduced serum albumin, and in 14 control subjects. Jejunal width was increased in patients with hypoalbuminemia and there was a highly significant correlation between jejunal width and the level of serum albumin (p less than 0.001). The level of serum albumin at which jejunal dilatation occurred ("albumin threshold") was found to be 27 g/l. Hypoalbuminemia was not found to be an important factor in the jenunal dilatation of celiac disease. There was a close correlation between the presence of edema and ascites and radiologic abnormality in the jejunum, suggesting that these appearances in nephrotic syndrome are due to intestinal edema. This study suggests that the serum albumin should be taken into account when interpreting the caliber of the small intestine.

Ascites↗
PubMed1979

Reintroduction of gluten in adults and children with treated coeliac disease.

Twenty-eight patients, thought to have coeliac disease and on gluten free diets, were put on a normal diet to confirm their diagnoses. Nineteen had been diagnosed in adult life (ACD) and nine in childhood (CCD). Patients were assessed on jejunal, morphological, and symptomatic parameters. Eighteen patients with ACD relapsed within seven weeks. Nine patients with CCD relapsed at variable times but five took longer than seven weeks, the longest period beint 10 months. Seven patients had no symptoms despite morphological deterioration during challenge and one patient, with ACD, did not relapse and was HLA B8 negative. This patient with ACD had subtotal villous atrophy on two jejunal biopsies and later showed morphological improvement on a gluten free diet. There was no correlation between the relapse time and time spent on a gluten free diet.

Adolescent↗
PubMed1978

Sprue.

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Adult↗
PubMed1976

Gastric lesion in dermatitis herpetiformis.

Five of 33 patients with dermatitis herpetiformis (DH) were found to have gastric parietal cell antibody in their sera, whereas it was not found in 30 healthy controls of comparable age distribution. Fifteen of the patients with DH underwent further studies to investigate the histological and functional state of their gastric mucosa. Atrophic gastritis was found in all five patients whose sera contained gastric parietal cell antibody and in three of 11 patients with no antibody in their sera. In addition, there was marked impairment of acid secretion in the DH group as a whole, but, apart from one patient with overt pernicious anaemia (PA), there was no evidence of malabsorption of B12.

Adolescent↗
PubMed1976

T cell depletion in untreated adult coeliac disease.

The proportional and absolute numbers of circulating thymus dependent lymphocytes (T cells) were reduced in untreated patients with coeliac disease but were normal after treatment with a gluten free diet. There was an inverse correlation between circulating T cell numbers and jejunal intraepithelial lymphocytes. This evidence suggests a possible role for T cells in the pathogenesis of coeliac disease and is a further example of disturbed cell mediated immunity in this condition.

Adult↗
PubMed1976

Cellular infiltrate of the jejunum after re-introduction of dietary gluten in children with treated coeliac disease.

Jejunal lamina propria plasma cells and eosinophils and intraepithelial lymphocytes were raised in coeliac children on gluten-containing diets, but only intraepithelial lymphocytes were increased in patients on gluten-free diets. In contrast, lamina propria lymphocytes were reduced in children with coeliad disease on gluten-containing diets but were normal in paitents on gluten-free diets. In children with coeliac disease who were studied serially, lamina propria plasma cells and eosinophils and intraepithelial lymphocytes increased, and lamina propria lymphocytes decreased, within three months of the reintroduction of gluten to the diet. These observations are essentially similar to those made in the adult form of the disease and suggest that more than one type of immunological reaction is involved in the pathogenesis of the jejunal lesion.

Adolescent↗
PubMed1976

Immunological phenomena in the jejunum and serum after reintroduction of dietary gluten in children with treated coeliac disease.

Jejunal mucosal immunoglobulin-containing cells of all three major classes (IgA, IgM, IgG) were increased in coeliac children on gluten-containing diets but only IgM cell numbers were raised in those on gluten-free diets. Patients with subtotal villous atrophy had greater numbers of immunoglobulin-containing cells than patients with normal mucosa. In previously treated patients studied before and after three months on a gluten-containing diet ther was an increase in all three classes of cell, IgM containing cells showing the greatest proportional rise. Basement membrane staining with anti-IgA serum occurred in coeliacs and was most intense in untreated patients. Apart from one patient with very low levels of serum IgA, serum immunoglobulins did not differ from normal. However, after reintroduction of gluten to the diet a significant fall in serum IgM concentrations occurred compared with levels in the same patients while on gluten-free diets. It seems probable that both IgA and IgM systems are important in the immunopathogenesis of the small intestinal lesion of childhood coeliac disease.

Adolescent↗
PubMed1976

Food antibodies in patients with dermatitis herpetiformis and adult coeliac disease - relationship to jejunal morphology.

Serum antibodies to a variety of dietary proteins were investigated in 26 patients with adult coeliac disease (ACD, 14 untreated and 17 treated with a gluten-free diet) and 38 patients with dermatitis herpetiformis (DH) with varying small bowel abnormalities. The incidence of one or more positive tests was highest in untreated ACD (73.4%) and DH with subtotal villous atrophy (57.4%). This incidence fell with morphological improvement, being 56.4% in treated ACD patients with partial villous atrophy (PVA), and 33.4% in DH with PVA, and 0% in DH with normal biopsies. The height of the serum antibody titre also fell with morphological improvement. These results show that there is an abnormally high incidence of dietary antibodies in patients with DH, and this correlates with the degree of small bowel damage.

Adult↗
PubMed1975

Ileal function in patients with untreated adult coeliac disease.

A double-lumen perfusion technique has been used to investigate jejunal and ileal absorption of glucose, water, and electrolytes in a group of patients with untreated adult coeliac disease. Correct positioning of the tube was confirmed by measuring the differential jejunal and ileal handling of bicarbonate. Eight control subjects and eight patients with coeliac disease were perfused with an isotonic electrolyte solution containing 50 mM glucose and 25 mM bicarbonate. The group of coeliac patients had impaired jejunal absorption of glucose (P less than 0.001), water (P less than 0.01), sodium (P less than 0.02), and chloride (P greater than 0.05) compared with the control group. In contrast the group of coeliac patients had normal ileal glucose and water absorption and increased ileal sodium (P greater than 0.01) and chloride (P greater than 0.05) absorption compared with the controls. Evidence for ileal adaptation was found in three individual patients who had absorptive values outside 2SD of the normal mean. The results indicate that the distal small intestine in coeliac disease has the ability to adopt to the damage and loss of absorptive capacity in the proximal small intestine.

Adolescent↗