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Biomedical subjects

A W Bullen

Publications and source records attributed to A W Bullen.

At least 19 recordsLinked to original sources
PubMed1982

Cell-mediated immunity to gluten within the small intestinal mucosa in coeliac disease.

Jejunal biopsies from controls and coeliac patients were maintained in organ culture in the presence of gluten fraction III. The culture media were assayed for evidence of lymphokine activity in a migration inhibition test using normal peripheral blood leucocytes. Significant inhibition of migration was produced by media from untreated coeliac patients compared with controls (P less than 0.005) or treated coeliac patients (P less than 0.001), indicating the production of a leucocyte migration inhibition factor (LIF) by untreated coeliac mucosa in response to gluten fraction III. The degree of inhibition correlated with the preculture interepithelial lymphocyte count in the coeliac biopsies (P less than 0.02). In six coeliac patients studied when on a normal diet and on a gluten-free diet, LIF was produced while on a normal diet, but not while on a gluten-free diet. These results suggest that a local cell-mediated immune reaction to gluten is present in the mucosa of patients with untreated coeliac disease but that this is reversed by treatment with a gluten-free diet.

Adult↗
PubMed1981

Serum beta 2-microglobulin in hepato-biliary diseases.

The levels of serum beta 2-m in hepato-biliary disease have been examined. Significant increase has been observed in various benign and malignant diseases of the liver, but not in jaundice due to acute pancreatitis. The age-dependent relationship of beta 2-m is present in controls, weaker in the malignant diseases and absent in the benign diseases. The level of beta 2-m is not influenced by jaundice. Serum beta 2-m levels have no role as a discriminant in liver disease.

Adolescent↗
PubMed1981

Simple method of assessing splenic function in coeliac disease.

1. Erythrocytes with membrane abnormalities seen on interference contrast microscopy ('pitted erythrocytes') were counted in venous blood samples from patients with treated coeliac disease and dermatitis herpetiformis, and from control subjects and patients who had had an elective splenectomy. 2. The percentage of 'pitted erythrocytes' was compared with the 99mTc-labelled heat-damaged erythrocyte clearance, and with the splenic size computed from scintiscans. 3. There was a significant correlation between percentage 'pitted erythrocytes' and the above methods of measuring splenic function and size. Increase in the percentage of 'pitted erythrocytes' above the control range indicated splenic hypofunction. 4. The number of coeliac patients with percentage 'pitted erythrocytes' above the control range increased with increasing age at which they started a gluten-free diet. 5. Counting of 'pitted erythrocytes' is a simple and sensitive method of assessing splenic hypofunction in treated coeliac disease. It avoids radiation exposure, and is applicable to all ages and repeatable without risk. 6. The incidence of splenic hypofunction in coeliac patients may be related to the duration of untreated disease.

Adolescent↗
PubMed1981

Hyposplenism, adult coeliac disease, and autoimmunity.

Functional hyposplenism is associated with a variety of disorders including coeliac disease. The aims of this study were to estimate the need for a small intestinal biopsy in the investigation of hyposplenism, and to assess the relationship of autoimmunity to hyposplenism and coeliac disease. During one year, the features of hyposplenism were found in blood films of 27 patients who had not had a splenectomy. Ten patients were already known to have coeliac disease. Intestinal biopsy was performed in another 13 patients; coeliac disease was diagnosed in six. Of the 23 patients biopsied, coeliac disease was present in 16 (70%). Autoantibodies were detected in significantly more patients with hyposplenism than in healthy controls (P less than 0.05), and in significantly more coeliacs with hyposplenism than coeliacs with normal blood films (P less than 0.01). The increased incidence of autoantibodies in coeliacs with hyposplenism compared with other coeliacs was not associated with a difference in the incidence of HLA-B8. Small bowel biopsy should be carried out in the investigation of unexplained hyposplenism. There may be a link between hyposplenism and the autoimmune manifestations of coeliac disease.

Adult↗
PubMed1981

In vitro diagnosis of coeliac disease: an assessment.

Jejunal biopsies from controls and coeliac patients were maintained in organ culture for up to 48 hours. The in vitro effect of gluten fraction III during the period of culture was assessed by measurement of the activity of the brush border enzymes alkaline phosphatase and alpha-glucosidase. Mucosa from controls and treated and untreated coeliacs behaved similarly and no reproducible in vitro effect of gluten was demonstrated. These results cast doubt on the in vitro diagnosis of coeliac disease by monitoring brush border enzyme activity.

Alkaline Phosphatase↗
PubMed1981

HLA-B8 and cell-mediated immunity to gluten.

The leucocyte migration inhibition (LMI) test was used as an indicator of cell mediated immunity to gluten fraction III in 30 healthy controls and 58 patients with adult coeliac disease and the results related to HLA status and duration of treatment with a gluten-free diet. HLA-B8 controls showed significantly lower leucocyte migration indices, indicating greater immune response, than non-HLA B8 controls. Untreated coeliacs showed no difference from HLA-B8 controls. There was no difference between results from HLA-B8 and non-HLA-B8 coeliacs. Leucocyte migration was even lower in coeliacs early in treatment but rose after treatment for over one year. These results may reflect an immune response gene for gluten in linkage disequilibrium with HLA-B8. The increased immune response to gluten as measured in this test cannot be the sole factor in aetiology of coeliac disease. Furthermore, it is necessary to re-evaluate earlier results of cell-mediated immunity in coeliac disease with reference to HLA status of the controls.

Celiac Disease↗
PubMed1981

Gluten sensitivity of small intestinal mucosa in vitro: quantitative assessment of histologic change.

In view of the importance to the patient of demonstrating mucosal sensitivity to gluten we have quantitated morphologic change during organ culture of small bowel mucosa by measuring enterocyte height. In 27 normal controls the mean preculture enterocyte height was 28.3 micrometer +/- 1.8 (+/- 1 SD), decreasing to 25.6 micrometer +/- 1.9 and 26.1 micrometer +/- 2.0 after 24 h culture in the absence and presence of gluten, respectively. Both these decreases were significant (p < 0.001), but there was no difference between culture with or without gluten. In 9 abnormal controls, the mean preculture enterocyte height was 27.0 micrometer +/- 2.7, decreasing significantly (p < 0.05) to 24.5 micrometer +/- 1.1 after 24 h culture without gluten, and to 25.4 micrometer +/- 2.3 with gluten (NS). In 17 untreated celiac patients, the mean preculture enterocyte height was 19.6 micrometer +/- 1.9 increasing significantly to 23.8 micrometer +/- 2.0 (p < 0.001) after 24 h culture without gluten but decreasing to 18.7 micrometer +/- 3.1 after 24 h culture with gluten (NS). There was a significant difference between culture with or without gluten (p < 0.001). In 21 treated celiac patients, the mean preculture enterocyte height was 28.1 micrometer +/- 1.9 decreasing to 25.4 micrometer +/- 2.0 and 24.2 +/- 1.9 in the absence and presence of gluten, respectively. Both these decreases were significant (p < 0.001), but more importantly there was a significant decrease (p < 0.001) after culture with gluten compared with culture without gluten. These data indicate that it is possible to quantify morphologic change during organ culture and to demonstrate gluten-sensitivity not only in untreated, but also in treated celiac mucosa. These studies have important implications as regards the diagnosis and further investigation of the etiology of celiac disease.

Caseins↗
PubMed1980

Splenic size and function in adult coeliac disease.

Splenic scintigraphy was performed after measurement of 99Tcm-labelled heat-damaged red cell clearance in 29 patients with treated coeliac disease. Good correlation was found between splenic size and function using these techniques. 99Tcm-labelled sulphur colloid scintiscans were also performed in 24 coeliacs. Splenic volumes computed from colloid scans correlated well with those computed from red cell scans. Almost 50% of adult patients with treated coeliac disease have impaired splenic function, the incidence rising with increasing age of starting treatment. Sulphur colloid scintigraphgy provides a simple quantitative method of assessing splenic function in treated coeliac disease which can be used in exploring the possibilities of avoidance of the adverse effects of hyposplenism.

Adult↗
PubMed1979

The diagnostic value of the oral pancreatic function test.

An oral pancreatic function test (PFT) using the synthetic peptide N-benzoyl-L-tyrosyl-p-aminobenzoic acid can assess pancreatic exocrine function, since urinary recovery of the ingested dose is an indirect index of chymotryptic activity. We have studied 34 subjects using this oral PFT, which correctly distinguished the control group (8 subjects) from the pancreatitis group (10 patients), results correlating well with Lundh test findings. However, the test was falsely abnormal on 9 out of 16 occasions in patients with bowel or liver disease. We therefore conclude that the present test cannot distinguish small-bowel disease from pancreatic disease, which is often the diagnostic problem, and is also frequently falsely abnormal in the presence of chronic liver disease.

4-Aminobenzoic Acid↗
PubMed1979

Improved diagnostic accuracy of a modified oral pancreatic function test.

The oral pancreatic function test (PFT) depends upon urinary recovery of p-aminobenzoic acid (PABA) released by chymotrypsin hydrolysis of orally administered N-benzoyl-L-tyrosyl-p-aminobenzoid acid. The diagnostic value of the test is limited because falsely abnormal results frequently occur in patients with bowel or liver disease in whom PABA recovery is impaired by abnormal absorption or hepatic conjugation, even though pancreatic function is normal. To overcome this problem, we have modified the oral PFT to correct for impaired PABA absorption and conjugation. Results of the oral PFT have been compared with urinary recovery of an equivalent dose of free PABA in order to derive a PABA excretion index (PEI). When the modified oral PFT is used, the PEI clearly distinguished patients with pancreatic disease from normal subjects. In patients with small-bowel or liver disease and normal exocrine pancreatic function, the PEI results were similar to those of normal subjects, although a previous oral PFT had been falsey abnormal. The modified test can therefore distinguish abnormal results due to pancreatic disease from the falsely abnormal results found in liver and small-bowel disease.

4-Aminobenzoic Acid↗
PubMed1978

Skin reactions caused by vitamin K in patients with liver disease.

Vitamin K and its analogues are frequently used in treatment of the hypoprothrombinaemia found in disease of the liver, biliary tract and small intestine. Most cases of cutaneous toxicity to vitamin K have been described in the French literature, but only two cases from Britain. This paper reports six patients with chronic liver disease who developed cutaneous reactions around the site of injection of vitamin K, and the results of investigations to futher understanding of the pathogenesis of the rash.

Adolescent↗
PubMed1978

Lymphocyte subpopulations in adult coeliac disease.

Rosetting techniques were used to estimate T and B cell subpopulations in the peripheral blood in patients with treated and untreated adult coeliac disease and in control subjects. In patients with untreated coeliac disease, T cell numbers were significantly lower than in controls or treated patients, although there was no difference in total lymphocyte counts. There was no significant difference in B cell numbers between treated and untreated patients, and the subpopulation which increased to replace the T cells in untreated patients comprised cells not identified by B or T cell markers. Total lymphocyte counts and lymphocyte subpopulations were affected by splenic atrophy. It is suggested that these effects might be caused by the loss of lymphocytes from the gastrointestinal tract in untreated coeliac disease.

Adult↗
PubMed1978

Cell-mediated immunity to gluten fraction III in adult coeliac disease.

A migration inhibition test was used to assess sensitisation of blood leucocytes, and thus cell-mediated immunity, to gluten fraction III in controls and patients with coeliac disease. Migration indices were significantly less (indicating sensitisation) in untreated and in treated patients than in controls, and significantly less in treated patients than in untreated patients. At a concentration of 1 mg/ml gluten fraction III, 13% of untreated patients and 54% of treated patients had migration indices in the sensitised range. At 2 mg/ml gluten fraction III, sensitisation was demonstrated in 8% of untreated patients and 48% of treated patients. After starting a gluten free diet, migration indices fell into the sensitised range in all patients followed. After at least nine months on a gluten free diet, migration indices were significantly higher in those patients with a normal interepithelial lymphocyte count than in those patients with a raised interepithelial lymphocyte count. Cell-mediated immunity to gluten fraction III can be detected in the peripheral blood of certain patients with coeliac disease. Detectable sensitivity is related to the time on a gluten free diet, and the interepithelial lymphocyte count.

Adult↗