Digestion of Gluten Peptides by Normal Human Jejunal Mucosa and by Mucosa from Patients with Adult Coeliac Disease

1970 ◽  
Vol 38 (1) ◽  
pp. 11-25 ◽  
Author(s):  
A. P. Douglas ◽  
C. C. Booth

1. The ability of homogenates of jejunal mucosa to liberate amino acids from a peptic-tryptic digest of gluten was assessed. Mucosal specimens were obtained from thirty-two control subjects without malabsorptive disease, from twenty-six patients with untreated adult coeliac disease and from nine patients with adult coeliac disease in whom the intestinal mucosa was histologically normal as a consequence of treatment with a gluten-free diet. In addition nine of the untreated patients were restudied after institution of a gluten-free diet. 2. The ability of the jejunal mucosa from the patients with untreated adult coeliac disease to liberate amino acids from the gluten peptides was significantly less than that of the mucosa from control subjects. 3. No significant difference from normal was found when jejunal mucosa from patients with treated adult coeliac disease was studied irrespective of whether or not the mucosa was histologically normal. 4. These results indicate that the impairment of jejunal mucosal digestion of gluten in untreated adult coeliac disease is a secondary phenomenon and do not support the hypothesis that coeliac disease is due to the absence from the intestinal mucosa of an enzyme normally concerned in the digestion of gluten.

1990 ◽  
Vol 27 (5) ◽  
pp. 536-536
Author(s):  
N Bonamico ◽  
P Lionetti ◽  
P Mariani ◽  
D D Alessandro ◽  
P Triqlione ◽  
...  

Gut ◽  
1974 ◽  
Vol 15 (11) ◽  
pp. 870-874 ◽  
Author(s):  
B. L. Chapman ◽  
K. Henry ◽  
F. Paice ◽  
N. F. Coghill ◽  
J. S. Stewart

2005 ◽  
Vol 64 (4) ◽  
pp. 434-450 ◽  
Author(s):  
Norma McGough ◽  
John H. Cummings

Coeliac disease is a lifelong intolerance to the gluten found in wheat, barley and rye, and some patients are also sensitive to oats. The disease is genetically determined, with 10% of the first-degree relatives affected and 75% of monozygotic twins being concordant. Of the patients with coeliac disease 95% are human leucocyte antigen (HLA)-DQ2 or HLA-DQ8 positive. Characteristically, the jejunal mucosa becomes damaged by a T-cell-mediated autoimmune response that is thought to be initiated by a 33-mer peptide fragment in A2 gliadin, and patients with this disorder have raised levels of anti-endomysium and tissue transglutaminase antibodies in their blood. Coeliac disease is the major diagnosable food intolerance and, with the advent of a simple blood test for case finding, prevalence rates are thought to be approximately 1:100. Classically, the condition presented with malabsorption and failure to thrive in infancy, but this picture has now been overtaken by the much more common presentation in adults, usually with non-specific symptoms such as tiredness and anaemia, disturbance in bowel habit or following low-impact bone fractures. Small intestinal biopsy is necessary for diagnosis and shows a characteristically flat appearance with crypt hypoplasia and infiltration of the epithelium with lymphocytes. Diet is the key to management and a gluten-free diet effectively cures the condition. However, this commitment is lifelong and many aisles in the supermarket are effectively closed to individuals with coeliac disease. Compliance can be monitored by measuring antibodies in blood, which revert to negative after 6–9 months. Patients with minor symptoms, who are found incidentally to have coeliac disease, often ask whether it is necessary to adhere to the diet. Current advice is that dietary adherence is necessary to avoid the long-term complications, which are, principally, osteoporosis and small bowel lymphoma. However, risk of these complications diminishes very considerably in patients who are on a gluten-free diet.


Author(s):  
Lorcan McGrogan ◽  
Mary Mackinder ◽  
Fiona Stefanowicz ◽  
Maria Aroutiounova ◽  
Anthony Catchpole ◽  
...  

Nutrients ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 947
Author(s):  
Anna Szaflarska-Popławska

Potential celiac disease (PCD) is a heterogeneous disease; only some patients develop full celiac disease (CD), characterised by advanced atrophic changes in the small intestine. Few accurate prognostic factors exist for the progression of PCD; therefore, therapeutic decisions should be made on an individual basis in each case. Patients with clinical gastroenterological or parenteral symptoms often benefit from a gluten-free diet, and those left on a diet containing gluten should receive clinical, serological and histopathological supervision.


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