Lymphoreticular dysfunction in idiopathic steatorrhoea.

McCarthy, C. F.; Fraser, I.D.; Evans, Kambria H.; Read, A. E.

doi:10.1136/gut.7.2.140

Cited by 117 publications

(38 citation statements)

References 26 publications

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“…This is indicated by the small spleen that may be found in adult coeliac disease and by the signs of splenic atrophy which are recognised in the blood, the presence of Howell-Jolly bodies being particularly striking. McCarthy et al (1966) have shown that there is a reduction in periph eral lymphoid tissue and it has also been shown that the lymphocytes in coeliac patients may show impaired transformation, whether they be circulating lym phocytes (Blecher et al, 1969) or lymphocytes teased out from mesenteric lymph nodes (Housley et al, 1969). All these findings suggest lymphoreticular dysfunction and this is supported by studies of the immunoglobulins in coeliac disease (Hobbs and Hepner, 1968) which have shown reduced levels of IgM in 60% of untreated patients.…”

Section: Immunological Abnormalities In Coeliac Diseasesupporting

confidence: 69%

Coeliac Disease

Booth¹

1977

Ann Nutr Metab

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In coeliac disease there is an abnormality of the intestinal mucosa which is caused by ingesting gluten. The intestinal lesion affects predominantly the proximal small intestine and the ileum is either normal or less severely involved than the jejunum. In some cases adaptive changes occur in the ileum, producing enhanced absorption in that region when there is malabsorption in the jejunum. The characteristic absorptive abnormality in coeliac disease is therefore jejunal malabsorption and Heal hyperabsorption. When such a situation develops it is possible that an individual with a flat jejunal mucosa may develop no symptoms of the disease, since the adaptive changes in the ileum compensate for the jejunal lesion. This may explain why in Western society there are probably more cases of coeliac disease undiagnosed in the community than have been treated by their doctors. The basic lesion in coeliac disease appears to be genetically determined and it is likely to be a failure to clear antigen which normally enters the lamina propria of the gut resulting in the formation of immune complexes with complement fixation at gut level.

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Section: Immunological Abnormalities In Coeliac Diseasesupporting

confidence: 69%

Coeliac Disease

Booth¹

1977

Ann Nutr Metab

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“…Despite the low concentration of IgM in serum, and despite the detection of decreased total body synthesis of IgM in this disease, as determined by turnover studies (24), the number of intestinal mucosal plasma cells containing IgM was found to be increased (20). The concentration of IgM in serum does not appear related to the severity of the disease (19,22) or to the presence of splenic atrophy (24,25).…”

Section: Discussionmentioning

confidence: 75%

Incorporation of l-leucine-14C into immunoglobulins by jejunal biopsies of patients with celiac sprue and other gastrointestinal diseases

Loeb¹,

Strober²,

Falchuk³

et al. 1971

J. Clin. Invest.

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“…The prevalence of hyposplenism in coeliac disease is disputed, ranging from 16% (McCarthy et al, 1966) to 77% (O'Grady et al, 1984). Its aetiology is unknown but the present case illustrates that these patients are at risk of overwhelming sepsis.…”

Section: Discussionmentioning

confidence: 99%