Slow and incomplete histological and functional recovery in adult gluten sensitive enteropathy.

Abstract

SUMMARY To assess the course of recovery ofgluten sensitive enteropathy in adults, histological and functional recovery was studied in 22 patients, aged 20-79 years. Biopsy specimens taken at the time of diagnosis were studied in 20; after adhering to a gluten free diet for nine to 19 (mean 14) months in 14; and after adhering to the same diet for 24-48 (mean 34) months in 10 patients. Histological recovery was assessed morphometrically in the proximal jejunum. Mucosal linings significantly improved over time, but did not completely return to normal with a gluten free diet: at diagnosis the surface:volume ratio was 22% of normal, increasing to 48% and 66% after nine to 19 and 24-48 months, respectively, ofa gluten free diet. Disaccharidase activities progressively increased. After 24-48 months maltase, sucrase, and isomaltase had returned to normal in the proximal jejunum; they were still significantly decreased in the distal duodenum. Duodenal and jejunal lactase activities were both below normal after 24 to 48 months.It is concluded that recovery of the intestinal mucosa of adults with gluten sensitive enteropathy during a gluten free diet continues beyond nine to 19 months and is still incomplete after two to four years. The recovery of disaccharidase activities extends from the distal to the proximal part of the small intestine, and is aligned to histological recovery.Gluten sensitive enteropathy or coeliac sprue is characterised by severe villous atrophy of the small intestinal mucosa; it responds favourably to the withdrawal of dietary gluten. Gross villous architecture and absorptive cells are severely damaged, and many enzymes, necessary for the digestive-absorptive process, are severely depleted. This is especially true for brush border enzymes like the disaccharidases maltase, sucrase, isomaltase, and lactase. To what degree the mucosa will recover during a gluten free diet is still a matter ofcontroversy: morphological changes occur and disaccharidases increase after gluten withdrawal. Most investigators have found that although some patients show complete histological and functional recovery during the diet, most still show some degree of histological and functional damage, even after adhering to the diet for several years.'Within days or weeks of starting a gluten free diet a clinical response can be detected. This is also true for some of the histological and functional abnormalities: soon after gluten withdrawal the height ofthe mucosal surface cells increases6 and partial return to normal of organelles is observed.7 The recovery of the villous Accepted for publication 17 March 1988 architecture is known to occur much more slowly, but so far no studies have emphasised the course of this slow recovery. Little is known with certainty about the rate and course of recovery of the disaccharidases and other brush border enzymes.There is good evidence to suggest that the most severe histological damage is found in the proximal small intestine in untreated coeliac disease28 and that during treatment, t...

Clinical and Immunologic Features of Ultra-Short Celiac Disease

“…21 Furthermore the gluten load is known to be highest in the proximal small bowel and there is evidence that the small bowel heals distally to proximally on a gluten free diet. 22,23 Some of the patients USCD group had Marsh 1 and 2 changes in more distal biopsies. These patients could be considered to belong to the celiac disease spectrum however these changes are non-specific.…”

Celiac disease in the Red Sea state of Sudan

“…28 However, complete histological resolution of small bowel inflammation may take up to 2 years in some individuals. 29 It can be challenge to avoid gluten in eastern Sudan. Poverty and ignorance are the major obstacles in such developing regions.…”

Involvement of macrophage migration inhibitory factor gene in celiac disease susceptibility

“…[18][19][20] Our data suggest that the reported MIF levels would not be a consequence of the inflammatory process, but they would be directly involved in the etiology of the disease. Functional studies on the role of the polymorphisms tested have been performed in the past with controversial findings reported in different cell types; [21][22][23] however, the (CAAT) 5 allele was associated with reduced basal and serum/forskolin-stimulated transcriptional activity in vitro [21][22][23] and the (CAAT) 7 and À173C alleles emerged as probable upregulators of transcriptional activity.…”