SUMMARY The cellobiose/mannitol (Ce/Ma) test is a non-invasive technique for investigating intestinal permeability. In coeliac disease there is a decreased absorption of small molecules and paradoxically increased absorption of large molecules. The simultaneous administration of cellobiose and mannitol as two probe molecules allows the permeability of the small bowel mucosa to be studied, eliminating extraneous factors such as gastric emptying, and incomplete urine collection. One thousand and ten patients presenting to a gastroenterology clinic with symptoms, signs, or biochemical indices compatible with coeliac disease had a Ce/Ma test. Eight hundred and seventeen had a normal test and of these 197 had a jejunal biopsy showing 148 normal mucosa, two coeliac disease, 43 non-specific abnormalities, four giardiasis. One hundred and ninety three had an abnormal test; of these 132 had a jejunal biopsy showing 62 normal mucosa, 48 coeliac disease, and 22 other abnormalities. Considering those who had jejunal biopsies, the sensitivity of the test for coeliac disease is 96%, specificity 70%, the predictive value of the positive 36%, and predictive value of the negative 99%. Eleven per cent of the patients with a 'false positive' test had abnormalities in the jejunal biopsy or a diagnosis which could explain the abnormal permeability.The Ce/Ma test is a non-invasive investigation of small bowel permeability. l 2 Cellobiose, a disaccharide (molecular radius 0.50 nm) and mannitol, a polyhydric alcohol (molecular radius 0-40 nm) are taken orally in hypertonic solution and a five hour urine collection is analysed for both probe molecules, the results being expressed as a ratio of the percentage recoveries.' In coeliac disease more cellobiose and less mannitol is absorbed than in normal subjects.' By expressing the results as a ratio there is good separation of coeliacs from normal subjects and the influence of certain non-intestinal factors acting similarly on both molecules such as renal impairment, gastric and bladder emptying and are eliminated.4Although results of the Ce/Ma test have been reported previously they relate to small numbers of
The cellobiose and mannitol differential sugar test is a non-invasive investigation of small bowel permeability, in which urinary recoveries of cellobiose and mannitol after a hyperosmolar oral load are expressed as a ratio to give a permeability index. Changes in the cellobiose:mannitol ratio often occur in coeliac disease, but some patients with abnormal permeability have normal jejunums by routine microscopy. Using computed morphometry the perimeter:lamina propria area index of jejunal biopsy samples was measured and compared with the cellobiose:mannitol ratio in three groups of patients: (i) those with coeliac disease with villous atrophy; (ii) those with normal jejunums and sugar test results: and (iii) those with normal jejunums but abnormal sugar test results. In addition to the expected difference in perimeter:lamina propria area index between patients with coeliac disease and those with normal findings (p less than 0.001), the index was also abnormal in patients with normal jejunums but abnormal sugar test results: (p less than 0.001 compared with group 1) and (0.01 greater than p greater than 0.001 compared with group 2). There was a significant overall correlation between the perimeter:lamina propria area index and cellobiose:mannitol ratio (p = 0.001). This study shows that computed jejunal morphometry can identify patients with subtle morphological changes that are related to abnormal intestinal permeability.
The pharmacokinetics of sulphasalazine and its principal metabolites in rheumatoid arthritis (RA) and inflammatory bowel disease (IBD) were compared. Patients with RA had a significantly greater concentration of plasma sulphapyridine than patients with IBD (medians 140 tg/ml and 7-4 pg/mI respectively). Patients with RA also tended to maintain a higher plasma sulphapyridine concentration with time, as determined by the area under the curve (AUC), but a lower plasma sulphasalazine AUC than patients with IBD. It is suggested that more sulphasalazine may be presented to the lower bowel for cleavage to sulphapyridine and 5-aminosalicylic acid in patients with RA than in IBD. Patients with RA may also have impaired metabolism of sulphapyridine as a consequence oftheir disease. Together these factors may contribute to higher peak circulating sulphapyridine concentrations and may be responsible for the higher incidence of side effects of sulphasalazine treatment in patients with RA than in patients with IBD.
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