Summary A retrospective clinical study was done of 38 infants with temporary monosaccharide intolerance who were admitted to hospital between November 1976 and August 1978. There were two clinical groups. Group 1 consisted of 31 infants who developed monosaccharide intolerance as a sequela to acute gastroenteritis (i.e., 4% of infants admitted with acute gastroenteritis). Rotavirus was the cause of gastroenteritis in 64% of cases of monosaccharide intolerance. Monosaccharide intolerance was easily managed by dietary manipulations and lasted a mean of 2.5 days. Group 2 consisted of seven infants who developed monosaccharide intolerance during the course of protracted diarrhoea. The monosaccharide in‐tolerance lasted up to 70 days, with a mean of 21 days, and required a period of total bowel rest followed often by complicated dietary manipulation.
Findings The patient ruptured the Achilles tendon working as a nurse and underwent an orthopaedic surgery primary repair. At 6 months post operatively the patient had developed chronic tendinopathy affecting over 80% of the Achilles tendon. The patient was referred for opinion and had been off work for over 6 months with limitation in activities of daily living. The patient underwent a surgical excision of a posterior calcaneal exostosis and debridement of the diseased Achilles tendon and harvest of tenocytes. 13 weeks postsurgery the tenocytes were injected into the Achilles tendon. The patient returned to full time work and normal activities of daily living at 8 weeks post injection. MRI studies were performed pre and post injection to assess diseased state of the tendon. Conclusions Autologous tenocyte injection provides the clinician with a tool for treatment of chronic tendinopathy, where other treatment options have failed.
Three children aged between 7 and 11 years, after an acute onset of diarrhoea and vomiting, developed protracted diarrhoea and severe loss of weight. None had been abroad. No significant aetiological agent was found. There was evidence of acute inflammatory disease on proximal small intestinal biopsy, and some evidence of more widespread gut involvement--of the rectum in Cases 1 and 2, and the terminal ileum in Cases 2 and 3. The disease resolved spontaneously and without relapse.
A retrospective clinical study was done of 38 infants with temporary monosaccharide intolerance who were admitted to hospital between November 1976 and August 1978. There were two clinical groups. Group 1 consisted of 31 infants who developed monosaccharide intolerance as a sequela to acute gastroenteritis (i.e., 4% of infants admitted with acute gastroenteritis). Rotavirus was the cause of gastroenteritis in 64% of cases of monosaccharide intolerance. Monosaccharide intolerance was easily managed by dietary manipulations and lasted a mean of 2.5 days. Group 2 consisted of seven infants who developed monosaccharide intolerance during the course of protracted diarrhoea. The monosaccharide intolerance lasted up to 70 days, with a mean of 21 days, and required a period of total bowel rest followed often by complicated dietary manipulation.
A new test for the detection of antibodies to gliadin in the sera of children who are gluten sensitive is described. This test is based on the observation that wheat protein binds selectively to connective tissue fibres in cryostat sections of mammalian tissues. Sera containing antibodies to gliadin give a reticulin pattern of staining on section pretreated with wheat gliadin if tested by indirect immunofluorescence. Antibodies to gliadin were detected in this manner in sera fom all of 32 children with coeliac disease, in 16 of whom a provisional diagnosis had been given and in 16 an established diagnosis confirmed by gluten challenge. The incidence of reticulin antibodies detected on untreated sections (in the absence of gliadin) was only 28%. Gliadin antibodies were also present in sera from 15% of 152 children with gastroenterological disorders other than coeliac disease, but most of these non-positive results for coeliac disease were in patients with transient gluten in tolerance, cows9 milk-sensitive enteropathy, or Crohn9s disease. This new test, although not specific for coeliac disease, promises to be of value as an indicator of gluten sensitivity, and when negative excludes a diagnosis of coeliac disease. It may also be useful in monitoring diet, and in determining when rebiopsy after gluten challenge in appropriate.
CMPI is a 20 th century disease. Until fairly recently it was not possible to feed safely large numbers of young infants other than by human breast milk. In our time, however, cow's milk protein is quantitatively the most important dietary protein in young infants.
Two hundred and seventy-eight duodenal biopsy specimens taken consecutively from children using either a single port paediatric Crosby capsule or a double port modification were examined both histologically and by dissecting microscopy, in order to determine the incidence of patchy mucosal lesions. One hundred and six specimens were abnormal and 49 of these were patchy. Patchy lesions occurred most commonly in cow9s milk sensitive enteropathy where 66% of 33 specimens were patchy; in comparison all children with undiagnosed coeliac disease taking a normal diet showed a uniformly flat mucosa. Twenty-two per cent of specimens taken using the double port and 10% using the single port capsule were patchy, a statistically significant difference (P = 0.01) using standard errors. Where lesions were uniform, grading by dissecting microscopy correlated well with histological grading; 18 (37%) of specimens were, however, recognised as patchy only on gross appearance. The high incidence of patchy lesions of the proximal small intestine reflected the prevalence of cow9s milk protein intolerance and the postenteritis syndrome in these children. The use of the double port capsule and of dissecting microscopy also contributed to the high incidence found.
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