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PAEDIATRICS
868
PAEDIATRICS
Peptic disease and childhood diabetes Since the introduction of fibreoptic endoscopy, oesophagitis, gastritis, and peptic ulceration are more commonly sought and identified as causes of recurrent abdominal pain, vomiting, and upper gastrointestinal blood loss in children. The younger the patient, the less likely that the pain will be localised; irritability and change in feeding
pattern may be the sole manifestations in infants and young children. The causes of peptic disease in childhood are poorly understood. Helicobacter pylori is causally associated with primary antral gastritis, often together with primary peptic ulcer disease; this organism probably accounts for about half the cases of primary gastroduodenitis in childhood,l being less important in children younger than 10 years.2 The role of duodenogastric reflux of bile acids in primary gastritis has been firmly established, but there may be specific histological features in gastric tissue from patients with bile-induced gastritis.3 A fruitful area of research in this respect would be disorders of gut motility in children since bile reflux is more likely in such patients. Pre-endoscopy-era epidemiological data on the incidence of peptic disease in childhood are highly suspect and the indications for endoscopy remain poorly defined. One study4 reported a 3-fold increase in incidence in children after the introduction of fibreoptic endoscopy. Despite these uncertainties, most paediatricians agree that peptic disease in childhood is uncommon. The observation by Burghen and colleagues6 that the condition may be not
present in
as
many
as
7% of diabetic children is therefore
important. Until now the estimated incidence of peptic disease in patients of all ages with insulin-dependent diabetes (IDDM) was thought to be lower than normal, or at least not elevated. Reduced acid secretion, in response to hyperglycaemia, was believed to provide some protection against duodenal ulceration.7 In a study spanning about 3 years, Burghen et al questioned 429 patients aged 5-19 years to elicit symptoms suggestive of peptic disease. Endoscopy was done in the 31 (7-2%) who had had symptoms for over a month, and appearances suggestive of gastritis were found in 29. Macroscopic appearances were suggestive of oesophagitis in 4, and of duodenitis in 12. Ulcers were noted in 11, although their location was not specified. Duodenogastric reflux was common. One-third had evidence of delayed clearance of food eaten 12-t8 h before the procedure. Histological studies were done in 27, and were said to show evidence of gastritis in 25 children with macroscopic evidence of the condition, and in 1 with no such evidence of gastritis. Surprisingly, none had H pylori identified histologically. These data are startling in several respects. The point prevalence of peptic disease, according to their criteria, is very high in the children with IDDM-about 7%. The absence of H pylori may signify a different aetiology from the primary peptic disease in children without IDDM. Although the researchers did not find a significant difference in glycosylated haemoglobin concentrations between diabetes with and without peptic disease, other criteria for control of diabetes indicated that IDDM is harder to regulate in patients with peptic disease, and that treatment of the peptic condition was associated with improved diabetic control. The admission rate fell by over
50 % and the number of emergency hospital admissions also fell slightly in the 18 months after treatment of peptic disease. Poor linear growth was common before diagnosis of peptic disease and may have improved with treatment. The researchers suggest that abnormal gut motility as a consequence of even mild hyperglycaemia8 may be important in the aetiology of peptic disease in this population of children. This hypothesis is supported by published observations of impaired gastric motility at serum glucose concentrations exceeding 7-7 mmol/L, and subnormal plasma motilin concentrations when serum glucose exceeds 9-7 mmol/L.8 The practical message is that gastrointestinal symptoms such as abdominal pain that were previously thought to be due to poor diabetic control or impending ketoacidosis may be due to peptic disease, especially if they recur and persist beyond one month. Since peptic disease may adversely affect diabetic control, children IDDM with (and their parents), should be questioned carefully for relevant symptoms, with a view to further investigation by endoscopy if necessary.
Ian W. Booth Andrew R. Magnay 1.
Kilbridge PM, Dahms BB, Czinn SJ. Campylobacter pylori-associated gastritis and peptic ulcer disease in children. Am J Dis Child 1988; 142:
1149-52. 2. Fiedorek SC,
epidemiology
Malaty HM, Evans DL. Factors influencing of Helicobacter pylori in children. Pediatrics 1991;
the 88:
578-82. 3. Dixon MF, O’Connor HJ, Axon A, King RFJ, Johnston D. Reflux gastritis: distinct histopathological entity? J Clin Pathol 1986; 39: 524-30. 4. Tam PKH, Lau TK. Diagnosis of peptic ulcer in children: the past nd present. J Pediatr Surg 1986; 21: 15-16. 5. Eastham EJ. Peptic ulcer. In: Durie P, Walker W, Hamilton JR, Walker-Smith JA, Watkins JB, eds. Pediatric gastrointestinal disease. Part 1. Philadelphia: BC Decker, 1991: 438. 6. Burghen GA, Murrell LR, Whitington GL, Klyce MK, Burstein S. Acid peptic disease in children with type I diabetes mellitus: a complicating relationship. Am J Dis Child 1992; 146: 718-22. 7. Dotevall G. Incidence of peptic ulcer in diabetes mellitus. Acta Med Scand 1959; 164: 463-77. 8. Barnett JL, Owyang C. Serum glucose concentration as a modulator of interdigestive gastric motility. Gastroenterology 1988; 94: 739-44.
Dr Heikki Peltola, Children’s Finland
Hospital, University of Helsinki,
Dr Michael S.
Caplan, Department of Pediatrics, Evanston Hospital, Evanston, IL, USA
Dr William A.
Gray, Division of Cardiology, Presbyterian Hospitals, Albuquerque, NM, USA
Dr Steen Seier Poulsen, Institute of Medical Anatomy, of Copenhagen, Denmark
University
Hughes, Chief Science Editor, Oxford English Dictionary, Oxford University Press, UK
Mr Alan
Prof lan W. Booth and Dr Andrew R. Magnay, Institute of Child Health, University of Birmingham, UK
PAEDIATRICS
Peptic disease and childhood diabetes Since the introduction of fibreoptic endoscopy, oesophagitis, gastritis, and peptic ulceration are more commonly sought and identified as causes of recurrent abdominal pain, vomiting, and upper gastrointestinal blood loss in children. The younger the patient, the less likely that the pain will be localised; irritability and change in feeding
pattern may be the sole manifestations in infants and young children. The causes of peptic disease in childhood are poorly understood. Helicobacter pylori is causally associated with primary antral gastritis, often together with primary peptic ulcer disease; this organism probably accounts for about half the cases of primary gastroduodenitis in childhood,l being less important in children younger than 10 years.2 The role of duodenogastric reflux of bile acids in primary gastritis has been firmly established, but there may be specific histological features in gastric tissue from patients with bile-induced gastritis.3 A fruitful area of research in this respect would be disorders of gut motility in children since bile reflux is more likely in such patients. Pre-endoscopy-era epidemiological data on the incidence of peptic disease in childhood are highly suspect and the indications for endoscopy remain poorly defined. One study4 reported a 3-fold increase in incidence in children after the introduction of fibreoptic endoscopy. Despite these uncertainties, most paediatricians agree that peptic disease in childhood is uncommon. The observation by Burghen and colleagues6 that the condition may be not
present in
as
many
as
7% of diabetic children is therefore
important. Until now the estimated incidence of peptic disease in patients of all ages with insulin-dependent diabetes (IDDM) was thought to be lower than normal, or at least not elevated. Reduced acid secretion, in response to hyperglycaemia, was believed to provide some protection against duodenal ulceration.7 In a study spanning about 3 years, Burghen et al questioned 429 patients aged 5-19 years to elicit symptoms suggestive of peptic disease. Endoscopy was done in the 31 (7-2%) who had had symptoms for over a month, and appearances suggestive of gastritis were found in 29. Macroscopic appearances were suggestive of oesophagitis in 4, and of duodenitis in 12. Ulcers were noted in 11, although their location was not specified. Duodenogastric reflux was common. One-third had evidence of delayed clearance of food eaten 12-t8 h before the procedure. Histological studies were done in 27, and were said to show evidence of gastritis in 25 children with macroscopic evidence of the condition, and in 1 with no such evidence of gastritis. Surprisingly, none had H pylori identified histologically. These data are startling in several respects. The point prevalence of peptic disease, according to their criteria, is very high in the children with IDDM-about 7%. The absence of H pylori may signify a different aetiology from the primary peptic disease in children without IDDM. Although the researchers did not find a significant difference in glycosylated haemoglobin concentrations between diabetes with and without peptic disease, other criteria for control of diabetes indicated that IDDM is harder to regulate in patients with peptic disease, and that treatment of the peptic condition was associated with improved diabetic control. The admission rate fell by over
50 % and the number of emergency hospital admissions also fell slightly in the 18 months after treatment of peptic disease. Poor linear growth was common before diagnosis of peptic disease and may have improved with treatment. The researchers suggest that abnormal gut motility as a consequence of even mild hyperglycaemia8 may be important in the aetiology of peptic disease in this population of children. This hypothesis is supported by published observations of impaired gastric motility at serum glucose concentrations exceeding 7-7 mmol/L, and subnormal plasma motilin concentrations when serum glucose exceeds 9-7 mmol/L.8 The practical message is that gastrointestinal symptoms such as abdominal pain that were previously thought to be due to poor diabetic control or impending ketoacidosis may be due to peptic disease, especially if they recur and persist beyond one month. Since peptic disease may adversely affect diabetic control, children IDDM with (and their parents), should be questioned carefully for relevant symptoms, with a view to further investigation by endoscopy if necessary.
Ian W. Booth Andrew R. Magnay 1.
Kilbridge PM, Dahms BB, Czinn SJ. Campylobacter pylori-associated gastritis and peptic ulcer disease in children. Am J Dis Child 1988; 142:
1149-52. 2. Fiedorek SC,
epidemiology
Malaty HM, Evans DL. Factors influencing of Helicobacter pylori in children. Pediatrics 1991;
the 88:
578-82. 3. Dixon MF, O’Connor HJ, Axon A, King RFJ, Johnston D. Reflux gastritis: distinct histopathological entity? J Clin Pathol 1986; 39: 524-30. 4. Tam PKH, Lau TK. Diagnosis of peptic ulcer in children: the past nd present. J Pediatr Surg 1986; 21: 15-16. 5. Eastham EJ. Peptic ulcer. In: Durie P, Walker W, Hamilton JR, Walker-Smith JA, Watkins JB, eds. Pediatric gastrointestinal disease. Part 1. Philadelphia: BC Decker, 1991: 438. 6. Burghen GA, Murrell LR, Whitington GL, Klyce MK, Burstein S. Acid peptic disease in children with type I diabetes mellitus: a complicating relationship. Am J Dis Child 1992; 146: 718-22. 7. Dotevall G. Incidence of peptic ulcer in diabetes mellitus. Acta Med Scand 1959; 164: 463-77. 8. Barnett JL, Owyang C. Serum glucose concentration as a modulator of interdigestive gastric motility. Gastroenterology 1988; 94: 739-44.
Dr Heikki Peltola, Children’s Finland
Hospital, University of Helsinki,
Dr Michael S.
Caplan, Department of Pediatrics, Evanston Hospital, Evanston, IL, USA
Dr William A.
Gray, Division of Cardiology, Presbyterian Hospitals, Albuquerque, NM, USA
Dr Steen Seier Poulsen, Institute of Medical Anatomy, of Copenhagen, Denmark
University
Hughes, Chief Science Editor, Oxford English Dictionary, Oxford University Press, UK
Mr Alan
Prof lan W. Booth and Dr Andrew R. Magnay, Institute of Child Health, University of Birmingham, UK