Prevalence of Gastrointestinal Symptoms in Children and Adolescents With Type 1 Diabetes
- 1Department of Pediatrics, Faculty of Nursing, University of Athens, P & A Kyriakou Children’s Hospital, Athens, Greece
- 2Institute of Child Health, University of Birmingham, Birmingham, U.K.
A wide variety of gastrointestinal (GI) symptoms have been reported to occur in adults with type 1 diabetes (1). Autonomic neuropathy or acute hyperglycemia have been implicated in the pathogenesis (2,3). In children with type 1 diabetes, GI symptoms are also frequently observed, although their prevalence and impact on glycemic control are poorly defined (4,5). The aims of this study were to determine the prevalence of GI symptoms in children and adolescents with type 1 diabetes and to assess their effect on diabetes control.
The study group was comprised of 118 consecutive children and adolescents (57 males, mean age 14.5 years and mean BMI 20.3 kg/m2) with type 1 diabetes (median duration of disease 5.2 years) attending the Diabetes Center for regular follow-up. The control group was comprised of 171 children and adolescents (75 males, mean age 13.6 years and mean BMI 20 kg/m2) who were either siblings of hospitalized children or patients with type 1 diabetes or offspring of the hospital staff. The sample size was calculated using the power analysis aimed at detecting an anticipated difference in the prevalence of GI symptoms ≥15% (α = 0.05 and power = 0.8). The study was approved by the Ethics Committee of the P & A Kyriakou Children’s Hospital, Athens, Greece.
The existence, frequency, and nature of GI symptoms in the control subjects and patients with type 1 diabetes were recorded after a single researcher interviewed the patients and their parents using a standard questionnaire. Recurrent abdominal pain (RAP), chronic dyspepsia (CD), and chronic constipation (CC) were defined according to previously published definitions. Weight, height, insulin requirements, and HbA1c were recorded. HbA1c concentrations at the previous three visits were also recorded. Nutritional status was expressed as BMI. Helicobacter pylori serum antibodies were detected by enzyme-linked immunosorbent assay. All of the seropositive patients were further investigated with upper-GI endoscopy and biopsies.
A total of 63 (36.8%) control subjects and 53 (44.9%) patients with type 1 diabetes manifested GI symptoms (P = 0.17). RAP, CD, and CC were present in 24 (20.8%), 14 (11.8%), and 19 (16.1%) of the type 1 diabetic patients compared with 23 (13.5%), 18 (10.5%), and 32 (18.7%) of the control subjects, respectively (P = 0.12, 0.52, and 0.57, respectively).
Patients with type 1 diabetes who manifested GI symptoms were comparable with patients who did not with respect to age, sex, duration of diabetes, BMI, insulin requirements, and mean HbA1c (last year) or current HbA1c levels (Table 1). The same was true for the various subgroups of patients with type 1 diabetes with and without RAP, CD, or CC.
Positive serum antibodies (both IgG and IgA) for H. pylori were detected in eight of the control subjects, all of whom had RAP, and in eight of the patients with type 1 diabetes (six with RAP and two with CD). The prevalence of antibody positivity was similar in control subjects and patients with type 1 diabetes (P = 1.00). H. pylori gastritis was diagnosed in all of the above 16 patients, by endoscopy and biopsies. No differences were found between type 1 diabetic children with and those without H. pylori gastritis with respect to duration of type 1 diabetes, BMI, insulin requirement, fasting glucose level, and HbA1c concentration. Furthermore, the 2-week treatment of H. pylori gastritis with clarithromycin (15 mg · kg–1 · day–1), metronidazole (20 mg · kg–1 · day–1), and omeprazole (1 mg · kg–1 · day–1) did not affect HbA1c concentration: the mean ± SD HbA1c pre- and 3 months posttreatment were 8.6 ± 2.2 vs. 7.8 ± 1.5%, respectively (P = 0.1).
The prevalence of CD and CC in adult patients with type 1 diabetes is controversial. Some researchers report increased prevalence of GI symptoms (1), whereas others do not (6). To our knowledge, this is the first controlled study to assess the prevalence of GI symptoms in children and adolescents with type 1 diabetes. Very few uncontrolled studies in children with type 1 diabetes focused on acid peptic disease (4,5).
In agreement with previous studies in adults, the current study showed that the prevalence of RAP was comparable between patients with type 1 diabetes and healthy control subjects (6). Furthermore, the frequency of H. pylori gastritis was similar in diabetic and nondiabetic children with RAP and/or CD, a finding in agreement with that previously reported in adult patients with diabetes (7). In an uncontrolled study, Burghen et al. (5) recently reported an increased (7%) prevalence of acid peptic disease in children with diabetes. According to the authors, children with peptic disease had poorer glycemic control and linear growth. We were unable to show any differences in nutritional status, insulin requirement, or HbA1c concentration between patients with type 1 diabetes who had H. pylori gastritis and those patients who did not. Furthermore, in agreement with Burghen’s study (5), our study showed that the treatment of H. pylori gastritis did not improve HbA1c concentration.
Poorer glycemic control in patients with diabetes and chronic dyspepsia has been attributed to gastric emptying delay, causing mismatch between the onset of insulin action and the absorption of carbohydrates. It should be noted, however, that gastric emptying delay does not occur in all of the patients with RAP and/or CD. In a large study in dyspeptic nondiabetic adults, gastric emptying of a solid meal, assessed by gastric scintigraphy, was reported to be normal in all of the dyspeptic patients who presented with epigastric pain and impaired in only 42% of dyspeptic patients with postprandial fullness and early satiety (8). Therefore, further studies assessing both GI motility in type 1 diabetic children with individual GI symptoms and the impact of possible motility abnormalities on glycemic control are required.
In conclusion, GI symptoms are as frequent in children with type 1 diabetes as in the general population and have no impact on diabetes control. The treatment of H. pylori gastritis does not affect glycemic control. GI symptoms in patients with type 1 diabetes should be investigated and treated as indicated in the nondiabetic individuals.
We acknowledge the valuable contribution of the statistician E. Kazazis.
Address correspondence and reprint requests to Dr. Andriani Vazeou, P.O. Box 17177, GR-10024, Athens, Greece. E-mail:.