Traditionally, gastrointestinal symptoms have been attributed to disordered motor function resulting from autonomic (vagal) neuropathy. More recently, impaired sensory function has been implicated as a trigger for gastrointestinal symptoms in dyspeptic patients. However, the predictive value of these abnormalities for the induction of chronic gastrointestinal symptoms is unknown.
A number of studies have shown that acute changes in blood glucose concentrations can have a profound effect on motor function throughout the gastrointestinal tract in both normal subjects and patients with diabetes mellitus. Recent studies have demonstrated that the blood glucose concentration may also modulate the perception of sensations arising from the gastrointestinal tract.
However, there is relatively little information about the mechanisms mediating the effects of the blood glucose concentration on gastrointestinal motility. While some studies have implicated impaired glycaemic control in the genesis of chronic gastrointestinal symptoms, this remains controversial.
Psychological factors may play a role in the generation and maintenance of gastrointestinal symptoms in the general population. Psychological factors are associated with both the symptoms of irritable bowel syndrome (IBS) and health care seeking by IBS sufferers. For example, patients with IBS have higher frequencies of psychiatric diagnoses and personality disturbances, such as neuroticism, than healthy volunteers. Further, those who see doctors for their IBS symptoms (consulters) appear to be psychologically more disturbed than those who did not seek medical attention (nonconsulters).
Psychological disorders are common in diabetics and psychological distress and poor glycaemic control are closely associated. It has thus been suggested that depression and hyperglycaemia may exacerbate one another. In patients with type 1 diabetes, abnormal anxiety ratings could be identified in up to 13% and psychological abnormalities were related to age and social class, but not to duration of diabetes or glycaemic control.
Moreover, in elderly patients with type 2 diabetes (mean age 70 years), mental distress (defined as an elevated score in a 12-item version of the General Health Questionnaire) and depression were associated with peripheral neuropathy, which may reflect worse metabolic control in the group who had depression. The presence of affective and anxiety disorders has also been associated with gastrointestinal motility abnormalities in diabetic and non-diabetic subjects.
Thus, out of 15 patients with diabetes mellitus who were found to have contraction abnormalities in the oesophageal body, such as an increased amplitude or abnormal motor response to swallowing, 13 (87%) had a psychiatric diagnosis.
It remains uncertain whether and to what extent psychological factors account for gastrointestinal symptoms in type 1 or type 2 diabetes mellitus, as this has not been systematically studied. Psychological distress could be the result of having a chronic illness and hence any association with symptoms could be spurious.
However, Clouse and Lustman found that psychiatric disturbances were more strongly related to gastrointestinal symptoms than autonomic neuropathy.
Helicobacter pylori infection
Helicobacter pylori causes chronic histological gastritis which can progress to gastric atrophy. H. pylori is now established to be a cause of chronic peptic ulcer and is classified as a class 1 carcinogen by the World Health Organisation.
An impaired immune response in diabetes that alters both humoral and cellular immunity, and the high prevalence of upper gastrointestinal symptoms described in some studies, have led to speculation that H. pylori may be linked to diabetes. In a recent Italian study, patients with diabetes with dyspepsia had a higher prevalence of H. pylori infection compared to dyspeptic controls. In another study, De Luis et al. reported that the seroprevalence of H. pylori increased with increasing duration of diabetes in patients with type 1 diabetes. However, others have failed to demonstrate any association between H. pylori and gastrointestinal symptoms in diabetes. Moreover, no studies have adequately assessed whether cure of H. pylori reverses upper gastrointestinal symptoms in diabetes.