Gastro Intestinal Manifestations of Diabetes Mellitus

Dysfunction of the autonomic nervous system is a well established long term complication of diabetes mellitus. Moreover, autonomic innervations is essential for appropriate functioning of the gastrointestinal tract, (GI), including the synchronicity between the motility induced peristaltic movement and the sphincters as well as the secretary capacity of the GI glands, i.e. salivary glands, pancreas, gallbladder. Therefore, several patients with diabetes mellitus of prolonged duration manifest chronic and recurrent clinical features related to the disordered motility of almost the whole GI tract including esophageal as well as epipharyngeal dysphagia, gastroparesis, constipation, diarrhoea, and fecal incontinence. Finally, acute cholecystitis secondary to biliary calculi or sometimes even in the absence of calculi, i.e. acalculus cholecystitis secondary to atonic gallbladder and dysfunction of the sphincter of Oddie, pancreatic maldigestion due to decreased secretion of pancreatic enzymes are also known to occur more frequently in subjects with diabetes when compared to the normal population. Alternatively, transient reversible disorders of gastrointestinal motility also occur during acute metabolic complications such as diabetic ketoacidosis and the hyperglycemic hyperosmolar state and are attributed to dehydration, altered acidbase status as well as imbalance of serum electrolytes secondary to urinary losses induced by osmotic diuresis. Therapeutic strategies in the management of chronic recurrent manifestations secondary to autonomic dysfunction include dietary manipulations, and several drugs including dopamine antagonists, antibiotics as well as hormones facilitating peristalsis. On the other hand, the gastrointestinal manifestations that occur during acute metabolic complications are self limited and respond promptly following restoration of a normal