Autonomic neuropathy is the main pathogenetic suspect. Neuropathological esophageal abnormalities have been reported by Smith (8), who observed swelling, irregularity of caliber, and disruption of parasympathetic fibers in the esophageal wall and in the extrinsic trunks. The myenteric plexus appeared normal except for a lym-phocytic infiltration within the ganglia. Hyperglycemia might also be involved, it will be shown later for a number of motor gut disturbances.
Esophageal motor dysfunction is common in patients with diabetes, but is usually asymptomatic (Table 1). The most frequent complaints are heartburn and dysphagia, but these symptoms are evidently nonspecific. Nishida et al. (9) reported that 25.3% of a group of 241 patients with diabetes mellitus had symptomatic gastroesophageal reflux disease (GERD) symptoms against 9.5% of a control group of patients with chronic hepatitis C. This figure approximates the 28% prevalence of abnormally elevated gastroesophageal reflux in diabetics, based on pHmetry studies, reported by Lluch et al. (10), although most patients in the latter group appeared to be asymptomatic. In any case, the presence of abnormal gastroesophageal reflux was associated with cardiovascular autonomic neurophathy (10). However, on the issue of reflux
Altered bowel habit
Gastric dysrhythmia, hypomotility
Incoordinated intestinal "bursts'
Fig. 1. Diagramatic representation of various gastrointestinal syndromes related to diabetes mellitus. Approximate symptom-regional relationships are noted.
Evaluation of Upper Gut Symptoms in a Patient With Diabetes
Esophageal symptoms Radiographic studies Endoscopy
Scintigraphy (esophageal transit or clearance) Esophageal manometry Psychological assessment Gastroparesis syndrome
Upper GI X-rays (only useful if showing manifest retention)
Gastroduodenoscopy, to exclude mechanical obstruction and to show retained residue Gastric emptying studies: radioscintigraphic (liquid and/or solid component); breath test;
ultrasound Upper gut manometry Electrogastrography (unproven reliability)
and autonomic neuropathy there are some conflicting reports. Jackson et al. (11) observed that among symptomatic GERD patients, those with diabetes mellitus often have normal 24-hour pHmetry, but abnormal autonomic functioning. In contrast to nondiabetics in whom the correlation between GERD symptoms and abnormal esophageal pHmetry is closer. It is quite possible that abnormal esophageal motility or sensitivity, or both, produce symptoms in diabetics with autonomic neuropathy that mimic acid reflux, but are not directly related to acid. This possibility should be considered in patients who do not respond as well as expected to antisecretory pharmacological therapy. These issues were also explored by Antwi et al. (12) who observed that endoscopic esophagitis was more prevalent among diabetics with auto-nomic neuropathy than without, whereas reflux like symptoms were similar with or without neuropathy. Further insight was provided by Kinekawa et al. (13) who showed that abnormal acid reflux on the basis of esophageal pHmetry correlated
with motor nerve conduction velocity, although not with the coefficient of variation of R-R intervals on the electrocardiogram.
Esophageal dysmotility usually consists of reduced or absent primary peristaltic waves, sporadic tertiary contractions, and delayed esophageal clearance. However, Loo et al. (14) were more impressed with the finding of multipeaked peristaltic wave complexes than with the aforementioned abnormalities, which they regarded as nonspecific. Esophageal motor dysfunction, measured manometrically, also appears to correlate with test evidence of neuropathy (13). Holloway et al. (15) explored the relationship between esophageal transit and esophageal dysmotility in patients with long-standing diabetes mellitus. He concurrently performed esophageal manometry and radionucleide transit measurement of solids and liquids in the esophagus. They observed a high prevalence of transit hold-ups in diabetics, significantly higher than in controls (both young and elderly, the latter being afflicted by a higher prevalence of dysmotility on account of presbiesophagus). The major mechanism responsible for esophageal bolus hold up in diabetics was peristaltic failure or focal low amplitude pressure waves, demonstrated manometrically.
Pitfalls in interpreting esophageal motor dysfunction as a cause of patients' symptoms do abound. A recent report of unsatisfactory symptomatic response to laparoscopic myotomy in a patient with diabetes with apparent achalasia diagnosed by manometry should be considered (16). Psychosomatic factors in the genesis of esophageal motor incoordination have also been postulated (17).
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