Ipan

sensory

ACh/SubP/ CGRP

motor

VIP/ NOS/ ATP/PACAP

Ascending contraction

Descending relaxation

ACh/SubP/ CGRP

Descending relaxation distention by bolus distention by bolus

FIGURE 1 Control of gastrointestinal motility. Note the extrinsic or autonomic nervous system modulates the function of the enteric nervous system, which controls smooth muscle cells through transmitters. Source: From Ref. 72.

Ascending contraction gastroparesis and only 0.6% had nocturnal diarrhea. This discrepancy has been addressed in other community-based epidemiological studies, which are discussed below.

Kassender recognized asymptomatic gastric retention in diabetics in 1958 (7) and coined the term "gastroparesis diabeticorum". Since the original report, the term gastroparesis has been used to reflect symptomatic as well as asymptomatic gastric retention. However, the presence of GI symptoms in people with diabetic autonomic neuropathy is not necessarily related solely to delayed gastric emptying. More recently, the term "diabetic dyspepsia" was used to reflect the spectrum of postprandial symptoms in diabetics that are attributable to upper GI dysfunction, including those associated with delayed gastric emptying (8). Thus, while nausea, vomiting and early satiation after meals were the classical symptoms of gastroparesis, the term diabetic dyspepsia reflects in addition bloating, fullness and pain in the upper abdomen (8).

Constipation among diabetic patients reflects the common etiologies: impaired rectal evacuation, slow transit or normal transit constipation (9). The extrinsic parasympathetic supply to the colon forms the ascending intracolonic nerves and is a major excitatory mechanism inducing transit of stool in the colon.

The pathogenesis of chronic diarrhea in patients with diabetes is incompletely understood. Several mechanisms may contribute to the development of the condition including anorectal dysfunction, intestinal dysmotility, abnormal intestinal secretion, bacterial overgrowth, bile acid diarrhea and exocrine pancreatic insufficiency (10). Celiac disease, which has been reported with increased frequency in type 1 diabetes, may also contribute to diarrhea.

The term "diabetic diarrhea" was first coined in 1936 by Bargen (11) at the Mayo Clinic to describe unexplained diarrhea associated with severe diabetes. Typically, patients with

- Gall bladder motility antral hypomotility pylorospasm

Anorectal dysfunction sensory neuropathy IAS-sympathetic EAS-pudendal neuropathy

GI manifestation of diabetes

- Gall bladder motility antral hypomotility pylorospasm v a2-adrenergic tone in enterocytes

Small bowel (SB) dysmotility

Colonic dysmotility

Anorectal dysfunction sensory neuropathy IAS-sympathetic EAS-pudendal neuropathy

Associated disease

Exocrine pancreatic insufficiency

Celiac sprue SB bacterial overgrowth

Bile acid malabsorption

Clinical presentation

Gall stones Gastric stasis, bezoars

Diarrhea, steatorrhea

Gastric or SB stasis or rapid SB transit

Constipation, or diarrhea

Diarrhea or incontinence

FIGURE 2 Gastrointestinal manifestations of diabetes mellitus. Source: From Ref. 73.

diabetic diarrhea have poorly controlled diabetes and evidence of diabetic neuropathy, usually peripheral neuropathy and frequently autonomic neuropathy Diarrhea is often nocturnal and may be associated with anal incontinence. Episodes of diarrhea may be alternate with constipation or normal bowel movements. Symptoms of delayed gastric emptying such as early satiety, nausea and vomiting are often experienced by such patients with diarrhea.

Fecal incontinence is experienced by a substantial percentage of patients with chronic diabetes mellitus referred to tertiary referral centers. This does not necessarily correlate with the presence of diarrhea, although patients may sometimes describe fecal incontinence as "diarrhea". Fecal continence is maintained by the internal and external anal sphincters and the puborectalis sling, which maintains the rectoanal angulation. Anorectal sensation and reflex contractions of the sphincter mechanisms are essential for continence. Wald et al. (12) and Schiller et al. (13) have demonstrated that patients with diabetes and incontinence have a higher threshold (that is reduced sensation) for rectal perception of balloon distention when compared to continent diabetics and healthy controls. Patients with diabetes and incontinence also exhibit decreased resting anal sphincter pressure when compared to continent patients with diabetes. This reflects loss of sympathetic nerve supply to internal anal sphincter. Daytime fecal incontinence aggravated by urgency or raised intra-abdominal pressure is suggestive of external sphincter weakness and pudendal neuropathy.

In summary, diabetic constipation, diarrhea and incontinence refer to the occurrence of these symptoms in the absence of any disorder other than diabetes or neuropathy. For example, in patients with "diabetic diarrhea", associated conditions such as celiac sprue and bacterial overgrowth are excluded. These disturbances of lower bowel function are closely linked with autonomic neuropathy. For example, colonic transit delay may result in constipation secondary to loss of extrinsic or intrinsic neural control of the colon, and diarrhea may result from loss of a adrenergic "tone" in enterocytes. Incontinence may result from loss of sensation, impaired sympathetic supply to the internal anal sphincter, or loss of pudendal innervation of the external sphincter.

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