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Secretory diarrhea is caused by abnormal ion transport across intestinal epithelial cells, which results in decreased ab-sorption, increased secretion, or both. It is typically caused by abnormal mediators, such as enteric hormones, bacterial en-terotoxins, or laxatives that affect intracellular levels of cAMP, cyclic guanosine monophosphate (cGMP), calcium, and/or protein kinase. These in turn cause a decrease in sodi-um chloride absorption or an increase in chloride secretion; the end result is increased water accumulation in the gut lumen. A classic example of secretory diarrhea is cholera. A toxin pro-duced by the organism binds to membrane receptors on entero-cytes, resulting in activation of guanine-nucleotide binding protein (G-protein) causing increased cAMP production. The increased concentration of cAMP inhibits the Na+/C1 co-transport mechanism, blocking NaC1 absorption, and at the same time induces chloride secretion by activating the C1-channel. These events can result in massive diarrhea, without evidence of cell injury, as shown by the ability of the cell to absorb Na+ if coupled to nutrients (Na+-glucose, Na+-amino acids). This is why cholera and other forms of secretory diar-rhea can be treated with oral solutions containing sodium and glucose.
Some of the causes of secretory diarrhea are listed in the Table(Table 2). In diseases such as celiac disease or any mal-absorptive syndrome, secretory and osmotic mechanisms coex-ist. For instance, fatty acids can inhibit fluid from both the small intestine and the colon, whereas bile acids can interfere with absorption of water and electrolytes or induce their secre-tion in the colon. Clinically, secretory diarrhea has two char-acteristics: @Diarrhea persists during fasting, and (2) the stool osmotic gap is small (< 50 mmol/L) because the product 2 (Na+ + K+ ) accounts for most of stool osmolality. Although these features are present in cases of pure secretory diarrhea, they may be absent when different mechanisms coexist.
TABLE 2 Classification of Diarrhea
| Type | Mechanism | Examples | Characteristics |
| Secretory | Increased secretion and/or de- | Cholera | Large volume,watery diarrhea. |
| creased absorption of Na+and | Vasoactive intestinal peptide- | No gas or pus | |
| C1- | secreting tumor | No solute gap | |
| Bile salt enteropathy | Little or no response to fasting | ||
| Fatly acid-induced diarrhea | |||
| Osmotic | Nonahsorbable molecules in gut | Lactose intolerance (lactase de- | Watery stool, no blood or pus |
| lumen | ficiency) | Improves with fasting | |
| Generalized malabsorption | Stool may contain fat globules or | ||
| (particularly carbohydrates) | meat fibers and may have an in- | ||
| Mg2+ -containing laxatives | creased solute gap | ||
| Inflammatory | Destruction of mucosa | Ulcerative colitis | Small frequent stools with blood and |
| Impaired absorpation | Shigellosis | pus | |
| Outpouring of blood, mucus | Amebiasis | Fever | |
| Decreased absorptive | Impaired reabsorption of dec- | Bowel resection | Variable |
| surface | trolytes and/or nutrients | Enteric fistula | |
| Motility disorder | Increased motility with decreased | Hyperthyroidism | Variable |
| time for absorption of dec- | Irritable bowel syndrome |
Malabsorption | |
| trolytes and/or nutrients | Scleroderma | ||
| Decreased motility with bacterial | Diabetic diarrhea | ||
| overgrowth |
