Clinical Information

The concentration of electrolytes in fecal water and their rate of excretion are dependent upon 3 factors:

-Normal daily dietary intake of electrolytes

-Passive transport from serum and other vascular spaces to equilibrate fecal osmotic pressure with vascular osmotic pressure

-Electrolyte transport into fecal water due to exogenous substances and rare toxins (eg, cholera toxin)

Fecal osmolality is normally in equilibrium with vascular osmolality, and sodium is the major effector of this equilibrium.(1) Fecal osmolality is normally 2 x (sodium + potassium) unless there are exogenous factors inducing a change in composition, such as the presence of other osmotic agents (magnesium sulfate, saccharides) or drugs inducing secretions, such as phenolphthalein or bisacodyl.

Chronic diarrhea with elevations in fecal chloride concentrations are caused by congenital chloridorrhea. This is a rare condition associated with a genetic defect in a protein responsible for transport of chloride ions across the mucosal membranes in the lower intestinal tract in exchange for bicarbonate ions. It plays an essential part in intestinal chloride absorption, therefore variants in this gene have been associated with congenital chloride diarrhea.(2.

Acquired chloridorrhea is a rare condition that has been described as causing profuse, chloride-rich diarrhea and a surprising contraction metabolic alkalosis rather than metabolic acidosis often associated with typical diarrhea. Contributors to acquired chloridorrhea include chronic intestinal inflammation and reduction of chloride/bicarbonate transporter expression in genetically susceptible persons post-bowel resection and ostomy placement. Acquired chloridorrhea is rare but may be an under-recognized condition in post-bowel resection patients.(3)