The cause of severe diarrhea in patients with systemic amyloidosis is obscure.
In this study, researchers from Texas evaluated 3 patients to determine the mechanism of amyloid diarrhea.
The team measured the epithelial cell absorption rate of electrolytes during steady state GI perfusion of a saline-mannitol solution.
In addition, they simultaneously measured GI transit time of polyethylene glycol (PEG), and absorption of radio-labeled bile acid while subjects ingested 3 meals per day.
|25% of the polyethylene glycol ingested was recovered in stool in 45 minutes.|
|American Journal of Gastroenterology|
The team compared transit time and bile acid absorption in normal subjects with diarrhea caused by milk of magnesia (MOM) ingestion.
The researchers found that diarrhea could not be explained by malabsorption of ingested nutrients, bacterial overgrowth, bile acid malabsorption, or epithelial cell malabsorption of electrolytes.
However, they found that 25% of the PEG ingested was recovered in stool in 45 minutes. This is 10 times faster than in normal subjects with equally severe diarrhea caused by ingestion of MOM.
The team found that all of the patients had autonomic neuropathy that remained unrecognized for 15 to 36 months after onset of chronic diarrhea. This may have been the cause of rapid transit.
Dr Michael Guirl's team concluded, "Severe chronic diarrhea in 3 patients with systemic amyloidosis was mediated by extremely rapid transit of chyme and digestive secretions through the intestine".