Pharmacomodulation of the Gut: Implications for the Enterally Fed Patient

Abstract

The level of nutrition support is mostly dictated by the functionality of the gastrointestinal tract. Native pathology and unavoidable iatrogenic disorders that affect gut function may be able to be managed via drug therapy so that the simplest level of enteral feeding may be used. Newer drug therapy modalities include the 5-hydroxytryptamine-3 (5-HT3) antagonists and propofol for nausea and vomiting, erythromycin for motility disorders, octreotide for refractory diarrhea, and naloxone for narcotic-induced constipation. The 5-HT3 antagonists have proven their superiority over all other agents for acute nausea and vomiting during highly emetogenic chemotherapy. Their use in anticipatory delayed nausea and vomiting in chemotherapy or with mild-to-moderate emetogenic chemotherapy is controversial. The use of 5-HT3 antagonists in postoperative nausea and vomiting is less clear. Propofol has demonstrated antiemetic properties, and its use as an anesthetic may decrease the incidence of nausea and vomiting and time in the recovery room. For both the 5-HT3 antagonists and propofol, costeffective analyses are important to determine their role in prevention of postoperative nausea and emetic events. Erythromycin has been used to attenuate motility disorders because it mimics motilin. In low doses, it may serve as an alternative to other promotility agents. Although pharmacologically similar to metoclopramide, it does not offer any advantage in an enteral feeding tube passage. Octreotide, a somatostatin analog, is being investigated to modulate endocrine function on the gastrointestinal tract and pancreas. Of note is its use in treating diarrhea associated with neuroendocrine tumors, acquired immunodeficiency syndrome, ileostomies, and chemotherapy. Finally, naloxone can reverse narcotic-induced constipation without interfering with effective pain management for most patients. This effect is due to antagonism of the gastrointestinal mu receptors by naloxone during its own absorption process and to a high first-passextraction for metabolism by the liver, which prevents appreciable systemic levels of this opioid antagonist.