5-Hydroxyindoleacetic acid and substance P profiles in patients receiving emetogenic chemotherapy

Abstract

Laboratory studies provide additional evidence that serotonin and SP are involved primarily, though not exclusively, in acute and delayed vomiting, respectively.

Evidence for a Re-Evaluation of the Neurochemical and Anatomical Bases of Chemotherapy-Induced Vomiting

“…258 A recent clinical study supports the latter findings, since changes in the plasma SP concentration of patients receiving high dose cisplatin had a similar profile of increases in both acute and delayed phase chemotherapy-induced vomiting. 8 The observed changes in the least shrew study seem to be region specific, since the shrew frontal cortex SP concentration during the delayed phase was decreased, while duodenal concentrations were unaffected in either phase. The changes in intestinal SP turnover in the periphery may affect induction of vomiting since the gastrointestinal tract can be another potential anatomical substrate for emesis.…”

Chemotherapy agent cisplatin induces 48-h Fos expression in the brain of a vomiting species, the house musk shrew (Suncus murinus)

“…Cisplatin or humoral factors might activate the AP directly. For example, systemic injection of cisplatin increases plasma levels of substance P and 5-HT (23,41), possibly derived from release of these factors from enteroendocrine cells of the gut. Direct application of 5-HT and substance P can activate neurons in the AP, and intracerebroventricular injection of cisplatin in the cat can produce emesis (11,67).…”

Nausea and vomiting with high-dose chemotherapy and stem cell rescue therapy: a review of antiemetic regimens

“…The investigational arm should maximize coverage for delayed nausea and vomiting by using two doses of palonosetron combined with an NK1 antagonist given for multiple days, as in the Bubalo studies. Initial investigations suggest that substance P levels continue to rise after highly emetogenic chemotherapy; 24,32 daily doses of an NK1 receptor antagonist through day 4 following the stem cell infusion may help to counteract the delayed effects of the events occurring up to the day of the stem cell infusion, as in the Bubalo studies. 20,21 Minimizing CINV should be a reasonable goal for those receiving these highly emetogenic therapies.…”

“…22 A variety of other neurotransmitters are involved in CINV and the emetic reflex including dopamine, acetylcholine, endorphins, gamma-aminobutyric acid and histamine. [23][24][25] Many of the other agents used to control CINV target the release of these other substances, which then trigger the emetic reflex. However, other agents such as steroids have an unknown mechanism controlling CINV, particularly in the clinical situation of highly emetogenic cisplatin during which some patients benefit from steroids alone.…”