Delayed chemotherapy-induced nausea is augmented by high levels of endogenous noradrenaline

Fredrikson, Mats; Hursti, Timo; Steineck, Gunnar; Fürst, C J; Börjesson, Sara I.; Peterson, Curt

doi:10.1038/bjc.1994.364

Cited by 32 publications

(17 citation statements)

References 22 publications

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“…In fact, urinary cortisol excretion was inversely related and noradrenaline excretion was directly related to the intensity of chemotherapy-induced delayed nausea [7,8]. The anti-inflammatory properties of cortisol may act as an antiemetic by preventing the release of serotonin in the gut or preventing the activation of 5-HT3 receptors in the gastrointestinal system [7].…”

Section: Introductionmentioning

confidence: 99%

Delayed emesis: incidence, pattern, prognostic factors and optimal treatment

Roila

Donati

Tamberi

et al. 2002

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Delayed emesis has been arbitrarily defined as vomiting and/or nausea beginning, or persisting for, more than 24 h after chemotherapy administration. Acute emesis is the most important prognostic factor for delayed emesis. Owing to the relatively high incidence and severity all patients treated with cisplatin > or = 50 mg/m(2) should receive antiemetic prophylaxis. In these patients a combination of dexamethasone plus metoclopramide or a 5-HT3 antagonist is the most efficacious regimen. All patients submitted to moderately emetogenic chemotherapy, such as cyclophosphamide, carboplatin, doxorubicin and epirubicin, should also receive antiemetic prophylaxis with oral dexamethasone to prevent delayed emesis.

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Section: Introductionmentioning

confidence: 99%

Delayed emesis: incidence, pattern, prognostic factors and optimal treatment

Roila

Donati

Tamberi

et al. 2002

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“…The first group contains the type of cytostatics used, the combination of different drugs and the chemotherapy dose. The second group contains gender, age, history of alcohol intake, susceptibility for motion sickness, chemotherapy experience and biochemically measurable parameters such as noradrenaline (Fredrickson et al, 1994) and cortisol (Fredrickson et al, 1992;Hursti et al, 1993). However, methodological problems of the latter studies make it difficult to draw final conclusions regarding the relation between cortisol metabolism and emesis.…”

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confidence: 99%

5-Hydroxyindoleacetic acid (5-HIAA) and cortisol excretion as predictors of chemotherapy-induced emesis

Bois

Vach²,

Wechsel³

et al. 1996

Br J Cancer

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Summary This study evaluated the relationship between prechemotherapy cortisol and 5-hydroxyindoleacetic acid (5-HIAA) excretion and chemotherapy-induced emesis. The urinary excretion of cortisol and the serotonin metabolite 5-HIAA in the night before chemotherapy administration were measured in 28 and 49 female patients receiving > 300 mg m-2 carboplatin. Vomiting and nausea were documented over a 3 day observation period. Lower basal cortisol excretion was significantly correlated with vomiting with or without nausea occurring within the observation period. 5-HIAA showed only a weak correlation with emesis on days 1-3, but low 5-HIAA excretion was correlated with a higher proportion of patients vomiting on days 2 -3 following chemotherapy. Low basal cortisol excretion might be useful as a predictor for chemotherapy-induced emesis and therefore should be evaluated prospectively in future studies.Keywords: cortisol; 5-hydroxyindoleacetic acid (5-HIAA); vomiting; emesis; chemotherapy; carboplatin Vomiting and nausea are distressing side-effects of cytostatic drug treatment (Coates et al., 1983) and efficient anti-emetic prophylaxis is mandatory for the maintenance of life quality and the patients' compliance with chemotherapy. Cisplatin, carboplatin and cyclophosphamide are widely used cytostatics which possess a remarkable emetogenic potential. Treatment without anti-emetic prophylaxis leads to emesis in the majority of patients (Gralla et al., 1981;Martin et al., 1990;Beck et al., 1993). The combination of 5-hydroxytryptamine-3-receptor (5-HT3) antagonists with corticosteroids represents the most effective anti-emetic treatment in platinum-based and cyclophosphamide-based chemotherapy (Roila et al., 1991;Italian Group for Antiemetic Research, 1995). These clinical experiences as well as experimental data (Cubeddu et al., 1990;Schworer et al., 1991;Miner et al., 1987;Fredrickson et al., 1992) indicate a role for serotonin and corticosteroid metabolism in the pathophysiology of emesis. The mechanism of anti-emetic action of the 5-HT3 antagonists mainly reflects their capability of blocking 5-HT3 receptors which are believed to play a crucial role in the afferent part of the emetic reflex. The mechanisms of the antiemetic action of corticosteroids are still unclear: increased 5-HT turnover or reduced 5-HT synthesis (Young, 1981;Munck et al., 1984) or an affection of the permeability of the blood -brain barrier (Livera et al., 1985) The aim of this study was to evaluate the relation between pre-chemotherapeutic 5-HIAA and cortisol excretion levels and chemotherapy-induced emesis in carboplatin-treated female patients. This analysis should add information about the role of 5-HT and cortisol metabolism in the pathophysiology of chemotherapy-induced emesis. Methods PatientsA total of 54 patients who received a carboplatin-based chemotherapy regimen gave informed consent and were enrolled into the study. Five patients were excluded because they had failed to complete the 12 h urine collection. Data from 49 patients we...

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“…A Swedish study supports the involvement of the adrenergic system [11]. Pretreatment night-time adrenaline and noradrenaline levels were measured in patients receiving chemotherapy.…”

Section: New Perspectivesmentioning

confidence: 99%

New perspectives in antiemetic treatment

Herrstedt

1996

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Though antiemetic therapy has improved markedly in the past 15 years, patients still regard nausea and vomiting as two of the most distressing adverse events during chemotherapy. A major progress was the development of the serotonin3 (5-HT3) receptor antagonists. A possible antiemetic effect, achieved by interference with the "serotonergic system", is not restricted to antagonism at 5-HT3 receptors, however, but also includes agonism at 5-HT1A and 5-HT2 receptors, and serotonin synthesis inhibitors. The number of receptors thought to be involved in the emetic reflex has been augmented by neurokinin1 receptors with substance P as the preferred ligand. Animal studies have demonstrated a broad antiemetic profile of substance P antagonists. The somatostatin analogue octreotide has an antiemetic effect in patients with gastrointestinal obstruction, but has not been investigated against chemotherapy-induced emesis. The next few years will disclose, whether the efficacy and safety profiles of one or more of these drugs will make it clinically useful in the treatment of chemotherapy-induced nausea and vomiting.

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Delayed chemotherapy-induced nausea is augmented by high levels of endogenous noradrenaline

Cited by 32 publications

References 22 publications

Delayed emesis: incidence, pattern, prognostic factors and optimal treatment

Delayed emesis: incidence, pattern, prognostic factors and optimal treatment

5-Hydroxyindoleacetic acid (5-HIAA) and cortisol excretion as predictors of chemotherapy-induced emesis

New perspectives in antiemetic treatment

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