Domperidone; secretion in breast milk and effect on puerperal prolactin levels

Hofmeyr, G Justus; Iddekinge, B. Van; Blott, J. A.

doi:10.1111/j.1471-0528.1985.tb01065.x

Cited by 53 publications

(32 citation statements)

References 14 publications

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“…Separate studies with intramuscular or oral domperidone indicated that the drug had the same potency as metoclopramide in inducing prolactin release. [102][103][104] Based on these findings, it is unlikely that the different prolactin levels caused by the various antagonists are due to different affinities at the dopamine D 2 receptor, as domperidone and clebopride have comparable affinities (see Table 1) 1 . It is also unlikely that the various antagonists can differently modulate the release of dopamine from the tuberoinfundibular pathway, as dopamine D 2 autoreceptors are absent in this pathway.…”

Section: Hyperprolactinaemiamentioning

confidence: 98%

Clinical implications of enteric and central D₂ receptor blockade by antidopaminergic gastrointestinal prokinetics

Tonini

Cipollina

Poluzzi

et al. 2004

Aliment Pharmacol Ther

256

207

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SUMMARYAntidopaminergic gastrointestinal prokinetics (bromopride, clebopride, domperidone, levosulpiride and metoclopramide) have been exploited clinically for the management of motor disorders of the upper gastrointestinal tract, including functional dyspepsia, gastric stasis of various origins and emesis. The prokinetic effect of these drugs is mediated through the blockade of enteric (neuronal and muscular) inhibitory D 2 receptors. The pharmacological profiles of the marketed compounds differ in terms of their molecular structure, affinity at D 2 receptors, ability to interact with other receptor systems [5-hydroxytryptamine-3 (5-HT 3 ) and 5-HT 4 receptors for metoclopramide; 5-HT 4 receptors for levosulpiride) and ability to permeate the bloodbrain barrier (compared with the other compounds, domperidone does not easily cross the barrier). It has been suggested that the serotonergic (5-HT 4 ) component of some antidopaminergic prokinetics may enhance their therapeutic efficacy in gastrointestinal disorders, such as functional dyspepsia and diabetic gastroparesis. The antagonism of central D 2 receptors may lead to both therapeutic (e.g. anti-emetic effect due to D 2 receptor blockade in the area postrema) and adverse (including hyperprolactinaemia and extrapyramidal dystonic reactions) effects. As the pituitary (as well as the area postrema) is outside the blood-brain barrier, hyperprolactinaemia is a side-effect occurring with all antidopaminergic prokinetics, although to different extents. Extrapyramidal reactions are most commonly observed with compounds crossing the blood-brain barrier, although with some differences amongst the various agents. Prokinetics with a high dissociation constant compared with that of dopamine at the D 2 receptor (i.e. compounds that bind loosely to D 2 receptors in the nigrostriatal pathway) elicit fewer extrapyramidal signs and symptoms. A knowledge of central and peripheral D 2 receptor pharmacology can help the clinician to choose between the antidopaminergic prokinetics to obtain a more favourable risk/ benefit ratio.

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Section: Hyperprolactinaemiamentioning

confidence: 98%

Clinical implications of enteric and central D₂ receptor blockade by antidopaminergic gastrointestinal prokinetics

Tonini

Cipollina

Poluzzi

et al. 2004

Aliment Pharmacol Ther

256

207

View full text Add to dashboard Cite

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“…In another study the same authors found that the concentrations in serum and in milk to be 8.0 and 0.24 ng/ml, respectively, with an M/P ratio of 0.03, 2 h after the administration of a single dose of 20 mg of domperidone. At 4 h post-dose the M/P ratio was 1.1 (32). After 5 days of treatment with domperidone (10 mg 3 times a day) Da Silva et al found an average serum and milk concentrations of 6.6 and 1.2 ng/ml respectively, with an M/P ratio of 0.18.…”

Section: Mechanism Of Actionmentioning

confidence: 99%

“…No of side effects has been reported in the infants whose mothers take domperidone (31,32,40,41). Mothers with cardiac diseases should avoid using this drug due to potential arrythmia (43).…”

Section: Side Effects For Mother and For Infantmentioning

confidence: 99%

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Safety and Efficacy of Galactogogues: Substances that Induce, Maintain and Increase Breast Milk Production

Zuppa¹,

Sindico²,

Orchi³

et al. 2010

J Pharm Pharm Sci

166

168

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Poor production of breast milk is the most frequent cause of breast lactation failure. Often, physician prescribe medications or other substances to solve this problem. The use of galactogogues should be limited to those situations in which reduced milk production from treatable causes has been excluded. One of the most frequent indication for the use of galactogogues is the diminution of milk production in mothers using indirect lactation, particularly in the case of preterm birth. The objective of this review is to analyze to the literature relating to the principal drugs used as galactogogues (metoclopramide, domperidone, chlorpromazine, sulpiride, oxytocin, growth hormone, thyrotrophin releasing hormone, medroxyprogesterone). Have been also analyzed galactogogues based on herbs and other natural substances (fenugreek, galega and milk thistle). We have evaluated their mechanism of action, transfer to maternal milk, effectiveness and potential side effects for mother and infant, suggested doses for galactogogic effect, and recommendation for breastfeeding.

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“…Domperidone administration is well known to induce hyperprolactinemia. This effect is attributable to domperidone blockade of pituitary dopamine D 2 receptors [24,25,[29][30][31][32][33] .…”

Section: Discussionmentioning

confidence: 99%

Dual Effects of Hyperprolactinemia on Carrageenan-Induced Inflammatory Paw Edema in Rats

Ochoa-Amaya

Malucelli

Cruz‐Casallas

et al. 2011

Neuroimmunomodulation

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Objectives: The effects of short-term 5-day and long-term 30-day hyperprolactinemia induced by domperidone (1.7 mg/kg/day, s.c.) or ectopic pituitary graft on the acute inflammatory response induced by carrageenan were evaluated in male rats. Both models of hyperprolactinemia effectively increased serum prolactin (PRL) levels. Methods: The volume in milliliters of inflammatory edema was measured by plethysmography 1, 2, 3, 4, 6, 8 and 24 h after carrageenan injection. The areas under the inflammatory time-response curves were compared. Additionally, the effects of hyperprolactinemia on body weight and serum corticosterone levels were evaluated. Results: In both domperidone-treated and pituitary graft-implanted animals, short-term 5-day hyperprolactinemia increased the inflammatory response, while long-term 30-day hyperprolactinemia had anti-inflammatory effects. Body weight was not affected by either short- or long-term hyperprolactinemia. Conclusion: These results show that PRL has biphasic effects on the carrageenan-induced inflammatory response.

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Domperidone; secretion in breast milk and effect on puerperal prolactin levels

Cited by 53 publications

References 14 publications

Clinical implications of enteric and central D₂ receptor blockade by antidopaminergic gastrointestinal prokinetics

Clinical implications of enteric and central D₂ receptor blockade by antidopaminergic gastrointestinal prokinetics

Safety and Efficacy of Galactogogues: Substances that Induce, Maintain and Increase Breast Milk Production

Dual Effects of Hyperprolactinemia on Carrageenan-Induced Inflammatory Paw Edema in Rats

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Domperidone; secretion in breast milk and effect on puerperal prolactin levels

Cited by 53 publications

References 14 publications

Clinical implications of enteric and central D2 receptor blockade by antidopaminergic gastrointestinal prokinetics

Clinical implications of enteric and central D2 receptor blockade by antidopaminergic gastrointestinal prokinetics

Safety and Efficacy of Galactogogues: Substances that Induce, Maintain and Increase Breast Milk Production

Dual Effects of Hyperprolactinemia on Carrageenan-Induced Inflammatory Paw Edema in Rats

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Clinical implications of enteric and central D₂ receptor blockade by antidopaminergic gastrointestinal prokinetics

Clinical implications of enteric and central D₂ receptor blockade by antidopaminergic gastrointestinal prokinetics