D O M P E R I D O N E
Use of
Domperidone is a synthetic benzimidazole compound that is
used as a prokinetic agent for treatment of upper gastrointestinal
(GI) motility disorders and as an antiemetic. This compound also
is gaining popularity as a galactagogue. Domperidone is a specific
dopamine2 receptor (D2) antagonist that does not cross the blood-
brain barrier. It exerts its effect at peripheral D2 receptors in the
GI tract; the chemoreceptor trigger zone (CRT), which is outside
the blood-brain barrier; and the pituitary.1-4 The basic pharma-
cology of domperidone and its use as a galactagogue have been
reviewed in this journal and elsewhere.5-7 This article provides back-
ground information for use of domperidone as an antiemetic, with a
focus on Parkinsons disease, and as a prokinetic agent, with a focus
on diabetic gastropathy.
Domperidone as An Antiemetic
Background
Vomiting is an organized process that is coordinated by an area
of the medulla called the vomiting center or central pattern genera-
tor. The vomiting center receives input from several sources, in-
cluding the CRT, GI tract (stomach and small intestine), higher
cortical centers of the brain and the labyrinths, and orchestrates the
gastromotor functions that result in vomiting. Domperidones
action as an antiemetic is thought to stem from antagonism of D2
receptors at the CRT.1,3,8,9
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Domperidone
as a Prokinetic
and Antiemetic
Lisa M. Albright, PhD
Austin, Texas
Parkinsons Disease
Parkinsons disease is a progressive movement disorder
characterized by degeneration of dopaminergic neurones in
the substantia nigra of the midbrain. Treatment is aimed at
increasing dopaminergic stimulation of the striatal neurons
involved in controlling movement, using dopamine-increas-
ing agents or dopamine agonists.10 Concomitant stimulation
of dopamine receptors at the CRT and, possibly, in the GI
tract results in the common side effects of nausea and vom-
iting. Domperidone is used prophylactically to counteract
these effects.11-12
Levodopa (L-Dopa), a precursor of dopamine, is a mainstay in
the treatment of Parkinsons disease. Oral domperidone (10 to 20 mg
3 times a day) has been shown to reduce levodopa-induced nausea
and vomiting.13
Domperidone (60 mg daily) reduced the incidence of nausea and
vomiting in a placebo-controlled study of patients receiving bromo-
criptine (a dopamine receptor agonist) therapy and allowed higher
doses of bromocriptine to be tolerated.14
Parkinsons disease is characterized by unpredictable off peri-
ods of poor drug response and increased parkinsonian symptoma-
tology. Management of off periods with apomorphine (intermittent
injections or continuous infusion), a short-acting dopamine receptor
agonist, was made practical by the use of domperidone to counter-
act apomorphines potent emetic effects. Domperidone pretreat-
ment (10 to 20 mg by mouth 3 times a day) is typically started 1 to
3 days before apomorphine treatment is begun. Patients can often
gradually reduce or stop domperidone after a few weeks, as toler-
ance develops to apomorphines emetic effects, possibly due to
down regulation of dopamine receptor sensitivity in the medulla
(vomiting center) after continuous dopaminergic stimulation.15-19
Domperidone (20 mg 3 times a day) has been used to allow
quicker titration of pergolide as an adjunct to L-Dopa therapy.20
Hobson et al21 suggest domperidone as an adjunct to ropinirol or
pramipexole therapy, two newer dopamine agonists that are rela-
tively specific for D2 receptors.
 D O M P E R I D O N E

Surgery-Postsurgical, Chemotherapy- or Radiation-Induced Emesis fullness, suggestive of underlying neuromuscular dysfunctions of

Early studies of domperidones utility for postsurgical, and the GI tract. Potential neuromuscular dysfunctions include gastro-
chemotherapy- or radiation-induced emesis used intravenous (IV) paresis (delayed gastric emptying), gastric dysrhythmias, antral-
or intramuscular administration (reviewed elsewhere).4 However, hypomotility and dilation, reduced antroduodenal coordination
parenteral forms of domperidone were withdrawn worldwide fol- and gastric tone dysfunction.26,36-37
lowing reports of severe adverse cardiac effects.12 Oral domperidone The correlation between upper GI symptoms and the rate of
has seen limited use in treatment and prevention of postoperative gastric emptying is relatively weak, thus gastroparesis is considered
nausea.22 In general, serotonin receptor antagonists are now recom- to be an indicator of gastroduodenal motor abnormality, rather than
mended as first-line treatment of chemotherapy- or radiation- the sole cause of the symptoms.3,26,29,36 Upper GI symptoms may
induced emesis; dopamine receptor antagonists may have a place as affect up to 50% of patients with diabetes, but symptoms do not
alternative or adjunct therapy.8,23-25 necessarily predict delayed gastric emptying.3,26,37 Conversely, pa-
tients with diabetes who have poor gastric emptying (up to 50% of
Prokinetic Activity of Domperidone patients with type 1 diabetes) may have no upper GI symptoms,
The stomachs function of receiving, preparing and delivering although they may experience poor glycemic control due to mis-
nutrients to the small intestine in a usable form is a complex process match of insulin administration with emptying of nutrients into the
in which the central, autonomic and enteric nervous systems all small bowel.3,26,36,37
play a role. Briefly, the main anatomical parts of the stomach are The etiology of diabetic gastropathy is not well understood.
the cardia, fundus, body and antrum. At the beginning of a meal, Autonomic neuropathy and hyperglycemia are thought to be two
the fundus relaxes to make room for the incoming food. After a lag dominant factors.
phase, regular contractions of the antrum mix food particles with Autonomic Neuropathy
acid and pepsin into a suspension called chyme, which is then emp- Vagal nerve impairment might alter antroduodenal motility,
tied through the pyloric sphincter into the duodenum, the first part gastroesophageal reflux activity and gastric secretory function.
of the small intestine. The gastric emptying rate depends upon the
physical and chemical characteristics of the stomachs contents;
typical gastric emptying time is 1 to 4 hours. In the interdigestive
period, four phases of spontaneous gastric contractions, some of
which are controlled by pacemaker cells of the stomach (interstitial
cells of Cajal), clear the stomach of undigestible solids.26
Dopamine is synthesized in the GI tract, spleen and pancreas
in humans; D1-like and D2-like receptors have been demon-
strated in several mammals at various GI sites. Dopamines effect
on the GI tract is primarily inhibitory, as evidenced by reduced
lower esophageal sphincter tone, reduced gastric tone and intragas-
tric pressure, and decreased antroduodenal coordination.1,3,26-28
Dopamine appears to directly inhibit gastric muscle contractions
via postjunctional muscular D2 receptors in the lower esophageal
sphincter, fundus and antrum.1,3,27 Domperidones prokinetic effect
is likely a result of blockade of D2 inhibitory receptors. It has been
shown to increase lower esophageal sphincter pressure, improve
antroduodenal coordination and gastric emptying and normalize
gastric dysrhythmias.28-32
Dopamine also has an indirect inhibitory effect via inhibition of
cholinergic transmission in the myenteric plexus, which regulates
the circular and longitudinal layers of smooth muscle. This inhibi-
tion was shown in isolated guinea pig stomach to be sensitive to
domperidone, indicating mediation by prejunctional D2 receptors
on postganglionic cholinergic neurons.33-34 However, domperidone
has not been shown to have procholinergic activity in isolated hu-
man stomach.1-3,35

Diabetic Gastropathy
Diabetic gastropathy is an umbrella term for a constellation of
upper GI symptoms in patients with diabetes, including nausea,
vomiting, bloating, abdominal discomfort and early satiety or

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 D O M P E R I D O N E
Although the association between gastroparesis and abnormal
autonomic function is relatively weak, it is thought to be a con-
tributing factor.26,36-37
Hyperglycemia/Glucose Toxicity
An inverse relationship has been shown between gastric empty-
ing and blood-glucose concentration both in healthy individuals and
in those with type 1 or type 2 diabetes. In addition, acute changes in
blood-glucose concentration can alter the perception of sensations
from the stomach and duodenum.26,36-37
Other Factors
Enteric neuropathy, altered postprandial release of hormones and
neurotransmitters, visceral hypersensitivity and psychological disor-
ders may potentially contribute to gastric dysfunction in patients
with diabetes. In addition, there are many other causes of gastro-
paresis besides diabetes.26,36-37
Evaluation of Patients
Evaluation of patients with diabetes who present with upper GI
symptoms should include a complete physical examination and
medical history. Other causes of upper GI symptoms and poor gas-
tric emptying, such as mechanical obstruction, poor glucose control
or medications that slow gastric emptying, eg, anticholinergics and
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dopaminergics, should be ruled out.26, 36-37 Gastric scintigraphy
(direct measure of the transit time of a radiolabeled meal) is the
most common, and considered to be the most accurate, way to
evaluate gastric emptying.36 Other methods for evaluating gastric
myoelectrical events include electrogastrophy, scintigraphic breath
tests, ultrasonography, magnetic resonance imaging and antroduo-
denal manometry.37
Treatment
Treatment focuses on improving upper GI symptoms, improv-
ing glycemic control and optimizing nutritional intake and quality
of life. Optimizing glucose control and avoiding drugs that can slow
gastric emptying, followed by dietary and lifestyle modifications,
are the usual initial course of treatment. Common recommenda-
tions include smaller, more frequent meals that are low in fat and
fiber (to avoid bezoar formation); and increased nutrient liquids,
although controlled trials have not proven this approach to be
effective. Moderate exercise is encouraged, as this accelerates gas-
tric emptying.26,36-37
Prokinetic agents are the mainstay of pharmacological treat-
ment. Mechanisms of action include dopamine D2 receptor block-
ade (domperidone and metoclopramide), stimulation of 5HT4
receptors (metoclopramide and cisapride) and stimulation of mo-
tilin receptors (erythromycin).36 Placement of a feeding jejunostomy
tube is a treatment of last resort.26,36-37
Efficacy
Numerous clinical trials have consistently shown oral domperi-
done, typically 20 mg 4 times a day, to improve symptom scores,
improve gastric emptying, correct gastric dysrhythmias, decrease
hospitalizations and improve the quality of life in patients with dia-
betic gastropathy or gastroparesis.2-3,26,29-30,38-44 The complex etiology
of diabetic gastropathy, and the weak association between more
objective measurements of gastroduodenal function (gastric empty-
ing, electrogastrographic measurements) and symptoms, complicate
interpretation of these studies. Domperidones antiemetic function
must also be considered in assessing symptom improvement.
Symptomatic improvement is the most common outcome evalu-
ated in clinical trials of domperidone efficacy. Other parameters
include measurement of gastric emptying, gastric myoelectrical
rhythm recording, health-related quality of life assessment and hos-
pitalization rates. Many studies have methodological limitations
related to one or more parameters: small study size, lack of report-
ing of patients blood glucose levels, lack of placebo control, lack of
randomization, unblinded treatment or nonvalidated measurement
of symptoms.29,36,38-39 A meta-analysis39 of clinical studies of four pro-
kinetics (cisapride, metoclopramide, domperidone and erythromy-
cin) showed that open-trial and single-blind studies showed greater
improvement in both symptom assessment and gastric emptying
times than did double-blind trials, indicating a substantial placebo
effect and/or bias. The use of domperidone and metoclopramide
in the treatment of gastroparesis is currently under review by the
Cochrane Upper Gastrointestinal and Pancreatic Diseases Group.45
The largest clinical trial40-42 used a two-phase withdrawal design
to enrich the trial with treatment responders. In phase I, 269 in-
sulin-dependent patients with diabetes who had symptoms of
 D O M P E R I D O N E

gastroparesis [8 out of 15 maximum in total symptom score (TSS)] Tolerability/Adverse Effects

received single-blind treatment with domperidone 20 mg 4 times a In one study of 17 patients with documented gastroparesis,
day for 4 weeks. Patients were classified as responders (n = 208, 77%) oral domperidone 40 to 120 mg/day was used for periods of up
if they showed statistically significant improvement in TSS at the to 4 years and was well tolerated.43-47 In the large study by Silvers
end of phase I (mean change from baseline 6.52; P <0.001).41 et al,41 the tolerability profile was similar to placebo. The most
Health-related quality of life (HRQOL) was evaluated using the common (occurring in as many as 10% to 20% of patients) ad-
Medical Outcomes Study Short-Form 36 (SF-36), with aggregation verse effects described in most studies are related to increased
into a physical component summary (PCS) or mental component prolactin levels due to antagonism of D2 receptors in the anterior
summary (MCS) index; higher scores indicate better HRQOL. Re- pituitary, including gynecomastia, galactorrhea, breast tenderness
sponders also experienced significant improvement from baseline or menstrual irregularities. 3,4,29 In a double-blind, nonplacebo-
in both PCS (+3.47; P <0.001) and MCS (+5.23; P <0.001) indexes controlled, comparison of domperidone and metoclopramide in
during phase I.40 93 insulin-dependent patients with diabetes, elicited CNS effects
Patients classified as responders in phase I were randomized for (somnolence, akathisia, asthenia, anxiety, depression and mental
phase II, a double-blind parallel-group 4-week withdrawal study acuity) were fewer and less severe for domperidone.49 Case re-
with either placebo (n = 103) or domperidone 20 mg 4 times a day ports describing extrapyramidal symptoms have been summarized
(n = 105). During phase II, both groups experienced deterioration elsewhere 3 and in general indicate that the risk of developing
in TSS. The placebo group experienced significantly greater extrapyramidal side effects is minimal when domperidone is
deterioration than the domperidone group (+1.84 placebo versus taken orally by adults at recommended doses.
+0.85 domperidone; between-group difference P = 0.025).41 Increased blood pressure and heart rate have been seen in
In phase II, responders receiving placebo demonstrated a signifi- patients treated with oral domperidone 10 mg 3 times a day in
cant decline in PCS (1.77; P = 0.20), while those receiving domperi- conjunction with continuous subcutaneous infusion of apomor-
done experienced a statistically insignificant change (+0.65; P = phine.50 Parenteral forms of the drug were withdrawn from the
0.361; between-group P = 0.050). Both groups MCS scores were
statistically unchanged in phase II.40
Patients were also evaluated by scintigraphy at the outset of
the study for gastric emptying rates and classified into delayed
gastric emptying (DGE; n = 126; 44%) and normal gastric empty-
ing (NGE) classes; criteria were not reported. No significant differ-
ence was seen between NGE and DGE groups in baseline TSS or
TSS improvement during phase I, nor in the deterioration of TSS in
phase II.41-42
Talley38 has suggested that the two-phase withdrawal design
might be suboptimal because of the open-trial design of the first
phase. In addition, a straightforward interpretation of the results of
the withdrawal phase depends on the assumption that the disease
relapses and remits, which may not be the pattern in diabetic gas-
troparesis. Silvers et al41 acknowledge that potential bias of investi-
gators in assigning total symptom scores at the end of phase I might
have been a factor in the deterioration of TSS by the domperidone
group in phase II. Talley38 suggests that double-blind, parallel
group studies remain the trial design of choice, using validated out-
come measures of both symptoms and quality of life.
GI Symptoms in Parkinsons
Patients with Parkinsons disease can experience upper GI symp-
toms as a result of cerebral degeneration, degeneration of the myen-
teric plexus and antiparkinsonian medication.46 Extended domperidone
therapy (20 mg 4 times a day, mean follow-up 3 years) has been shown
to improve upper GI symptoms and gastric emptying.13,47
Gastroesophageal Reflux Disease
Domperidone has not been shown conclusively to reduce the
number of reflux episodes or improve gastroesophageal reflux dis-
ease (GERD) symptoms. At this time, acid-suppressive agents have
become the drugs of choice for GERD.48

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 D O M P E R I D O N E
market in 1984 due to QT prolongation, ventricular arrhythmia
and cardiac arrest in patients receiving high IV doses.3,12 Physio-
logically relevant concentrations of domperidone have been
shown to prolong cardiac repolarization in isolated guinea pig
hearts, indicating the potential for association with QT prolon-
gation and ventricular arrhythmia clinically. 51 No clinically
important changes in vital signs or electrocardiographic activity
were observed in 286 patients using domperidone 20 mg 4 times
a day for 4 weeks and in 105 patients who were treated for 8 weeks.41
Summary
Domperidone is a dopamine D2 receptor antagonist with anti-
emetic properties and localization outside the blood-brain barrier
that have made it a useful adjunct in therapy for Parkinsons dis-
ease. There has been a renewed interest in antidopaminergic pro-
kinetic agents since the withdrawal of cisapride, a 5-HT4 agonist,
from the market. 1 Domperidone continues to be an attractive
alternative to metoclopramide because it causes fewer CNS side
effects. Patients receiving domperidone or other prokinetic
agents for diabetic gastropathy or gastroparesis should also be
managing diet, lifestyle and other medications to optimize gastric
motility.
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