American Journal of Gastroenterology ISSN 0002-9270


C 2007 by Am. Coll. of Gastroenterology doi: 10.1111/j.1572-0241.2007.01255.x
Published by Blackwell Publishing

CLINICAL REVIEWS

Domperidone: Review of Pharmacology and Clinical

Applications in Gastroenterology
Savio C. Reddymasu, M.D., Irfan Soykan, M.D., and Richard W. McCallum, M.D.
Department of Medicine, Center for Gastrointestinal Motility, Division of Gastroenterology and Hepatology,
University of Kansas Medical Center, Kansas City, Kansas

Domperidone is a dopamine-2 receptor antagonist. It acts as an antiemetic and a prokinetic agent through its
effects on the chemoreceptor trigger zone and motor function of the stomach and small intestine. Unlike
metoclopramide, it does not cause any adverse neurological symptoms as it has minimal penetration through the
blood-brain barrier. It thus provides an excellent safety profile for long-term administration orally in the
recommended doses. Domperidone is widely used in many countries and can now be officially prescribed to
patients in the United States by an investigational new drug application for the treatment of gastroparesis and any
condition causing chronic nausea and vomiting. In view of this additional clinical exposure of domperidone to a
new generation of gastroenterologists and other specialists, the purpose of this timely review is to revisit the
pharmacology, clinical application, and safety profile of this beneficial medication.
(Am J Gastroenterol 2007;102:2036–2045)

INTRODUCTION had been enrolled in controlled clinical trials to make sta-

Domperidone is a dopamine (D) antagonist with particular
affinity for the D2 subtype receptors in the brain and the pe-
ripheral nervous system including the gastrointestinal (GI)
tract. Since it was first synthesized in 1974, it has been used
both as a research tool for investigating the molecular actions
of dopamine and dopamine receptors and as a therapeutic
agent with several specific clinical applications in gastroen-
terology.
Domperidone is structurally related to the butyrophenones
(Fig. 1). Its most notable effect in the GI tract is antagonism
of apomorphine- and dopamine-induced changes in GI func-
tion. Stimulation of dopaminergic receptors inhibits gastric
motility, resulting in a variety of GI symptoms including post-
prandial bloating and pain, premature satiety, and nausea and
vomiting. Dopamine antagonists, such as domperidone and
metocloprarnide, have the potential to negate this dopamin-
ergic effect and thereby prevent subsequent GI symptoms.
Unlike metoclopramide, which also has both central and pe-
ripheral effects, domperidone does not cause significant cen-
tral nervous system (CNS) side effects as it minimally crosses
the blood-brain barrier. Domperidone is currently available
in 58 countries, including Canada, and there is worldwide
experience in utilizing this agent, both as a treatment of gas-
troparesis as well as a general antiemetic. While a number
of preclinical and early trials were conducted using an in-
travenous (IV) form, domperidone is now only available for
oral or suppository administration. Although domperidone
was evaluated by the Food and Drug Administration (FDA)
in 1989, the agency withheld approval at that time because
it was determined that an inadequate number of patients
tistically valid evaluations of its efficacy (1). Over the last
2 yr, domperidone has been available in the United States
through a compassionate clearance program. The FDA al-
lows physicians to prescribe domperidone for gastrointesti-
nal symptoms that are refractory to standard medical manage-
ment by requesting and initiating an investigational new drug
application (IND) permitting administration of investiga-
tional drugs to humans. More information could be obtained
at http://www.fda.gov/cder/news/domperidone.htm. Import-
ing, interstate shipment, and oral administration of domperi-
done are legal as long as they are obtained via an IND. On
the same note, the FDA deems compounding domperidone
felonious in the United States. The process of obtaining an
IND for domperidone starts by applying and obtaining ap-
proval from the local institutional review committees. After
the institution permits the use of domperidone, an informed
consent should be obtained from the patient after obtaining
an EKG and serum potassium. The IND should be renewed
annually and the EKG and serum potassium repeated on a
yearly basis. Medication can then be purchased from a list of
approved sites.
This agent is therefore being utilized more frequently
by gastroenterologists in the United States and will also
be encountered by endocrinologists, emergency department
physicians, internists, neurologists, primary care physicians,
nurses, and paramedical personnel. Hence, it is important to
be familiar with this agent as it evolves into more extensive
clinical use in the United States as well as highlight new dos-
ing strategies for physicians outside the United States already
utilizing this agent. The purpose of this article is to review
the pharmacology, mechanisms of action, and summarize the

2036

Figure 1. Molecular structure of domperidone.
current literature on its efficacy in the treatment of a variety
of gastrointestinal motility disorders and other conditions.
A computerized literature search was conducted using the
MEDLINE database for English language journals between
the time period of January 1975 and June 2006 using the
following key words “domperidone,” “gastroparesis,” “nau-
sea,” “vomiting,” “dyspepsia,” and “gastroesophageal reflux
disease.”
PHARMACOLOGIC EFFECTS
Domperidone has a molecular weight of 425.9. Depending
on intramuscular (IM) or oral administration peak plasma
levels of domperidone occur anywhere from 10 to 30 min.
Peak levels after rectal administration of suppositories are
usually achieved in 1–2 h. Bioavailability is high after IM ad-
ministration (90%), and much lower with oral administration
(13–17%) (2). This is probably a result of both incomplete
absorption (3) and a first-pass effect with oral administration.
The bioavailability of oral domperidone is further decreased
by increasing the pH of the stomach via antacid medications
(2). A comparison of plasma concentrations following differ-
ent routes of administration is shown in Table 1.
Domperidone binds to striatal dopamine receptors more
specifically and selectively than tritiated spiperone, the clas-
sic ligand used to study the central nervous system model (4,
5). Nevertheless, IV administration of domperidone, even
at high doses, does not result in displacement of labeled
spiperone in the brain in animal models—a finding that is
consistent with poor penetration of the blood-brain barrier
(6). In contrast to other labeled neuroleptic drugs known to
cross the blood-brain barrier, recovery of tritiated domperi-
done from brain tissue after IV administration is very low
(6). In an experimental model in which the blood-brain bar-
Table 1. Plasma Concentrations After Single-Dose Administration
of Various Forms of Domperidone (2)
Peak Plasma Time to
Administration Dose Concentration Peak
Intramuscular 10 mg 40 ng/mL 10–30 min
Oral (tablet) 10 mg 23 ng/mL 30 min
Oral (drops) 60 mg 102 ng/mL 30 min
Rectal (suppository) 60 mg 20 ng/mL 60 min
Review of Domperidone 2037
rier was breached by protamine sulfate, the activity of dom-
peridone inhibiting apomorphine-induced ACTH release was
increased over normal conditions (7). Domperidone has a
high affinity for GI tissue and high concentrations of the drug
are found in the esophagus, stomach, and small intestine (8).
A number of preclinical studies have indicated that domperi-
done blocks dopaminergic inhibition of GI transit and this
effect is mediated primarily through D2 receptors (9–11).
Domperidone is strongly bound to plasma proteins and is
rapidly metabolized by the liver to inactive metabolites. Fol-
lowing oral administration, 32% of the drug is excreted in
the urine. Urinary excretion rates parallel the plasma con-
centration curves. Sixty-six percent of the drug is found in
the feces after oral administration and the elimination half-
life is approximately 7.5 h in healthy subjects (12). In patients
with severe renal dysfunction, the elimination half-life may
increase to 20 h. However, since renal clearance is a small
portion of the total clearance, prolongation of urinary excre-
tion should not occur with renal dysfunction (13). Most of
the drug is extensively metabolized to an inactive product
(13–15).
In plasma, approximately 92% of domperidone is bound
to plasma proteins (14). There are limited data on drug dis-
tribution in humans, but studies in comparable rat models
demonstrate wide distribution of the drug in all body tissues
except the central nervous system. Small amounts of radio la-
beled domperidone have been shown to cross the placenta in
this model (13, 16). It may also be secreted in small quantities
in breast milk (17).
Domperidone’s prokinetic efficacy is based on its ability to
increase the amplitude of esophageal motor function, enhance
antral-duodenal contractions, and better coordinate peristal-
sis across the pylorus with subsequent acceleration of gastric
emptying (18, 19). Effects of domperidone on the small bowel
(beyond the duodenum) and on colon motility and transit have
not been reported. Early studies established that administra-
tion of domperidone increased gastric emptying of liquids and
solids, both in patients with dyspepsia and healthy subjects
(20). Despite its low degree of CNS activity, domperidone is
an effective antiemetic (12). This efficacy reflects its activity
at the chemoreceptor trigger zone (CTZ), which is located in
the fourth ventricle of the brain but outside the blood-brain
barrier (Fig. 2). Domperidone is distinguished from other
prokinetic agents in that it has no cholinergic activity and its
action is not inhibited by atropine (21).
Electrophysiological research indicates that the D2 recep-
tor may play a role in the activity of gastric electrical patterns
(22), and that dopamine may inhibit calcium-dependent cur-
rents at the cellular level in melanotrophs of the rat pars in-
termedia (23). A study of 14 human subjects showed that
administration of dopamine disrupted normal motor patterns
in the stomach through inhibition of antral waves and the mi-
grating motor complexes (24). Pretreatment of subjects with
domperidone completely prevented this dopamine-mediated
effect, suggesting that D2 receptors are involved in regulation
of normal motility patterns.
2038 Reddymasu et al.
Figure 2. Mechanisms of action of domperidone.
Dopamine is one of the neurotransmitters involved in me-
diating receptive relaxation of the stomach and dopamine
antagonists partially block reflexly induced receptive relax-
ation. The finding that dopamine is a mediator of changes
in intragastric pressure and gastric emptying in humans after
vagotomy provides one basis for the known beneficial ef-
fect of dopamine antagonists on delayed gastric emptying of
solids after vagotomy (25, 26).
The ability of domperidone to modulate gastric emptying
of both liquid and solid meals has been documented (20, 26).
These observations have stimulated continued clinical inter-
est in the role of domperidone in the treatment of a wide
range of gastrointestinal motility disorders, including gastro-
paresis, gastroesophageal reflux, and nonspecific dyspepsia.
Domperidone has not been shown to have other significant
effects on gastrointestinal physiology. Studies in healthy sub-
jects with duodenal ulcer indicate that domperidone does not
alter gastric acid secretion, secretory volume, intragastric pH,
or serum gastrin concentration (18).
CLINICAL TRIALS AND USES
Domperidone has been extensively evaluated in the treatment
of a variety of gastrointestinal motility disorders (Tables 2–5).
Much of the clinical work on domperidone was undertaken in
the late 1970s and early 1980s in Europe. More recent studies
performed in the 1990s will also be examined. These stud-
Table 2. Clinical Trials Involving Domperidone in Dyspepsia
Study Number
Design of Patients
1 Double-blind, randomized 54
2 Double-blind, placebo-controlled 40
3 Double-blind, placebo-controlled, crossover 41
4 Double-blind, placebo-controlled 14
5 Double-blind, placebo-controlled 16
6 Double-blind, placebo-controlled, crossover 44
7 Double-blind, placebo-controlled 20
8 Double-blind, placebo-controlled 20
9 Double-blind, placebo-controlled 71
ies usually measured changes in symptom scores and global
assessment. Most of these studies showed that domperidone
could alleviate dyspeptic symptoms in a wide variety of GI
disorders; however, many of these studies had a small number
of patients and conclusions are limited because of deficien-
cies in study design.
GASTROPARESIS AND DIABETIC GASTROPATHY
A number of GI and systemic disorders may impair gas-
tric motility with resultant gastroparesis. Symptoms usually
include nausea, vomiting, postprandial fullness, early sati-
ety, and abdominal pain. Approximately one-third of patients
with this condition have idiopathic gastroparesis, that is, no
identifiable underlying cause. However, a number of these
patients (25–50%) might be related to a postviral syndrome
(27). Of the remaining spectrum of gastroparesis, 24% of
cases are attributed to diabetes mellitus and 19% are postsur-
gical (28).
Prokinetic agents are commonly used to treat gastroparesis
and the first-line agent is often the dopamine antagonist meto-
clopramide. Currently, metoclopramide is the only prokinetic
with FDA approval for this indication in the United States. It
stimulates gastric emptying and provides symptomatic relief
in many, but not all, patients with gastroparesis. The clinical
utility of metoclopramide, especially for long-term use, is
further diminished by its potential for adverse effects, which
may occur in up to 40% of patients combining data from
short- and long-term clinical use (29). About 20% of patients
receiving metoclopramide initially experience CNS adverse
effects such as drowsiness, akithesia, restlessness, insomnia,
lassitude, and fatigue. About 10–20% of patients experience
extra-pyramidal reactions such as acute dystonia (including
torticollis) initially and with chronic use, Parkinsonian symp-
toms, tardive dyskinesia, and depression can evolve (30).
Domperidone has been extensively utilized throughout
the world over the past 25 yr for gastroparesis. However,
there are only a few well-controlled, double-blind studies
of patients with gastroparesis directly comparing the effi-
cacy of domperidone with other prokinetic agents such as
metoclopramide and cisapride (31). The clinical efficacy of
Dose (mg/day) Result Reference
30 Positive effect but not (83)
superior to itopride
30 Superior to placebo (84)
30 Superior to placebo (85)
60 Superior to placebo (48)
60 Superior to placebo (35)
30 Superior to placebo (86)
20 Positive effect (87)
80 Superior to placebo (97)
60 Superior to placebo (98)

Table 3. Clinical Trials Involving Domperidone in Postoperative Nausea and Vomiting
Number Dose
Study Design of Patients (mg/day)
1 Double-blind, placebo-controlled 106 10–60
2 Double-blind, randomized, comparative 195 30
3 Double-blind, randomized, placebo-controlled, 176 4–10
comparative
4 Double-blind, placebo-controlled 100 10
5 Double-blind, randomized, placebo-controlled 77 10
6 Double-blind, placebo-controlled, comparative 60 10
7 Double-blind, randomized, placebo-controlled, 199 20
comparative
8 Double-blind, randomized, placebo-controlled, 200 20
comparative
domperidone has, however, been well documented in
placebo-controlled trials (18, 32–35). As with metoclo-
pramide, it is not clear how much of the symptomatic im-
provement could be attributed to improved gastric and upper
GI motility, and how much was related to its antiemetic effect
(31).
The long-term efficacy of domperidone in gastroparesis
has not been established, but there is no evidence that symp-
tomatic improvement diminishes with chronic therapy. A con-
trolled study of 12 patients with delayed gastric emptying
showed that after 35 to 51 days administration, domperidone
continued to have a significant effect on increasing liquid
emptying (P < 0.025), and symptoms significantly improved
over the treatment period (P < 0.001) (33).
A study in six insulin-dependent diabetic patients with
nausea and vomiting indicated that gastric dysrrhythmias re-
solved, and upper GI symptoms were significantly reduced
during 6 months of domperidone treatment (36). In an-
other multicenter randomized control trial of 93 patients with
insulin-dependant diabetes mellitus, domperidone and meto-
clopramide were both effective in alleviating symptoms, but
the domperidone group had a reduced incidence of central
nervous system side effects (37).
Estimates of the incidence of GI symptoms in patients with
diabetes range from 10% to as high as 76% (38–40). In di-
abetic patients with symptoms of dyspepsia and indigestion
but without objective evidence of gastroparesis, the etiology
of symptoms appears to be multifactorial and is thought to
be one or more of the following: abnormal gastric electri-
cal rhythms, impaired relaxation of the fundus with redis-
Table 4. Clinical Trials Involving Domperidone in Diabetic Gastroparesis
Number
Study Design of Patients
1 Double-blind, randomized 93
2 Double-blind, placebo-controlled, randomized 6 10
3 Double-blind, placebo-controlled 12
4 Open-label 6 80
5 Double-blind, placebo-controlled 208
Review of Domperidone 2039
Result Reference
Superior to placebo (88)
Superior to placebo, no significant (89)
difference from other medications
Superior to placebo and other medications (90)
Superior to placebo (56)
No significant difference from other medications (91)
Superior to placebo, inferior to other medications (92)
Superior to placebo, inferior to other medications (93)
Superior to placebo, inferior to other medications (94)
tribution of the meal to a distended antrum, loss of antral-
duodenal coordination, and pyloric “spasm.” The effects of
hyperglycemia on neuromuscular gastric function indicate
that acute elevations of glucose (>200 mg/dL) might induce
acute changes in electrical rhythm of the stomach (41) lead-
ing to nausea and also inhibit antral and duodenal motor
function. This spectrum of possible disturbances of gastric
motility is best termed gastropathy. Diabetic gastropathy re-
sults in both chronic and intermittent symptoms and also
can interfere with glucose control by affecting nutrient ab-
sorption, and hence patients can present with either hypo- or
hyperglycemia. It has been estimated that 80% of gastropa-
thy patients will require long-term maintenance therapy with
prokinetic and antiemetic agents; and 20% require periods of
nutritional support (28).
A multicenter, two-phase withdrawal study in the United
States involving over 200 insulin-dependent diabetic patients
showed that domperidone is effective in treating moderate
to severe upper GI symptoms independent of their gastric
emptying status (42). This study also investigated two health-
related quality of life measures of physical and mental com-
ponents. Results at the end of the single-blind phase indi-
cated that patients with a symptomatic response to domperi-
done also experienced significant improvements in health-
related quality of life from baseline as measured by physical
and mental component summary scores. Patients continuing
on domperidone during the double-blind withdrawal phase
maintained their clinical and health-related quality of life
gains. In contrast, those in the placebo group experienced
more gastroparetic symptoms and a decline in the quality
Dose (mg/day) Result Reference
80 Equal efficacy (37)
as metoclopramide
Superior to placebo (32)
120 Superior to placebo (33)
Had a positive effect (36)
80 Had a positive effect (42)
2040 Reddymasu et al.
Table 5. Clinical Trials Involving Domperidone in Other Miscellaneous Conditions
Number
Indication Study Design of Patients
Chemotherapy-induced Double-blind, comparative
nausea/vomiting
Nausea/vomiting associated Single-blind, placebo-controlled
with Parkinson’s disease
Nausea/vomiting associated Open-label
with Parkinson’s disease
Pediatric gastroenteritis Double-blind, placebo-controlled,
comparative
Gastroparesis (any etiology) Open-label
of life summary score. Literature indicates that domperidone
might be a useful agent in addressing the symptoms attributed
to the neuromuscular and myoelectrical abnormalities de-
scribed in diabetic gastropathy.
Gastroesophageal Reflux Disease (GERD)
In one 8-wk trial, domperidone 80 mg daily was not more
effective than placebo in decreasing the severity of reflux in
23 patients with GERD (43). A 6-wk randomized compari-
son of ranitidine (150 mg twice daily), domperidone (20 mg
three times daily), or both showed that all three regimens were
equally effective in reducing symptoms, and promoting endo-
scopic and histological healing of esophagitis in 45 patients
with GERD (44). The published trials of domperidone’s use
in GERD preceded the proton pump inhibitor (PPI) era and
it would be fair to say that its role in control of heartburn
would not be comparable to a PPI since a significant percent-
age of patients with GERD also have an accompanying delay
in gastric emptying (45, 46). There is an indication for the
use of prokinetic agents, specifically domperidone as com-
plimentary to a PPI. The gas-bloat syndrome is common after
fundoplication and is more of a problem if there has been a
background of slow gastric emptying. After fundoplication,
patients can develop symptoms suggestive of gastroparesis
possibly secondary to vagal nerve injury. Both of these set-
tings could benefit from domeperidone.
Dyspepsia
The symptoms of dyspepsia include intolerable postprandial
fullness, epigastric pain, burning, early satiety, and nausea
(47), (48). An open-label study involving more than 200 pa-
tients suffering from chronic dyspepsia revealed that 78% of
subjects benefited significantly from a dose of 30–60 mg/day
of domperidone. A double-blind study of domperidone in
the symptomatic treatment of chronic postprandial upper
GI distress in 41 patients demonstrated that oral domperi-
done (30 mg/day) would considerably reduce the degree of
postprandial distress associated with chronic dyspepsia (49).
Two double-blind placebo-controlled studies have indicated
that domperidone significantly reduced the GI symptoms
of patients with chronic dyspepsia (35, 48). About 30% of
patients with functional dyspepsia have delayed gastric emp-
tying (50), an equal number of patients also have gastric ar-
Dose
(mg/day) Result Reference
62 60 Inferior to other medications (95)
20 150 Superior to placebo (60)
11 80 Had a positive effect (62)
60 30 Superior to placebo and other (52)
medications
17 40–120 Had a positive effect (96)
rhythmias (50). Along with its prokinetic effect, domperidone
also helps in the resolution of gastric dysrhythmias (36). It
would seem likely that this subset of patients might benefit
from domperidone; however, when these results were sub-
ject to a meta-analysis, there were concerns about the quality
of some of these studies, raising some reservations about
recommending the use of domperidone in all patients with
functional dyspepsia (51).
Nausea and Vomiting
The antiemetic properties of domperidone are well docu-
mented.
In patients experiencing postoperative nausea and vomit-
ing, IV domperidone was more effective than placebo (52–
56). Neither domperidone nor metocloprarnide is more effec-
tive than placebo when given prophylactically before induc-
tion or near the end of anesthesia, for preventing postoperative
emesis (13, 57).
Nausea and vomiting associated with cytotoxic drug ther-
apy has been effectively controlled by domperidone when
administered immediately before the cytotoxic regimen. It
is more effective than placebo and compares favorably with
metoclopramide in controlling vomiting as a result of moder-
ately emetic cytotoxic drugs (58, 59). As might be expected,
nausea and vomiting accompanying the use of strongly emetic
drugs such as mustine (e.g., mechlorethamine, nitrogen mus-
tard) and dacarbazine are not as well controlled (57).
MISCELLANEOUS NAUSEA AND VOMITING
Domperidone has been used to treat nausea and vomiting as-
sociated with other conditions including dysmenorrhea, head
injury and intracranial lesions, hemodialysis, radiotherapy,
and migraine headaches. However, most of the studies were
open trials and there are few controlled data demonstrating
efficacy for these indications.
Parkinson’s Disease
The management of patients who need anti-Parkinsonian
drugs and other centrally acting dopamine agonists is of-
ten hampered by the peripheral effects of nausea, vom-
iting, anorexia, and postprandial fullness caused by these
agents. Domperidone may prove especially useful in this situ-
ation, because it suppresses peripheral dopaminergic activity

without inhibiting central dopamine agonism. Studies have
shown that oral domperidone (60–150 mg daily) decreases
the incidence of nausea and vomiting in patients treated
with bromocriptine, allowing them to tolerate higher doses
of bromocriptine (12, 60, 61). Domperidone also improved
gastric emptying and alleviated GI symptoms, including nau-
sea, vomiting, anorexia, and abdominal bloating, induced by
levodopa. There is also an associated improvement in gastric
emptying which was delayed by levodopa (62). The benefi-
cial central effects of the anti-Parkinsonian drugs were not
inhibited by domperidone, and no extra-pyramidal side ef-
fects attributable to domperidone were reported in any of
these studies (62).
PEDIATRIC USE OF DOMPERIDONE
Nausea and Vomiting
Domperidone has been used to treat nausea and vomiting
because of various causes in children. One open study and
one randomized crossover study confirmed the efficacy of
domperidone in preventing pediatric nausea and vomiting
induced by cytotoxic drugs (63, 64).
Domperidone has also reduced pediatric postprandial vom-
iting. In a double-blind comparison with metoclopramide, a
solution of 0.3 mg/kg domperidone resulted in either rapid
or complete disappearance of symptoms or marked improve-
ment in children with chronic vomiting or regurgitation (65).
Both open and placebo-controlled studies have indicated that
domperidone helps control vomiting associated with condi-
tions such as gastroenteritis, gastritis, ketosis, upper respira-
tory tract infection, and infectious hepatitis (52, 66).
Available literature, however, does not support the use of
domperidone as a first-line antiemetic agent in pediatric nau-
sea and vomiting.
Reflux Disease
In an open-label study reflux-associated symptoms improved
significantly after domperidone therapy. Postprandial reflux
time (defined as esophageal pH < 4.0) and percent peri-
staltic esophageal contractions improved significantly indi-
cating that domperidone may be a useful and safe agent for
the treatment of symptomatic reflux disease in children with
upper GI motility abnormalities (67).
SAFETY
Domperidone has been well tolerated and has caused rel-
atively few side effects in clinical trials to date. Cardiac
arrhythmias were reported after IV administration of high
doses of domperidone and, therefore, this route of adminis-
tration was discontinued (68–70). Domperidone has electro-
physiological properties similar to class III antiarrhythmic
agents and can prolong the QT interval and predispose to
ventricular arrhythmias. This effect seems to be more pro-
nounced in the presence of hypokalemia (71). A general
Review of Domperidone 2041
recommendation is to obtain a baseline electrocardiogram
(ECG) and serum potassium prior to initiation of domperi-
done. As with other class III antiarrhythmic agents, a QT
interval of >450 ms in males and 470 ms in females on the
baseline ECG or sustained hypokalemia settings would be a
contraindication to domperidone therapy (72).
Unlike metoclopramide, it has poor penetration of the
blood-brain barrier and therefore rarely causes CNS symp-
toms. No extra-pyramidal side effects have been reported dur-
ing controlled therapeutic trials with domperidone, although
there have been a few anecdotal reports of such effects (73–
76). Side effects with oral administration occur in fewer than
7% of patients and include headaches, dry mouth, diarrhea,
anxiety, and prolactin-related findings (77). Like metoclo-
pramide, domperidone can elevate serum prolactin concen-
trations, and so may induce breast tenderness and enlarge-
ment, galactorrhea (uncommon), and menstrual irregularities
including amenorrhea (2, 12, 77). Gynecomastia in men is
infrequently seen. Often these side effects are more inconve-
nient than serious, and patients who benefit from the drug are
generally willing to accept them (77). Domperidone stimu-
lates thyroid-stimulating hormone, but this does not seem to
have any clinical ramifications (78, 79). Plasma concentra-
tions of 18-hydroxycorticosterone, cortisol, and plasma renin
angiotensin are not altered by domperidone. Domperidone
does not stimulate aldosterone secretion in man (80).
Dopamine antagonists should not be given in conjunction
with monoamine oxidase (MAO) inhibitors. Stimulation of
DA2 receptors causes an inhibition of norepinephrine release
from presynaptic nerve terminals. Antagonists of the DA2
receptor would be expected to cause decreased inhibitory
control, facilitating the release of norepinephrine. Concomi-
tant administration of a MAO inhibitor would thereby impair
the body’s ability to metabolize this increased level of en-
dogenous norepinephrine. Because dopamine is broken down
by MAO, it is possible that during long-term treatment with
MAO inhibitors, dopamine could accumulate in sympathetic
nerve terminals leading to exaggerated end organ response
(81).
Dosage
In gastroparesis, and chronic nausea and vomiting, a maxi-
mal daily dose of 120 mg of domperidone is often required
and must be taken for at least a month before its efficacy
can be judged. Worldwide, domperidone is distributed as 10-
mg tablets. A liquid preparation and suppositories are also
available. Suppository forms of the drug are valuable for pa-
tients with nausea and vomiting who may not need hospital
admission but vomiting precludes any predictable absorption
from the oral route. The usual starting dosage is 20 mg taken
15 to 30 min before meals and at bedtime. This dosage can
be quickly increased to 30 mg q.i.d. if adequate control is
not experienced within a 2–4 wk period. An oral suspension
(1 mg/mL) may be used in a dosage of 0.3 mg/kg of body
weight three times a day and at bedtime for children. For
nausea and vomiting associated with agents for the treatment
2042 Reddymasu et al.
of Parkinson’s disease, the recommended adult dosage is up
to 20 mg four times a day. Patients with renal impairment
need to be dosed once or twice daily instead of four times a
day. No dose adjustment is needed in liver dysfunction (12).
Domperidone is available in the form of a tablet and can be
crushed and dissolved for administration through nasogastric,
gastrostomy, or jejunostomy tubes.
COMBINATION THERAPY
In a randomized double-blind trial of eight patients with dys-
pepsia combining cisapride (2.5 mg) with domperidone (10
mg three times daily), domperidone improved gastric empty-
ing more effectively than cisapride plus placebo (82). Com-
bining peripherally acting prokinetic agents with different
pharmacologic mechanisms, such as motilin receptor ago-
nists (erythromycin) and 5HT-4 agonists (tegaserod), with
a centrally acting adjunctive agent like domperidone would
seem to be clinically appropriate and a practical approach for
controlling nausea and vomiting while accelerating upper GI
motility.
SUMMARY
Domperidone is a prokinetic and antiemetic agent that is
useful in the management of gastrointestinal motility dis-
orders; the bulk of data supports its role in the management
of gastroparesis, particularly diabetic gastropathy. Its ther-
apeutic profile is similar to that of metoclopramide, but it
results in essentially no adverse CNS events, including extra-
pyramidal side effects. Domperidone is a safe alternative to
metoclopramide for patients who require long-term treatment
to control chronic GI symptoms, particularly where nausea
and vomiting are predominant. Domperidone could be used
to treat nausea and vomiting associated with anti-Parkinson
therapy and is also safe for use in children. By combining
its unique brain-gut mechanisms, domperidone should be a
valuable addition to our currently limited pharmacologic ar-
mamentarium for functional bowel diseases.
KEY POINTS
r Domperdione is a central and peripheral dopaminergic an-
tagonist but, unlike metoclopramide, it has no effects on
the central nervous system.
r Domperidone is an effective antiemetic, and improves gas-
tric motility, and is an alternative to metoclopramide.
r Domperidone can be used to help symptoms of gastro-
paresis and nausea and vomiting of any etiology including
that accompanying therapy for Parkinson’s disease.
r Domperidone is available in most of the countries world-
wide.
r Domperidone can be used in the United States by applying
for an investigational new drug program through the FDA.
r Domperidone dosing is 10 to 30 mg before meals and at
bed time and maximal doses of 120 mg/day should be
taken for at least one month to determine clinical efficacy.
r Side effects are related to increased prolactin, secretion
and occur in approximately 10% of patients, ranging form
gynecomastia to lactation and amenorrhea.
Reprint requests and correspondence: Richard W. McCallum,
M.D., Center for Gastrointestinal Motility, Division of Gastroen-
terology and Hepatology, The University of Kansas Medical Center,
3901 Rainbow Boulevard, MS-1058, Kansas City, KS 66160-7350.
Received October 30, 2006; accepted March 5,2007.
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CONFLICT OF INTEREST
Guarantor of the article: Richard W. McCallum, M.D.
Specific author contributions: Savio C. Reddymasu and
Irfan Soykan reviewed literature and drafted the manuscript.
Richard W. McCallum, as the senior author, edited the paper
for important intellectual content and supervised this project.
Financial support: None.
Potential competing interests: None.