Domperidone

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Not to be confused with Dom Pérignon or droperidol.
Domperidone
Domperidone 2D structure.svg
Domperidone ball-and-stick model.png
Clinical data
Trade names Motilium, many others
AHFS/Drugs.com Micromedex Detailed Consumer Information
Pregnancy
category
  • Not classified (US)
Routes of
administration		 Oral, intramuscular, intravenous (d/c'd), rectal[1]
ATC code A03FA03 (WHO) QP51AX24 (WHO)
Legal status
Legal status
  • Not approved for use or sale: US; prescription medicine (POM): India, Australia, Canada, Israel, Belgium; over-the-counter: UK (Prescription Only Medicine as of 4 September 2014), Egypt, Ireland, Italy, Japan, Netherlands, South Africa, Switzerland, China, Russia, Slovakia, Ukraine,[2] Thailand, Malta, South Korea, and Romania[3]
Pharmacokinetic data
Bioavailability Oral: 13–17%[1][4]
Intramuscular: 90%[1]
Protein binding ~92%[1]
Metabolism Hepatic (CYP3A4/5) and intestinal (first-pass)[1][5]
Metabolites All inactive[1][5]
Biological half-life 7.5 hours[1][4]
Excretion Feces: 66%[1]
Urine: 32%[1]
Breast milk: small quantities[1]
Identifiers
CAS Number 57808-66-9 YesY
PubChem (CID) 3151
IUPHAR/BPS 965
DrugBank DB01184 YesY
ChemSpider 3039 YesY
UNII 5587267Z69 YesY
KEGG D01745 YesY
ChEBI CHEBI:31515 YesY
ChEMBL CHEMBL219916 YesY
ECHA InfoCard 100.055.408
Chemical and physical data
Formula C22H24ClN5O2
Molar mass 425.911 g/mol
3D model (Jmol) Interactive image
Melting point 242.5 °C (468.5 °F)
  (verify)

Domperidone (INN, USAN, BAN, JAN) (brand name Motilium, many others) is a peripherally selective dopamine D2 receptor antagonist developed by Janssen Pharmaceutica that is used as an antiemetic, gastroprokinetic agent, and galactogogue.[1][6][7] It may be administered orally or rectally, and is available in the form of tablets, orally disintegrating tablets (based on Zydis technology),[8] suspension, and suppositories.[9] The drug is used to relieve nausea and vomiting; to increase the transit of food through the stomach (by increasing gastrointestinal peristalsis); and to promote lactation (breast milk production) by release of prolactin.[1][7]

Medical uses[edit]

The uses or indications of domperidone vary between nations. For instance, in Italy it is used in the treatment of gastroesophageal reflux disease and in Canada, the drug is indicated in upper gastrointestinal motility disorders and to prevent gastrointestinal symptoms associated with the use of dopamine agonist antiparkinsonian agents.[10] In the United States, domperidone is not currently a legally marketed human drug and it is not approved for sale in the U.S. On 7 June 2004, FDA issued a public warning that distributing any domperidone-containing products is illegal.[11] In the United Kingdom, domperidone is only indicated for the treatment of nausea and vomiting and the treatment duration is usually limited to 1 week.

It was reported in 2007 that domperidone is available in 58 countries, including Canada.[12]

Nausea and vomiting[edit]

There is some evidence that domperidone has antiemetic activity.[13] It is recommended in the Canadian Headache Society's guidelines for treatment of nausea associated with acute migraine.[14]

Gastroparesis[edit]

Gastroparesis is a medical condition characterised by delayed emptying of the stomach when there is no mechanical gastric outlet obstruction. Its cause is most commonly idiopathic, a diabetic complication or a result of abdominal surgery. The condition causes nausea, vomiting, fullness after eating, early satiety (feeling full before the meal is finished), abdominal pain and bloating.

Domperidone may be useful in diabetic and idiopathic gastroparesis.[15][16]

However, increased rate of gastric emptying induced by drugs like domperidone does not always correlate (equate) well with relief of symptoms.[17]

Parkinson's disease[edit]

Parkinson's disease is a chronic neurological condition where a decrease in dopamine in the brain leads to rigidity (stiffness of movement), tremor and other symptoms and signs. Poor gastrointestinal function, nausea and vomiting is a major problem for people with Parkinson's disease because most medications used to treat Parkinson's disease are given by mouth. These medications, such as levodopa can cause nausea as a side effect. Furthermore, anti-nausea drugs, such as metoclopramide, which do cross the blood–brain barrier may worsen the extra-pyramidal symptoms of Parkinson's disease.

Domperidone can be used to relieve gastrointestinal symptoms in Parkinson's disease, because, even though it blocks dopamine receptors (which would be expected to worsen Parkinson's disease), it does not cross the blood–brain barrier (the barrier between the blood circulation of the brain and the rest of the body).[18] In addition to this, domperidone may enhance the bioavailability (effect) of levodopa (one of the main treatments in Parkinson's disease).[19]

Although these features make domperidone a useful drug in Parkinson's disease, caution is needed due to the cardiotoxic side effects of domperidone especially when given intravenously, in elderly people and in high doses (> 30 mg per day).[20] A clinical sign of domperidone's potential toxicity to the heart is the prolongation (lengthening) of the QT interval (a segment of the heart's electrical pattern).[21]

Functional dyspepsia[edit]

Domperidone may be used in functional dyspepsia in both adults and children.[22][23]

Lactation[edit]

The hormone prolactin stimulates lactation (production of breast milk). Dopamine, released by the hypothalamus stops the release of prolactin from the pituitary gland. Domperidone, by acting as an anti-dopaminergic agent, results in increased prolactin secretion, and thus promotes lactation (that is, it is a galactogogue). In some nations, including Australia, domperidone is used off-label, based on uncertain and anecdotal evidence of its usefulness, as a therapy for mothers who are having difficulty breastfeeding.[24][25] In the United States, domperidone is not approved for this or any other use.[26][27] A study called the EMPOWER trial has been designed to assess the effectiveness and safety of domperidone in assisting mothers of preterm babies to supply breast milk for their infants.[28]

To induce lactation, domperidone is used at a dosage of 10 to 20 mg 3 or 4 times per day by mouth.[29] Effects may be seen within 24 hours or may not been seen for 3 or 4 days.[29] The maximum effect occurs after 2 or 3 weeks of treatment, and the treatment period generally lasts for 3 to 8 weeks.[29]

Pediatric reflux[edit]

Domperidone has been found effective in the treatment of pediatric reflux.[30] However some specialists consider it to be an excessively powerful drug for treating babies with reflux.[31]

Side effects[edit]

Side effects associated with domperidone include dry mouth, abdominal cramps, diarrhea, nausea, rash, itching, hives, and hyperprolactinemia (the symptoms of which may include breast enlargement, galactorrhea, breast pain/tenderness, gynecomastia, hypogonadism, and menstrual irregularities).[29] Due to blockade of D2 receptors in the central nervous system, D2 receptor antagonists like metoclopramide can also produce a variety of additional side effects including drowsiness, akathisia, restlessness, insomnia, lassitude, fatigue, extrapyramidal symptoms, dystonia, Parkinsonian symptoms, tardive dyskinesia, and depression.[1][7] However, this is not the case with domperidone, because, unlike other D2 receptor antagonists, it minimally crosses the blood-brain-barrier, and for this reason, is rarely associated with such side effects.[1][7]

Excess prolactin levels[edit]

Due to D2 receptor blockade, domperidone causes hyperprolactinemia.[32] Hyperprolactinemia can suppress the secretion of gonadotropin-releasing hormone (GnRH) from the hypothalamus, in turn suppressing the secretion of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) and resulting in hypogonadism (low sex hormone (e.g., testosterone, estradiol) levels).[33] As such, male patients may experience low libido, erectile dysfunction, and impaired spermatogenesis.[33] Also in accordance with hyperprolactinemia, 10–15% of female patients have been reported to experience mammoplasia (breast enlargement), mastodynia (breast pain/tenderness), galactorrhea (inappropriate or excessive milk production/secretion), and amenorrhea (cessation of menstrual cycles) with domperidone treatment.[32] Gynecomastia has been reported in males treated with domperidone,[34] and galactorrhea could occur in males as well.[33]

Rare reactions[edit]

Cardiac reactions[edit]

Domperidone use is associated with an increased risk of sudden cardiac death (by 70%)[35] most likely through its prolonging effect of the cardiac QT interval and ventricular arrhythmias.[36][37] The cause is thought to be blockade of hERG voltage-gated potassium channels.[38][39] The risks are dose-dependent, and appear to be greatest with high/very high doses via intravenous administration and in the elderly, as well as with drugs that interact with domperidone and increase its circulating concentrations (namely CYP3A4 inhibitors).[40][41] Conflicting reports exist, however.[42] In neonates and infants, QT prolongation is controversial and uncertain.[43][44]

UK drug regulatory authorities (MHRA) have issued the following restriction on domperidone in 2014 due to increased risk of adverse cardiac effects:

Domperidone (Motilium) is associated with a small increased risk of serious cardiac side effects. Its use is now restricted to the relief of nausea and vomiting and the dosage and duration of use have been reduced. It should no longer be used for the treatment of bloating and heartburn. Domperidone is now contraindicated in those with underlying cardiac conditions and other risk factors. Patients with these conditions and patients receiving long-term treatment with domperidone should be reassessed at a routine appointment, in light of the new advice.

However, a 2015 Australian review concluded the following:[41]

Based on the results of the two TQT (the regulatory agency gold standard for assessment of QT prolongation) domperidone does not appear to be strongly associated with QT prolongation at oral doses of 20 mg QID in healthy volunteers. Further, there are limited case reports supporting an association with cardiac dysfunction, and the frequently cited case-control studies have significant flaws. While there remains an ill-defined risk at higher systemic concentrations, especially in patients with a higher baseline risk of QT prolongation, our review does not support the view that domperidone presents intolerable risk.

Possible central toxicity in infants[edit]

In Britain a legal case involved the death of two children of a mother whose three children had all had hypernatraemia. She was charged with poisoning the children with salt. One of the children, who was born at 28 weeks gestation with respiratory complications and had a fundoplication for gastroesophageal reflux and failure to thrive was prescribed domperidone. An advocate for the mother suggested the child may have suffered neuroleptic malignant syndrome as a side effect of domperidone due to the drug crossing the child's immature blood-brain-barrier.[45]

Interactions[edit]

Domperidone is almost exclusively metabolized by CYP3A4, and for this reason, inhibitors and inducers of this enzyme may alter the metabolism and concentrations of domperidone. Moreover, domperidone has been identified as a modest mechanism-based (irreversible) inhibitor of CYP3A4 (Ki = 12 μM), and it has been estimated that it may increase the serum concentrations of CYP3A4 substrates by approximately 50%.[46]

Itraconazole and ketoconazole, both used to treat fungal infections, are potent CYP3A4 inhibitors and increase the plasma concentration of domperidone.[47][48] In healthy volunteers, ketoconazole increased the Cmax and AUC concentrations of domperidone by 3- to 10-fold.[49] This was accompanied by a QT interval prolongation of about 10–20 milliseconds when domperidone 10 mg four times daily and ketoconazole 200 mg twice daily were administered, whereas domperidone by itself at the dosage assessed produced no such effect.[49] As such, domperidone with ketoconazole or other CYP3A4 inhibitors is a potentially dangerous combination.[49]

Erythromycin and certain other macrolide antibiotics are CYP3A4 inhibitors and inhibit the metabolism of domperidone (in vitro), thus increasing the concentration of domperidone and potential side effects of the drug. This is of concern as both drugs may be used to treat gastroparesis.[50]

There is evidence that domperidone should not be taken with grapefruit juice, which is a known CYP3A4 inhibitor.[51]

Contraindications[edit]

Pharmacology[edit]

Pharmacodynamics[edit]

Domperidone is a peripherally selective dopamine D2 and D3 receptor antagonist.[7] It has no clinically significant interaction with the D1 receptor, unlike metoclopramide.[7] The drug provides relief from nausea by blocking receptors at the chemoreceptor trigger zone (a location in the nervous system that mediates nausea) at the floor of the fourth ventricle (a location near the brain). It increases motility in the upper gastrointestinal tract to a moderate degree and increases[53] lower esophageal sphincter pressure by blocking dopamine receptors in the gastric antrum and the duodenum. It blocks dopamine receptors in the anterior pituitary gland increasing release of prolactin which in turn increases lactation.[54][55] Domperidone may be more useful in some patients and cause harm in others by way of the genetics of the person, such as polymorphisms in the drug transporter gene ABCB1 (which encodes P-glycoprotein), the voltage-gated potassium channel KCNH2 gene (hERG/Kv11.1), and the α1D—adrenoceptor ADRA1D gene.[56]

Effects on prolactin levels[edit]

A single 20 mg oral dose of domperidone has been found to increase mean serum prolactin levels (measured 90 minutes post-administration) in non-lactating women from 8.1 ng/mL to 110.9 ng/mL (a 13.7-fold increase).[7][57][58][59] This was similar to the increase in prolactin levels produced by a single 20 mg oral dose of metoclopramide (7.4 ng/mL to 124.1 ng/mL; 16.7-fold increase).[58][59] After two weeks of chronic administration (30 mg/day in both cases), the increase in prolactin levels produced by domperidone was reduced (53.2 ng/mL; 6.6-fold above baseline), but the increase in prolactin levels produced by metoclopramide, conversely, was heightened (179.6 ng/mL; 24.3-fold above baseline).[7][59] This indicates that acute and chronic administration of both domperidone and metoclopramide is effective in increasing prolactin levels, but that there are differential effects on the secretion of prolactin with chronic treatment.[58][59] The mechanism of the difference is unknown.[59] The increase in prolactin levels observed with the two drugs was, as expected, much greater in women than in men.[58][59] This appears to be due to the higher estrogen levels in women, as estrogen stimulates prolactin secretion.[60]

For comparison, normal prolactin levels in women are less than 20 ng/mL, prolactin levels peak at 100 to 300 ng/mL at parturition in pregnant women, and in lactating women, prolactin levels have been found to be 90 ng/mL at 10 days postpartum and 44 ng/mL at 180 days postpartum.[61][62]

Effects on TSH levels[edit]

Along with prolactin, domperidone has, to a lesser extent, been found to increase the secretion of thyroid-stimulating hormone (TSH), even in patients with hypothyroidism.[58] A single 4 mg intravenous dose of domperidone produced peak TSH levels of 1.9-fold above baseline and peak prolactin levels of 23-fold above baseline (which occurred at 30 minutes post-administration) in women with hypothyroidism.[58] Levels of TSH and prolactin decreased to 1.6-fold and 17-fold above baseline, respectively, at 120 minutes post-administration.[58]

Pharmacokinetics[edit]

With oral administration, domperidone is extensively metabolized in the liver (almost exclusively by CYP3A4/5, though minor contributions by CYP1A2, CYP2D6, and CYP2C8 have also been reported)[63] and in the intestines.[5] Due to the marked first-pass effect via this route, the oral bioavailability of domperidone is low (13–17%);[1] conversely, its bioavailability is high via intramuscular injection (90%).[1] The terminal half-life of domperidone is 7.5 hours in healthy individuals, but can be prolonged to 20 hours in people with severe renal dysfunction.[1] All of the metabolites of domperidone are inactive as D2 receptor ligands.[1][5] The drug is a substrate for the P-glycoprotein (ABCB1) transporter, and animal studies suggest that this is the reason for the low central nervous system penetration of domperidone.[64]

Chemistry[edit]

Domperidone is a benzimidazole derivative and is structurally related to butyrophenone neuroleptics like haloperidol.[65][66]

History[edit]

  • 1974 – Domperidone synthesized at Janssen Pharmaceutica[67] following the research on antipsychotic drugs.[68] Janssen pharmacologists discovered that some of antipsychotic drugs had a significant effect on dopamine receptors in the central chemoreceptor trigger zone that regulated vomiting and started searching for a dopamine antagonist that would not pass the blood–brain barrier, thereby being free of the extrapyramidal side effects that were associated with drugs of this type.[68] This led to the discovery of domperidone as a strong anti-emetic with minimal central effects.[68][69]
  • 1978 – On 3 January 1978 Domperidone was patented in the United States under patent US4066772 A. The application has been filed on 17 May 1976. Jan Vandenberk, Ludo E. J. Kennis, Marcel J. M. C. Van der Aa and others has been cited as the inventors.
  • 1979 – Domperidone marketed under trade name "Motilium" in Switzerland and (Western) Germany.[70]
  • 1999 – Domperidone was introduced in the forms of orally disintegrating tablets (based on Zydis technology).[71]
  • Janssen Pharmaceutical has brought domperidone before the United States Federal Drug Administration (FDA) several times, including in the 1990s.
  • 2014 – In April 2014 Co-ordination Group for Mutual Recognition and Decentralised Procedures – Human (CMDh) published official press-release suggesting to restrict the use of domperidone-containing medicines. It also approved earlier published suggestions by Pharmacovigilance Risk Assessment Committee (PRAC) to use domperidone only for curing nausea and vomiting and reduce maximum daily dosage to 10 mg.[9]

Society and culture[edit]

Availability[edit]

Domperidone is available over-the-counter to treat gastroesophageal reflux and functional dyspepsia in many countries, such as Ireland, the Netherlands, Italy, South Africa, Mexico, Chile, and China.[72] Domperidone is not approved for use in the United States, but is prescribable and limitedly available in this country for use in people with treatment-refractory gastrointestinal symptoms under an FDA Investigational New Drug application.[1] In 2007, it was reported that domperidone was available in 58 countries.[1]

Formulations[edit]

Nation Manufacturer Brand Formulations
Australia Janssen–Cilag Motilium 10 mg scored tablets[52]
Belgium and the Netherlands - Motilium From 2013 only by prescription in Belgium.[73]
Bangladesh Square Motigut 10 mg scored tablets
Bangladesh Astra Pharma Domperon 10 mg scored tablets
Bangladesh - Ridon -
Canada - Motilium (1985–2002) Generic brands available
France Mylan Dompéridone 10 mg tablets
India Salius Pharma Escacid DXR pantoprazole 40 mg and domperidone SR 30 mg
India Medley pharmaceuticals Dompan pantoprazole 40 mg and domperidone 10 mg
India Rhubarb pharmaceuticals - domperidone 5, 10 and 20 mg tablets.
India Ipca Laboratories, Mumbai Domperi suspension domperidone 1 mg/ml, 30 ml suspension.[74]
India Torrent pharmaceuticals Domstal - [75]
India Ozone pharmaceuticals and chemicals Pantazone-D 10 mg domperidone and 40 mg pantoprazole
India Chimak Health Care Pancert D 10 mg Domperidone and 40 mg pantoprazole
India Draavin Pharma Draaci-XD Pantaprazole 40 mg and Domperione 30 mg
Iran Abidi Pharmaceutical Co. MOTiDON 10 mg tablet
Ireland McNeil Healthcare Motilium 10 mg orally disintegrating tablet (ODT)
Italy - Peridon domperidone 10 mg tablets; 30 ml suspension
Lithuania Johnson & Johnson Motilium -
Pakistan Johnson & Johnson Pakistan Motilium-v domperidone 10 mg tablets; 30 ml suspension
Pakistan ATCO Laboratories Limited Vomilux domperidone 10 mg tablets
Philippines Health Saver Pharma Abdopen -
Philippines United Laboratories, Inc. GI Norm -
Portugal Medinfar Cinet domperidone 1 mg/ml oral suspension (200 ml)
Russia Janssen Pharmaceutica Motilium domperidone 10 mg film-coated tablets & ODT; 1 mg/ml suspension (100 ml)
- OBL Pharm Passagix domperidone 10 mg film-coated tablets & chewable tablets
- Dr. Reddy's Laboratories Omez D domperidone/omeprazole (10 mg/10 mg)
Saudi Arabia JamJoom Pharmaceuticals Dompy Domperidone 10 mg tablets
Spain Laboratorios Dr. Esteve, SA Motilium domperidone 1mg/ml oral suspension (200 ml)
Sweden Ebb medical Domperidon Ebb (2013) domperidone 10 mg ODT and peppermint
Taiwan - Dotitone -
Thailand - Motilium M -
Turkey Saba Motinorm -
- GlaxoSmithKline Motinorm -

See also[edit]

References[edit]

  1. ^ a b c d e f g h i j k l m n o p q r s t Reddymasu, Savio C.; Soykan, Irfan; McCallum, Richard W. (2007). "Domperidone: Review of Pharmacology and Clinical Applications in Gastroenterology". The American Journal of Gastroenterology. 102 (9): 2036–2045. doi:10.1111/j.1572-0241.2007.01255.x. ISSN 0002-9270. 
  2. ^ "БРЮЛІУМ ЛІНГВАТАБС" [BRULIUM LINGUATABS]. Нормативно-директивні документи МОЗ України (in Ukrainian). 2014-03-18. Retrieved 2015-05-29. 
  3. ^ "Domperidone". Retrieved 2013-06-30. 
  4. ^ a b Suzanne Rose (October 2004). Gastrointestinal and Hepatobiliary Pathophysiology. Hayes Barton Press. pp. 523–. ISBN 978-1-59377-181-2. 
  5. ^ a b c d Simard, C.; Michaud, V.; Gibbs, B.; Massé, R.; Lessard, É; Turgeon, J. (2008). "Identification of the cytochrome P450 enzymes involved in the metabolism of domperidone". Xenobiotica. 34 (11-12): 1013–1023. doi:10.1080/00498250400015301. ISSN 0049-8254. 
  6. ^ Index Nominum 2000: International Drug Directory. Taylor & Francis. January 2000. pp. 366–. ISBN 978-3-88763-075-1. 
  7. ^ a b c d e f g h Barone JA (1999). "Domperidone: a peripherally acting dopamine2-receptor antagonist". The Annals of Pharmacotherapy. 33 (4): 429–40. PMID 10332535. 
  8. ^ "MOTILIUM INSTANTS PL 13249/0028" (PDF). Medicines and Healthcare Products Regulatory Agency. 23 February 2010. Archived (PDF) from the original on 31 October 2014. Retrieved 2014-10-31. 
  9. ^ a b "CMDh confirms recommendations on restricting use of domperidone-containing medicines: European Commission to take final legal decision". European Medicines Agency. 25 April 2014. Archived from the original on 30 January 2016. Retrieved 2014-10-31. 
  10. ^ "Domperidone - heart rate and rhythm disorders." Canadian adverse reactions newsletter. Government of Canada. January 2007 17(1)
  11. ^ "How to Obtain". Food and Drug Administration. 10 February 2015. Retrieved 24 February 2016. 
  12. ^ Reddymasu SC, Soykan I, McCallum RW (2007). "Domperidone: review of pharmacology and clinical applications in gastroenterology". Am. J. Gastroenterol. 102 (9): 2036–45. doi:10.1111/j.1572-0241.2007.01255.x. PMID 17488253. 
  13. ^ Swann IL, Thompson EN, Qureshi K (November 1979). "Domperidone or metoclopramide in preventing chemotherapeutically induced nausea and vomiting". British Medical Journal. 2 (6199): 1188. doi:10.1136/bmj.2.6199.1188 (inactive 2015-01-12). PMC 1597274Freely accessible. PMID 519355. 
  14. ^ Worthington I, Pringsheim T, Gawel MJ, Gladstone J, Cooper P, Dilli E, Aube M, Leroux E, Becker WJ (September 2013). "Canadian Headache Society Guideline: acute drug therapy for migraine headache". The Canadian Journal of Neurological Sciences. 40 (5 Suppl 3): S1–S80. PMID 23968886. 
  15. ^ Stevens JE, Jones KL, Rayner CK, Horowitz M (June 2013). "Pathophysiology and pharmacotherapy of gastroparesis: current and future perspectives". Expert Opinion on Pharmacotherapy. 14 (9): 1171–86. doi:10.1517/14656566.2013.795948. PMID 23663133. 
  16. ^ Silvers D, Kipnes M, Broadstone V, Patterson D, Quigley EM, McCallum R, Leidy NK, Farup C, Liu Y, Joslyn A (1998). "Domperidone in the management of symptoms of diabetic gastroparesis: efficacy, tolerability, and quality-of-life outcomes in a multicenter controlled trial. DOM-USA-5 Study Group". Clinical Therapeutics. 20 (3): 438–53. doi:10.1016/S0149-2918(98)80054-4. PMID 9663360. 
  17. ^ Janssen P, Harris MS, Jones M, Masaoka T, Farré R, Törnblom H, Van Oudenhove L, Simrén M, Tack J (September 2013). "The relation between symptom improvement and gastric emptying in the treatment of diabetic and idiopathic gastroparesis". The American Journal of Gastroenterology. 108 (9): 1382–91. doi:10.1038/ajg.2013.118. PMID 24005344. 
  18. ^ Shindler JS, Finnerty GT, Towlson K, Dolan AL, Davies CL, Parkes JD (December 1984). "Domperidone and levodopa in Parkinson's disease". British Journal of Clinical Pharmacology. 18 (6): 959–62. doi:10.1111/j.1365-2125.1984.tb02571.x. PMC 1463696Freely accessible. PMID 6529536. 
  19. ^ Nishikawa N, Nagai M, Tsujii T, Iwaki H, Yabe H, Nomoto M (2012). "Coadministration of domperidone increases plasma levodopa concentration in patients with Parkinson disease". Clinical Neuropharmacology. 35 (4): 182–4. doi:10.1097/WNF.0b013e3182575cdb. PMID 22751085. 
  20. ^ Lertxundi U, Domingo-Echaburu S, Soraluce A, García M, Ruiz-Osante B, Aguirre C (February 2013). "Domperidone in Parkinson's disease: a perilous arrhythmogenic or the gold standard?". Current Drug Safety. 8 (1): 63–8. doi:10.2174/1574886311308010009. PMID 23656449. 
  21. ^ Malek NM, Grosset KA, Stewart D, Macphee GJ, Grosset DG (June 2013). "Prescription of drugs with potential adverse effects on cardiac conduction in Parkinson's disease". Parkinsonism & Related Disorders. 19 (6): 586–9. doi:10.1016/j.parkreldis.2013.02.004. PMID 23522959. 
  22. ^ Xiao M, Qiu X, Yue D, Cai Y, Mo Q (2013). "Influence of hippophae rhamnoides on two appetite factors, gastric emptying and metabolic parameters, in children with functional dyspepsia". Hellenic Journal of Nuclear Medicine. 16 (1): 38–43. doi:10.1967/s002449910070 (inactive 2015-01-12). PMID 23529392. 
  23. ^ Huang X, Lv B, Zhang S, Fan YH, Meng LN (December 2012). "Itopride therapy for functional dyspepsia: a meta-analysis". World Journal of Gastroenterology. 18 (48): 7371–7. doi:10.3748/wjg.v18.i48.7371. PMC 3544044Freely accessible. PMID 23326147. 
  24. ^ Grzeskowiak LE, Lim SW, Thomas AE, Ritchie U, Gordon AL (February 2013). "Audit of domperidone use as a galactogogue at an Australian tertiary teaching hospital". Journal of Human Lactation. 29 (1): 32–7. doi:10.1177/0890334412459804. PMID 23015150. 
  25. ^ Donovan TJ, Buchanan K (2012). "Medications for increasing milk supply in mothers expressing breastmilk for their preterm hospitalised infants". The Cochrane Database of Systematic Reviews. 3: CD005544. doi:10.1002/14651858.CD005544.pub2. PMID 22419310. 
  26. ^ da Silva OP, Knoppert DC (September 2004). "Domperidone for lactating women". CMAJ. 171 (7): 725–6. doi:10.1503/cmaj.1041054. PMC 517853Freely accessible. PMID 15451832. 
  27. ^ "FDA warns against women using unapproved drug, domperidone to increase milk production." U.S. Food and Drug Administration 7 June 2004.
  28. ^ Asztalos EV, Campbell-Yeo M, daSilva OP, Kiss A, Knoppert DC, Ito S (2012). "Enhancing breast milk production with Domperidone in mothers of preterm neonates (EMPOWER trial)". BMC Pregnancy and Childbirth. 12: 87. doi:10.1186/1471-2393-12-87. PMC 3532128Freely accessible. PMID 22935052. 
  29. ^ a b c d Henderson, Amanda (2003). "Domperidone: Discovering New Choices for Lactating Mothers". AWHONN Lifelines. 7 (1): 54–60. doi:10.1177/1091592303251726. ISSN 1091-5923. 
  30. ^ Kapoor, A.K.; Raju, S.M. (2013). "7.2 Gastrointestinal Drugs". Illustrated Medical Pharmacology. JP Medical Ltd. p. 677. ISBN 9350906554. Retrieved 2014-10-31.  (Google Books)
  31. ^ Rebecca Smith (1 August 2014). "Fear that reflux treatment for babies will be denied under new Nice guidance". The Daily Telegraph. Archived from the original on 31 October 2014. Retrieved 2014-10-31. 
  32. ^ a b Elliott Proctor Joslin; C. Ronald Kahn (2005). Joslin's Diabetes Mellitus: Edited by C. Ronald Kahn ... [et Al.]. Lippincott Williams & Wilkins. pp. 1084–. ISBN 978-0-7817-2796-9. 
  33. ^ a b c Edmund S. Sabanegh, Jr. (20 October 2010). Male Infertility: Problems and Solutions. Springer Science & Business Media. pp. 83–. ISBN 978-1-60761-193-6. 
  34. ^ Gerald G. Briggs; Roger K. Freeman; Sumner J. Yaffe (28 March 2012). Drugs in Pregnancy and Lactation: A Reference Guide to Fetal and Neonatal Risk. Lippincott Williams & Wilkins. pp. 442–. ISBN 978-1-4511-5359-0. 
  35. ^ Leelakanok N, Holcombe A, Schweizer ML (2015). "Domperidone and Risk of Ventricular Arrhythmia and Cardiac Death: A Systematic Review and Meta-analysis". Clin Drug Investig. doi:10.1007/s40261-015-0360-0. PMID 26649742. 
  36. ^ van Noord C, Dieleman JP, van Herpen G, Verhamme K, Sturkenboom MC (November 2010). "Domperidone and ventricular arrhythmia or sudden cardiac death: a population-based case-control study in the Netherlands". Drug Safety. 33 (11): 1003–14. doi:10.2165/11536840-000000000-00000. PMID 20925438. 
  37. ^ Johannes CB, Varas-Lorenzo C, McQuay LJ, Midkiff KD, Fife D (September 2010). "Risk of serious ventricular arrhythmia and sudden cardiac death in a cohort of users of domperidone: a nested case-control study". Pharmacoepidemiology and Drug Safety. 19 (9): 881–8. doi:10.1002/pds.2016 (inactive 2015-01-12). PMID 20652862. 
  38. ^ Rossi M, Giorgi G (2010). "Domperidone and long QT syndrome". Curr Drug Saf. 5 (3): 257–62. doi:10.2174/157488610791698334. PMID 20394569. 
  39. ^ Doggrell SA, Hancox JC (2014). "Cardiac safety concerns for domperidone, an antiemetic and prokinetic, and galactogogue medicine". Expert Opin Drug Saf. 13 (1): 131–8. doi:10.1517/14740338.2014.851193. PMID 24147629. 
  40. ^ Marzi, Marta; Weitz, Darío; Avila, Aylén; Molina, Gabriel; Caraballo, Lucía; Piskulic, Laura (2015). "Efectos adversos cardíacos de la domperidona en pacientes adultos: revisión sistemática". Revista médica de Chile. 143 (1): 14–21. doi:10.4067/S0034-98872015000100002. ISSN 0034-9887. 
  41. ^ a b Buffery PJ, Strother RM (2015). "Domperidone safety: a mini-review of the science of QT prolongation and clinical implications of recent global regulatory recommendations". N. Z. Med. J. 128 (1416): 66–74. PMID 26117678. 
  42. ^ Ortiz, Arleen; Cooper, Chad J.; Alvarez, Alicia; Gomez, Yvette; Sarosiek, Irene; McCallum, Richard W. (2015). "Cardiovascular Safety Profile and Clinical Experience With High-Dose Domperidone Therapy for Nausea and Vomiting". The American Journal of the Medical Sciences. 349 (5): 421–424. doi:10.1097/MAJ.0000000000000439. ISSN 0002-9629. 
  43. ^ Djeddi D, Kongolo G, Lefaix C, Mounard J, Léké A (November 2008). "Effect of domperidone on QT interval in neonates". The Journal of Pediatrics. 153 (5): 663–6. doi:10.1016/j.jpeds.2008.05.013. PMID 18589449. 
  44. ^ Günlemez A, Babaoğlu A, Arisoy AE, Türker G, Gökalp AS (January 2010). "Effect of domperidone on the QTc interval in premature infants". Journal of Perinatology. 30 (1): 50–3. doi:10.1038/jp.2009.96 (inactive 2015-01-12). PMC 2834362Freely accessible. PMID 19626027. 
  45. ^ Coulthard MG, Haycock GB (January 2003). "Distinguishing between salt poisoning and hypernatraemic dehydration in children". BMJ (Clinical Research Ed.). 326 (7381): 157–60. doi:10.1136/bmj.326.7381.157. PMC 1128889Freely accessible. PMID 12531853. 
  46. ^ Chang SY, Fancher RM, Zhang H, Gan J (2010). "Mechanism-based inhibition of human cytochrome P4503A4 by domperidone". Xenobiotica. 40 (2): 138–45. doi:10.3109/00498250903406762. PMID 20082577. 
  47. ^ Yoshizato T, Kotegawa T, Imai H, Tsutsumi K, Imanaga J, Ohyama T, Ohashi K (September 2012). "Itraconazole and domperidone: a placebo-controlled drug interaction study". European Journal of Clinical Pharmacology. 68 (9): 1287–94. doi:10.1007/s00228-012-1258-x. PMID 22418831. 
  48. ^ Boyce MJ, Baisley KJ, Warrington SJ (March 2012). "Pharmacokinetic interaction between domperidone and ketoconazole leads to QT prolongation in healthy volunteers: a randomized, placebo-controlled, double-blind, crossover study". British Journal of Clinical Pharmacology. 73 (3): 411–21. doi:10.1111/j.1365-2125.2011.04093.x. PMC 3370345Freely accessible. PMID 21883386. 
  49. ^ a b c Jeffrey K. Aronson (27 November 2009). Meyler's Side Effects of Antimicrobial Drugs. Elsevier. pp. 2244–. ISBN 978-0-08-093293-4. 
  50. ^ Ung D, Parkman HP, Nagar S (October 2009). "Metabolic interactions between prokinetic agents domperidone and erythromycin: an in vitro analysis". Xenobiotica. 39 (10): 749–56. doi:10.1080/00498250903096121. PMID 19575604. 
  51. ^ "Grapefruit, Medicine Interaction Warning Expanded". ABC News. 26 November 2012. Archived from the original on 31 October 2014. Retrieved 2014-10-31. 
  52. ^ a b Swannick G. (ed.) "MIMS Australia." December 2013
  53. ^ Bron B, Massih L (1980). "Domperidone: A drug with powerful action on the lower esophageal sphincter pressure". Digestion. 20 (6): 375–8. doi:10.1159/000198476. PMID 7409348. 
  54. ^ Saeb-Parsy K. "Instant pharmacology." John Wiley & Sons, 1999 ISBN 0471976393, 9780471976394 p216.
  55. ^ Sakamoto Y, Kato S, Sekino Y, Sakai E, Uchiyama T, Iida H, Hosono K, Endo H, Fujita K, Koide T, Takahashi H, Yoneda M, Tokoro C, Goto A, Abe Y, Kobayashi N, Kubota K, Maeda S, Nakajima A, Inamori M (2011). "Effects of domperidone on gastric emptying: a crossover study using a continuous real-time 13C breath test (BreathID system)". Hepato-gastroenterology. 58 (106): 637–41. PMID 21661445. 
  56. ^ Parkman HP, Jacobs MR, Mishra A, Hurdle JA, Sachdeva P, Gaughan JP, Krynetskiy E (January 2011). "Domperidone treatment for gastroparesis: demographic and pharmacogenetic characterization of clinical efficacy and side-effects". Digestive Diseases and Sciences. 56 (1): 115–24. doi:10.1007/s10620-010-1472-2. PMID 21063774. 
  57. ^ Gabay MP (2002). "Galactogogues: medications that induce lactation". J Hum Lact. 18 (3): 274–9. PMID 12192964. 
  58. ^ a b c d e f g Hofmeyr GJ, Van Iddekinge B, Blott JA (1985). "Domperidone: secretion in breast milk and effect on puerperal prolactin levels". Br J Obstet Gynaecol. 92 (2): 141–4. PMID 3882143. 
  59. ^ a b c d e f Brouwers JR, Assies J, Wiersinga WM, Huizing G, Tytgat GN (1980). "Plasma prolactin levels after acute and subchronic oral administration of domperidone and of metoclopramide: a cross-over study in healthy volunteers". Clin. Endocrinol. (Oxf). 12 (5): 435–40. PMID 7428183. 
  60. ^ Fujino T, Kato H, Yamashita S, Aramaki S, Morioka H, Koresawa M, Miyauchi F, Toyoshima H, Torigoe T (1980). "Effects of domperidone on serum prolactin levels in human beings". Endocrinol. Jpn. 27 (4): 521–5. PMID 7460861. 
  61. ^ Jan Riordan (January 2005). Breastfeeding and Human Lactation. Jones & Bartlett Learning. pp. 76–. ISBN 978-0-7637-4585-1. 
  62. ^ Kenneth L. Becker (2001). Principles and Practice of Endocrinology and Metabolism. Lippincott Williams & Wilkins. pp. 147–. ISBN 978-0-7817-1750-2. 
  63. ^ Youssef AS, Parkman HP, Nagar S (2015). "Drug-drug interactions in pharmacologic management of gastroparesis". Neurogastroenterol. Motil. 27 (11): 1528–41. doi:10.1111/nmo.12614. PMID 26059917. 
  64. ^ Stan K. Bardal; Jason E. Waechter; Douglas S. Martin (2011). Applied Pharmacology. Elsevier Health Sciences. pp. 184–. ISBN 1-4377-0310-0. 
  65. ^ Hospital Formulary. HFM Publishing Corporation. 1991. p. 171. Domperidone, a benzimidazole derivative, is structurally related to the butyrophenone tranquilizers (eg, haloperidol (Haldol, Halperon]). 
  66. ^ Giovanni Biggio; Erminio Costa; P. F. Spano (22 October 2013). Receptors as Supramolecular Entities: Proceedings of the Biannual Capo Boi Conference, Cagliari, Italy, 7-10 June 1981. Elsevier Science. pp. 3–. ISBN 978-1-4831-5550-0. 
  67. ^ Wan EW, Davey K, Page-Sharp M, Hartmann PE, Simmer K, Ilett KF (2008-05-27). "Dose-effect study of domperidone as a galactagogue in preterm mothers with insufficient milk supply, and its transfer into milk". British Journal of Clinical Pharmacology, August 2008. 66 (2): 283–289. doi:10.1111/j.1365-2125.2008.03207.x. PMC 2492930Freely accessible. PMID 18507654. 
  68. ^ a b c Sneader, Walter (2005). "Plant Product Analogues and Compounds Derived from Them". Drug discovery : a history. Chichester: John Wiley & Sons Ltd. p. 125. ISBN 0-471-89979-8. 
  69. ^ Corsini, Giovanni Umberto (2010). "Apomorphine: from experimental tool to therpeutic aid". In Ban, Thomas A; Healy, David & Shorter, Edward. The Triumph of Psychopharacology and the Story of CINP. CINP. p. 54. ISBN 9634081819. Archived from the original (PDF) on 2014-11-01. 
  70. ^ "Domperidone". Pharmaceutical Manufacturing Encyclopedia, 3rd Edition (Vol. 1-4). William Andrew Publishing. 2013. p. 138. ISBN 9780815518563. Retrieved 2014-12-12. 
  71. ^ Rathbone, Michael J.; Hadgraft, Jonathan; Roberts, Michael S. (2002). "The Zydis Oral Fast-Dissolving Dosage Form". Modified-Release Drug Delivery Technology. CRC Press. p. 200. ISBN 9780824708696. Retrieved 2014-10-31. 
  72. ^ Fais, Paolo; Vermiglio, Elisa; Laposata, Chiara; Lockwood, Robert; Gottardo, Rossella; De Leo, Domenico (2015). "A case of sudden cardiac death following Domperidone self-medication". Forensic Science International. 254: e1–e3. doi:10.1016/j.forsciint.2015.06.004. ISSN 0379-0738. 
  73. ^ "De Standaard: "Motilium from now on only with prescription"". standaard.be. 2013-05-07. Retrieved 2013-10-03. 
  74. ^ "ipcalabs.com". ipcalabs.com. Retrieved 2013-06-30. 
  75. ^ "torrentpharma.com". torrentpharma.com. Retrieved 2013-06-30. 

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