UTIL Capsule

Known hypersensitivity to Esomeprazole, substituted benzimidazoles or any of the excipients.

Uncommon

Peripheral oedema, Insomnia, Dizziness, Paraesthesia, Somnolence, Vertigo, Dry mouth, Increased liver enzymes, Dermatitis, Pruritus, Rash, Urticaria

Common

Headache Abdominal pain, Constipation, Diarrhoea, Flatulence, Nausea/Vomiting.

Rare

Leukopenia, Thrombocytopenia, Hypersensitivity reactions (e.g. Fever, Angioedema and Anaphylactic reactions/shock), Hyponatraemia, Agitation, Confusion, Depression, Taste disturbance, Blurred vision, Bronchospasm, Stomatitis, Gastrointestinal candidiasis, Alopecia, Photosensitivity, Arthralgia, Myalgia, Increased sweating.

Very rare

Agranulocytosis, Pancytopenia, Aggression, Hallucinations, Hepatic failure, Encephalopathy in patients with pre-existing liver disease, Erythema multiforme, Stevens-Johnson syndrome, Toxic Epidermal Necrolysis (TEN), Muscular weakness, Interstitial nephritis.

Concomitant use of atazanavir and nelfinavir with proton pump inhibitors is not recommended.

Esomeprazole may potentially interfere with CYP2C19, the major Esomeprazole metabolizing enzyme. Co-administration of Esomeprazole 20mg and diazepam, a CYP2C19 substrate, resulted in a 45% decrease in clearance of diazepam. Avoid concomitant administration of Esomeprazole with clopidogrel. When using Esomeprazole, consider use of alternative anti-platelet therapy.

Drug-induced decrease in gastric acidity results in enterochromaffin-like cell hyperplasia and increased Chromogranin A levels which may interfere with investigations for neuroendocrine tumors.

Co-administration of Esomeprazole, clarithromycin, and amoxicillin has resulted in increases in the plasma levels of Esomeprazole and 14-hydroxyclarithromycin.

Pregnancy

For Esomeprazole, clinical data on exposed pregnancies are insufficient.

Lactation

Esomeprazole is likely present in human milk. Esomeprazole is the S-isomer of omeprazole and limited data indicate that maternal doses of Esomeprazole 20mg daily produce low levels in human milk. Caution should be exercised when Util is administered to a nursing woman.

In the presence of any alarm symptom (e.g. significant unintentional weight loss, recurrent vomiting, dysphagia, haematemesis or melaena) and when gastric ulcer is suspected or present, malignancy should be excluded, as treatment with Util may alleviate symptoms and delay diagnosis. Patients on long-term treatment (particularly those treated for more than a year) should be kept under regular surveillance. Patients on on-demand treatment should be instructed to contact their physician if their symptoms change in character. When prescribing Esomeprazole for on demand therapy, the implications for interactions with other pharmaceuticals, due to fluctuating plasma concentrations of Esomeprazole should be considered. When prescribing Esomeprazole for eradication of Helicobacter pylori possible active substance interactions of all components in the triple therapy should be considered. Patients with rare hereditary problems of fructose intolerance, glucose-galactose malabsorption or sucrose-isomaltase insufficiency should not take this medicine.

Esomeprazole is a proton pump inhibitor that suppresses gastric acid secretion by specific inhibition of the H+/K+-ATPase in the gastric parietal cell. The S- and R-isomers of omeprazole are protonated and converted in the acidic compartment of the parietal cell forming the active inhibitor, the chiral sulphonamide. By acting specifically on the proton pump, esomeprazole blocks the final step in acid production, thus reducing gastric acidity. This effect is dose-related up to a daily dose of 20mg to 40mg and leads to inhibition of gastric acid secretion.

PHARACOKINETICS

Esomeprazole is a compound that inhibits gastric acid secretion and is indicated in the treatment of gastroesophageal reflux disease (GERD), the healing of erosive esophagitis, and H-pylori eradication to reduce the risk of duodenal ulcer recurrence. Esomeprazole belongs to a new class of antisecretory compounds, the substituted benzimidazoles, that do not exhibit anticholinergic or H2 histamine antagonistic properties, but that suppress gastric acid secretion by specific inhibition of the H+/K+-ATPase at the secretory surface of the gastric parietal cell. By doing so, it inhibits acid secretion into the gastric lumen. This effect is dose-related and leads to inhibition of both basal and stimulated acid secretion irrespective of the stimulus.