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Dosage and Directions for Use :
In Peptic Ulceration:

The usual dosage is 150 mg twice daily, taken in the morning and before retiring, or a single bedtime dose of 300 mg. It is not necessary to time the dose in relation to meals. In most cases of duodenal ulcer and benign gastric ulcer, healing may occur in four weeks. Ulcers that do not heal within 4 weeks may require a further course of treatment. In ulcers following non-steroidal anti-inflammatory therapy or associated with continued non-steroidal anti-inflammatory agents, 8 - 12 weeks treatment may be necessary

For the prevention of non-steroidal anti-inflammatory agent associated ulcers:
RANITIDINE 150 mg twice daily may be given concomitantly with non-steroidal anti- inflammatory therapy.
For ulcers associated with Helicobacter pylori infection:
RANITIDINE may be used in combination with appropriate antibiotics.
Maintenance Treatment :
For patients with peptic ulceration who have responded to short-term therapy, particularly those with a history of recurrent ulcer, extended maintenance treatment at a reduced dosage of 150 mg at bedtime is advised. Smoking is associated with a higher rate of ulcer relapse. Patients should be advised to stop smoking. In patients unable to stop smoking, a dose of 300 mg at night provides additional therapeutic benefit in these patients over the 150 mg dosage regimen.
In Reflux Oesophagitis :
To help in the management of reflux oesophagitis, the recommended course of treatment is 150 mg twice daily or 300 mg at bedtime for up to 8, or if necessary, 12 weeks. In patients with moderate to severe reflux oesophagitis, the dosage may be increased to 150 mg four times daily for up to 12 weeks. For the long-term management of reflux oesophagitis the recommended adult oral dose is 150 mg twice daily
In Zollinger-Ellison Syndrome :
In patients with very high gastric acid secretion (eg. Zollinger-Ellison Syndrome) the starting dose is 150 mg three times daily and this may be increased as necessary, to within the range of 600 mg to 900 mg per day.
In Anaesthesia :
For premedication prior to anaesthesia in order to reduce the volume and acid content of gastric secretion, a dose of 300 mg given at least 2 hours before induction is indicated to minimise the consequences of the acid aspiration syndrome. Alternatively, a dose of 150 mg given 12 hours prior, followed by a further 150 mg 2 hours prior to anaesthesia, is effective in suppressing gastric secretion
Oral Dose 150mg / 300mg :

Foreign studies have shown that patients heal equally well with
150 mg b.i.d. and 300 mg h.s. (85% versus 84%, respectively)
during a usual 4-week course of therapy.

If patients require extended therapy of 8 weeks, the healing rate may be higher for 150 mg b.i.d. as compared to 300 mg h.s. (92% versus 87%, respectively).

IV and IM Injection, not for Direct Infusion :
Serum concentrations necessary to inhibit 50% of stimulated gastric acid secretion are estimated to be 36 to 94 ng/ml. Following single IV or intramuscular (IM) 50-mg doses, serum concentrations of ranitidine HCl are in this range for 6 to 8 hours.

Following IV injection, approximately 70% of the dose is recovered in the urine as unchanged drug. Renal clearance averages 530 ml per minute, with a total clearance of 760 ml per minute. The volume of distribution is 1.4 l/kg, and the elimination half-life is 2 to 2.5 hours.

Four patients with clinically significant renal function impairment (creatinine clearance 25 to 35 ml per minute) administered 50 mg of ranitidine intravenously had an average plasma half-life of 4.8 hours, a ranitidine clearance of 29 ml per minute, and a volume of distribution of 1.76 l/kg. In general, these parameters appear to be altered in proportion to creatinine clearance.

After IM injection, Ranitidine HCl is absorbed very rapidly. Mean peak levels of 576 ng/ml occur within 15 minutes or less following a 50-mg IM dose. Absorption from IM sites is virtually complete, with a bioavailability of 90% to 100% compared with IV administration. Following oral administration, the relative bioavailability of ranitidine HCl tablets is 50%.

In humans, the N-oxide is the principal metabolite in the urine; however, this amounts to less than 4% of the dose. Other metabolites are the S-oxide (1%) and the desmethyl ranitidine (1%). The remainder of the administered dose is found in the stool.
Studies in patients with hepatic dysfunction (compensated cirrhosis) indicate that there are minor, but clinically insignificant, alterations in ranitidine half-life, distribution, clearance, and bioavailability.
Serum protein binding averages 15%.

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