Pharmacology for Dentistry

Antacids and Antiulcer Agents 265

persists for much longer as it strongly binds
to H+ K+ ATPase. The disposition is not
altered in patients with renal disease or in
those undergoing haemodialysis. Increased
age and liver disease delays plasma clearance
of the drug but this does not necessitate
dosage adjustment in these patients.

It is indicated in:

• Treatment of duodenal ulcer.


• Treatment of gastric ulcer.


• Treatment of reflux oesophagitis.


• For control of acid secretion in patients
  of Zollinger-Ellison syndrome.
  It is well tolerated. Nausea, headache,
  diarrhoea, constipation and flatulence have
  been reported occasionally, Rarely skin rash
  has occurred in few patients.

RABEPRAZOLE

Rabeprazole belongs to substituted ben-
zimidazole proton-pump inhibitors. In
gastric parietal cells, rabeprazole is proto-
nated, accumulates and is transformed to
an active sulfenamide.

Following oral administration of 20 mg,
rabeprazole is absorbed and can be detected
in plasma by one hour. Rabeprazole is 96.3%
bound to plasma proteins.

Rabeprazole is extensively metabolized.
The thioether and sulfone are the primary
inactive metabolites. 90% of the drug is
eliminated in the urine, primarily as
thioether carboxylic acid, its glucuronide
and mercapturic acid metabolites.

It is indicated in erosive and ulcerative
gastroesophageal reflux disease, healing of
duodenal ulcers and Zollinger Ellison syndrome.

Adverse effects include nausea, diarr-

hoea, skin eruptions, headache and dizziness.

Other proton pump inhibitors e.g., lanso-

prazole is more potent than omeprazole and

has higher bioavailability, rapid onset of ac-

tion and longer duration of action.

Pantoprazole is the new H+K+ATPase inhibi-

tor with similar properties and action to

omeprazole.

PROSTAGLANDIN ANALOGUES

PGE 2 and PGI 2 are the main prostaglandins

synthesized by gastric mucosa. They decrease

acid secretion and improve mucosal defense

mechanism by:

• Stimulation of synthesis and release of
  mucus.


• Enhance bicarbonate production.


• Enhancement of tight junctions of cell
  membrane architecture.


• Inhibit gastrin production.


• Stimulation of a number of cellular
  transport processes.


• Stimulation of DNA content in
  damaged gastric mucosa by a process
  termed as cytoprotection.
  The important use of prostaglandin
  analogues is in the arthritic patients who are
  on chronic use of NSAID’s and are not
  responding to H 2 receptor antagonists.

MISOPROSTOL

200 μg QID was of similar efficacy to

cimetidine 300 mg TDS in healing duodenal

and gastric ulcer. Pain relief occurred more

slowly than with cimetidine. Shown to heal

erosions, ulcers due to NSAIDs.