Talk on gastic disorders and rabeprazole

Gastric Acid Disorders

Effective treatment

using Rabeprazol

Dr Anshu P Gokarn MBBS, MD(Pharmacology)

How my talk is structured

1. Physiology of Gastric acid secretion

2. Overview of Gastric Acid-Related

Disorders

3. Gastroesophageal Reflux Disease

4. Drugs used in GERD – proton pump

inhibitors

5. Rabeprazol

22 Dr Anshu P Gokarn

Part 1

Part 2

Part I

3 Dr Anshu P Gokarn


Effective treatment

using Rabeprazol





Disorders



inhibitors

5. Rabeprazol


Stomach

Main Functions

Storage

Preparing the chyme for digestion in the

small intestine

Absorption of water and lipid-soluble

substances (alcohol and drugs)


Stomach


Stomach

Types of Gland (located in gastric mucosa):

Cardiac Glands

Pyloric glands (many G cells)

Oxyntic glands (most abundant, found in

fundus and corpus)


Chief Cell

Surface Mucous Cell

Mucous Neck Cell

Panetal Cell

Endocrine Cell

Isthmus

Gastric Pit (Ioveola)

Oxyntic Gland

Neck

Base


Stomach Cells

Types of Cells

Parietal cells

most distinctive cells in stomach (HCl &

intrinsic factor)

Chief cells

pepsinogen

Mucus neck cells:

- HCO3-

- Mucus


Types of Cells

G Cells: Gastrin (hormone) ---> HCl secretion

D Cells: Somatostatin (antrum)

Enterochromaffin-like cell: Histamine


Types of Cells


Gastric juices

HCl (hydrochloric acid)

Pepsinogen

Electrolytes

Intrinsic factor

Mucus (mucus gel layer)

pH ~4


Gastric motility

Functions

1. Allows the stomach to serve as

reservoir

2. Breaks food to small particles and mix

it with gastric juice

3. Empties gastric contents at a

controlled rate


Gastric motility

Reservoir part

fundus + 1/3 corpus

(tonic contraction)

Antral pump

2/3 corpus + antrum & pylorus

(phasic contraction)



Gastric motility

Anatomic Regions Functional Motor

Regions

Mixing & emptying of gastric contents

Gastric contents may remain unmixed (1h)

Fat takes a longer time for empty

Liquids are emptied easier and first

Major mixing activities are in the antrum

Retropulsion



Mixing & emptying of gastric contents


Constriction of pyloric sphincter

Constriction of pyloric sphincter

Hormones promote constriction

1. CCK

2. Secretin

3. Gastrin

4. GIP

Sympathetic innervation


Regulation of gastric emptying

Acidity (stomach) Secretin antral contraction

Fat (monoglycerides) CCK, GIP gastric emptying

Hyperosmotic solutions gastric emptying

Amino acids G cells Gastrin contraction of sphincter



Gastric reservoir

Functions:

To maintain a continuous compression

To accommodate the received food with

out significant gastric wall distention or

pressure


Receptive relaxation

- triggered by swallowing reflex

Adaptive relaxation

- triggered by stretch receptors (vago-vagal

reflex)

- lost in vagotomy

- threshold of fullness and pain

Feedback relaxation

- triggered by chyme in small intestine

Relaxation in gastric reservoir


Gastric juices

HydroChloric Acid (HCl) Secretion

Secreted by parietal cells

Fundus

Body


Gastric juices – HCl Secretion


HCl Secretion (cont)

Mechanism of HCl production:

H/K ATPase

Inhibited by: omeprazole

H/K pump depends on [K]out

[HCl] drives water into gastric content to

maintain iso-osmolality

During gastric acid secretion:

amount of HCO3- in blood = amount of HCl

being secreted

Alkaline tide


Neural & Hormonal Control of Gastric

Secretion

Vagus nerve (neural effector)

Gastrin (hormonal effector)

Enterochromaffin-like cellsHistamine ---

H2 receptor (parietal cells) acid secretion

Cimetidine (H2 receptor blocker) peptic ulcer and

gastroesophageal reflux




Secretion


Secretion


Phases of Acid Secretion

Cephalic phase(30%): Smelling, Chewing and swallowing

Stimulates parietal G-Cells

GRP

Gastric phase (60%): gastric distention

proteins

Intestinal phase (10%):

digested proteins


Regulation of Acid Secretion


Inhibition of Acid Secretion

Inhibitory hormones (Enterogastrones):

Somatostatin (D-cells) in antrum

Secretin (S-cells) in duodenum

Glucose-dependent insulinotropic peptide

(GIP) in duodenum


Mechanism of gastric acid secretion

Gastrin Histamine

Acetylcholine

Ca2+

HCI

Protein kinases Protein kinases Protein kinases Protein kinases

Ca2+ Ca2+

Release of Ca2+ from

intracellular stores

Release of Ca2+ from

intracellular stores

cAMP cAMP

Protein

kinases

Protein

kinases

Release of Ca2+ from intracellular stores

Release of Ca2+ from intracellular stores

ACh (M3)

Ca2+ Ca2+

H

K

K

Cl

Cl

HCl

AcidAcid pumppump



Activation of H1K ATPase




Disorders



inhibitors

5. Rabeprazol


Aspirin and other NSAIDs

PROTECTIVE FACTORS

Mucus layer

Ionic gradient

Bicarbonate layer

Prostaglandins

Surface epithelial cells

Mucosal blood supply

H. pylori Pepsin Gastric

acid

AGGRESSIVE FACTORS

Aspirin and other NSAIDs

Prostaglandin production

Bicarbonate production

Mucus production

Acidic environment

Neutral environment

Gastric acid plays a central role in

NSAID-associated gastroduodenal damage


Helicobacter pylori


IL-8

Proteolytic

enzymes

O2 radicals

Infection with H. pylori results in an

acute inflammatory reaction

Epithelial cell

Polymorph





Disorders



inhibitors

5. Rabeprazol


Gastroesophageal reflux disease


Gastroesophageal reflux

disease (GERD) is a chronic,

relapsing condition with

associated morbidity and an

adverse impact on quality of

life. The disease is common,

with an estimated lifetime

prevalence of 25 to 35

percent.



An approximated 2% of

the adult population

suffer from GERD all

over the world.

The incidence of GERD

increases markedly

after the age of 40.

Dr Anshu P Gokarn 46


Complications of GERD

Barrett’s esophagus

Esophageal strictures

Carcinomas

Barrett’s esophagus

Gastric Cancer Esophageal strictures 4747 Dr Anshu P Gokarn

Lifestyle modification should be initiated and

continued throughout the course of GERD

therapy

Antacids and over-the-counter acid

suppressants are appropriate, initial patient-

directed therapy for GERD.

Acid suppression by PPIs which provide

symptomatic relief and healing of esophagitis

Guidelines for management of GERD

DeVault RK et al,The American Journal of Gastroenterology 1999:94(6): 1434-42


Guidelines contd.

Chronic proton pump inhibitor therapy is an

effective and appropriate form of maintenance

therapy in many patients.

Antireflux surgery, performed by an

experienced surgeon, is a maintenance option

for the patient with well-documented GERD.

DeVault RK et al,The American Journal of Gastroenterology1999:94(6):1434-42





Disorders


4. Drugs used in GERD

5. Proton Pump Inhibitors - Rabeprazol


Proton-pump inhibitors (PPIs) - pronounced and long-

lasting reduction of gastric acid production

Most potent inhibitors of acid secretion available.

Largely superseded another group of pharmaceuticals

called H2-receptor antagonists.

Biological target Hydrogen potassium ATPase

Proton pump inhibitors


Proton pump inhibitors


End of Part – I

any questions ?any questions ?

Part II

59 Dr Anshu P

Gokarn


Effective treatment

using Rabeprazol





Disorders



inhibitors

5. Rabeprazol


Part 1

Part 2

MODERN ZEN


Rabeprazole

• Novel Proton pump inhibitor

• Acid suppression with once-daily dosing

• Consistent symptom control

• Significantly effective healing rates in erosive

GERD.

Prakash A., Faulds. D .Rabeprazle, Drugs 1998 Feb; 55 (2),28,260-6


Chemistry

Substituted benzimidazole sulfoxide

Empirical Formula C18H20N3NaO3S

Molecular weight 381.43


• Produrg

• Transformed at low pH to a more reactive

species, a Sulfenamide.

• Sulfenamide reacts with thiol group on

gastric (H+K+)-ATPase.

Structure activity relationship

Yun Hee jang, Hojing Kim; Quantam Chemical study of proton pump inhibiting activity of Substituted

2-Sunfinylbenimidazoles; Korean Jour. Of Med. Chem., VOl 2, No. 2, 1992


Reduced side effect profile

• Irreversible disulphide bond with the enzyme

(ATPase)

• Binding to the Proton Pumps is partially

reversible.



Pyridine nitrogen and the nitrogen near

benzimidazole 2-position – responsible for

the activity of rabeprazole.

Yun Hee jang, Hojing Kim; Quantam Chemical study of proton pump inhibiting activity of

Substituted 2-Sunfinylbenimidazoles; Korean Jour. Of Med. Chem., VOl 2, No. 2, 1992


Pharmacokinetics

Peak plasma levels occur 2-5 hours

after oral administration

Oral bioavailability is approximately

52%.

Plasma elimination half life is 1-2

hours


Rapid onset of action

Rapid dissociation to active tetracyclic

sulfenamide.1

Faster Rate of inhibition of proton pump

Faster and greater effect on the

intragastric pH2.

1. Besancon M, Simon A, Sachs G, Shin JM,.Sites of reaction of th egastric H,K-ATPase with extracytoplasmic thiol reagents. J Biol Chem 1997;272(36):22438-22446c

2. Langtry HD, Markham A.Rabeprazole :A review of its use in acic related gastrointestinal disorders. Drugs 1999;58(4):725-742


To produce the same degree of inhibition

Rabeprazole takes 5 minutes

Omeprazole takes 30 minutes,

Lansoprazole takes 30 minutes,

Pantoprazole takes 60 minutes

Besancon M, Simon A, Sachs G, Shin JM,.Sites of reaction of th egastric H,K-ATPase with extracytoplasmic thiol reagents. J Biol Chem

1997;272(36):22438-22446c

Faster acid inhibition


Activation time

Activation time

(minutes)

pH 1.2

pH 5.1

1.3

7.2

Percent inhibition of

the H+/K+-ATPase

At 10 minutes

At 45 minutes

100%

100%

At pH 5.1,the

activation time

is faster for

rabeprazole

compared to

other proton

pump

inhibitors.


Increases gastric mucin

Omeprazole reduces gastric mucin and

prevents mucin synthesis

Lansoprazole that has no effect on mucin,

Rabeprazole significantly increases

gastric mucin.

and thus rapid ulcer healing



Antisecretory potency of Rabeperazole

Vs Omeprazole

Significantly greater decrease in intragastric

acidity over the 24-hour period

Significantly low Intragastric acidity at night and

during 3 of 4 meal related periods

American Pharmaceutical Assoc.,Special Report:The use of proton pump

inhibitors in acid-peptic Disorders 1999


331

160

640

218

0

200

400

600

800

Intr

ag

as

tric

ac

idit

y

mm

ol.h

/L

Rabeprazole Omeprazole

Faster onset of antisecretory activity than

Omeprazole

Intragastric acidity -Day 1 Intragastric acidity- Day 8


Most Patients Treated With Rabeprazole Reported

Day And Night time Symptom Relief After One Day

No. of patients treated : 2,500

Data presented at the American College of Gastroenterology (ACG) meeting, Oct 16 2000

significantly improved symptoms of both daytime and nighttime heartburn after the first day.

80 % patients with moderate to severe symptoms reported satisfactory symptom relief on day one for both daytime and nighttime heartburn.

By day seven,

91.2 % patients reported satisfactory symptom relief for daytime heartburn,

91.7 percent reported satisfactory symptom relief for nighttime heartburn.**


•Calabrese et al. studied the effect of a 3-day course of antibiotics including azithromycin used either at the initiation of 7 days of PPI therapy or at the conclusion of the PPI treatment.

Cure Rate was:

86% (antibiotics at the initiation of PPI therapy)

88% (antibiotics at the end of PPI therapy)

Calabrese C, DiFebo G, Areni A, Scialpi C, Biasco G, Miglioli M. Pantoprazole, azithromycin and tinitazole: short duration triple therapy for eradication of Helicobacter pylori infection. Aliment Pharmacol Ther. 2000;14(12):1613-1617.

Rabeprazole

Short Course Therapy


Intrinsically greater reduction in

gastric acid secretion

Intrinsic specificity advantage (binds

to proton pump)

Advantage over H2 antagonists

Yun Hee jang, Hojing Kim; Quantam Chemical study of proton pump inhibiting activity of Substituted

2-Sunfinylbenimidazoles; Korean Jour. Of Med. Chem., VOl 2, No. 2, 1992


Does not suppress collagen regeneration

unlike H2 receptor antagonists

Does not delay healing of gastric lesions.


Increases Collagen regeneration


Pharmacological advantages

over older PPI’s

More potent than other PPI’s

Faster onset of action due to quicker

dissociation.

Complete inhibition of H+K+ATPase.



Greater increase in mucin synthesis.

Significantly greater anti H. pylori activity.

Does not produce conformational changes in

proton pump


Pharmacological advantages over

older PPI’s contd…


Does not alter prostaglandin levels

Increases prostaglandin synthesis

Prevents stress induced increase in gastric

mucosal peptide –leukotriene


Does not alter testosterone levels

NoNo effecteffect onon steroidogenesissteroidogenesis unlikeunlike omeprazoleomeprazole


Indications

Duodenal ulcer

GERD

Gastric ulcer

Reflux oesophagitis

Zollinger- Ellison Syndrome

H. pylori eradication

Rabeprazole, Clinical Pharmacology 2000, Customised monograph


Consistent symptomatic

relief

More consistent symptomatic relief H2

receptor antagonists or other PPIs

Superior to omeprazole and ranitidine in

prevention of symptoms in patients with

healed GERD.



Nocturnal symptom relief

Greater reduction in frequency and severity

of symptoms especially nighttime heartburn.

Significantly lower Intragastric acidity at

night. 1

Nocturnal acid control consistent after 8

days of once daily doses.2

1. American Pharmaceutical Assoc.,Special Report:The use of proton pump inhibitors in acid-peptic Disorders 1999

2. Williams MP et al,Aliment Pharmacol Ther 1998 Nov;12(11):1079-89


Higher rate of healing

Higher healing rates as compared to

omeprazole

Significantly greater improvement in

daytime pain.

Dekkers CP, Beker JA, Thjodleifsson B, Gabryelewicz A, Bell NE, Humphries TJ. Ignatius Hospital, Breda, the Netherlands.Comparison of rabeprazole 20 mg versus omeprazole 20 mg in the treatment of active duodenal ulcer: a European multicentre study. Aliment Pharmacol Ther 1999 Feb;13(2):179-86


Cloud ML et al,Dig.Dis.Sci.1998;43;993-1000

9384 85

120

20

40

60

80

100

% h

ea

lin

g r

ate

s

Rabeprazole

10 mg

Rabeprazole

20 mg

Rabeprazole

40 mg

Placebo

Healing Rates of Ulcerative GERD with different

doses of rabeprazole compared to placebo


Rabeprazole Vs Omeprazole

in healing of Duodenal ulcer

69 62

98 93

0

20

40

60

80

100

% H

EA

LIN

G

After 2 weeks After 4 Weeks

Rabeprazole 20 mg Omeprazole 20 mg

Dekkers CPM,et al, comparison of rabeprazole 20mg vs omeprazole 20mg in the treatment of active duodenal ulcer,Aliment Pharmacol Ther.1999;13;179-86


Rabeprazole Vs Ranitidine

in management of active duodenal ulcer disease

0

10

20

30

40

50

60

70

80

90

%

Healing Rates Complete resolution

of pain

Night time pain

severity

improvement in

overall well being

Rabeprazole 20 mg OD Ranitidine 150 mg D

Breiter JR et al. Am J Gastroenterol 2000 Apr; 95(4): 936-42


Improvement in symptoms of

gastric ulcer

Dekkers CP et al. Aliment Pharmacol Ther 1999 Jan; 13: 49-57

69 61

98 93

84

68

0

20

40

60

80

100

% s

ym

pto

m r

eli

ef

Day pain After 2

weeks

Day pain after 4

weeks

Night pain after

4 weeks

Rabeprazole 20 mg Omeprazole 20 mg


Intrinsic Anti H. pylori activity

Highly effective inhibitor of gastric acid

secretion in subjects infected with H. pylori.

Ohara T, Goshi S, Taneike I, Tamura Y, Zhang HM, Yamamoto T..Inhibitory action of a novel proton pump inhibitor, rabeprazole, and its thioether derivative against the growth and motility of clarithromycin-resistant Helicobacter pylori. Helicobacter 2001 Jun;6(2):125-9

Irreversibly inhibits urease enzyme produced by

H. pylori

Thus exerts a potent antibacterial activity

Inhibits Urease enzyme


Thioether derivative of Rabeprazole has the

strongest inhibitory action against both the

growth and motility of CRPH

1. Park JB, Imamura L, Kobashi K, Kinetic studies of H. pylori urease inhibition by a novel PPI, Rabeprazole, Biol

Pharm Bull 1996 Feb;19:182-7

Potential novel agent for

Clarithromycin resistant H. pylori

(CRPH) eradication.


4-day triple therapy in combination with

clarithromycin and amoxicillin - highly effective

Well tolerated in patients with gastric and

duodenal ulcer disease.

Eradication rate- 90%

Comparable with the established 7-day triple

therapy regimens.

Luth S, Teyssen S, Kolbel CB, Singer MV. Department of Medicine IV Gastroenterology/Hepatology), University Hospital of Heidelberg at Mannheim.4-day triple therapy with rabeprazole, amoxicillin and clarithromycin in the eradication of Helicobacter pylori in patients with peptic ulcer disease--A pilot study. Z Gastroenterol 2001 Apr;39(4):279-81, 284-5

Triple therapy for eradicating H.pylori


1. Rapid onset of H+K+ATPase inhibition than

omeprazole,

2. Greater effect on intragastric pH after the

first dose1.

3. More potent inhibitor of proton pump than

omeprazole2.

Rabeprazole vs. Omeprazole

1. Prakash A., Faulds. D .Rabeprazle, Drugs 1998 Feb; 55 (2),28,260-6

2. Langtray HD, Markham A. Rabeprazole:A review of its use in Acid related gastrointestinal

disorders, Drugs 199;58(4):725-742



3. More consistent symptom relief

4. Faster rate of healing

5. Lower potential for interaction with

cytochrome P450 enzyme system- Lesser

drug interactions

• Prakash A., Faulds. D .Rabeprazle, Drugs 1998 Feb; 55 (2),28,260-6

• Humphries TJ, Spera AC, Laurent L, Spanyers SA. Rabeprazole sodium (E3810) 20 mg daily does not affect the

pharmacokinetics of Phenytoin sodium in normal volunteers, AM J Gastroenterol 1996;91:1914



contd.

6. Two to ten fold greater antisecretory

activity.1

7. Significantly increases the production of

gastric mucin2.

1. Prakash A., Faulds. D .Rabeprazle, Drugs 1998 Feb; 55 (2),28,260-6

2. Takiuchi H, Asada S, Umegaki E et al. Effects of proton pump inhibitors, omeprazole,

lansoprazole and E-3810, on th egastrin mucin. 10th World Congress of

Gastroenterology; 1994 Oct

96 Dr Anshu P GokarnDr Anshu P Gokarn

8. Irreversibly inhibits the enzyme

urease produced by H. pylori

9. Potent anti-H.pylori activity


contd.

1. Bell NE, Humpries TJ, Comparision of fasting gastric levels in 634 patients treated with either rabeprazole 20 mg or omeprazole 20mg once daily in 3 double blind therapeutic trials, Gasteroenterology 197;112(4) Suppl:A 70

2. Park JB, Imamura L, Kobashi K, Kinetic studies of H. pylori urease inhibition by a novel PPI, Rabeprazole, Biol Pharm Bull 1996 Feb;19:182-7


Rabeprazole vs. Esomeprazole

Esomeprazole 40 mg results in 10%-15% higher

healing rates in GERD patients, compared to 20 mg

omeprazole racemate.

Same difference is found when the 20 & 40 mg

omeprazole racemate are compared to each other.

The chiral PPI prodrug is converted by acid into an

achiral cyclic sulfenamide which only then reacts with

the proton pump.

Therefore no pharmacodynamic argument in favour of

any single enantiomer formulation of any PPI. Kromer W. Relative efficacies of gastric proton-pump inhibitors on a milligram basis: desired and undesired SH reactions. Impact of chirality. Scand J Gastroenterol Suppl 2001;(234):3-9


Rabeprazole vs.

Esomeprazole

Lower incidences of Drug-Drug

interactions

Faster rate of H+K+ATPase inhibition


Rabeprazole Vs Lansoprazole

Comparable Ulcer healing rates with

Lansoprazole 30 mg

Lower potential for drug interactions

Earlier and better symptom relief

American Pharmaceutical Assoc.,Special Report:The use of proton pump inhibitors in acid-peptic

Disorders 1999


Cure Rates of H.pylori infection with

Lansoprazole and Rabeprazole

82.7

85.6

87

808182838485868788

Cure rates

Perc

ent cure

rate

s

LAC

RAC

R1/2AC

Miwa H et al,Efficacy of reduced dosage of rabeprazole in PPI/AC therapy for Helicobacter pylori infection: comparison of 20

and 40 mg rabeprazole with 60 mg lansoprazole.Dig Dis Sci 2000 Jan;45(1):77-82

Key: LAC: Lansoprazole 30mg bid with amoxicillin and clarithromycin

RAC:Rabeprazole 20mg bid with amoxicillin and clarithromycin

R1/2AC:10mg bid with amoxicillin and clarithromycin


Safety profile

Similar short term side effect profile to

other PPIs

Safe for long-term use.

Serious side effects rare

Welage SL,Journal of the American Pharmaceutical association 1999:40:1


Well tolerated

Very well tolerated as compared to

omeprazole and H2-receptor

antagonists.

No dose adjustments required for

special populations

Thjodleifsson and Cockburn,Alimentary Pharmacology & Therapeutic 1999 ; 13 s5 ; 17


Dosage and administration

Adults:

Usual dosage: 20mg/day

Route of administration: Oral

Frequency of administration: Once daily

For GERD



For pathological hyper secretory

conditions including Zollinger-Ellison

syndrome Adults:

Usual Dosage: 60mg/day

(Dosage should be adjusted based on clinical

response and should be continued as clinically

indicated. Doses up to 100 qd or 60 mg bid have

been administered).

Duration of therapy: some patients with

Zollinger-Ellison Syndrome have been treated

continuously for up to one year.



Maximum dosage limits

Adults:

GERD, Duodenal ulcer, Gastric ulcer: 40 mg qd

Zollinger-Ellison Syndrome: 120mg qd

Elderly:

GERD, Duodenal ulcer, Gastric ulcer:40 mg qd

Zollinger-Ellison Syndrome: 120mg qd

Adolescents and Children:

Safe and effective use has not been established.



Hepatic impairment No dosage adjustment required

Renal impairment No dosage adjustment is necessary

Intermittent haemodialysis

Extensively protein bound Not readily haemodialysable



Maximum dosage limits

Overdose

No experience to date with

deliberate overdose.

Dosages of up to

120mg/day have been well

tolerated.

Product details, Pariet , Eisai, http://www.eisai.co.uk/pariet.htm


Contraindications

Known hypersensitivity to rabeprazole,

other substituted benzimidazoles

(e.g.,lansoprazole, omeprazole)


Gastric cancer

Hepatic disease

Children

Elderly

Japanese (AUC values were seen to be

50-60% greater)

Precautions



Pregnancy

No data is available in human

pregnancy.

Studies in rats and rabbits have revealed

no evidence of impaired fertility or harm

to the foetus

Contraindicated during pregnancy.


Lactation

It is not known whether rabeprazole sodium

is excreted in human breast milk.

No studies in lactating women have been

performed.

Excreted in rat mammary secretions.

Should not be used during breast feeding.


Low potential for drug

interactions

Not complicated by clinically significant drug-

drug interactions with medications

metabolized by CYP 2C19

Humphries TJ, Spera AC, Laurent L, Spanyers SA. Rabeprazole sodium (E3810) 20 mg daily does not affect the pharmacokinetics of

Phenytoin sodium in normal volunteers, AM J Gastroenterol 1996;91:1914


Drug interactions

Cyclosporine: metabolism is inhibited

Digoxin: AUC and Cmax is increased

Warfarin: No interaction

Antacids: Not clinically significant

Theophylline: No interaction

Diazepam: No interaction



Salient Features

Rapid onset of action

Higher rate of healing

Consistent Symptomatic relief

Increases gastric mucin, Heals mucosa

No effect on Steroidogenesis or endocrine functions


Salient Features

The conformation of pump not altered as done by

Omeprazole.

Brings acid production level back to normal baseline

within 2 days as compared to 4 days with Omeprazole

Intrinsic anti H.pylori action

Low potential for drug interactions

Prevents stress induced increase in gastric mucosal

peptide – leukotriene content without altering mucosal

prostaglandin level.





Disorders


4. Drugs used in GERD – protein pump

inhibitors

5. Rabeprazol


Concluding Remarks

Thank You

Queries ?

[email protected]@gmail.com

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