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
Part 1
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
Part 2

5. Rabeprazol

Dr Anshu P Gokarn 2

Effective treatment
using Rabeprazol

Part I

Dr Anshu P Gokarn

Dr Anshu P Gokarn 3

Disorders
inhibitors
5. Rabeprazol

Dr Anshu P Gokarn 4

Stomach

Main Functions
 Storage
 Preparing the chyme for digestion in the
small intestine
 Absorption of water and lipid-soluble
substances (alcohol and drugs)

Dr Anshu P Gokarn 5

Stomach

Dr Anshu P Gokarn 6

Stomach
Types of Gland (located in gastric mucosa):
 Cardiac Glands
 Pyloric glands (many G cells)
 Oxyntic glands (most abundant, found in
fundus and corpus)

Dr Anshu P Gokarn 7

Stomach Cells
Surface Mucous Cell

Gastric Pit
(Ioveola)

Isthmus
Mucous Neck Cell

Neck

Panetal Cell
Oxyntic Gland

Endocrine Cell

Chief Cell Base

Dr Anshu P Gokarn 8

Types of Cells

Parietal cells
 most distinctive cells in stomach (HCl &
intrinsic factor)
Chief cells
 pepsinogen
Mucus neck cells:
- HCO3-
- Mucus

Dr Anshu P Gokarn 9

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

D Cells: Somatostatin (antrum)

Enterochromaffin-like cell: Histamine

Dr Anshu P Gokarn 10

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


Relaxation in gastric reservoir
 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


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 cellsHistamine ---
H2 receptor (parietal cells)  acid secretion

 Cimetidine (H2 receptor blocker) peptic ulcer and
gastroesophageal reflux


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
HCI

HCl
H Cl
Protein
Protein kinases K kinases
Acid
Ca2+ pump Ca2+
Cl
Release of K Release of Ca2+
Ca 2+ from
Ca2+ from
intracellular Protein intracellular
stores kinases stores
cAMP
ACh (M3)

Gastrin Acetylcholine
Histamine

Activation of H1K ATPase


Disorders
inhibitors
5. Rabeprazol


Gastric acid plays a central role in
NSAID-associated gastroduodenal damage

PROTECTIVE
Acidic AGGRESSIVE FACTORS
FACTORS environment Aspirin
H. pylori
Mucus layer and other Gastric Pepsin
NSAIDs acid
Ionic gradient
Bicarbonate layer Neutral environment

Prostaglandins

Surface epithelial
cells

Mucosal blood
supply Aspirin and
other NSAIDs

Prostaglandin Bicarbonate Mucus
production productionproduction


Helicobacter pylori


Infection with H. pylori results in an
acute inflammatory reaction

Epithelial cell

O2 radicals
IL-8

Proteolytic
enzymes 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.


Complications of GERD

 Barrett’s esophagus

 Esophageal strictures

 Carcinomas
Barrett’s esophagus

Gastric Cancer Esophageal strictures
 Dr Anshu P Gokarn 47

Guidelines for management of GERD
 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
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
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

End of Part – I

any questions ?


Effective treatment
using Rabeprazol

Part II

Dr Anshu P Gokarn

59
Dr Anshu P

Part 1

Disorders
inhibitors
Part 2

5. Rabeprazol


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


Structure activity relationship
• Produrg
• Transformed at low pH to a more reactive
species, a Sulfenamide.

• Sulfenamide reacts with thiol group on
gastric (H+K+)-ATPase.

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
68
Dr Anshu P Gokarn

Faster acid inhibition
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


Activation time
Activation time At pH 5.1,the
(minutes)
activation time
pH 1.2 1.3 is faster for
pH 5.1 7.2
rabeprazole
Percent inhibition of
the H+/K+-ATPase
compared to
At 10 minutes other proton
100%
At 45 minutes 100%
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


Faster onset of antisecretory activity than
Omeprazole

800
Intragastric acidity
mmol.h/L

600

640
400

200 331

160 218

0
Rabeprazole 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.**

Rabeprazole
Short Course Therapy
•Calabreseincluding azithromycin usedaeither at the initiation of
antibiotics
et al. studied the effect of 3-day course 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.


Advantage over H2 antagonists
 Intrinsically greater reduction in

gastric acid secretion

 Intrinsic specificity advantage (binds

to proton pump)
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


Increases Collagen regeneration

 Does not suppress collagen regeneration

unlike H2 receptor antagonists

 Does not delay healing of gastric lesions.



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.



Pharmacological advantages over
older PPI’s contd…

 Greater increase in mucin synthesis.

 Significantly greater anti H. pylori activity.

 Does not produce conformational changes in

proton pump



Does not alter prostaglandin levels
 Increases prostaglandin synthesis

 Prevents stress induced increase in gastric

mucosal peptide –leukotriene

Does not alter testosterone levels
 No effect on steroidogenesis unlike omeprazole



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


Healing Rates of Ulcerative GERD with different
doses of rabeprazole compared to placebo

100
80 93
% healing rates

84 85
60
40

20
12
0
Rabeprazole Rabeprazole Rabeprazole Placebo
10 mg 20 mg 40 mg
Cloud ML et al,Dig.Dis.Sci.1998;43;993-1000


Rabeprazole Vs Omeprazole
in healing of Duodenal ulcer
100
% HEALING

80
98 93

60
69 62
40

20

0
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

90
80
70
60
50
%
40
30
20
10
0
Healing Rates Complete resolution Night time pain improvement in
of pain severity 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
100
98 93
80
% symptom relief

84
60 68
69 61
40

20

0
Day pain After 2 Day pain after 4 Night pain after
weeks weeks 4 weeks

Rabeprazole 20 mg Omeprazole 20 mg
Dekkers CP et al. Aliment Pharmacol Ther 1999 Jan; 13: 49-57


Intrinsic Anti H. pylori activity
 Highly effective inhibitor of gastric acid
secretion in subjects infected with H. pylori.

Inhibits Urease enzyme
 Irreversibly inhibits urease enzyme produced by
H. pylori

 Thus exerts a potent antibacterial activity
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


Potential novel agent for
Clarithromycin resistant H. pylori
(CRPH) eradication.
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


Triple therapy for eradicating H.pylori
 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


Rabeprazole vs. Omeprazole
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.
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

Dr Anshu P Gokarn
96

contd.
8. Irreversibly inhibits the enzyme

urease produced by H. pylori

9. Potent anti-H.pylori activity

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

88 87
Percent cure rates

87 85.6
86
LAC
85
84 82.7 RAC
83 R1/2AC
82
81
80
Cure rates
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
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


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
For GERD
Adults:

Usual dosage: 20mg/day

Route of administration: Oral

Frequency of administration: Once daily



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.



Maximum dosage limits
Hepatic impairment
No dosage adjustment required
Renal impairment
No dosage adjustment is necessary

Intermittent haemodialysis
 Extensively protein bound
 Not readily haemodialysable



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)


Precautions
 Gastric cancer

 Hepatic disease

 Children

 Elderly

 Japanese (AUC values were seen to be
50-60% greater)


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
3. Concluding Remarks
Gastroesophageal Reflux Disease
4. Drugs used in GERD – protein pump
inhibitors
5. Rabeprazol


Thank You

Queries ?
anshu.gokarn@gmail.com

Talk on gastic disorders and rabeprazole

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