Empirical Treatment With PPI in Acid Related Disease

EMPERICAL TREATMENT WITH P.P.I.
IN ACID RELATED DISEASE
RIFAI AMIRUDIN
Div. of Gastroentero-Hepatology, Department of Internal Medicine

Medical Faculty of Hasanuddin University, Makassar
P.P.I. Symposium in NSAID Gastropathy, March 5, 2006

INTRODUCTION
Pattern of U.G.I. Disease
1900
Malignancy Peptic Ulcer Dyspepsia GERD

2000
Relationships of the forces attacking and defending
the mucosa in health and disease
GASTRIC ACID-PEPSIN
HCL-PEPSIN
HISTAMINE
GASTRIN
ACETYLCHOLINE
VAGUS RECEPTOR
CENTRAL STIMULUS LOCAL STIMULUS

(EMOTION, ANXIETY) (CHEMIST, ALCOHOL)
GASTRIC MUCOSAL DAMAGE
GASTRIC JUICES
H +
HISTAMINE
HISTAMINE
MAST CELL
CAPILLARY DILATATION / EDEMA

H.P INFECTION AND
GASTRIC ACID SECRETION
HELICOBACTER PYLORI INFECTION AND PEPTIC ULCER
CHRONIC INFLAMMATION
DISINTEGRATION OF MUCOSA
ATROPHY OF MUCOSA
GASTRIC METAPLASIA
INTESTINAL METAPLASIA
Gastric ulcer : 60 – 70% Duodenum ulcer : 90 – 100%

H.P (+)  NOT ALWAYS PEPTIC ULCER
Pathogenicity of H.P strain

Host factor
NSAID
– Widely used :
» Pain killer
» Rheumatic disease
» Anti inflammatory
– Consumption is increased :
» OTC
» Population of the elderly
» Traditional medicine of rheumatic disease / pain killer
• Gastrointestinal adverse effects  NSAID
gastropathy (from erosion to ulcer) with wide range of
symptoms (dyspepsia, upper G.I. bleeding)
• NSAID gastropathy requires adequate treatment and

prevention
Scope of NSAID Gastropathy
• NSAID related G.I. toxicity is the most common
serious drug-induced toxicity reported to regulatory
authorities
• Dyspepsia occurs in about 15% of patients
• Prevalence of upper G.I. ulcer is 15 – 31%, higher
risk of developing gastric than duodenal ulcers
• Risk of complications increased 4 fold
Hawkey, Gastroenterology 2000;119:521-35

Epidemiology of NSAID Gastropathy
• USA :
– long term use of NSAID  ulcer 25 %
» Gastric ulcer 15%
» Duodenal ulcer 10%
– FDA (1995) :
• 130.000.000 patients with NSAID use
 200.000 hospitalization
• Glasgow (Center for Rheumatic Disease)
– Prevalence of ulcer, upper G.I. bleeding and perforation
were increased with the increase of NSAID use
– Prevalence of gastric ulcer / duodenal ulcer among

patients with arthritis : 5 – 15 times than general
population
Risk Factors of NSAID Gastropathy
1. History of previous peptic ulcer

2. Age of > 60 years
3. High dose of NSAID / multiple NSAID
4. H. Pylori infection
5. Comorbidity with other chronic systemic disease
6. Alcoholism
Pathogenesis of NSAID-induced
ulcers
PROTECTIVE
FACTORS AGGRESSIVE FACTORS
Prostaglandins
Acid + pepsin H. pylori
Mucus layer
Bicarbonate
Surface
epithelial
cells
Mucosal blood
supply
Seager & Hawkey, BMJ 2001; 323: 1236–9.

ulcers
PROTECTIVE
+
Prostaglandins
NSAIDs Acid + pepsin H. pylori
Mucus layer
Bicarbonate
Surface epithelial
cells
Mucosal blood
supply

ulcers
PROTECTIVE
+
Prostaglandins
NSAIDs Acid + pepsin H. pylori
Mucus
layer
Bicarbonate
Surface epithelial
cells
Mucosal blood
supply

Management of NSAID Gastropathy
• NSAID gastropathy should be considered among all

NSAID users
• Endoscopy :
– All long term NSAID user
– Risk factor
– Alarm sign : anaemia, U.G.I bleeding, severe dyspepsia
MANAGEMENT OF PEPTIC ULCER
• Purposes :
• Pain relief
• Ulcer healing
• Prevent recidif
• Resting (physical and emotional)
• Diet
• Antacids / anticholinergic
• H2 receptor blokade
• Proton Pump inhibitor
Goal Treatment
• To relief the symptoms
• To heal the lesion
• To prevent ulcer and ulceration
• To prevent ulcer recurrence
NSAID users with Dyspepsia
• Mild symptoms or asymptomatic

• Endoscopy : hyperaemic lesion to superficial
erosion
• Treatment :
• H2RA
• Cytoprotective agent
• P.P.I
• H2RA
– less effective in prevention of complication
• P.P.I
– the most effective to treat NSAID gastropathy
(drug of choice)
NSAID users with
Gastric / Duodenal Ulcer
• NSAID should be discontinued  change to simple
analgetic / doesn’t affect prostaglandin synthesis
• H2RA
• Cytoprotective agents Heal the lesion
• P.P.I after 8 – 12 weeks
P.P.I THE MOST EFFECTIVE DRUG

Figure. Healing rate of NSAID-associated gastric ulcer
(%)
( ):%
100
50/62 (80.6)
70/103 (68.0)
Healing rate
32/52 (61.5)
31/62 (50.0)
50
22/52 (42.3)
33/103 (32.0)
4 8 Weeks
: H2 blocker (52 lesions)
: H2 blocker + cytoprotective drugs(52 lesions)
Maeda dkk. 1998. Therapeutic Research : PPI (62 lesions)
Figure. Healing rate of NSAID-associated
gastric ulcer (Omeprazole vs Lansoprazole)
(%)
( ):%
100
32/37 (86.5)
18/25 (72.0)
Healing rate
20/37 (54.1)
50
11/25 (44.0)
4 8 Weeks
: Omeprazole (25 lesions)
: Lansoprazole (37 lesions)
Maeda dkk. 1998. Therapeutic Research
Figure. Cumulative rates of healing at 4 and 8 weeks during treatment with
ranitidine hydrochloride, 150 mg twice daily; 15 mg once daily; o rlansoprazole,
30 mg once daily, among intent-to-treat patients
(%)
100 Gastric ulcers
90
80
(%) Healed
70
: Ranitidine Hydrochloride
60 : Lansoprazole, 15 mg
: Lansoprazole, 30 mg
50
40
30
20
10
4 8 Week
Naurang. dkk. 2000. Arch Intern Med

P.P.I.
• More effective than H2RA and misoprostol in the
prevention of NSAID gastropathy / NSAID
induced ulcer
• Lesser side effect
• Drug of choice
Recommendation
• NSAID treatment only for strict indication
• Avoid high dose of NSAID
• Avoid co-therapy with anticoagulant / corticosteroid
• High risk patients

Preventive treatment
• Long term users
P.P.I is the drug of choice
Conclusions
• NSAID gastropathy is the most frequent side effect in

NSAID users with the wide range of clinical
manifestation
• Dual mechanism of the pathogenesis of NSAID

gastropathy / NSAID induced ulcer : topical and
systemic effect
Conclusions (2)
• P.P.I is the most effective drug in the treatment of
NSAID induced ulcer / NSAID gastropathy and in the
prevention of ulcer complication and ulcer recurrence
• Avoid high dose and multiple NSAID co-therapy with

anticoagulant / corticosteroid and choose the less
side effect NSAID
Severe erosive gastritis
Erosion of the pylorus
Deep oesophageal ulcer
Severe erosive gastritis
Several acute erosion of the duodenal bulb
Large duodenal ulcer
Large ulcer with blood clot
Ulcer of the duodenal bulb
THANK YOU

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EMPERICAL TREATMENT WITH P.P.I.

IN ACID RELATED DISEASE

Div. of Gastroentero-Hepatology, Department of Internal Medicine

P.P.I. Symposium in NSAID Gastropathy, March 5, 2006

Malignancy Peptic Ulcer Dyspepsia GERD

CENTRAL STIMULUS LOCAL STIMULUS

CAPILLARY DILATATION / EDEMA

Gastric ulcer : 60 – 70% Duodenum ulcer : 90 – 100%

Pathogenicity of H.P strain

• NSAID gastropathy requires adequate treatment and

Hawkey, Gastroenterology 2000;119:521-35

– Prevalence of gastric ulcer / duodenal ulcer among

1. History of previous peptic ulcer

Acid + pepsin H. pylori

Seager & Hawkey, BMJ 2001; 323: 1236–9.

NSAIDs Acid + pepsin H. pylori

Seager & Hawkey, BMJ 2001; 323: 1236–9.

NSAIDs Acid + pepsin H. pylori

Seager & Hawkey, BMJ 2001; 323: 1236–9.

• NSAID gastropathy should be considered among all

• Mild symptoms or asymptomatic

P.P.I THE MOST EFFECTIVE DRUG

Naurang. dkk. 2000. Arch Intern Med

• Lesser side effect

• High risk patients

• NSAID gastropathy is the most frequent side effect in

• Dual mechanism of the pathogenesis of NSAID

• Avoid high dose and multiple NSAID co-therapy with

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