DRUG INDUCED GASTROPATHY

Masita
FARDAH AKIL
INTRODUCTION

The use of "gastropathy" should be used to mark a condition in which the

damage to epithelial or endothelial lining of the stomach without evidence of
inflammation

Gastropathy caused by bile reflux and NSAID gastropathy is often referred

to as chemical or reactive gastropathy

three categories of chemical gastropathy :: bile reflux after partial gastrectomy,

bile reflux as part of gastrointestinal dysmotility syndrome and the chronic
nonsteroidal anti-inflammatory drugs.
EPIDEMIOLOGY

Nonsteroidal anti-inflammatory drugs (NSAIDs) are among the most commonly

prescribed drugs worldwide

In the United States, 5-10% of the adult population (15-25 million people)
use of NSAIDs, In Europe, NSAIDs reached 7.7% of all prescription.

In Indonesia : Makassar 71%, Jakarta 67.7% , Surabaya, 6%, and Malang 21%.
CLASSIFICATION OF NSAID
RISK FACTOR
PATHOMECANISM
CLINICAL MANIFESTATION

Asymptomatic

Symptomatic : epigastric pain, nausea, vomiting

GIT bleeding : hematemesis, coffee grounds emesis,

melena, perforation.
DIAGNOSE

HISTOPATOLOGY
• Epitelial cell degradation, foveolar hyperplasia,
neutrofil infiltration, mononuclear cell
inflammation, lymphoid folickel atrophy, intestinal
metaplasia, endokcrine hyperplasia, parietal cell
damage, smooth cell expansion to mucosa.

ENDOSCOPY
• Small mucosal erosions congestion, sometimes
accompanied by bleeding. Such lesions can heal
itself. More severe lesions can be multiple
erosions and ulcers, extensive bleeding, and
perforation of the gastrointestinal tract
DIFFERENTIAL DIAGNOSE

Ulcer like
• Dyspepsia • Variceal esofagus,
fungsional • Gastric tumor, • Gastric carcinooma,
• Gastroesofageal • Zollinger-Ellison
reflux Syndrom

Abdominal
GI bleeding
discomfort
TREATMENT
RISK
STRATIFI
CATION

COX-2 MISOPROST
inhibitor OL

REBAMIPIDE PPI

H2-RA
RISK STRATIFICATION
MISOPROSTOL

Prostaglandine sintetic analogue

In MUCOSA study, misoprostol 200 mcg QID  ↓ NSAID

induced complication for 40%

Side effect : abdominal pain, nausea, diarea, and avoided

to lactation woman
H2 RECEPTOR ANTAGONIST

first drugs effectively to heal reflux oesophagitis as well as peptic ulcers

Doubling the standard dose (famotidine 40 mg twice daily) significantly ↓

the 6-month incidence of GU

H2-receptor antagonists can no longer be recommended

to prevent NSAID gastropathy
 PROTON PUMP INHIBITOR

standard therapy : peptic ulcers and gastro-oesophageal reflux-

disease(GERD)

Specifically block the parietal cellH+/K+-ATPase  significantly

inhibiting the gastric acid secretion

Omeprazole (20 mg QD), more effective in the prevention of GU

than ranitidine (150 mg BID) / misoprostol (200mg BID)

20 and 40 mg of esomeprazole  relieve upper GI symptoms in

patients continuing NSAID / COX-2inhibitors
REBAMIPIDE

Rebamipide : an gastroentero-protective drug

1st announced in Japan, 1990.

Mecanism of action : stimulate production endogenous PG,

eliminate free radical oxydative, decrease intestinal
proinflammation cytokine
COX-2 INHIBITOR

Incidences of GI symptoms : lower in patients on rofecoxib /celecoxib

compared with unselective COX-inhibitors

Large prospective outcome studies : the VIGOR study comparing rofecoxib 50

mg with naproxen 1 g daily demonstrated a reduction of all upper GI events in
54%

preferentially inhibit COX-2 but exhibited

the anti-inflammatory, antipyretic, and analgesic activities of
NSAIDs
TREATMENT
Thank you