NON-ULCER DYSPEPSIA: current concepts in diagnosis & management

DR. RAJARSHI KUMAR

dyspepsia
Often a symptom of other diseases

Characterised by vague abd discomfort

Sense of fullness after eating ,eructation, nausea,

vomiting & loss of appetite. Organic cause: 40-50% pts

D/D of dyspepsia
Peptic ulcer

NUD
GERD & esophagitis Abd malignancy(gastric, pancreatic)

Drug-induced gastritis(NSAIDs,iron,

antibiotics,metronidazole) Alcohol-induced gastritis Stress-induced

 Cholelithiasis& choledocholithiasis

Chr pancreatits
Intestinal parasites( hookworm,tapeworm,

roundworm) Carbohydrate malasorption Systemic disorders( diabetes, thyroid, adrenal disorders)

NON-ULCER DYSPEPSIA
Functional dyspepsia

Defn: pain/discomfort localised to upper abdomen

without any identifiable cause Criteria: chronic or recurrent, upper abd pain or discomfort for a period of at least 1m, symptoms present > 25% of time, and absence of clinical,biochemical, endoscopic & ultrasonographic evidence of organic ds accounting for the symptoms

Clinically- 2 broad categories

Uicer-like dyspepsia: pain- predominant symptom

Dysmotility-like dyspepsia: bloating, fullness, early

satiety as main complaint

ETIOLOGICAL FACTORS
GASTRIC ACID SECRETION : not increased

GASTRIC MUCOSAL SENSITIVITY: pts with NUD

more sensitive i.e. volume thresholds for fullness,discomfort & pain in response to distension : 40-50% lower than normal controls or pts with organic causes ABNORMAL GASRIC EMPTYING: delayed gastric emptying in~ 30-70% of pts

 Recent scintigraphic studies: differences in

distribution of gastric contents Ingestion of solid meal-> bulk accumulated in fundus -> relaxes to accommodate In NUD: most of the meal accumulated in antrum: failure of fundus to relax / antral hypomotility: mechanism not known Experiments suggest role of vagal afferent neurons in upper abd hyperalgesia

 PSYCHOLOGICAL FACTORS: higher scores for

depression & anxiety compared to healthy controls HELICOBACTER PYLORI: Clinical studies have documented higher prevalence in dyspeptic pts To assess role of H.pylori , various trials showing effect of eradication therapy in NUD

Trials showing effect of eradication of H.pylori in NUD

STUDY TYPE YEAR NUMBER PERIOD RESULT

McColl et al RCT
McCarthy et al Jakkimaine n et al Laheij et al Talley et al

1994-6

318
83 5 trials 10 trials 337

1 yr
1 yr NA NA 1 yr

Improves symptoms
,, ,, ,, No significant improvemnt ,, ,,

Prospective 1994 Metaanalysis Metaanalysis RCT 1999 1996 1999

Koskenpato RCT et al Laine et al Metaanalysis

2001 1995-99

51 10 trials

1 yr NA

 Studies conducted to evaluate role of virulent strains

in NUD: Marker for virulence: Cag A GENE Virulent strains more prevalent in NUD CagA status depends on geographical regions WESTERN STUDIES: lower Cag A +ve rate ASIAN STUDIES: higher prevalence of Cag A +vity in NUD cases

Dietary factors
Not clear whether plays any imp role in causation

Some evidence:high fat intake

Caffeinated products -> higher incidence of

dyspeptic symptoms in NUD but not in DU / healthy controls.

Approach to diagnosis
Diagnosis is one of exclusion

Presence of alarm symptoms: wt. loss, upper

g.i.bleeding,dysphagia & h/o chr intake of NSAIDs indicate organic disorders Upper g.i. endoscopy to rule out organic cause Indications: Wt loss/recurrent vomiting/dysphagia/ g.i. bleeding/anaemia/strong family history / abd mass

 Chronic users of NSAIDs

Older pts(>45 yrs)

Pts who fail to respond to empirical therapy

EMPIRICAL THERAPY: young pts with typical chr h/o dyspepsia dont have alarm symptoms or take NSAIDs

 Other investigations done:

USG abd to rule out biliary pathology

LFT for liver ds Stool examn for parasites

MANAGEMENT
In un-investigated dyspepsia, AGA recommends

non-invasive testing (serology/ urea breath test) for H.pylori : H.pylori +ve: Hpylori eradication therapy Rationale: cure of ulcer ds Follow-up in 4-8 wks-> failure to respond/ recur/ alarm features-> UGIE

 Un-investigated dyspepsia: H.pylori ve:

AGA recommends a trial of antisecretory therapy or

prokinetic for 1 m -> symptoms persist after 8 wks of t/t or rapidly recur on stopping t/t -> UGIE

 REASSURANCE:1st step after exclusion of organic

cause ANTISECRETORY AGENTS: H2 receptor antagonists, PPIs Studies have shown PPIs to be superior to placebo in relieving dyspepsia Recent Cochrane review: PPIs significantly more effective than antacids or H2 antagonists in initial management of dyspepsia

 PROKINETIC AGENTS:

Decrease GER,improve gastric emptying

Domperidone, dopamine antagonist Mosapride,shown to improve symptoms & quality of

life Tegaserod, new 5-HT4 agonist, shown to accelerate gastric emptying & relax gastric fundus

 ANTI-HELICOBACTER PYLORI THERAPY:

Value controversial
Pts with ulcer-like dyspepsia, also +ve for CagA

(virulent H.pylori ) significant symptomatic improvement ANTIDEPRESSANTS: Mechanism of action unclear

 Symptom relief independent of psychiatric effects

Low dose amitryptiline/ nortryptiline-> if successful,

cont for 6m-> taper off At present ,no consensus on exact durn of t/t

 ALTERNATE THERAPIES:

Psychotherapy & hypnotherapy tried

-chr relapsing nature of NUD -lack of good efficacy of drugs Currently insufficient evidence of efficacy

SUMMARY
Diagnosis of exclusion

Most cases: mild&intermittent symptoms,

Respond to reassurance Antisecretory agents(PPIs) benefit reflux-like & ulcer-

like dyspepsia: t/t for 4-6 wks Dysmotility-like dyspepsia: limited options Prokinetic agents tried but prolonged usage avoided

 A trial of low-dose antidepressants in non-

responders A minority of pts refractory to all forms of therapy: - psychiatric evaluation& counselling - Alternate therapies

THANK YOU