Disclosures None 1 Heartburn and Barretts Esophagus Heartburn - - PDF document
Heartburn and Barretts Esophagus Christian Mathy, MD University of California, San Francisco 2015 Disclosures None 1 Heartburn and Barretts Esophagus Heartburn and GERD GERD therapy Extraesophageal GERD Barretts
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Prevalence (%) 20 40 60 80 25–34 35–44 45–54 55–64 65–74 Age (years)
Any episode
At least weekly episodes of GERD sxs Females Males
Locke GR et al Gastro 1997
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Hypertension, untreated Normal female Angina pectoris Duodenal ulcer, untreated Psychiatric disease
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Normal male Heart failure (mild) Esophagitis, untreated
PGWB Index score
60 70 80 90 100
Dimenas E Scand J Gastroenterol 1993
Typical/ Esophageal
Atypical/ Extraesophageal
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lower chest up towards the neck”
n=196
Study patients dx’d with functional dyspepsia
Reflux questionnaire with heartburn definition specified 42% identified heartburn as main symptom
42%
Carlsson R et al Scand J Gastroenterol 1998
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GERD
NERD 60-70% Erosive Esophagitis 20-30% Barrett’s Esophagus 6-10%
NERD: Non-Erosive Reflux Disease
Functional chest pain (< 10%)
Mechanisms of GERD
Esophagus LES Diaphragm Pylorus Stomach Angle
UES
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> 30
↓ BMI 3.5 ↓ 40% GERD sxs Global elimination not recommended
– Dysphagia, bleeding, emesis
– Male age > 50 – Sxs > 5-10 yrs – Obesity
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Normal
– Grade A: < 5mm, < 2 folds – Grade B: ≥ 5mm, < 2 folds – Grade C: ≥ 2 folds, < 75% – Grade D: ≥ 75%
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Normal
Smout el al APT 1997
Heartburn
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– Faster, more complete sx relief – Superior healing of esophagitis
(vs H2 blockers)
– 70-80% vs 60% sx relief
Gastro 1997
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– Healing at 8 wks: 84% PPI vs 52% H2B – Sx response better
(Chiba et al Gastro 1997)
– % pts with sx relief: qday = BID – If persistent sxs, only 20% improve with BID (or new PPI) (Fass et al J Aliment Pharm Ther 2000)
– ~ 100% relapse by 6 mos
– PPI use may decrease dysplasia
– 66% have recurrent sxs – On-demand PPI same sx control as PPI daily
(Pace et al Aliment Pharm Ther 2007)
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6-12 months Continuous Intermittent On demand = symptom recurrence
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– 46% refractory GERD pts taking PPI correctly (Alim Pharm Ther 2006)
– New or BID: 20% improve
– Biopsy for eosinophilic esophagitis
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pH, impedance-pH
reflux vs no reflux
with reflux events Persistent sxs on therapy
(Mainie et al Gut 2006)
Rebound acid hypersecretion Bone disease Clopidogrel and CV events Enteric infections ??? ??? ??? ??? PPI use contributes to . . .
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PPI
X 8 wks
compared pre- vs post-treatment
Gastro 1999
3.0 6.8
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for 8 weeks
7, 14, 28, 42 and 56 dys Gastro 2004
**Wean off slowly 32% 16% YES
hip fx IF another risk factor (Corley Gastro 2010) – Dose dependent, can occur at 2 yrs
(Targownik et al Gastro 2010)
Kind of …
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– Competitive inhibition of P450-2C19 (least: pantoprazole) – Retrospective studies (JAMA 2009) – FDA alert 2009
Probably not
(Katz et al AJG 2013)
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– Salmonella, Campylobacter, C difficile, others – Systemic review: OR 2.05, 95%, CI 1.47-2.85 (Am J Gastro 2007)
– Nosocomial, community, initial, recurrent
YES
Rebound acid hypersecretion Bone disease Clopidogrel and CV events Enteric infections YES Kind of … Probably not YES PPI use contributes to . . .
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gastric fundus
chronic PPI use
– Medical failure predicts surgical failure
necessary
– At 5 yrs, 62% on PPIs Spechler et al JAMA 2001
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pain
symptoms
similar sxs
Controversial association:
GER sxs
endoscopic changes
acid suppression
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mucous production, bronchoconstriction – Esopha-bronchial cough reflex bronchoreactivity
– Cough, decreases PEF
– ~ 51% asthmatics have abnl pH tests – What causes what?
– 60% do not have typical sxs
(Irwin et al Chest 1993)
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– Also from smoking, alcohol, allergies, voice abuse, viral
– No benefit with PPI – No benefit with fundoplication
(Am J Gastro 2006, Clin Gastro Hep 2006)
– Helpful:
– Asthma: EGD abnl in ~ 30% pts – Laryngeal sxs: EGD abnl in ~ 25% pts
(Gut 1992, Aust J Otolaryg 1999)
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– Daily vs BID – Observational, uncontrolled data for BID
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extent
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– IM LGD/HGD EAC – Risk of progression varies:
0.4%/yr
1.5%/yr
(Rees et al Cochrane Database Sys Rev 2010)
Increasing Genetic Changes
Injury:
Acid & bile reflux Nitrous oxide
Basal layer stem cells
exposed to gastric contents abnl differentiation
Evolution of Barrett’s to Carcinoma
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– Fundic vs cardia vs intestinal with goblet cells? – Most EAC associated with intestinal
histology”
Most recent AGA review: BE is “any extent of metaplastic columnar epithelium that predisposes to cancer development”
(Spechler et al Gastro 2010)
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– 40% EAC pts have no GERD hx – Only 10% EAC pts have BE dx
– Chronic GERD sxs AND – One or more EAC risk factors
– If no Barrett’s, no further screening
Screening EGD/bx shows BE No Dysplasia LGD HGD Expert confirmation of path EGD every 3-5 yrs EGD every 6-12 mos OR Eradication Endoscopic eradication
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Esophagus Melanoma Colorectal Lung/Breast Prostate
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– If mod/severe asthma (2 inhalers) – If GER sxs, nocturnal asthma – “Success”: 20% ↑ PEF or ↓ po steroid; ↓ sxs
– ↑ QOL, ↓ flares – ↔ PEF, FEV1 (Littner et al Chest 2005)
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