This is the latest update on irritable bowel syndrome and gastroesophageal reflux by Associate Professor Reuben Wong from gutCARE. This is presented during the latest GP symposium

1. What’s new in…
Irritable Bowel Syndrome
Gastroesophageal Reflux
Reuben K Wong
Gastroenterologist
Adj Associate Professor

2. What you need to know about…
1. Epidemiology
• Have your patients changed?
2. Diagnosis
• Changes in diagnostic criteria
• The rationale for change
• Does it really matter?
3. Management
• What’s NEW
• What’s OLD
• Should I change the way I treat my patients?

3. What’s New in Rome IV
for Irritable Bowel Syndrome

4. Epidemiology of IBS…

5. Who gets IBS…

6. Diagnosis of IBS
IBS
Relief w
defecation
Change in
frequency or
stool
consistency
Associated with
straining/urgency.
mucus

7. A walk through History
“The bowels are at one time constipated and the other lax,
in the same person…. How the disease has two such
different symptoms I do not profess to explain….” : 1849
“irritable colon syndrome,” “spastic colon,” or “mucous
colitis.” : 1940 -1950
that patients be categorized into three clinical patterns:
painful spastic colon, painless diarrhea, and alternating
diarrhea and constipation (or alternators) : 1970 – 1980

8. • Distinguishing symptoms
• Abdominal distension
• pain relief with BM
• loose / frequent BM with pain onset
1978
Manning
• Biological indices and Symptoms
• Symptoms
• Leucocytosis, anaemia, blood in stool
1984
Kruis

10. What is IBS – According to Rome III
10% of the time
Shorter time of onset to diagnosis

11. What’s in Rome IV?

13. Frequency of symptoms
• From 3 days / month to 1 day a week
• Increase based on the Rome Normative GI Symptom Survey
Nature of symptoms
• No more “Discomfort”
• Linguistics/language issue
• Confusion

14. The “poop” link remains!
BUT notice the subtle change….
It’s now “related to” and NOT “relieved by” defecation
• Many patients do not feel better after pooping
• Some actually feels worse
“Onset” has also been removed
• The direct temporal association is not always seen (no “Ahhhhh…” moment!)

16. IBS Subtyping
Subtyping
• IBS-C >25% BSS 1/2 & <25% 6/7
• IBS-D >25% BSS 6/7 & <25% ½
• IBS-M >25% BSS 1/2 & 3/4
Clinical common-sense prevails!
Emphasis is on “abnormal” BMs
• Reduction in number of IBS-Us

18. Treatment: IBS-Diarrhea

19. Treatment : IBS - Constipation

20. Treatment : Abdominal Pain

21. Motility Myoelectrical Marker
Brain-Gut Interactions
Visceral Hypersensitivity
Mechanisms
Inflammation
Microflora
Stress affects
GI function
Meals
Pain/Motility
Pain
sensitivity
3 cpm
motility
Clustered
contractions
CNS/ENS
Autonomic
reactivity
Visceral
hypersensitivity
Postinfection
IBS
CNS
Brain Imaging
Probiotics
Food and Diet
FODMAP
Gluten
Rome
Criteria
19701960 1980 1990 2000 2010 20141950
Neuroplasticity
and Neurogenetics
Food and Diet

22. IBS Update : Summary
1. Who’s likely to get IBS
2. Changes in the definition of IBS
3. Clarity of the sub-classification
4. Overlap of diagnoses
5. Treatment Options

23. 23

24. 24

25. 25

26. What’s New in dealing with
GERD

28. Epidemiology of GERD

29. Reflux rates in Singapore
Prevalence of Heartburn…
Singapore Community Survey
• Jurong Estate
• 1994 – 4.6%
• 2000 – 10.5%
Increasing incidence that indicates we are
catching up with rates in the West • Increasing Obesity
• Lifestyle & Stress
• Ethanol
• Fatty Food
• Less H. Pylori
Ho KY et al. Amer Journ Gastroenetrol 1998
Lim SL, Ho KY et al. Journ Gastroenterol & Hepatol 2001

30. Reflux Esophagitis
Direct physical evidence of acid reflux
Lundell et al 1999; published with permission
from Professor G Tytgat and Professor J Dent

31. You’ve sent a patient for a gastroscopy….
What will it show?

32. Asian Data :
Esophagitis tends to be mild ( Grade A )
RK Wong et al. Jour Gastroenterol Hepatol 2009;24(1):103-106

33. NERDs Rule!

34. What happens if PPIs fail?

35. How prevalent is the problem…
• Persistent Reflux Symptoms in China = 37.9%
• Primary care and community = 45%

36. Fass R. Gut 2009
Causes for Refractory GERD

38. Compliance to medication
Hatlebakk JG. Aliment Pharmacol Ther 2000

40. PPIs
Proton Pump Inhibitors (PPIs)
• Most potent gastric acid-suppressing agents
for GERD2
• Patients with reflux symptoms should receive
initial treatment with full-dose PPIs for one
month2
• Maintenance therapy for GERD is recommended
at the lowest effective dose33
• Patients with chronic cough and laryngitis and
typical GERD symptoms should be offered
twice-daily PPI therapy after exclusion of
non-GERD etiologies2
Inhibition
of acid
secretion
Parietal
cell
Canalicular
space
Proton pump
Inhibition of
proton
pump
Activation
Concentration
PPI
(inactive)
H+
Blood
Gastric gland
PPIs control acid secretion by directly inhibiting the
proton pump32
2. Fock et al. J Gastroenterol Hepatol. 2008;23(1):8-22.
32. Richardson et al. Drugs. 1998;56(3):307-35.
33. Bruley et al. Best Pract Res Clin Gastroenterol. 2010;24(6):905-21.
GERD, gastroesophageal reflux disease

41. Histamine - RAs
H2-receptor Antagonists (H2RAs)
• Commonly used for episodic heartburn, primarily for
postprandial heartburn2
– H2RAs are better than antacids2
– Simultaneous consumption of an H2RA and an antacid
provides better control of esophageal acid exposure and
heartburn symptoms26
• Best if used before bedtime27
– Histamine regulated spontaneous acid secretion at night
– NAB controlled with H2RAs added to twice-daily PPI28
• Limitations29,30
– H2RAs are not effective in esophagitis healing
– Maintenance therapy with standard doses of H2RAs
cannot prevent relapses
Proton pump
Signal
transduction
to activate proton
pump
H
+
Acid
secretion Parietal cell
Histamine receptor
H2RAs
Histamine
Inhibition of
histamine receptor
Gastric gland
Blood
H2RAs inhibit signal transduction to the proton pump31
GERD, gastroesophageal reflux disease;
NAB, nocturnal acid breakthrough
2. Fock et al. J Gastroenterol Hepatol. 2008;23(1):8-22.
26. Robinson et al. Aliment Pharmacol Ther. 2001;15(9):1365-74.
27. Tutuian and Castell. Am J Med Sci. 2003;326(5):309-18.
28. Peghini et al. Gastroenterology. 1998;115(6):1335-9.
29. Colin-Jones. Aliment Pharmacol Ther. 1995: 9(suppl 1): 9-14.
30. Chiba et al. Gastroenterology. 1997;112(6):1798-810.
31. Huang and Hunt. Best Pract Res Clin Gastroenterol.
2001;15(3):355-70.

42. The Acid pocket
• Gastric juice in the
proximal stomach
escapes the buffering
effect of food, and
remains acidic
• This acidic pocket
traverses the SCJ, onto
the distal esophagus
Fletcher J et al. Gastroenterology 2001; 121: 775-83
pH step-up
Acid pocket

43. Neutralise the Acid
Antacid
Antacid + Alginate
The ‘alginate raft’:
• Displaces the acid pocket1,2
• Traps pepsin and bile3
• Impedes the reflux of
gastric contents2
1. Kwiatek et al. Aliment Pharmacol Ther. 2011:34(1):59-66. 2. Rohof W et al. Clin Gastroenterol Hepatol. 2013; S1542-3565(13)00621-6. 3. Strugala V et al. J Pharmacy and Pharmacol. 2009:1021-1028

44. P-CABs and PPIs:
Main Differences in the Mechanism of Action
P-CABs PPIs
Acts directly (after protonation) on the
H+,K+-ATPase enzyme
Requires transformation to the active
form, sulphenamide
Super-concentrates in parietal cell acid
space (100,000-fold higher than in
plasma)
Concentrates in parietal cell acid
space (1000-fold higher than in
plasma)
P-CABs binds competitively to the K+
binding site of to H+,K+-ATPase
Sulphenamide binds covalently to
H+,K+-ATPase
Reversible binding to the proton pump
Irreversible binding to the proton
pump
Duration of effect related to half-life of
drug in plasma
Duration of effect related to half-life of
the sulphenamide-enzyme complex
Full effect from the first dose Full effect after repeated doses
[Scarpignato & Hunt, Aliment Pharmacol Ther 2015; 42: 1027-1029]

45. Help… My patient is not getting better!

46. 48hr Wireless pH testing

47. pH-Impedance Testing

48. Extent of reflux
Type of reflux

50. Risks of long-term acid suppression

52. What is Barrett’s Esophagus

53. How likely am I to have a
Barrett’s patient?

54. The 3 BIG Barrett’s Questions…
1. Do I need to take long term medication?
2. I heard it’s a precancerous condition, do I need to
have surveillance?
3. Shall I send my family for screening?

55. Do I need to take long term medication?

56. I heard it’s a precancerous condition, do I need to
have surveillance?

57. Shall I send my family for screening?

58. Reflux Update : Summary
1. Rise of Reflux
2. NERDs > GERDs
3. Tackling Refractory Reflux
4. Battling Barrett’s

59. UPDATES:
IBS
REFLUX
Reuben KM Wong
Gastroenterologist
Adj Associate Professor