Update in GI

Posted by admin

January 22, 2012

AGA conference

Barrett's Esophagus :

Define Barretts's as C2M5
5% with Long BE and 8% with Short BE
There maybe other causes of BE besides reflux
Study by Doug Rex – free EGD with colonoscopy.
? role of EGD with screening colonoscopy
4 quadrant biopsy. After each bx, suction the air!
Adherence 51% to the 4 quad bx
BIT – Barrett's inspection time! Higher BIT more the detection.
3 min versus 5 min versus 7 min. At 7 min 69% detection rate
Capsule endoscopy is not ready for Barrett's diagnosis.
Capsule that dissolved in the stomach and then use brushings. Trial from UK

Eosinophilic Esophagitis

S/S dysphagia, odynophagia, Food impaction
IN children vomiting, feeding intolerance, failure to thrive feeding aversion
IN adults epigastric pain, chest pain, refractory GERD
Ringed esophagus, white specks, linear furrows, stricture. NOT Pathognomonic
Dx more than 15 eosinophils per HPF and basal zone hyerplasia and dilated intercellular spaces. Again NOT pathognomonic. Rule out GERD then the above is acceptible as diagnosis and EoE
New definition – chronic immune antigen mediated eso disease.
Remember GERD and EoE now thought to be mutually exclusive.
High eosinophils present both in GERD and EoE. Some patients with GERD have more than100 eos per HPF
Trial of PPI is recommended for all EoE
PPI responsive EoE (confirmed by bx and neg 24 hr pH)
Is it possible that PPI have an anti inflammatory response besides controlling pH

Whats new in GERD and motility

Non responders to PPI – Medications don't help regurgitation
Dyspeptic symptoms – pain in epigastric area or burning
Regurgitation – acid taste in mouth or unpleasant movement of material from the stomach
Cough – top 3 causes are sinusitis, asthma and GERD. (60%, 60% and 40%)
Efficacy of GERD relief is 60-75% with NERD and esophagitis
Chest pain with neg pH response is 25%
Chronic cough response rate with PPI is less than 10 %
PPI does not work for regurgitation, wheeze, globus or throat clearing.
GERD plus epigastric pain – 20% response rate less (?) Usually additional symptoms makes response rate lower to PPI
Lastly concept of hypersensitivity of esophagus.
LNF works best for volume reflexurs – even if partial response to PPI.
Hypersensitivity esophagus DO NOT DO Laproscopic fundoplication (LFP)

Newer Techniques for Barrett's Ablation

EMR but associated with stricturing
Phobar trial for PDT – 52% complete eradication of Barrett's
"Buried Barrett's" – 25% of patients have sub-squamous intestinal metaplasia.
Cryotherapy machines for BE. There are different kinds of cryotherapy machines including balloon based. Liquid nitrogen. Efficacy is 97% complete response.
Esophagectomy 30 day mortality is 18% to 8% (depending on skills and number of surgeries done by surgeon).
Endoscopic therapy is therapy of choice of HGD Barrett's.
If EMR shows submucosal invasion – needs surgery.
Even after ablation – regular follow up is needed – every 3 months of HGD and 6 months to a year for LGD.
EMR for nodular lesions.

Probiotics

Coined by IlieMetchinikoff in 1907 and got a nobel prize in 1908 – Longer survival in Bulgaria which he thought was from probiotics.
It may help in constipation, C diff, H pylori eradication, lactose intolerance, antibiotic associated diarrhea, infectious diarrhea in children (best data) and IBD.
Bacteria in GUT can cause pro or anti inflammatory effects in colon.
It enhances barrier function – increased mucos, increased surface cell effects and can produce chemicals that are antibiotic like substances, serotonin like substances.
Unfortunately it is NOT held to any standards in production.
So, many of the products may not be viable after it passing through stomach pH, or viable in the capsule etc.
On the packaging there is "no claims" they make.
Constipation benefits – B lactis DN shortens colonic transit, L rhamnosus, B lactis and inulin stimulate bowel motility. It should be considered investigational.
Lactobacillus paracasei (published in Alim. Pharm) – 20 patients 15 day trial (L. paracasei enriched with artichokes) statistically significant benefit with chronic constipation.
VSL # 3 decreased bloating.
Funnel plot asymmetry – trial bias
Bifidobacterium, Lactobacillus, Streptococcus, by themselves no study has shown clear benefit but pooled study shows a trend that to benefit.
Bifidobacterium infantis 35264 is beneficial for IBS.
Lactobacillus salivarius 4331 is not helpful in IBS
Bifidobacterium infantis 35264 improved pain, bloating, incomplete evacuation, straining.
B. infantis 35264 – for non-patients with mild symptoms – there was no benefit.
VSL # 3 slows bowel motility and improved flatulence
Bifidobacterium lactis (animalis or rapidis) – has shown some benefits in IBS-C.
Another study showed Lactobacillus paracasei helped IBS-D in another trial not IBS-C!
Probiotics are supplementary.
Results with one strain cannot be applied to another.
Combination can be additive in some cases and antagonistic in other situations.
Get medication from good supplier and stick with evidence.
Chronic constipation – L paracasei, B lactis DN (activia)
IBS – D/M B. infantis 35264 (align)
IBS-C B. lactis DN 1 container 3 times a day for 3 weeks before effect or benefits is seen.
Gas and bloating – VSL #3, B. infantis 25624?
Probiotics in IBD -
Body weight is 1-2 kg is from 100 trillion bacteria.
400-500 species.
Most bacteria is in colon – 10 to the power 11 and in distal ileum 10 raised to 8.
Active probiotic should contain more than 100 million per dose but less than a trillian bacteria.
Extremely rare but infections have occurred in immunosuppressed pts.
Pouchitis VSL # 3, helpful in maintenance.
UC – VSL # 3 probably helpful and E coli Nissle maybe helpful in induction but helpful in maintenance. (as adjunctive Rx)
Crohns – uncertain if E coli Nissle or S. boulardii, LGG is helpful.

Future of GI

New generation stool DNA tests 100% sensitivity and specificity. (2 meth markers) (for cancer detection)
Detection rate was 64 % sensitivity for 1 cm, 79% for 2 cm and 91% for 3 cm polyps.
No difference between proximal or distal location
Screening is suggested q 2 years and after 3 years of screening the detection rate is 95%
DNA markers in Plasma – plasma septin 9. CRC sensitivity is 50-90% (58%) but not good for polyps. (ARUP lab)
ANother blood test is sDNA (Exact Sciences lab)
Conceptual model – Large pre-cancerous polyp best test would be stool makers.
Stage 4 cancer – blood test is better.
Role is "interval test" for every 10 year colonoscopy screening.

Surveillance Colonoscopy

Reason is Interval cancer
New fast growing lesions, incomplete removal occurs in 20 to 27% as cause
Missed lesions occurs in 17% of polyps – polyps greater than 1 cm. Even when done by expert colonoscopists. Thus it underestimates the rate of missed lesion in general population
Risk of interval cancer is - 1.7-2.8 cancers /100 person years or 0.3-0.9% in 3-5 years
2-9 % of cancers were interval cancers in Canadian registry
Interval cancers were more likely to be proximal, in women and advanced stage.
Interval cancers have high micro-satellite instability and are more aggressive.
30% of GI physicians suggested repeat colonoscopy even in hyper-plastic polyps
Advanced adenomas and more than 3 adenomas need more frequent colonoscopies
2006 Guidelines, 3 adenomas, 3 year colonoscopy, more than 1 cm, repeat in 3 years, villous adenoma 3 year colonoscopy,
If adenomatous or villous adenomas surveillance guideline is 3 years.
Cancer surveillance is 1 year.
Serrated polyp is 20% of CRC. Hard to detect esp. if sessile and often covered with mucous. During colonoscopy – look carefully for synchronous polyps.
Hyperplastic polyposis syndrome more than 5 and 2 of them more than 1 cm – repeat in 1 year
serrated polyp with dysplasia or more than 1 cm – 3 cm
So high risk polyps, continue every 3 years and if neg after 1 – change to 5.
Poor prep colonoscopy – repeat colonoscopy.
If FOBT + after colonoscopy – individualized approach.
Above is proposed but not approved (all the above guidelines)

New approaches for better colonoscopy

Spend at least 6-8 min, look behind folds and attentive to flat mucosal changes
Colonoscopy reduces it by 76-90% reduction rather than 100%. Reason is MISSED lesion
Canadian study shows there is no reduction in right colon cancer but substantial reduction in left CRC. However it was done by non – GI and 66-83 % cecal intubation rate. Cecal intubation should be more than 95%
German study showed reduction in both left and right colon cancer but more in left colon compared to right colon.
15% and 25 % detection rate for female and males. % screening / surveillance
Low adenomatous detection rate is associated with higher colon cancer in next 5 years.
New technology improves polyp detection rate by 3-4%
cap assisted colonoscopy, look behind folds
Increasing WT does not improve polyp detection. What is needed is better visualization.
Use Peer pressure by having statistics on display of detection rate.
Yellow golden mucous suggests sessile serrated polyp under it.
Fold deformity suggests polyp behind it, lack of vascular marking and yellow mucous suggests it.
High definition colonoscopy – 3.5% increase in polyp detection based on meta-analysis.
NBI – if there is any advantage it is very slight.
clear caps – studies are very variable to helpful, no help and worsens polyp detection.
MAKE A COMMITMENT TO IMPROVE YOUR PERFORMANCE
Experience of nurse in room helps to improve polyp detection rate.

HNPCC

Risk of cancer with Lynch is 70-80%
Autosomal dominant
40-50 years old, 2 generations, and usually in proximal colon.
MSH2, MLH1, MSH6, PMS2
stomach cancer 13% life time risk, endometrial cancer is 4-60% risk renal is less than 5%, Surveillance for stomach cancer every 1-4 years
Muir_Torre syndrome – Lynch plus kerato-acanthomas and sebaceous neoplasms.
Anyone with CRC before 50 think Lynch.
Start screening at 20-25 and interval is 1-2 years. AFter 40 every year.
CRC repeat colon in 1 year and then 3 years and then every 5 years.
De Novo germ line mutation occurs in 30% of patients for FAP / Gardeners.

IBD

70% endoscopic healing with immunomodulators vs 14% on imuran
The healing was maintained at 3 and 4 years.
Top down is better than conventional (73% vs 30% remission)
Optimizing Imuran therapy
30-40% rates of remission overall
It may alter course of CD natural history.
Syngergistic effect of imuran with immunomodulators.
SONIC study – advantage is 10% added benefit
He believes infliximab level guided therapy makes sense
SONIC was only 26 week study (that was published)
Advantage of imuran is lower CRP and higher trough of infliximab.
Loss of response to IFX with time. 22.9% for IFX, 20% for adalimumab,
Do not use episodic treatment and combination is better.

IBD and Pregnancy

Fertility is NOT affected by IBD.
Fertility is dropped by 30% with creating pouch
Disease should be in remission before they conceive.
If active disease and they get preganant – 1/3 get better, 1/3 no change and 1/3 get worse
Higher change of prematurity, low body weight and need for C section.
Active perianal disease or active CD – go for C section
Safe medications in pregnancy -
Azathioprine or 6 MP is a category B.
The greatest risk to pregnancy is active disease not the medications
Asacol is a category C, but other aminosalicylates are category B.
Steroids are category B/C – higher incidence of oral clefts, overall risk of malformations is low., adrenal suppression in newborn, premature rupture of membranes. Entocort does not share these problems.
Immunomodulators are all category B.
DO NOT GIVE ANY LIVE VACCINE – TO ANY BABIES BORN OF MOTHERS WHO RECEIVED IMMUNOMODULATORS. (ROTAVIRUS, MMR, BCG)
Breast feeding contraindicated with flagyl cipro, methotrexate and cyclosporine
Post partum period is when they often have flareup of CD / IBD

Toxicity of IBD Medications

Bad prognostic markers of IBD – onset at young age, fistulizing disease, perianal disease, early need for steroids, severe endoscopic disease, positive serologies for CD are more likely to need surgery.
Combination therapy is much better!
Recurrent use of steroids or use of steroids is associated with twice the mortality.
In contrast – IFX or Mtx or 6 – MP does not increase mortality.
6 MP can cause allergic reaction, nasuea, hepatitis, pancreatitis, serious infections and non hodgkins lymphoma.
Patients with low tPMT have EARLY leukopenia
Any drop in WBC even if in normal range, WARNING sign of low TPMT activity.
NHL 2-4% on imuran. It is discovered within 8 weeks of treatment.
Best study for risk of NHL is the French study.
Cesame trial – Old men pass the age of 50 get NHL.
Risk of NHL on anti TNF – 6.1 per 100,000 pt years. Usually it is in older patients
HSTCL _ hepatosplenic T cell lymphoma from anti TNF
Quality measures – if patient on steroids more than 60 days, check C diff, TB, Hep B screening, and yearly BDM, pneumonia and flu vaccination.
HPV vaccination in young women
Avoid varicella and MMR vaccination.

Surgery in IBD

1/3 patients with UC need surgery
2/3 of patients with CD need surgery.
Surgical rate has not changed in spite of newer medications between 1-2% however the trend is you may need it less likely. Probably because they already had tissue damage by the time they started treatment.
Post op IFX – endoscopic recurrence was 0-10% versus it was 85-100% in placebo at 1 year
Post op anti TNF works the best is the most effective.
Mucosal healing is the most important.
Data suggests that start treatment after surgery even if no endoscopic mucosal lesions. Waiting for disease to come back after surgery is probably not the best thing.

Hepatitis C

Anemia is more severe in triple therapy and more serious. Recommend ribavarin ? role of epo. Reducing ribavarin dose dos not affect SVR
Rash use topical steroids and antihistamines
Stop statins, sildefnafil, versed, rifampin, ergots cisapride, st. Johns wort,
Largest increment in SVR is for CT/TT patients
Modest increase in SVR in CC naives
IL28B use for fine tune discussions and more useful in naive patients than non responders.
HCV resistance in patients who fail triple therapy. They are V36, T54, R155, A156 types.
End of IFN era / – DAA-1 plus DAA-2. NS5A plus Protease inhibitor works well even in null responders
Next step will be quad combo and then interferon free regimen. DAA protease inhibitor and DAA polymerase inhibitors.

Strategies for Hep B treatment

High viral load associated with higher chance of hepatoma.
Type C is associated with highest chance of hepatoma
Older the age higher the chance of hepatoma
ALT more than 45 – risk of hepatoma is higher
Cirrhosis also higher chance of hepatoma
New concept is HBsAg level than HBV DNA level correlates better with ccc DNA in liver.
Use HBsAG levels (<1000) and HBV DNA (<2000) gives best result of inactive carrier validation.
HBsAg loss after 2-5 years of treatment is less common (less than 5%. One study showed 11%)
Traditionally we start treatment based on elevated ALT, inflammation on liver biopsy and presence of serum HBV DNA level.
AASLD guidelines suggests Rx when ALT > 2 x ULN and HBV DNA > 20,000 level. Exception Lower threshold for pt > 4, active fibrosis and clinical evidence of cirrhosis. Then start treatment earlier. Borderline ALT or HBV DNA do liver biopsy and monitor.
Resistance more likely in nucleosides or tides and no mutations in interferon treatment.
TDF and ETV should be initial Rx choice (entecavir or tenofovir).
Genotype A favor interferon treatment.
HBe Ag neg – Lack of HBsAG and HBV DNA decline at week 12 – futility rule for genotype D-HBV. Hb e Ag+ pt, decline in HBs AG at week 12 and 24 predicts sustained response.
PEG treatment for 1 year. May need longer for Hbe Ag neg.
Likelihood of HBeAg seroconversion 50% after 5 years treatment

NASH

2 types Micro and Macro
NAFLD – 30% of the US population has it
NASH occurs in up to 10% of US population
NAFLD increases risk of death – from liver, cardiovascular and cancer causes.
Fat in liver is an independent risk factor for CV death!
Nash with high activity score, DM, obesity and fibrosis have worse prognosis.
Caspase-3 generated fragments are seen in NASH.
CK-18 level in blood -? Diagnostic value for NASH
Rx for NASH – lifestyle changes
PIVENs study – vitamin E 800 IU/day was helpful and pioglitazone was not helpful
TONIC is other study which showed vitamin E helped. But weight loss is most important
Pioglitazone associated with risk of fracture and CV risk.
Rx of Vitamin E can increase risk of prostate cancer and 0.04% increase in risk of mortality from all causes.
? role of gastric bypass.
Pentoxyfylline maybe helpful for NASH
PUFA on NASH – data is pending could be helpful.

HCC

AASLD slide recommendation
If mass is less than 1 cm, repeat US every 3 months. If it remains stable repeat every 6-12 months. If it grows follow 1-2 cm recommendation
If more than 2 cm – dynamic CT or or MRI. If typical for HCC – proceed with treatment for HCC WITHOUT bx. Most transplant centers recommend proceed without bx
If between 1-2 cm, get CT and MRI. If concordant proceed accordingly. If findings not concordant proceed with bx.
Staging based therapy – number, size, symptoms of HCC, cirrhosis presence and
If one lesion, less than 2 cm, and no cirrhosis, surgery is curative.
Look at slides in book.
RF ablation has 50% 5 year survival.

Biliary dyskinesia

Biliary and pancreatic SOD
SOD evaluation – invasive and non invasive
Hopkins scintographic score for biliary SOD dynfunction. 100% sensitivity and specificity. Drawback is does not evaluate pancreatic SOD.
Secretin stimulated MRCP – 0.5 cm increase in PD size suggests pancreatic SOD.
ERCP 30% of patients will develop pancreatitis in SOD. DO NOT DO ERCP.
Chronic abd. pain – 60% of them had SOD. 10% isolated biliary SOD, 20% had ioslated pancreatic SOD and 30% had both.
Rx is antispasomodics – smooth muscle relaxants, botox injections, CCBs
Gold standards is biliary sphincterotomy.
Type 2 and type 3 biliary – do sphincterotomy.
Causes of pain after sphincterotomy – residual SODor pancreatic SOD or chronic pancreatitis or non pancreaticobiliary cause.
Should patients get pancreatic sphincterotomy with biliary sphincterotomy ? On going study.

Cysts of Pancreas

1.2% of general population has it on routine imaging.
serous cystadenoma, mucinous cystic neoplasm, IPMN, cystic islet cell tumor, pseudocyst, solid papillary neoplasm
IPMN in male, head of pancreas, variable malignancy risk, All other cysts are more common in women.
Pseudocyst – may not always have history of pancreatitis. It is 15-30% of all cysts
Islet cell tumor – 17% is cystic and more common in MEN 1
Serous cystadenoma – usually large, innumerable small cysts with central calcification. There is a macrocystic variant, usually females in 6th or 7 th decade and can be symptomatic, frothy, and very bright on EUS, low malignant potential.
Mucinous cystic neoplasm – has ovarian stroma in it, malignant potential and usually in women
IPMN – 29% malignant risk in 10 years. Can present as unexplained pancreatitis with dilated PD, jaundice and diabetes. Cancer risk is if size more than 3 cm,mural nodules. Fish mouth appearance of IPMN – with mucous. Amylase in pseudocyst in cystic fluid is more than 250. CEA less than 5 unlikely to be cancer and more than 800 in fluid is probably malignant.
PANDA study – DNA analysis of cystic fluid. Moderate accuracy and does not add much to current tests
Mucinous cysts – inject with ethanol or paclitaxel. Cyst resolution is 33-79%. 10% pancreatitis risk and 20% abd. pain.
Cyst more than 1 cm and symptomatic consider surgery. If more than 1 cm and no symptoms do EUS.
If cyst less than 1 cm, repeat imaging in 1 year.

Chronic Pancreatitis

Pain occurs from PD obstruction or ischemia of pancreas or pseudocyst formation or inflammation or duodenal and CBD obstruction.
Mx from enzymes, analgesics, octreotide, antioxidants, nerve blocks, endoscopic therapy, ESWL and surgery.
Pancreatic surgery – islet autotransplantation.
Endoscopic treatment involves ESWL, EUS and ERCP. Pancreatic and biliary sphincterotomy. Often needs a screw dilator, shock wave lithotripsy and then stone extraction
Pancreatic stone extraction – less than 30-40% extraction rate

Familial Pancreatic Cancer

2 or more patients with pancreatic cancer in family.
10% of all pancreatic cancers are familial.
High risk FPC. Families with > 3 members with cancer.
Hereditary Pancreatic cancer BRCA1/2, p16 mutations or FAMMM, Lynch syndrome, PJ syndrome, hereditary pancreatitis (cationic trypsinogen gene)
Hereditary breach and ovarian cancer HBOC BRCA 1 and BRCA2
PJ syndrome higher risk of colon cancer and should be monitored for pancreatic cancer also. Moreover risk of gastric cancer, ovarian, breast, cervical and endometrial cancer
FAMM (familial atypical multiple mole melanoma). p16/CDKN2A gene. They have atypical melanocytic nevi, autosomal dominant
Lynch – SB cancer, ureter cancer, renal pelvis cancer, brain, ovary and pancreatic cancer. Age 50 1.3% and Age 70 4% risk of pancreatic cancer
HBOC syndrome – autosomal dominant. Some patient family may have pancreatic cancer but no breast or ovarian cancer !!!!
BRCA mutation in Jewish patients.
PALB-2 Multiple family members with pancreatic cancer. Also increased risk of breast cancer
Johns Hopkins, Mayo clinic, Creighton Univ, Mt Sinai, Anderson CC, – sites for familial cancers
Screening with EUS, dedicated MRI / MRCP or dedicated pancreatic protocol CT, aggressive evaluation of cysts. ????prophylactic pancreatectomy.
PanINs lesions – intraepithelial neoplasia (similar to colon cancer from adenoma). High grade PanIN3 and more dense, different Kras mutations.
Thus 2 ways to develop pancreatic cancer PanIN or IPMN.
3 D reconstruction for pancreatic neoplasm
MRI has no radiation advantage.
EUS not widely available and high inter observer variability. Requires extra training.
Start screening at 50 or 10 years younger. PJ start at 35

Celiac disease

Best combo is t Tg Ig A and DGP.
neg serology in 15% of patients
Hemolysis reduces anti tTG titer
Bx is gold standard.
Marsh Classification
Patchy disease.
Need 4-6 biopsies during endoscopy.
Bulb biopsies increased diagnosis of celiac by 13%
4-6 bx from SB and 2 bx from duodenal bulb
Genetic testing DQ2/DQ8 – 100% of patients with celiac disease have this genotype.
Thus genetic has 100% negative predictive value.
Gluten free diet. Support groups CDF, GIG, CSA/USA
Increased mortality in celiac is from lymphoma (T and B lymphoma and extraintestinal), other cancers are also increased. Increased breast, cervical endometrial cancer also. They should get pneumovaccine also.
Gluten free diet is protective against malignancy
Poorly responsive celiac disease – wrong diagnosis, bacterial overgrowth, lactose or fructose intolerance, microscopic colitis, pancreatic insufficiency and refractory celiac disease.
Refractory celiac disease – type 1 and 2 based on intra epithelial immunohistochemistry. Intra epithelial lymphocytes do not have surface markers then it is type 2 refractory celiac disease. Type 2 is poor prognosis. ALso can do flow cytometry and PCR to differentiate. Type 1 use immonomudolators including steroids, imuran etc. Do not use steroids in type 2 because it increases risk of lymphoma.
Children should get gluten when being breast fed to reduce their chance of developing celiac disease.

Bariatric surgery in Obesity

Roux – en – Y(RYGP).
Endoluminal bariatric interventions.
Complications of bariatric surgery – gallstones, PUD, GERD, food impaction, band displacement, band erosion. RYGP compllications includes biliopancreatic diversion
Gastric bypass – late complications are stomal stricture, stomal ulceration, marginal ulcer, stomal ulcer, staple line disruption, internal hernia. Pouch is 3-5 cm long.
Anastomotic ulcer in RYGP – 3-20% of patients. They have nausea, vomiting and epigastric pain. Ulcers on jejunal side usually. Remember to wash well. Anastomotic ulcer can occur within a few cm of the anastomosis also.
Treatment PPI high dose, carafate, eradicate Hp. Use carafate suspension not tablet. Rare cases will require resection.
Anastomotic stricture – less common than ulcer. Non wire guided dilatation with balloon. Try to dilate to 1 cm. Usually diagnostic scope will not traverse.
RYGP – staple line fistula or disruption. Fistula is between gastric pouch and gastric remnant. (gastro gastric fistula). S/S weight gain and reflux are symptoms. Contrast radiologic study.
Cutaneous fistulas can also occur.
May need to remove anastomotic suture material with applying traction and cutting suture material. This way you can see the ulcers etc better.
GI bleeding is uncommon in RYGP fortunately. If DU, can be hard to reach it endoscopically.
Laproscopic adjustable gastric banding – dome seen on retroflexion. Complications include food impaction, band displacement or slippage, band erosion, gastric pouch dilatation, esophageal dilatation.
Sleeve gastrectomy complication – Long staple line 10-12 cm long!
Endoscopic Mx of post bariatric surgery – CBD stone, Can be very difficult to remove the stones.
If EGD does not give answer – then do CT, SBFT and MRCP or EUS. Role of WCE is questionable. Consider Agile patency capsule.
Suture scissors maybe needed.

IBS

ROME 3 – change in frequency / consistency and pain relieved with BM and occuring 3 times in a year
IBS -C , IBS – D, mixed, IBS – U
Patients with IBS migrate from C to D to A(lternating)or mixed.
Physical activity helps improve IBS! Encourage patients to exercise.
Food intolerance – 2/3 of patients associate IBS triggered by some foods!
Also fermentation plays a role. Gas handling is different in IBS patients than normal patients.
Later on patients have a conditioned response to food later on – Psychological factors.
Food elimination helps reduce IBS symptoms.
Gluten sensitivity – Consider that in patients.
Lactose intolerance. More likely to be carbohydrate intolerance.
FODMAPs diet – fermentable oligo, di, monosaccharides and polyols. Avoid fructose, fructan containing vegetables, wheat based products, sorbitol and lactose containing foods, raffinose containing foods (legumes, lentils,cabbage, brussels sprouts).
FODMAPs diet – you must have a trained dietitian.
Patients with severe symptoms will follow FODMAPs diet. This information is from UK and Australia. No US data yet.
Consider anti depressants in some patients with IBS – TCA and SSRI.
No data for IBS-C for using PEG or miralax !
Rifaximin – 10% therapeutic gain with treatment. Improvement is it related to SIBO?

Allergies and EoE

Physiological food reaction – large volume leads to distension and regurgitation.
Fatty food delay gastric emptying
Legumes, cruceferous vegetables, garlic, onions, leads to flatus.
Non absorbable or poorly absorbed sugars and carbohydrates can lead to diarrhea, bloating, flatulence etc.
Normal flatus is 14 x/day !!!!
Gas becomes a problem in crohns, gastroparesis etc.
Food hypersensitivities, celiac, hypersensitivity to food protein enteropathies (usually in pediatrics)
Food allergy – 4-5% of patients have it. 50% of anaphylaxis in USA is due to food!
ARF (adverse reaction to food) occurs in IBS, IBD also.
Big 8 foods – milk, soy, eggs, wheat, peanuts, tree nuts, fish and shelfish.
Outgrows in egg, milk and peanuts by the age of 5. Milk – they outgrow in 80% of cases by 5.
Increased risk on those taking b blockers and Ace Inhibitors. (for food allergies)
Oral allergy symptoms – cross reactivity between raw fruit and vegetables and pollens. Itching and swelling and tingling on lips. Patients with seasonal rhinitis are more likely to get it.
Latex food allergy syndrome – Foods are kiwi, potato, tomato, avocado, chestnut and banana.
GI disorders associated with eosinophilia – EoE, E gastritis, enteritis, colitis.
Lactose intolerance – secondary lactase insufficiency occurs after gastroenteritis, crohns and celiac. Genetic usually more common in asians, africans, native NA and mediterranean areas.
Lactose intolerance – can tolerate upto 12-15 g lactose (8oz milk a day). Yogurt, hard cheese are lactose free. Better if you take it in small frequent amounts. Lactase supplements are helpful. Triacylglycerol content of many milk products can cause GI symptoms unrelated to lactse insufficiency or cows milk protein allergy.
(FODMAPs diet) (see table).
3 types of ARF (food hypersensitivity, food protein enteropathy and food intolerance).

Update on new treatments for IBS

Rifaximin is helpful in IBS – bloating associated symptoms. Rx is 550 mg tid for 2 weeks.
Linaclotide – submitted for approval. Effective for IBS-C. guanylate cylcase -C agonist.
Others in the same class of GC-C is guanilib.
5-HT3 antagonist – ramostron.
Crofelemer CFTR inhibitor
Asimadoline – k opiod receptor agonist
Tryptophan hydroxylase 1 inhibitor.

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