Category Archives: Gastroenterology

Will NOTES come to pediatrics?

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Natural orifice translumenal endoscopic surgery (NOTES) has been receiving increasing attention and is being considered as a potential alternative to laparascopic surgery; but it will be a long time before NOTES comes to pediatrics.  Initial studies for several indications have been published in the last few years and this experience has recently been reviewed (Gastroenterology 2012; 142: 704-10).

Potential operations include the following:

  • Cholecystectomy.  This has been accomplished transgastric and transvaginally.  One multicenter study published experience with 362 transgastric cases and another with 551 transvaginal cases.
  • Thyroidectomy via a translingual approach.
  • Esophageal myotomy via a transesophageal approach.
  • Appendectomy via a transvaginal approach.
  • Rectal cancer resection via a transrectal approach.

Thus far, complications have been low & no deaths; only infrequently has a laparascopic or open procedure been needed to salvage the operation.  The main limitation to further use of NOTES has been adequate instrumentation and a critical mass of investigators to explore this technique.  As expertise develops in this area, a much larger number of procedures will be undertaken.  In many ways, NOTES is akin to laparascopy in its early days.  Potential advantages of decreased pain and faster recovery are the motivation to continue to work on NOTES.

Preventing Cancer in patients with Barrett’s Esophagus

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Though Barrett’s esophagus is rare in pediatric gastroenterology, concerns about esophageal cancer are fairly frequent.  In addition, some conditions that increase the risk of esophageal adenocarcinoma start in childhood.

One way to lessen the risk of Barrett’s esophagus in adults is through the use of medications (Gastroenterology 2012; 142: 442-52).  This study was a pooled analysis of six population-based trials with a total of 1226 esophageal adenocarcinoma (EAC) patients and 1140 esophagogastric junctional adenocarcinoma (EGJA) patients.  NSAIDs (aspirin and nonaspirin) lowered the risk of both EAC and EGJA, with OR of 0.68 and 0.83 respectively.

Although this study suggests a possible role for NSAIDs in preventing cancer in patients with Barrett’s esophagus, the risks and benefits for this intervention need to be individualized.

Related previous blog post: More bad news for smokers

Additional references:

  • -Gastroenterology 2011; 141: 2000. Lower risk of Barrett’s in pts taking NSAIDs & statins. n=570.
  • -Gastroenterology 2011; 141: 1179. Overall, patients with BE and LGD have a low annual incidence of EAC, similar to nondysplastic BE. There are no risk factors for progression and there is significant interobserver variation in diagnosis, even among expert pathologists.
  • -NEJM 2011; 365: 1375. Large Danish study, n=11028. Lower incidence of Barrett’s than previous estimates. Relative risk of 11.3 compared to general population for adenoca of Esophagus with absolute annual risk of 0.12%. Barrett’s patients have the same life expectancy as general population (ed. pg 1437). Detecting cancer only ~1 in 1460 scopes with screening whereas Barrett’s detected in 10% of pts.
  • -Gastroenterology 2011; 141: 417, 460. Durable effects of ablation, n=127..
  • -Gastroenterology 2011; 140: 1084. AGA statement on Barrett’s . Recs screening only in those with multiple risk factors (age 50, male, chronic GERD, white, incr BMI)
  • -Clin Gastro & Hep 2010; 8: 565. Guidelines suggest that screening for Barrett’s is not justified w/o alarm symptoms (dysphagia, odynophagia, wt loss, anemia, hematemesis)
  • -Gastroenterology 2010; 138: 2260. n=11,823. Decrease risk of esophageal adenoCa in patients taking NSAIDs & statins.
  • -Gastroenterology 2010; 138: 854. Nice review.
  • -Gastroenterology 2010; 138: 5. Survival equivalent to general population according to Mayo study, n=366. In Barrett’s patients, leading cause of death was cardiovascular (28%). Esophageal cancer resulted in 7% of deaths. Study presented at ACG Oct 26, 2009.
  • -Clin Gastro & Hepatology 2009; 7: 1266. no benefit from surgery for Barrett’s & unclear if chemoprevention works.
  • -Gastroenterology 2009; 137: 763. Suggests surveillance with Barrett’s is not beneficial.
  • -NEJM 2009; 360: 2277, 2353.. Radiofrequency ablation can be effective.
  • -Gut 2008; 57: 1200-06. Utility of endoscopic Rx.
  • -Clin Gastro & Hep 2008; 6: 1206; editorials: 1180, 1181, 1183.. n=2107 with Barrett’s. 79 w surgery and 80 w endoscopic Rx.
  • -Gastro & Hep 2006; 2: 468. 2-8% of pts in general population have Barrett’s. >90% of ptsc Barretts will never develop cancer. Screening has not been proven to be effective in lowering rate of death from cancer. ~40% of US population has heartburn; only 8000-9000/yr develop esoph adenoCa. Also, the presence of Barrett esophagus does not decrease life expectancy.
  • -Gastroenterology 2005; 129: 1825-31. 1.6% incidence of BE in adult Swedish population. Alcohol, smoking increase risk.

Disruption of KLF4 is the real villain for gastric cancer

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The only reason I’m posting this article is the word “Villin” in the title of the article (Gastroenterology 2012; 142: 531-42); I wondered what this was.  In this study, the authors show that “disruption of KLF4 in villin-positive gastric progenitor cells promotes the formation and progression of tumors in the antrum of mice.”  For the uninitiated,  an editorial on pages 424-27 of the same issue explains the entire article and the significance of the findings.

Kruppel-like factor 4 (KLF4) is a protein in multiple tissues that is important in cell differentiation, inflammation, and carcinogenesis.  Villin is an actin-bundling protein found in the apical brush border of absorptive tissue.  Villin-expressing gastric progenitor cells are typically quiescent but undergo division during inflammatory insults.

This is important in understanding gastric cancer because for a long time it was unclear why cancer would develop in the stomach where there is frequent turnover of the mucosa.  It is likely that more quiescent cells live long enough to accumulate cancer-promoting mutations/changes.  This study adds support to this hypothesis, at least in mice.

Gluten sensitivity without celiac disease

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Gluten free is big business.  In a range of conditions, eliminating gluten has been advocated to improve symptoms.  The most frequent problem in which a gluten-free diet (GFD) may be beneficial is irritable bowel syndrome (IBS).  A selected summary in Gastroenterology discusses this topic (Gastroenterology 2012; 142: 664-73).

This review highlights an article that showed improvement in a double-blind randomized trial (Am J Gastroenterol 2011; 106: 508-14) & then reviews the topic more broadly.  The study is the first randomized controlled trial that suggests that nonceliac IBS patients may improve with a GFD.  The study looked at 34 patients with IBS who had improved with a GFD & had no evidence of celiac disease (either negative HLA-DQ2/DQ8 or duodenal biopsy).  Then 19 patients had 16g of gluten per day reintroduced; control patients were offered equivalent food that was gluten-free.  The gluten products in the study were free of fermentable oligo-, di-, monosaccharides and polyols to avoid confounders (What to make of FODMAPs).  The patients who continued a GFD had less reported pain, bloating and tiredness.  The GFD group reported good control of symptoms the previous week in 68% vs. 40% in the study group.

The commentary notes that ‘gluten sensitivity’ is big business, accounting for 1.3 billion in 2011 expenditures.  Companies like General Mills, Betty Crocker, PF Chang’s, and Subway are offering gluten-free choices.  Since immune activation and low-grade inflammation may be important for IBS, it is possible that some foods trigger these processes.  At the same time, individuals with reported gluten sensitivity have not been shown to have increased intestinal permeability; this is in contrast to celiac disease (BMC Med 2011; 9; 23).

There may be more patients with IBS who will benefit from a GFD due to gluten sensitivity than patients with celiac disease.

Additional references:

  • -Nutr Clin Pract. 2011;26:294-299.  A gluten-free diet (GFD) is commonly recognized as the treatment for celiac disease. It also has been investigated as a treatment option for other medical conditions, including dermatitis herpetiformis, irritable bowel syndrome, neurologic disorders, rheumatoid arthritis, diabetes mellitus, and HIV-associated enteropathy. The strength of the evidence for the use of a GFD in these nonceliac diseases varies.
  • -Clin Gastro & Hep 2007; 5: 844. GFD in IBS pts (w/o celiac)
  • -Am J Gastro 2009; 104: 1587. Gluten sensitivity in IBS (w celiac)
  • -Gastroenterology 2011; 141: 1187. Prevalence of celiac similar in IBS as general population though higher number (7%) with celiac antibodies (esp gliadin).
  • -Am J Gastro 2008; 103: S472 (abstract P687) Serology for Celiac in IBS patients same as in controls. n=566. n=555 controls.
  • -Clin Gastro & Hep 2007; 5: 844. d-IBS patients may respond to gluten-free diet, especially if positive HLA-DQ2 expression or positive celiac serology.
  • -Lancet 2001; 358: 1504-08. n=300 uninvestigated pts w IBS criteria & 300 controls. 66 w positive serology; 14 w biopsy-proven celiac dz, 43 w normal biopsies. Odds ratio of 7 to have celiac compared to control group (2 w biopsy-proven disease).

HEROES trial

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HEROES is definitely a catchy acronym (Arch Intern Med 2011; 171: 1929-36); HEROES is short for Helicobacter eradication relief of dyspeptic symptoms.

In pediatric practice, when Helicobacter pylori infection is identified, efforts are made to eradicate it.  However, studies have not been conclusive about whether this is beneficial for individuals with ‘functional dyspepsia.’  A 2006 Cochrane review of 21 trials found only 6 were positive for eradication.  Previous trials had not focused on primary care patients who may be more prone to respond.  As such, the investigators randomly assigned 404 patients (adults with average age of 46 years) into a group (n=201) treated with antibiotics and a control group (n=203); this was a randomized double-blind placebo-controlled clinical trial at a single center.  All eligible patients had to meet the Rome III criteria for functional dyspepsia and have H pylori infection.  Individuals with heartburn and irritable bowel were excluded. The antibiotic group received omeprazole, amoxicillin, and clarithromycin whereas the control group received omeprazole and placebo –both groups received treatment for 10 days.

In the antibiotic group, 49% achieved at least a 50% reduction in symptoms at 12 months; the control group had a 36.5% response.  Overall, 78.1% of the antibiotic cohort improved compared with 67.5% in the control cohort.

Although the findings of the study indicate improvement with a course of antibiotics, what to do with these results is not clear.  Worldwide, at least 50% of the population is infected by H pylori.  In addition, dyspeptic symptoms afflict up to 40% of the adult population in Western countries.  Due to the enormity of these problems, translating the results of this study into practical treatment strategies is difficult.

Additional references:

  • -JPGN 2011; 52: 387. Impact of Rome III criteria on yield. Still 2.8% w/o alarm symptoms that had significant endoscopic findings.
  • -Clin Gastro & Hep 2008; 6: 746. Antidepressant venlafaxine not effective in functional dyspepsia in double-blind, randomized, placebo-controlled study. n=160.
  • -Cochrane Database Syst Rev 2006; (2): CD002096. Rx of H pylori in functional dyspepsia.
  • -Gastroenterology 2007; 133: 799. Natural hx of functional disorders: 20% persist w same Sx, 40% develop other Sx, 40% get better. Large study from Olmstead county (n=1365)
  • -Gastroenterology 2007; 132: 1684.  Changes in cerebral blood flow during gastric balloon distention in dyspepsia.
  • -Gastroenterology 2006; 130: 1466-79. Functional gastroduodenal d/o. Acid suppression is 1st line Rx.
  • -Gastroenterology 2005; 129:1753-55, 1756-80, 1711. Mgt & guidelines for dyspepsia. In pts < 55 w/o alarm sx, test for H pylori and rx c PPI. In pts who don’t respond, consider EGD. Other Rx unclear: prokinetics, anticholinergics, antidepressants.
  • -Gastroenterology 2004; 127; 1239. Review of functional dyspepsia. Rx initial c acid-blocker/prokinetic reasonable, if not helpful, consider tricyclic, or clonidine. Eliminate H pylori. Sumatriptan may help
  • -J Pediatr 2005; 146: 448, 500.  Dyspepsia in children often associated with delayed GE and reduced gastric volumes
  • -Gastroenterology 2003; 125: 1219-26. Algorithm suggested:1. chech H pylori 2. Rx c PPI/H2RA.  3. If persists, EGD.  If EGD neg, consider elavil
  • -Clinical Gastro & Hepatology 2003; 1: 356. Increased Mast cells noted.
  • -Gastroenterology 2002; 123: 1778, 2132. Use of hypnosis for NUD.
  • -Ann Intern Med 2001; 134: 361-369. Meta-analysis of H pylori & NUD. Non-significant/minor improvement c eradication.

TNF antagonists and UC

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In my fellowship (15 years ago), the use of thiopurines (eg. azathioprine, 6-mercaptopurine) for ulcerative colitis was debated.  Many physicians urged colectomy rather than using these drugs which could have long-term consequences.  At the time, the risk of thiopurines was less well-understood.  Over time, the use of these agents has become common when mesalamine products were ineffective.  The same issue comes up with TNF antagonists versus colectomy.

A recent study provides more information on the effectiveness of adalimumab for patients with moderate-to-severe UC but does not settle this debate (Gastroenterology 2012; 142: 257-65).  In this study, termed ‘ULTRA-2’ (Ulcerative colitis long-term remission and maintenance with adalimumab 2), the  efficacy of adalimumab for induction & maintenance of remission was studied in 494 patients.  This was a randomized, double-blind, placebo-controlled study; average age was 40 years.

Clinical remission in the adalimumab group were 16.5% at 8 weeks (9.3% placebo).  At 52 weeks, 17.3% in the adalimumab group were in remission (8.5% placebo).  Among patients naive to anti-TNF agents, the response rate was 21.3% at week 8 & 22% at week 52.  Safety overall was similar in both groups; however, in the adalimumab group one patient developed gastric cancer and one developed squamous cell carcinoma.

The authors conclude that adalimumab is safe and more effective than placebo in inducing and maintaining remission among patients with moderate-to-severe UC.

A second study, also published this past month, looks at the use of infliximab for maintenance therapy for UC (Inflamm Bowel Dis 2012; 18: 201-11).  Patients who had achieved benefit from ACT-1 and ACT-2 studies were followed for three years.  Dosage of infliximab could be adjusted.  A total of 229 patients entered the study.  During the study, 70 patients (30.6%) discontinued infliximab due to adverse effects (10.5%), lack of efficacy (4.8%) or other reasons (15.2%); the majority were able to continue infliximab.  The authors indicate that no new safety issues were identified. Yet, there were two deaths among the infliximab group including a 19 year-old nonsmoker who developed lung cancer and a lethal case of histoplasmosis.

Because the improvement compared to placebo is modest with both of these agents, the question about whether to use these medications or proceed to surgery in UC patients is unanswered.

Additional references:

  • -Aliment Pharmacol Ther. 2008 Oct 15;28(8):966-72. Epub 2008 Jul 24.  Long-term outcome of adalimumab therapy for ulcerative colitis with intolerance or lost response to infliximab: a single-centre experience.
  • -Am J Gastroenterol (Oussalah A et al) 2010; 105: 2617-25. Multicenter study of IFX for UC
  • -Gastroenterology 2010; 138: 2282. Severe pediatric UC. 25/33 responded to IFX. colectomy rate 19% at 1 year.
  • -Gastroenterology 2009; 137: 1204 (ed), 1250. lower colectomy rates at 54wks in IFX vs placebo (+concomitant meds): 10% vs. 17%.
  • -Clin Gastro & Hep 2008; 6: 1112. Do NOT use CYA post infliximab and vice versa. n=19. 1 death due to sepsis. Remission rates occur in ~1/3rd but are of short duration.
  • -NEJM 2005; 2462. 69% clinical response @ 8 weeks (vs. 37% placebo) & 45% at week 54 (vs. 20% placebo).
  • -JPGN 2004; 38: 298. 82% short-term response, 63% sustained response; n=16.

More bad news for smokers

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Add two more cancer risks for tobacco smoke (Gastroenterology 2012: 142: 233-40, 242-47).  There is now evidence linking tobacco smoke to 18 different cancers and tobacco smoke is probably the most preventable cause of death in the world.

In the first study, the investigators examined 3167 patients with Barrett’s esophagus.  This retrospective study followed patients for 7.5 years.  Patients who were current smokers (any form of tobacco) had double the risk of developing high-grade dysplasia or cancer compared to those who had never smoked.  Former cigarette smokers had a hazard ratio of 1.53.

In the second study, 386 patients with Lynch syndrome were analyzed during a 10 month period.  The hazard ratio for developing colorectal adenomas was 6.13 for current smokers and 3.03 for former smokers compared with patients who never smoked.  In addition, the authors identified a trend for developing adenomas based on pack-years.

Two more reasons to quit smoking.  On a side note, my grandmother said quitting smoking was the easiest thing that she ever did.  So easy, she did it a thousand times.

Additional references:

  • -Gastroenterolgy 2005; 129: 1825-31.  1.6% incidence of BE in adult Swedish population. Alcohol & smoking increase risk.
  • -NEJM 2011; 365: 1222. Treating smokers -useful review.
  • -NEJM 2011; 365: 1193. Cytisine -inexpensive- helps with smoking cessation (8.4% success vs 2.4%in placebo)
  • -NEJM 2008 358; 2249. Smoking and role of social networks.
  • -Gastroenterology 2011; 141: 2000. Lower risk of Barrett’s in pts taking NSAIDs & statins. n=570.
  • -Gastroenterology 2011; 141: 1179. Lower risk of Barrett’s in pts with low-grade dysplasia than previously noted -similar to non-dysplastic Barrett’s.
  • -NEJM 2011; 365: 1375. Large Danish study, n=11028. Lower incidence of Barrett’s than previous estimates. Relative risk of 11.3 compared to general population for adenoca of Esophagus with absolute annual risk of 0.12%. Barrett’s patients have the same life expectancy as general population (ed. pg 1437). Detecting cancer only ~1 in 1460 scopes with screening whereas Barrett’s detected in 10% of pts.
  • -Gastroenterology 2011; 140: 1084. AGA statement on Barrett’s . Recs screening only in those with multiple risk factors (age 50, male, chronic GERD, white, incr BMI)
  • -NEJM 2005; 352: 1851. Cases of Lynch can be missed when following screening guidelines.
  • -Gastroenterology 2010; 138: 207-2177 (entire issue) Colon cancer, Lynch syndrome
  • -Gastroenterology 2008; 135: 380.  Review of colon cancer screening and prevention -2008 up-to-date- literature review
  • -Gastroenterology 1967; 53: 517-27.  Seminal article.  Lynch HT showed gene-related cancer in family cancer syndrome -different than polyposis syndromes.

What to make of FODMAPs

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Consumption of FODMAPs (fermentable oligosaccharides, disaccharides, monosaccharides and polyols) may trigger irritable bowel syndrome (IBS) symptoms.  Some research indicates that a diet low on FODMAPs may be beneficial (J Hum Nutr Diet 2011; 24: 487-95).  This study tried to assess whether a low FODMAPs diet which had been reported from a single center in Australia would be effective for IBS.

In this study, consecutive patients with IBS were divided into two groups.  39 received standard dietary advice based on UK National Institute for Health and Clinical Excellence (NICE) guidelines.  43 patients were placed on a low FODMAP dietary advice.  Patients were selected into each group consecutively (not randomized). This study reported a 76% satisfactory symptom response in the FODMAP group vs a 54% response in the control group (p=0.038).  Overall, 86% of FODMAP group had improved composite score compared with 49% of standard treatment group. Specific improvements were noted in bloating, abdominal pain, and flatulence.  The average age of the study population was 38 and 71% were females.  60% had diarrhea-predominant IBS.

NICE guidelines for IBS:

  • Healthy eating principles: regular eating, taking time to eat
  • Limit high fat foods and fizzy drinks
  • Limit insoluble fiber for diarrhea and gradually increase for constipation
  • Limit sugar-free sweets and foods with sorbitol
  • Limit fruit to 3 portions/day
  • Avoiding ‘resistant’ starch may be useful (eg. sweetcorn, green bananas, part-baked and reheated bread)
  • Addition of oats and linseeds may be helpful

Low FODMAP diet

  • Reduce high fructan foods (eg wheat and onion)
  • Reduction in high galactooligosaccharide foods (eg chickpeas, lentils)
  • Reduce high polyol foods and polyol-sweetened sources.  Replace with suitable fruits and vegetables
  • In patients with lactose malabsorption, reduce high lactose foods (eg milk, yoghurt) to smaller volumes or substitute lactose-free products
  • In those with fructose malabsorption, decrease excess fructose

Of course, reading the author’s description of a low FODMAP diet is confusing.  Translation:

Include more bananas, blueberries, lettuce, potatoes, gluten-free breads or cereals, rice, oats, hard cheeses, lactose-free milk, sugar, molasses, and artificial sweeteners that do not end in “ol.”

Avoid/eliminate apples, pears, canned fruits in natural juices, high-fructose corn syrup, cows’ milk (due to lactose), soft cheese, broccoli, cabbage, pasta, bread, baked goods from wheat/rye, mushrooms, and sweeteners like sorbitol or others that end in “ol.”

Since this diet has attracted more widespread attention, basic familiarity is important for all physicians who treat IBS.  A useful resource to explain this diet is the Wall Street Journal:

http://online.wsj.com/article/SB10001424052970204554204577023880581820726.html

This link has a good table illustrating the recommended dietary choices.

Whether FODMAPs will be superior to other dietary advice for IBS is still uncertain.  Though, given the limited number of effective treatments for IBS, this small study is a promising development.

Additional references:

  • -Clin Gastro & Hep 2009; 7: 706. n=17. 13 responded to very low carb diet (<20g/day)
  • -Clin Gastro & Hep 2008; 6: 765. Dietary triggers for IBS include fructose/fructans: honey, high fructose corn syrup, wheat, fruits.
  • -IBD 2006; 13: 91. Dietary guidelines for IBS.
  • -Clin Gastro Hepatol 2005; 10: 992-996. Obesity increases IBS symptoms; diet with low fat, high fruit/fiber have fewer symptoms
  • -Gut 2004; 53: 1459-1464. Food elimination based on IgG antibodies. Patients did better on diet with implicated foods than with control diet (diet was blinded/randomized).
  • -Am J Gastro 2011; 106: 508-514. randomized, double-blind trial showing efficacy of GFD for non-celiacs.  60% vs 32& placebo response.
  • -Nutr Clin Pract. 2011;26:294-299.  GFD for non-celiacs.
  • -Gastroenterology 2011; 141: 1941./Am J Gastro 2011; 106: 915.  Exercise improves IBS symptoms.

Holes in the fiber theory

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Since the 1970s, it has been accepted that diverticular disease is related to low fiber intake and the Western diet.  Problem is that this might not be right (Gastroenterology 2012; 142: 205-10).  In this observational cross-sectional study (n=2104), low dietary fiber was not associated with diverticulosis; just the opposite.  High fiber intake, after adjusting for other factors, had an adjusted prevalence ratio of 1.3.  Due to the nature of the study, there may be potential bias that would not be present with a prospective study, especially with regard to dietary recall.  An editorial in the same issue (pg 205-07) lists three other studies; two of these also could not demonstrate a protective effect of fiber.  In addition to these findings, this study did not find an association between fat, red meat, physical activity and diverticulosis.

Although these data throw a big question mark regarding the pathogenesis of diverticular disease, this does not mean you should throw away your fiber bars quite yet.  Although low fiber may not cause diverticular disease, several large prospective studies have been completed which convincing show an association with lower complications/hospitalizations among individuals with higher fiber intake.  In addition, increased fiber in the diet has been shown to lower cardiovascular complications.

Additional references:

  • -Br Med J 1971; 2: 450-54.  Seminal article on diverticular disease and association with Western countries with low fiber intake.
  • -Am J Clin Nutr 1994; 60: 757-64.  Prospective study showing benefits of fiber in preventing diverticular complications (n=47,888); RR=0.58 for developing symptomatic diverticulitis.
  • -BMJ 2011; 343: d4131.  EPIC study, n=47,033, showing benefit of fiber in reducing hospitalizations due to diverticular dz over 12yrs (0.59 RR)
  • -NEJM 1999; 340: 169. fiber does not decrease Colon Ca risk.
  • -NEJM 2000; 342: 1149 & 1159. fiber does not decrease risk of recurrent adenomas.
  • -Am J Clin Nutr 2000; 70: 1433-1438. Fiber lowers cholesterol & can decrease risk of heart attack by 15%.

Pain changes brain

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For several years, there has been research showing changes in PET scans and functional MRI in association with functional abdominal pain.  A recent article goes a step further showing microstructure  brain changes in patients with chronic pancreatitis (Gut 2011; 60: 1554-62).

This study examined 23 patients with pain due to chronic pancreatitis and 14 controls.  Using a 3T MR scanner, apparent diffusion coefficients (ADC) and ‘fractional anistotropy’ (FA) values were assessed in numerous parts throughout the brain.  This new technology, uses an MRI for diffusion tensor imaging which assesses changes in white and grey matter microstructure not evident with more conventional imaging.  Chronic pancreatitis patients had increased ADC in the amygdala, cingulate cortex, and prefrontal cortex.  In addition, FA values were reduced in the cingulate cortex and secondary sensory cortex.  These areas of the brain with these changes are known to be involved in the processing of visceral pain.  Microstructural changes were correlated to patients’ clinical pain scores.  Some of the changes can be influenced by other factors including alcohol usage, depression, Alzheimer’s or diabetes.

This study echoes findings from others that demonstrate structural reorganization of the brain in association with chronic pain.

Additional references:

  • -Gastroenterology 2010; 139: 1310. n=15 IBS women, 12 controls.  IBS pts have emotional modulation of neural responses to visceral stimuli (eg rectal stimulation) –based on functional MRI studies.
  • -Gastroenterology 2006; 130: 26 & 34. Functional MRI measured in response to barostat show increased sensitivity in pts c IBS. Also, altered 5-HT signaling in IBS-D & IBS-C.
  • -J Pediatr 2001; 139: 838-843. Pts c IBS, RAP more sensitive to visceral perception in rectum and stomach respectively.
  • -Gastroenterology 2005; 128: 1819. Brain response to visceral aversive conditioning –>similar cortical responses between actual and anticipated stimuli.
  • -Cereb Cortex 2010; 20: 1409-19.  Changes in brain anatomy associated with neuropathic pain following spinal cord injury.
  • -J Am Acad Child Adolesc Psychiatry 2010; 49: 173-83.  White matter microstructure changes in adolescents with major depression.