Author Archives: gutsandgrowth

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About gutsandgrowth

I am a pediatric gastroenterologist at GI Care for Kids (previously called CCDHC) in Atlanta, Georgia. The goal of my blog is to share some of my reading in my field more broadly. In addition, I wanted to provide my voice to a wide range of topics that often have inaccurate or incomplete information. Before starting this blog in 2011, I would tear out articles from journals and/or keep notes in a palm pilot. This blog helps provide an updated source of information that is easy to access and search, along with links to useful multimedia sources. I was born and raised in Chattanooga. After graduating from the University of Virginia, I attended Baylor College of Medicine. I completed residency and fellowship training at the University of Cincinnati at the Children’s Hospital Medical Center. I received funding from the National Institutes of Health for molecular biology research of the gastrointestinal tract. During my fellowship, I had the opportunity to work with some of the most amazing pediatric gastroenterologists and mentors. Some of these individuals included Mitchell Cohen, William Balistreri, James Heubi, Jorge Bezerra, Colin Rudolph, John Bucuvalas, and Michael Farrell. I am grateful for their teaching and their friendship. During my training with their help, I received a nationwide award for the best research by a GI fellow. I have authored numerous publications/presentations including original research, case reports, review articles, and textbook chapters on various pediatric gastrointestinal problems. In addition, I have been recognized by Atlanta Magazine as a "Top Doctor" in my field multiple times. Currently, I am the vice chair of the section of nutrition for the Georgia Chapter of the American Academy of Pediatrics. In addition, I am an adjunct Associate Clinical Professor of Pediatrics at Emory University School of Medicine. Other society memberships have included the North American Society for Pediatric Gastroenterology Hepatology and Nutrition (NASPGHAN), American Academy of Pediatrics, the Food Allergy Network, the American Gastroenterology Association, the American Association for the Study of Liver Diseases, and the Crohn’s and Colitis Foundation. As part of a national pediatric GI organization called NASPGHAN (and its affiliated website GIKids), I have helped develop educational materials on a wide-range of gastrointestinal and liver diseases which are used across the country. Also, I have been an invited speaker for national campaigns to improve the evaluation and treatment of gastroesophageal reflux disease, celiac disease, eosinophilic esophagitis, hepatitis C, and inflammatory bowel disease (IBD). Some information on these topics has been posted at my work website, www.gicareforkids.com, which has links to multiple other useful resources. I am fortunate to work at GI Care For Kids. Our group has 17 terrific physicians with a wide range of subspecialization, including liver diseases, feeding disorders, eosinophilic diseases, inflammatory bowel disease, cystic fibrosis, DiGeorge/22q, celiac disease, and motility disorders. Many of our physicians are recognized nationally for their achievements. Our group of physicians have worked closely together for many years. None of the physicians in our group have ever left to join other groups. I have also worked with the same nurse (Bernadette) since I moved to Atlanta in 1997. For many families, more practical matters about our office include the following: – 14 office/satellite locations – physicians who speak Spanish – cutting edge research – on-site nutritionists – on-site psychology support for abdominal pain and feeding disorders – participation in ImproveCareNow to better the outcomes for children with inflammatory bowel disease – office endoscopy suite (lower costs and easier scheduling) – office infusion center (lower costs and easier for families) – easy access to nursing advice (each physician has at least one nurse) I am married and have two sons (both adults). I like to read, walk/hike, bike, swim, and play tennis with my free time. I do not have any financial relationships with pharmaceutical companies or other financial relationships to disclose. I have helped enroll patients in industry-sponsored research studies.

Improve Care Now

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Several years ago, “ImproveCareNow” Network was established with a goal of improving the quality of care children with inflammatory bowel disease. https://improvecarenow.org/ (http://www.youtube.com/watch?v=beG2eMROWqg)

Documentation of some outcomes of this effort have now been published (Pediatrics 2012; 129: e1030-e1041).  In this study from six U.S. centers, data from 843 children with Crohn’s disease and Ulcerative Colitis were available.  Centers were eligible to participate if they did not have extensive quality improvement (QI) experience and if they were able to enroll >75% of their IBD patients.  During the course of the study (2007-2010), there were increases in the proportion of patients with measurement of thiopurine methyltransferase (TPMT) before initiation of thiopurines, increased percentage of individuals receiving an appropriate thiopurine dosage, and an increased percentage of patients with inactive disease.  In Crohn’s disease, the number with inactive disease changed from 55% to 68%; in ulcerative colitis, the number increased from 61% to 72%.  

This study shows significant progress in these patients and the potential benefit of a more-structured approach.  However, some of the improvements in these outcomes may not be to process improvements. 

Study limitations:

  • The study does not document the rate of inactive disease in non-participating centers; thus there is not an adequate control population.  Given more widespread use of biologic therapies, this may account for much of the improvement in outcomes.   In fact, the study does not describe the percentage of patients receiving thiopurines or biologic agents.
  • The use of the physician global assessment (PGA) as indicative of disease activity.  The authors acknowledge that “PGA ….is a relatively subjective measure.”  A more reliable measure of disease activity like a stool calprotectin, endoscopy, or imaging study improvement would have been helpful.  
  • Better documentation or better outcomes? It is not clear whether some of the improvement reflects better documentation or improved care delivery.

Despite the limitations of this study, it is a good starting point.  The goal of improving the care of patients is shared by almost all physicians.  One way to start making a difference is measuring specific outcomes and targeting specific goals/checklists. Going forward with QI there are many QI hurdles: 

  • Defining optimal care is nearly impossible, there are few trials comparing efficacy & difficult to judge risk/benefit ratio of many therapies.
  • Difficulty selecting appropriate outcome measures -indications for hospitalization and surgery are not clear-cut in many cases.  Surgery may be an appropriate treatment rather than a negative outcome. 
  • Risk adjustment is an imperfect science.

Goals with Quality Improvement:

  • Plan-Do-Study-Act cycles.
  • Learning from high-performing centers -benchmarking

Warranted vs unwarranted variations:
Unwarranted: selecting inadequate dosing of medications, failure to check for TB before remicade/biologics, failure to consider drug interactions, failure to discuss options with families
Warranted: variation due to differences in disease (eg budesonide for ileitis but not pancolitis), variation driven by patient preferences (eg. using NG instead of corticosteroids)

“When you can measure what you are speaking about and express it in numbers, you know something about it; but when you cannot express it in numbers, your knowledge is of a meagre and unsatisfactory kind” –Lord Kelvin 1883

“Not everything that counts can be counted, and not everything that can be counted counts.” –Albert Einstein

Additional references on quality improvement:

  • Free Self Management Handbook endorsed by ImproveCareNow:

https://improvecarenow.org/patients/self-management-handbook

  • -JPGN 2009; 49: 272.  Review of quality measures/history.
  • -Kohn LT, et al. To Err is Human: Building Safer Health System.  Nat’l Academy Press; 2000
  • -Crossing the quality chasm.  Wash DC: Nat’l Academy Press; 2001.
  • -Clin Gastro & Hep 2010; 8: 709.  Quality indicator sets in cirrhosis.
  • -J Pediatr 2005; 146: 744-50.  Bucuvalas JC et al.  Adjusting calcinerin inhibitor dosing
  • -IBD guidelines: www.cincinnatichildrens.org/svc/alpha/health-policy/ev-based/ibd.htm
  • -JPGN 2009; 49: 297.  Variation in care in pediatric Crohn disease. (Our center participated in this study)
  • -J Pediatr 2009; 154: 582.  Ventilator assoc pneumonia reduced w bundle of hand hygiene, elevated HOB, not changing ventilator circuits except when soiled & mouth care
  • -“The Learning Curve”(Atul Gawande) in The Best American Essays 2003 -some CF ctrs outperform, extending life expectancy ~14yrs.
  • -” A Surgeons Notes on Performance-Atul Gawande
    -NEJM 2007; 357: 2652.  Nice editorial.
  • www.icsi.org
  • www.qualityforum.org
  • www.ambulatoryqualityalliance.org
  • www.ncqa.org
  • www.cms.hhs.gov/hospitalqualityinit

Comments from lead author forwarded to blog:

Thanks for including our recent paper in your blog.  I agree with the study limitations as you mentioned, but wanted to put a couple of things in context.  We actually thought very hard about the issue of a control group, and specifically how to determine what the remission rate would be without the intervention.  We could not come up with a reasonable comparator (very few people/groups outside of ICN even know what the remission rate of their population is).  One very rough measure (which we did not feel was legitimate to include) is the rate of remission for new sites as they are joining the collaborative.  Established sites with complete participation have better outcomes than newer sites or sites that participate less fully, suggesting that at least a significant portion of the effect is due to the QI intervention rather than secular trend.  As far as the objective measures for outcomes, I know you realize that we are not able to mandate specific objective evaluations for a QI/observational research study, so we may never be able to use mucosal healing (for example) as our measure of remission.  However you probably noticed in the paper that we did demonstrate improvements in objective measures including sPCDAI, PUCAI and use of corticosteroids.  Certainly improvements in process measures may have been due in part to better documentation, but it is unlikely that objective outcome measures improved due to documentation. Thanks again for sharing our work with your audience.

Bleeding due to vitamin K deficiency

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With cholestasis in infancy, Bill Balistreri taught me that there were four potential emergencies:

  • Bleeding due to vitamin K deficiency or coagulopathy
  • Hypoglycemia
  • Sepsis
  • Metabolic poisoning with formula (in patients with galactosemia)

Once these issues have been considered, then it is appropriate to start investigating the etiology of the cholestasis.

One of the more dramatic complications is intracranial hemorrhage (ICH). While ICH is a well-recognized complication of cholestasis in infancy, the long-term outcomes are not well-characterized. A report from Japan adds some insight (JPGN 2012; 54: 552-57).

Among a retrospective review of 83 infants with biliary atresia (BA) between 1979 to 2009, ICH occurred in 8% despite oral vitamin K prophylaxis (2 mg).  The onset of ICH was between 47-76 days after birth and was prior to surgery.  Coagulopathy was noted in all cases, which improved with vitamin K intravenously.  Two infants required craniotomy.  In 5 of 7 cases, neurologic sequelae were noted including developmental delay in three, epilepsy in one, and mild hemiparesis in two.

Additional references:

  • Blood Rev 2009; 23: 49-59.  Review of vitamin K deficiency.
  • Pediatrics 2008; 121:e857.  Vitamin K deficiency common in cholestatic breastfed babies.  Can be prevented with 1mg po each week or single IM dose of 2mg.
  • Eur J Pediatr Surg 2005; 15: 295-9.  Bleeding disorder as 1st symptom of BA.
  • Pediatr Neurosurg 2006; 42: 362-7.  ICH due to vitamin K deficiency.
  • Pediatrics 2006; 118: e1657.  dose of 0.2mg effective for median of 25days (w/o toxicity/accumulation of K1O) in infants <32weeks gestation.

Pierre Robin and what else?

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In a large pediatric center, patients with Pierre Robin Sequence (PRS) are routinely seen by genetics and for good reason.  Underlying syndromic features were present in 60% of a recent retrospective review (J Pediatr 2012; 160: 645-50).

Most common syndromes with PRS include the following:

  • Stickler syndrome (22% pf all cases)
  • 22q11.2 deletion syndrome/velocardiofacial syndrome
  • Marshall syndrome
  • Moebious syndrome
  • Cornelia de Lange syndrome
  • Treacher Collins syndrome
  • Fetal alcohol syndrome
  • Van der Woude syndrome
  • Oculo-auricular-vertebral spectrum

For gastroenterologists, the article notes that 43% of the San Diego cohort required tube feeding whereas 79% of the Cleveland cohort needed tube feedings.  Overall, average was 52% needing tube feeds.

Additional references:

  • -J Pediatr 2011; 159: 887.  Feeding problems common in UAO/Robin-like phenotype.
  • -Burstein FD, Williams JK.  Mandibular distraction. Plast Reconstr Surg 2005; 115: 61-7.
  • www.vcfsef.org
  • www.sticklers.org
  • -J Pediatr 2002; 140: 719.  Frequent upper esophageal/oral motor dysfxn (24/28)
  • -J Pediatr 2001; 139: 588. n=117.  descriptive study.  35% c syndrome, 48% isolated, 17% c associated anomalies.
  • -JPGN 2001; 32: 297.  Frequent oroesophageal motor disorders in these patients.  86% required prolonged NG feeds.

Increased ferritin predicts poor response in Hepatitis C

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Serum ferritin levels were independently shown to be a risk factor for poor response to treatment in hepatitis C virus (HCV) infection (Hepatology 2012; 55: 1038-47).  This article adds additional information to previous work which has shown that increased iron can be a comorbid factor in chronic viral hepatitis and other liver diseases.

This study used the Swiss Hepatitis C Cohort Study (SCCS) (n=3648).  In this group, the success of treatment with pegylated interferon alpha and ribavirin were correlated with clinical and histological features.

Ferritin levels ≥ the sex-specific median values was one of the strongest pretreatment predictors of treatment failure (OR 0.45). It had a similar predictive effect as the IL28B genotype.  In addition, higher ferritin levels were associated with severe liver fibrosis (OR 2.67) and steatosis (OR 2.29).  For women the sex-specific median for ferritin level was 85 μg/L and for men it was 203 μg/L.  The authors note that these cutoffs are quite close to the upper limits of normal of the general population (150 and 300 respectively).

Mechanistically, HCV interferes with the host’s iron metabolism leading to iron accumulation in the liver.  Part of this is explained by down-regulation of hepcidin (Help with hepcidin).  Part is due to ferritin acting as an acute phase reactant to inflammation.  Ultimately, excess iron promotes liver inflammation, oxidative stress and mitochondrial dysfunction.

How important ferritin will be with newer therapies is not clear.  It is likely that patients that are less responsive to dual therapy (pegylated interferon/ribavirin) will have poorer response as well to triple or quadruple therapies.

Additional references/previous related posts:

Recurrent pancreatitis and genetic underpinnings

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While the absolute number of patients with genetic causes of pancreatitis is small, due to frequent hospitalizations, this remains a significant problem.  This month additional information on genetic predisposition for pancreatitis is available (JPGN 2012; 54: 645-50).

Sultan et al (Milwaukee, WI) reviewed the charts of children <18 years with recurrent acute pancreatitis (RAP) and patients with chronic pancreatitis (CP) from 2000-2009.   RAP was considered if patient had a minimum of two distinct episodes of acute pancreatitis.  Acute pancreatitis was considered the diagnosis if patient had typical symptoms associated with 3-fold elevation of amylase or lipase or imaging changes consistent with acute pancreatitis. CP was defined as a minimum of 2 episodes of acute pancreatitis associated with pancreatic duct abnormalities or pancreatic insufficiency.

Among this cohort of 29 children, 23 (79%) had mutations which have been associated with genetic pancreatitis (GP).  Family history was positive in only five patients.

  • CFTR mutation in 14 (48%): two had homozygous mutations, six heterozygous, and four had 5 T variants.  The importance of a single CFTR mutation in contributing towards pancreatitis is unclear.  However, the Wisconsin population has a carrier frequency of 1:32; the striking difference in frequency  indicates that even a single mutation may be important in the pathogenesis of RAP.
  • SPINK1 (serine protease inhibitor Kazal type 1) in 8 (27%).  SPINK1 mutations occur in 1-3% of the general population.  It is often a modifying factor rather than an isolated causal factor in the development of RAP.  Four of the patients with SPINK1 mutations also had a CFTR mutation.
  • PRSS1 (cationic trypsinogen gene) in 7 (24%).  Individuals with these mutations are considered to have hereditary pancreatitis, an autosomal disease with incomplete penetrance.
  • Only one patient was tested for chymotrypsin C gene (CTRC) –tested negative.

Seven patients with RAP did not undergo genetic testing & were excluded from the study.  These patients had other known causes of RAP: 3 had gallstones, 2 had pancreas divisum, 1 had a metabolic disorder, and 1 had a medication-induced pancreatitis.  The authors note, however, that patients with pancreas divisum have had genetic mutations identified in other studies.

Additional References:

  • www.uni-leipzig.de/pancreasmutation. This link will take you to the hereditary pancreatitis database where you can search for the specific mutation you identified and find articles dealing with a variety of aspects of that particular mutation.
  • 2011 Naspghan Postgraduate Course:
    Pancreatitis Workup
    -1st bout, check U/S, trig
    -if 2nd bout, suggested to check MRI, genetics (SPINK1, PRSS1, CFTR), sweat test, fecal elastase, possibly IgG4/ANA
  • OMIM#167800/276000
  • -Gastroenterology 2006; 131: 1844.  Mouse model w R122H Trypsiongen expression.
  • -Whitcomb DC. Gut 2004; 53: 1710-17. test for PRSS1 (cationic trypsinogen), SPINK1 (Serine protease inhibitor, Kazal Type 1), and CFTR gene.
  • -JPGN 2002; 34: 1A pg 444. n=108 with hereditary or idiopathic pancreatitis. (28% had + fhx)  12 c PRSS1 mutation, 24 c SPINK1 (21 s fhx); 22 had + CFTR mutation.
    -Pancreatology 2001; 1: 405-415.  Consensus guidelines for testing for H. Pancreatitis. PRSS1 gene -cationic trypsinogen
    http://www.pancreas.org/assets/pdfs/Pancreatology/HPgeneTestConsensus.pdf
  •  David Whitcomb’s laboratory at the University of Pittsburgh. The test is commercially available there. Their web site for the forms is:
    http://www.pitt.edu/~whitcomb/HPINFO/MolGenTest.html
  • -JPGN 2011; 52: 262. Review.
  • -J Pediatrics 2011; 158: 612.  Acute pancreatitis can result in diabetes.
  • -Clin Gastro & Hep 2010; 8: 410-416, 417. REVIEW of acute pancreatitis.  Rec NJ generally over TPN.
  • -Clin Gastro Hep 2010; 8: xxii.  Anomalous pancreatobiliary jxn as a cause.
  • -JPGN 2009; 49: 137.  Pancreatitis assoc w celiac
  • -Clin Gastro & Hep 2009; 7: 702.  Harmless Acute pancreatitis score.  Nonsevere when NL hgb, NL creatitine, and no rebound tenderness/guarding
  • -Alim Pharm Ther 2008; 28: 777-781.  Use of a low fat diet helped shorten hospital stay among adult pts with acute pancreatitis.
  • -Clin Gastro & Hep 2008; 6: 1070, 1077.   Fluids and imaging in acute pancreatitis.  With imaging, CT probably best.
  • – J Pediatrics 2008; 152: 106.  Acute pancreatitis in young children

Related blog entry:

Indomethacin to prevent post-ERCP pancreatitis

How much radiation from your CT scanner?

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Our children’s hospital, along with many others, has made a concerted effort to reduce radiation exposure by adjusting CT scan settings.  Even a single abdominal CT scan may confer a small but real risk of developing cancer.  The trade-off with low-dose CT techniques has been a concern about poor image quality.  New research indicates that low-dose CT scan is not inferior to standard-dose CT with respect to detecting appendicitis (NEJM 2012; 366: 1596-605).

This single-center study examined 441 patients assigned in a single-blind fashion to low-dose CT (median dose: 116 mGy-cm) in comparison to 447 patients receiving a standard-dose CT (median dose: 521 mGy-cm).  All patients had CT for suspected appendicitis.  The negative appendectomy rate was 3.5% in the low-dose group and 3.2% in the standard-dose group.  There was no significant difference in appendiceal perforation rate or proportion of patients needing more imaging.

How much radiation do your patients receive with a CT scan?

Related newspaper article:

FDA issues guidelines to lower radiation exposure in children:

http://www.ajc.com/health/child-sizing-radiation-doses-1434081.html

Related posts:

Magnetic resonance enterography for Crohn’s disease

More imaging needed?

Additional references:

  • -NEJM 2010; 363: 1, 4. Safety of CT.  Can have overdose of radiation and even standard doses could cause complications.  Also, a big issue is downstream unnecessary testing due to incidental findings.
  • -JPGN 2011; 52: 280. Documents high exposure to radiation in large IBD pediatric cohort.
  • -J Clin Gastroenterol 2011; 45: 34-39. High levels of ionizing radiation thru CT scan in pts with IBD.
  • -Pediatr Radiology 2002; 32: 217-313. Minimizing radiation exposure, risk/benefit of CT. Proceedings from conference.
  • -Pediatr Radiology 2002; 32: 700-706. Risk of CT for young child: ~ 1 in 1000 risk of fatal cancer later in life.

Good care 24/7

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In hospital settings, there have been concerns about clinical care at night or weekends (see references below).  At least with liver transplantation, 24/7 care appears to be the rule rather than the exception (Liver Transpl 2012; 18: 558-65). 

Using the UNOS database, this study analyzed 94,768 transplants from 1987-2010.  Survival rates at 30, 90, and 365 days for nighttime operations: 96%, 93%, and 86% respectively.  For weekends, the respective rates were 95%, 92%, and 86%.  These rates did not differ from weekday rates.  Graft failure rates were modestly increased for weekend transplants at 365 days (HR 1.05, 95% confidence interval 1.01-1.11) but not for 30 days or 90 days.  In addition, there was no difference in graft failure between nighttime and weekday transplantations.

Additional reference:

  • -Clin Gastroenterol & Hepatol 2009; 7: 296., 303.  n>400,000 discharges.  OR 1.2 for mortality of UGI bleed if on weekend. 
  • NEJM 2001; 345: 663-668.   3,789,917 admissions (in Canada).  Weekend admissions were also associated with significantly higher mortality rates for 23 of the 100 leading causes of death and were not associated with significantly lower mortality rates for any of these conditions.

Proton pump inhibitors–infection risk with cirrhosis

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In a previous post (The Medical Pendulum and Gastroesophageal Reflux), I note that enthusiasm for proton pump inhibitors has started to wane.  In addition, a significant number of reported of potential side effects were referenced.  Another potential adverse effect is increasing the rate of spontaneous bacterial peritonitis (SBP) in patients with cirrhosis (Clin Gastroenterol Hepatol 2012; 10: 422-27).

This retrospective study examined 65 hospitalized cirrhotic patients with paracentesis-proven SBP between 2006-2009 and compared them to 65 contemporaneous hospitalized cirrhotic patients without SBP.   Patients with SBP had a higher incidence of use of PPI within previous 7 days: 71% versus 42%.  Of patients with SBP receiving PPI, the authors state that 68% did not have a documented indication for PPI use.

Additional references/previous posts:

  • –Treating reflux does not help asthma
  • -Risk of Hypomagnesemmia -2011. http://www.fda.gov/drugs/drugsafety/ucm245011.htm
  • –Gastroenterology 2010; 139: 1115.  Review of safety of PPIs.
  • –Gastroenterology 2010; 139: 93. n=167,000. PPIs associated with hip fracture risk, OR 1.3, in patients with other risk factors.
  • –Gastroenterology 2010; 138: 896-904. 5 yrs of PPI -no increase risk in hip/spine fx.
  • –Arch Intern Med 2010; 170: 765-71, 747 (ed). PPI not related to hip fx (n=161,806) women 50-79. INCREASE risk of spine fx, hazard risk 1.47
  • –Arch Intern Med 2010; 170: 772-8. PPIs increase risk of Clostridium difficile infection (hazard ratio 1.42 –42% increase in risk), n=1166.
  • –Arch Intern Med 2010; 170: 784-90. n=101,796. OR 1.74 for daily PPI, OR 2.36 if BID Rx; thus ~70% increase risk of nosocomial infection.
  • –Clin Gastro & Hep 2010; 8: 504. Increased bacterial overgrowth with PPI use.
  • -JAMA 2009; 301: 2120-2128. Use of PPIs associated with INCREASED hospital acquired pneumonia by ~30%. Could result in 180,000 HAP cases/yr with ~33,000 deaths. n+ 63,878 admissions, 52% on PPIs or H2RAs (83% PPIs, 17% H2RAs). H2RAs NOT associated with HAP cases.

Does it make sense to look for parasites in RAP?

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Probably not, in the absence of other symptoms.  A small study from Switzerland shows that treatment of Blastocystis hominis does not help recurrent abdominal pain (RAP) more than placebo (JPGN 2012; 54: 677-79).

This study result is not surprising.  A previous study of 157 RAP pediatric patients (JPGN 2007; 44: 524-26) showed that testing for ova and parasites was unnecessary as the incidence of parasitic infections in this population was not increased in RAP patients compared with controls. In this 2007 study, stool samples were positive for parasitic infection in 15 children, with no difference in prevalence between children with chronic abdominal pain (6/87; 7%) and healthy control children (9/70; 13%).

The current study had 37 patients complete the study.  The pain index (PI) for all patients improved in the study; however, there was no difference between patients who received antibiotics (trimethoprim-sulfa was used as first-line agent) compared to those who received placebo.

Regarding the methodology, the PI was either a visual analog scale with numbers from 0 to 10 or a standardized face scale; the specific scale was determined by the patient age.  Also, among the 20 patients who received antibiotics, 13 continued with B hominis in their stool tests after an initial round of therapy.  Yet the change in pain was virtually identical.  In antibiotic-treated patients, initial PI was 7.1.  After treatment, those with persistent B hominis detected in the stool had a PI of 4.2 whereas those with negative stool specimens had a PI of 4.1.  The placebo patients started with a PI of 7.4; after placebo treatment, a similar proportion cleared the B hominis from their stool –in this group, at the conclusion of the placebo treatment the PI was 2.4; the placebo group with persistent detection of B hominis had a PI of 3.2 at the conclusion of the study.

Although the potential pathogenicity of B hominis in humans remains unclear, it is not unusual in clinical practice for patients with this finding to receive treatment.   Besides trimethoprim-sulfa, metronidazole is frequently administered. Based on this study, placebo would be as helpful as an antibiotic in improving clinical symptoms.

Related blog entries:

What to make of FODMAPs

Pain changes brain

Treating diabetes with surgery

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Two articles in the New England Journal of Medicine point to the role of bariatric surgery in  treating type 2 diabetes in obese patients (NEJM 2012; 366: 1567-76 & 1577-85).  Type 2 diabetes looms as one of “the most challenging contemporary threats to public health.”

The first study was a randomized nonblinded single-center trial with 150 patients; mean BMI 36 with 34% having a BMI less than 35.  Intensive medical therapy was compared to Roux-en-Y gastric bypass or sleeve gastrectomy.  Mean patient age was 49 years. 42% of the gastric bypass group, 37% of the sleeve-gastrectomy group, and 12% of the medical treatment group achieved the primary end-point of a glycated hemoglobin level of ≤6% by the 12 month followup; the average starting glycated (HgbA1C) hemoglobin was 9.2%.  At the conclusion of the study, the average HgbA1C was 6.4, 6.6, and 7.5 respectively in the three groups.

The second study used a similar trial with 60 obese patients; all had BMI >35  At 2 years, diabetes remission occurred in 75% of their gastric bypass group, 95% of their biliopancreatic-diversion group and in no patients receiving intensive medical therapy patients. HgbA1C had similar rates of improvement as the 1st study: 6.3 in gastric-bypass, 4.9 in biliopancreatic-diversion group, and 7.7 in medical-therapy group.

While surgery has risks (see related material below), its benefits are likely to alter future treatment strategies with surgery being contemplated prior to exhausting all medical treatments.

Additional References:

  • -JAMA 2012; 307: 56-65.  Bariatric surgery and long-term cardiovascular events.
  • -JAMA 2011 [doi: 10.1001/jama.2011.817]). Large study failed to show that roux-en-Y gastric bypass prolonged life. n=850 VA pts to 41,244 controls. Same group showed no cost savings during initial 3 yrs: Med Care 2010; 48: 989-98.
  • -NEJM 2011; 365: 1365. Increased frequency of bariatric surgery in adolescents.
  • -NEJM 2009; 361: 445/520. perioperative safety.
  • -NEJM 2007; 357: 741, 753, 818. Bariatric surgery improves mortality rate.
  • NEJM 2007; 356: 2176. Review

Complications from surgery:

  • Early: bowel obstruction, DVT, GI bleed, leaks, pulmonary embolism, wound infection
  • After 30 days: anastomotic stricture, bowel obstruction, gallstones, dehiscence, fistula, Bleeding, Incisional hernia, nutrient deficiencies (iron, B12; calcium, Vit D (w RYGB), folate, B6/riboflavin).
  • Complications from gastric band: food impaction, erosion (now banned in Finland!), band slippage, gastric volvulus, band too tight, port infection
  • Roux-y gastric bypass:
    anastomotic leak 1.2%, anastomotic ulcers/stricture
  • Nutrient Monitoring–every 3months x 3, then yearly: Vitamin A, B12, Folate, Ceruloplasmin, Vit D-25OH, Iron studies, Zinc, thiamine, Selenium, Intact PTH, Mg, PT/PTT
  • Suggested supplements: Calcium c vitamin D 1200-2000mg, Iron at least 18-27mg/day, MVI with zinc/selenium
  • Also if duodenal switch, add Vitamin A 10,000 IU, and Vitamin D3 1200units daily or 50,000 units weeekly, Vitamin K 300 mcg,

Potential nutritional deficiencies:

  • B12, B6 (pyridoxine), Riboflavin (B2), B1 (Thiamine), Folate (B9)
  • Vitamins A,D,E, K
  • Calcium, Copper, Iron, Selenium, Zinc

Recommendations from NASPGHAN Post-Graduate Course 2011:

  • If post-op pain: epigastric –>do EGD & if neg do ‘RUQ w/u’, RUQ –> check U/S, LFTs possibly CT
  • If post-op vomiting –>do EGD
  • If post-op nausea –>Rx PPI and EGD if not improving
  • Anastomotic stricture in stomach –>dilate to 10-12mm in 1 session

Related blog posts (includes additional references)

Cardiovascular disease for the entire family

Staggering cost of obesity

A liver disease tsunami

Lower leptin with physical activity