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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.

HAV vaccination: how long will it take?

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Despite the availability of a safe and effective vaccine, immunization rates in the U.S. remain poor (Pediatrics 2012; 129: 213-221).

In this study which included data from the 2009 National Immunization Survey-Teen, hepatitis A virus (HAV) vaccination  coverage was examined in adolescents 13-17 years of age.  The national coverage for at least 1 dose was 42%; 70% of these vaccinees completed the 2-dose series.  For Georgia, the rates were similar to national data: the 1-dose receipt % was 42.5% and the 2-dose receipt % was 26.3%; 62% completion of 2 doses.

More specific breakdown of coverage rates:

  • 74.3% from 11 states that recommended universal HAV vaccination since 1999
  • 54% from 6 states that recommended consideration of HAV vaccination since 1999 & universal coverage since 2006
  • 27.8% for 33 states that recommended universal vaccination since 2006

While acute HAV rates have been declining, in 2009 there were 1987 reported cases; the CDC estimates that the total number of cases was 21,000 (due to underreporting and asymptomatic cases).  The highest rates of disease were in young adults between 20-29 years of age.

This data is disappointing. Yet, extrapolation from this data indicates that national coverage in seven years, when all states will have had 10 years to implement universal vaccination to young children, could be markedly better.

Additional references:

  • -NEJM 2007; 357: 1685. HAV vaccine effective in preventing cases of HAV after exposure (as good as IVIG). Low rates of HAV c postexposure prophylaxis c HAV vaccine (4.4%) or immune globulin (3.3%). n=1090.
  • -MMWR 2007; 56: 1080-84. Updated recs for IVIG -use only for exposures in infants <12months, immunocompromised persons, persons with chronic liver disease, or persons w contraindications to HAV vaccine.
  • -Pediatrics 2007; 120: 189. Recs from AAP. Recs for vaccine — all children at 1 year of age in US w 2-dose regimen; w/in 1 mo of 1st dose 97% of children & 95% of adults develop protective antibody. VAERS (adverse rxns) 800-822-7967 for forms.
  • -Pediatrics 2007; 119; e12, e22. HAV vaccine is cost-effective.
  • -MMWR 2007; 56: No. SS-3. drop in new infections by 80% compared to previous nadir; HAV 1.5/100,000 & HBV 1.8/100,000
  • -Hepatology 2006; 44: 1589. Decreasing incidence of fulminant HAV ; between 1988-2005, decrease of HAV in UNOS database from 0.7% to 0.1%. Risk factors for severe disease: creatinine >2, ALT <2600, intubation, pressors.
  • -J Pediatr 2004; 144: 327. Maternal antibody decrease HAV vaccine response when administered at 2, 4 & 6 months.
  • -Am J Gastroent 2002; 97: 721-8. ? cost-effective to vaccinate HCV pts; however, ~35% FHF risk if secondarily infected.

Test your knowledge of Clostridium difficile

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While Clostridium difficile (C diff) is a common infection, there is a lot to know.  A thorough but brief review is a good place to test your knowledge (Clin Gastroenterol Hepatol 2012; 10: 581-92).

  • a. When was C diff discovered?
  • b. When was C diff identified as a cause of antibiotic-associated diarrhea?
  • c. What antibiotics have been associated with a surge in severity and frequency of C diff infections?
  • d. Which C diff strains are the predominant cause of severe C diff?
  • e. How many C diff infections are occurring yearly in hospitalized patients in U.S.?
  • f. What are the most important risk factors?
  • g. How does the risk profile change for multiple antibiotics?
  • h. What time of year sees the greatest number of infections?
  • i. What does C diff smell like?
  • j. What % of antibiotic-associated diarrhea is due to C diff?
  • k. What clinical parameters may indicate severe infection and which ones indicate fulminant infection?
  • l. How much does a nucleic acid amplification test (NAAT) cost compare to enzyme immunoassay (EIA)?  How does this test work? What are the advantages/disadvantages?
  • m. How to treat severe infection?
  • n. What instructions should be given to prevent C diff in hospital?

Answers:

  • a. 1935
  • b. 1970s
  • c. Fluoroquinolones
  • d. BI/NAP1/027.  This strain has hypersecretion of toxins A & B, the presence of binary toxin, and resistance to fluoroquinolones.
  • e. CDI present in 300,000 hospitalized patients in 2005 (vs. 85,000 in 1993)
  • f. Hospitalization, older age (>65 years), and receipt of antibiotics (especially during 1st two months).
  • g. Hazard ratio 2.5 for two antibiotics, HR 9.6 for exposure to five antibiotics
  • h. Winter
  • i. “Horse stable”
  • j. 15-25%
  • k. Severe: WBC>15,000, Creatinine >1.5 fold patient’s baseline.  Also, albumin <2.5, admission to ICU, pseudomembranes on endoscopy, comorbid diseases.  Fulminant: (50% mortality) colon >6cm in diameter/toxic megacolon, WBC >50,000, lactate >5 mmol/L.
  • l. ~10 times the cost.  Works by identifying genes that encode toxins by PCR or loop-mediated amplification of DNA.  Test is very sensitive and rapid but may have false-positives.  Some recommend using a less expensive test for screening to decrease costs.
  • m. Vancomycin up to 500mg QID (NG/PO) plus metronidazole.  If complete ileus, vancomycin can be given rectally
  • n. Hand hygiene (not alcohol): either soap or chlorhexidine, contact precautions, cleaning environment –chlorine solutions effective (1000-5000 ppm), antimicrobial stewardship (especially reducing clindamycin and fluoroquinolones)

How many did you get right?

Related posts:

Clostridium difficile -Current Battlelines

Proton pump inhibitors–infection risk with cirrhosis

A cautionary vitamin D tale?

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A recent case report indicates that pharmacologic doses of vitamin D can cause hypercalcemia and hypervitaminosis D (Pediatrics 2012; 129: e1060-63).  The three cases all document good reasons for instituting therapy: craniotabes, hypocalcemic seizures, and tibial bowing.  The total dose that the patients received over 7-12 weeks ranged from 112,000 IU to 168,000 IU.  The ages of the patients ranged from 2 weeks to 33 months.   The peak abnormal calcium for all three patients was 11 mg/dL and the peak 25-hydroxy vitamin D was 102 ng/dL.  There were no clinical symptoms in these three patients due to increased calcium.  A fourth oh-by-the-way patient was described as well.  This patient was receiving vitamin D for an “inappropriate indication” (failure to thrive) and had received 3.6 million IU without monitoring.  This led to the development of a multitude of symptoms associated with a calcium level of 17.4 mg/dL.

My take-home points:

  • If giving generous doses of vitamin D, obtain a followup calcium several weeks into therapy. However, pharmacologic doses of vitamin D for valid indications pose a very low risk.
  • Excessive doses of vitamin D can be detrimental. (This last statement may be akin to the warning “hot coffee might cause a burn.”)

Related blog entries:

Common to be “D-ficient”

Vitamin D, IBD, and Causality

Colonic disease and PSC

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While primary sclerosing cholangitis (PSC) has been associated with inflammatory bowel disease, and ulcerative colitis (UC) in particular, the pathogenesis of this relationship has not been established.  A fascinating observation on this relationship is that an inflamed colon is important in PSC development (Clin Gastroenterol Hepatol 2012; 10: 439-41).

In this study which reviewed 2754 Irish patients with IBD, 59 (2.2%) had PSC.  PSC incidence correlated with increasing colonic involvement.  Among the 13 patients with Crohn’s disease, none had isolated small bowel disease.  The second part of the study involved a review of 82 separate PSC patients attending the Irish National liver transplant unit.  The majority of ulcerative colitis patients had a pancolitis; all 10 PSC patients with Crohn’s disease had colonic involvement.

Since PSC occurs without IBD, colonic inflammation is not necessary for PSC development.  However, in patients with IBD, colonic inflammation is very important.  In fact, in a previous study of 53 PSC-IBD patients, no UC patient status post a colectomy had recurrent liver disease following liver transplantation whereas seven patients with intact colons had recurrent disease following liver transplantation.

The authors speculate that bacterial translocation along with subsequent portal bacteremia may be an important step in pathogenesis among these patients.

Additional references/previous posts:

Salmonella by mail-order

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Sometimes patients are amazed that hemoccult cards can be sent by mail.  Now, I learned something new: you can mail-order live poultry and thereby spread salmonella far and wide (NEJM 2012; 366: 2065-73).  This study identified 316 cases in 43 states.

Key findings:

  • 36 hospitalized (23%)
  • 38 had chicks as pets (42%); of these, 22 (69%) said the pet owner was a child <5 years
  • Salmonella enterica serotype Montevideo subtype
  • 81% of infections identified as coming from a hatchery in Western U.S.
  • After identification of problem, owners implemented recommendations which lowered salmonella contamination.  After these measures, outbreak strain still detected in 7% of samples
  • Hatcheries mail live poultry to all 50 states –4 million birds are produced annually for this purpose. Approximately 250,000 birds are shipped each week, usually within 24 hours of hatching; each costing about $5 each.

Because only a portion of salmonella infections are identified with laboratory tests, there are likely thousands more infections associated with this outbreak.  Overall, nontyphoidal salmonella infections are estimated to cause 1 million illnesses, 19,000 hospitalizations, and 370 deaths annually.  Most infections are acquired as foodborne illnesses.  Though contact with animals, as this report indicates, is another mechanism.  These birds can appear healthy and intermittently shed salmonella.

Individuals wishing to reduce their risk of illness should practice careful hand hygiene around animals.  See link for helpful advice:

http://www.cdc.gov/healthypets/resources/salmonella-baby-poultry.pdf

The poultry business can help by adhering to sanitary practices, by avoiding artificially coloring chicks (which targets children), and by warning recipients of the danger of salmonella infection.

More on perinatal HBV

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In addition to a recent blog entry (How to stop HBV vertical transmission), several other recent articles add information about HBV vertical transmission:

  • Gastroenterology 2012; 142: 773-81.  Data from 2386 Taiwanese children born to HBsAg-positive mothers were examined.  HBeAg-positivity increased the likelihood of having an HBV-infected infant (9.26%) despite appropriate immunization & HBIG.  Since HBeAg-posiitivity is associated with higher HBV DNA levels, this is logical based on previous studies. Fulminant HBV developed in 1 of 1050 children who did not receive HBIG; in this study, the majority of mothers with HBeAg-negative HBV did not receive HBIG.
  • Pediatrics 2012; 129: 609-16.  This study examined HBV prevention in the U.S. from 1994-2008.  The CDC created the US Perinatal Hepatitis B Prevention Program (PHBPP) to accelerate progress at eliminating perinatal HBV transmission.  While the number of infants born to HBsAg-positive women with HBV increased from 19,208 to 25,600, the incidence of infants with chronic hepatitis B virus infection among tested infants decreased from 2.1% in 1999 to 0.8% in 2008.  This is due to the fact that 94.4% of PHBPP-managed infants received HBV vaccine and HBIG within 1 day of birth.  Yet, gaps remain.  The number of infants who completed the vaccine series by 12 months actually declined from 86% (1994) to 77.7% (2008). And, in 2008 only one-quarter of CDC’s 25,6000 infants born to HBsAg-positive women had known serologic outcomes.

Related previous post: Looking for trouble

Food choices, FODMAPs, and gluten haters

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Given the frequency of functional gastrointestinal diseases (FGID), including irritable bowel syndrome (IBS), dietary treatments that may improve symptoms receive a lot of attention.  A recent review of the role of food choices in the development and management of FGIDs is a useful reference (Am J Gastroenterol 2012; 107: 657-66 -thanks to Ben Gold for forwarding this article).

This review details specific dietary advice as well as the following specific physiologic effects of FODMAPs:

  • Osmotic effects
  • Bacterial fermentation
  • Motility effects
  • Prebiotic effects
  • Systemic effects –mild depression, tiredness
In addition, the review looks at other potential foods which could serve as a trigger for IBS symptoms, like gluten & summarizes why some IBS patients are gluten haters.  The authors acknowledge that gluten sensitivity, in the absence of celiac disease, does not have a known mechanism.  Until a reliable marker becomes available, the importance of gluten sensitivity for FGIDs is unknown.
Related posts:

What to make of FODMAPs

Gluten sensitivity without celiac disease

Is a biopsy necessary in Celiac disease?

Alive and well? 10 years after liver transplantation

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As survival has improved with liver transplantation (LT), long-term health outcomes have become more important.  Reported 5-year survival rate after pediatric LT in North America is >85%.  More data on long-term health consequences are provided in a review of 167 10-year survivors from a North American Database (Studies of Pediatric Liver Transplantation –SPLIT) (J Pediatr 2012; 160: 820-6).

Ng VL et al report on frequency of comorbidities as well as quality of life.  Of the 10-year survivors who were included in this study: 85 (50.9%) were transplanted in the first year of life; 69 (41.3%) received transplants between 1-7.9 years.  Biliary atresia accounted for 55.1% of the transplanted cohort; the remainder were due to the following: metabolic liver disease 23 (13.8%), acute liver failure 18 (10.8%), other cholestatic conditions 17 (10.2%), tumor 6 (3.6%), and other 11 (6.6%).

First allograft survival rates were 94% at 1 year and 88% at 10 years.   Health-related quality of life (HRQOL) as assessed by the PedsQL 4.0 Generic Core Scales revealed lower patient self-reported total scale scores for LT survivors compared with healthy children (77.2 vs 84.9, P<.001).  14% had HRQOL >2 SDs below that of a matched healthy population.  Other specific post-LT morbidities included the following:

  • Impaired linear growth (23% <10th percentile); ongoing steroid therapy was associated with increased risk of poor linear growth.
  • Renal dysfunction (9%) –defined as calculated glomerular filtration rate <90 mL/min/1.73 m2.
  • Hyperlipidemia: 20% with hypercholesterolemia, and 26% with hypertriglyciridemia
  • Lymphoproliferative disease (5%).  EBV seroconversion occurred in 46 (47%) of 97 who had been EBV-negative prior to LT.  25 (15%) developed symptomatic EBV infection.
  • School performance: 32 (23%) had repeated a grade or were held back at least 1 school year.
  • Liver fibrosis: at 10 years, elevated aminotransferases were noted in 11% and increased gamma gluatmyl transpeptidase in 15%.  Previous studies from SPLIT indicate fibrosis is common in long-term survivors even with good clinical outcomes.

Alive and well?  While survival has improved remarkably, better outcomes are still needed.

Related posts:

Picking winners and losers with liver transplantation allocation

Good care 24/7

Big gift, how much risk

Additional references:


  • -Pediatrics 2008; 122: 1128-35.  Outcomes of 461 pediatric LT.
  • -Am J Transplant 2008; 8: 2506-13.  Improving long-term outcomes of LT.
  • -Hepatolog 2009; 49: 880-6.  LT-Liver fibrosis at 10 year followup.
  • -JPGN 2008; 47: 165. ~50% below 1.3 SD of adult height. Many show partial catch up growth.
  • -Liver Transplant 2006; 12: 1310. Review article on nutrition for OLTx patient.

New caustic danger from detergent pods

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“Brightly colored little packets that combine laundry detergent with other cleaning agents are a new convenience for consumers — and a new danger for kids.”

See more complete story at attached links that follow:

http://www.washingtonpost.com/national/poison-control-centers-field-increased-number-of-calls-of-children-ingesting-detergent-packets/2012/05/24/gJQAaiSZnU_story.html

http://yourlife.usatoday.com/health/healthyperspective/post/2012-05-24/new-kid-danger-swallowing-candy-colored-laundry-packets/701134/1

Does pancreas divisum cause pancreatitis?

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The role of pancreas divisum (PD) as a cause of either acute recurrent or chronic pancreatitis (AR/CP) remains a matter of debate.  A recent study suggests that pancreas divisum serves as a cofactor but does not cause pancreatitis independently (Am J Gastroenterol 2012; 107: 311-17).

PD occurs due to failure of fusion of the dorsal and ventral pancreatic buds during gestation.  The frequency of PD has been estimated to be between 5-10% of the general population based on large post-mortem studies.  There is an increased frequency of PD in patients with idiopathic pancreatitis (12-26%).  The referenced study from France examined the frequency of genetic mutations vis-a-vis relationship with PD.  PD was determined using MRCP.

Findings–percentage with PD among subgroups:

  • 7% of subjects without pancreatic disease, n=45
  • 7% of alcohol-associated pancreatitis patients, n=29
  • 5% of idiopathic pancreatitis patients, n=40
  • 16% of patients with PRSS-1-associated pancreatitis, n=19
  • 16% of patients with SPINK-1-associated pancreatitis, n=25
  • 47% of patients with CFTR-associated pancreatitis, n=30

The study has several limitations.  Overall, the numbers of patients with pancreatitis are fairly low.  In addition, these genetic mutations are not typically examined in individuals without pancreatitis.  As such, the effect of these mutations with PD still is difficult to know in comparison to a larger population.

Additional references:

  • Recurrent pancreatitis and genetic underpinnings (previous blog post)
  • -Clin Gastro & Hep 2009; 7:141.  Review -case of recurrent pancreatitis -suggests checking ANA, Trig, IgG4 (also TTG)
  • – J Pediatr 2008; 152: 106.  Acute pancreatitis in young children; 109 cases.  systemic dz in 29, drugs in 7, gallstones in 3, annular pancreas in 1, trauma in 7, infections in 16, CF in 2, Idiopathic in 15.
  • -NEJM 2006; 354: 2142.  Review of acute pancreatitis mgt.
  • -Clin Gastro & Hep 2006; 4: 455.  Elevated pancreatic enzymes frequently identified in celiac disease.
  • -Clin Gastro & Hep 2007; 5: 1347. Celiac is a risk factor for acute & chronic pancreatitis. n=14,239 & 69,381 reference population (Sweden).
  • -Pediatrics 2005; 115: e463. CF & pancreatitis
  • -JPGN 2003; 37: 5591. Systemic dz 14%, Trauma 14%, drugs 12%, metabolic 6%, structural 5%, infectious 8%, ERCP 6%, Biliary 12%, Familial 3% (but accounted for 20% of episodes) Transplant 8%, idiopathic 8%
  • -Clin Perspectives in Gastro 2002; 5: 73. Pancreas divisum