Category Archives: Nutrition

Where is the Journal Editor?

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A recent article is titled “Determination of Bone Age in Pediatric Patients with Crohn’s Disease Should Become Part of Routine Care” (Inflamm Bowel Dis 2013; 19: 61-65). (Thanks to Ben Gold for suggesting this reference.)

Does the study merit the authors’ conclusion that ‘determination of bone age (BA) should become the standard of care in pediatric Crohn’s disease (CD) patients, allowing clinically meaningful interpretation of growth…leading to improved treatment recommendations?’

No.  This small study (n=49, 84% Caucasian) simply showed that a lot of pediatric CD patients have a delayed bone age.  This is not a novel finding.

Specifically, the mean BA Z score was -1.40 ± 1.5 in this population and 41% had a BA Z score of < -2.0.  This cross-sectional study was conducted between 2007-2009.  Patients were consecutively approached for enrollment during this time period.

Clinical factors associated with delayed bone age included Caucasian race, Tanner stage 1-3, history of steroid exposure, colonic disease location, azathioprine/6-mercaptopurine usage, and female sex.  Interestingly, these variables are not entirely consistent with prior studies in which male sex was associated with delayed bone age.

The reason why the conclusion is a far-reach is that there is no data in the study showing how bone age influences any clinical decision-making in these patients.  There is no information on cost-effectiveness of their proposed “standard of care.”  There is no longitudinal data to suggest that the delayed BA or the recognition of a delayed BA  resulted in a different outcome.

My conclusion:

Many pediatric patients with CD have delayed BA and some may benefit from a BA determination.  I think extrapolating a much broader conclusion from this study is not warranted.

Vitamin D deficiency and metabolism in pediatric Crohn’s disease

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As noted in previous blog posts (see links below), vitamin D has received a great deal of attention with a number of chronic diseases.  In this latest study from CHOP, the incidence and mechanisms of vitamin D deficiency in pediatric Crohn’s disease are explored (Inflamm Bowel Dis 2013; 19: 45-33).

At diagnosis (2002-2005), Crohn’s disease (CD) participants (n=78) had their serum vitamin D assays and parathyroid hormone (PTH) levels checked.  Then, these values were sequentially followed at 6 months, 12 months, and a median of 43 months later (n=52). The average age of the CD patients was 12.7 years.

Key findings:

  • 42% of CD participants were 25-OH D deficient (<20 ng/mL) with an odds ratio of 2.1 compared with controls.
  • Among patients with 25-OH D <30 ng/mL, CD patients had a lower PTH than controls.
  • At final visit, 3% remained 25-OH D deficient and PTH levels corrected.
  • Risk factors, besides CD, for vitamin D deficiency: black race (OR 10.4), visit in winter (OR 2.4), age 12 to <15 (OR 2.7), age >15 (OR 3.2).  Greater disease activity was associated with lower vitamin D levels at baseline.

Implications of this study:

  1. Vitamin D deficiency normally causes secondary hyperparathyroidism.  With newly-diagnosed CD, there was a relative hypoparathyroidism that resolved with therapy.  “It is conceivable that proinflammatory cytokines associated with CD …prevent an appropriate PTH response.”
  2. The authors state that ‘vitamin D deficiency likely contributes to the pathogenesis of CD through effects on T and B lymphocyte, macrophage, and dendritic cell regulation.”  Correcting vitamin D deficiency may improve CD treatment response in addition to potential improvements in bone health.

Related posts:

Challenging the Obesity Myths

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A recent provocative article highlights the myriad misconceptions regarding obesity (NEJM 2013; 368: 446-54).

According to the authors, many of the obesity recommendations are fallacies:

  • Myth: “Small sustained changes in energy intake will produce large long-term weight changes.” Fact: Because of changes in body mass, the energy requirements change which results in only modest improvement.
  • Myth: “Setting realistic goals for weight loss is important.” Fact: Setting realistic goals has not been shown to improve outcomes over more ambitious goals.
  • Myth: “Rapid weight loss is associated with poorer long-term weight-loss outcomes, as compared with slow, gradual weight loss.”  Fact: Ultimate success in terms of body weight is better with greater initial weight loss.
  • Myth: “It is important to assess…diet readiness.” Fact: Readiness does not predict the magnitude of weight loss or treatment adherence among those who sign up for behavioral programs or undergo weight loss surgery.
  • Myth: “Physical-education classes…play an important role in reducing or preventing childhood obesity.” Fact: Physical education, as typically provided, has not been shown to reduce or prevent obesity.
  • Myth: “Breast-feeding is protective against obesity.” Fact: “Studies with better control for confounding..involving more than 13,000 children who were followed for more than 6 years provided no compelling evidence of an effect of breast-feeding on obesity.”
  • Myth: “Sexual activity burns 100-300 kcal for each participant.” Fact: “Incremental benefit of one bout…is plausibly on the order of 14 kcal.”  (This is going to dampen the all-you-need-to-lose weight is to become a pornography star craze.)

Presumptions -also not proven:

  • Eating breakfast is protective against obesity
  • Early childhood learning regarding exercise and eating influence our weight throughout life
  • Eating more fruits and vegetables will result in weight loss
  • Snacking contributes to weight gain
  • Availability of parks and sidewalks influence the development of obesity

Facts:

  • Reducing energy intake (dieting) can be effective.
  • Increased exercise improves health.
  • Programs that involve parents promote greater weight loss.
  • Some pharmaceutical agents can help.
  • Bariatric surgery can be lifesaving treatment in some cases.
  • Heritability is not destiny.  Moderate sustained environmental changes can be effective.

 

Some related links:

Avoid breastfeeding to lower the risk of HIV

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AAP recommends against breastfeeding infants of HIV-infected mothers:

http://pediatrics.aappublications.org/content/early/2013/01/23/peds.2012-3543.abstract?papetoc

“It is critical that physicians are aware of the HIV transmission risk from human milk and the current recommendations for feeding HIV-exposed infants in the United States. Because the only intervention to completely prevent HIV transmission via human milk is not to breastfeed, in the United States, where clean water and affordable replacement feeding are available, the American Academy of Pediatrics recommends that HIV-infected mothers not breastfeed their infants, regardless of maternal viral load and antiretroviral therapy.”

Thanks to Mike Hart for sharing this link.

Outgrowing the growth charts

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Unfortunately, there is a need for extreme growth charts (Pediatrics 2012; 130: 1136-40).

The authors of this study designed growth charts for morbidly obese children.  The reason for these charts is that there are many pediatric patients who cannot be plotted using the CDC  growth chart which has a maximum BMI of 36 kg per meter-squared.  The CDC charts are based on a preobesity epidemic population data set (1963-94) and has sparse data for those above the 97th percentile.  The manuscript describes how these initial charts were derived.

These new growth charts calculate the BMI as a percentile of the 95th percentile.  For example, multiplying the BMI 95th % by 1.2 would yield a result of 120% of the 95th%.  The authors calculated 1.1 through 1.9 multiples of the 95% for all ages between 2 and 20 years.  On their curve, a BMI as high as 64 kg per meter-squared can be plotted.  This allows easier visual tracking of a patient’s progress.

Drawbacks:

  • Difficult to explain to parents due to confusing phraseology –use of two percentages
  • Many of the patients are now on the growth curve and could appear to be graphically normal despite being morbidly obese

The authors note that their growth charts were incorporated into their electronic medical record (Epic software).

Related blog entry:

Visual Acuity and LCPUFA

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Long-chain polyunsaturated fatty acids (LCPUFA) have been examined due to their potential to affect infant cognition (Long–chain polyunsaturated fatty acids, breastmilk … – gutsandgro).  A recent meta-analysis has reviewed 19 studies with regard to LCPUFA supplementation and infant visual acuity (Pediatrics 2013; 131: e262-72 -thanks to Mike Hart for sharing this reference).

Since 75% of U.S. infants are formula fed by 1 year of age and there is widespread dependence on formula for nutritional completeness, these formulas have been designed to mimic breast milk composition.  Docosahexaenoic acid (DHA) and arachidonic acid (ARA) are the two main LCPUFAs and are integral to  the structural membranes of cells in the central nervous system and retina.  DHA comprises >50% of the phospholipid content of the retinal membrane bilayer.

These 16 studies (in the abstract it erroneously states 19 studies), identified by a literature search, involved 1949 infants.  Overall, a significant benefit of LCPUFA supplementation on infants’ visual acuity was noted at 2, 4, and 12 months of age when assessed by visual evoked potential.  A benefit was also seen at 2 months of age by using behavioral methods.  Studies were included if they were randomized control trials comparing LCPUFA supplementation to unsupplemented formula.  Initially, 286 citations were identified but most did not meet inclusion criteria.

This study findings differ from two recent Cochrane reviews on the effect of LCPUFA on visual acuity.  The Cochrane reviews failed to combine trials that  measured “visual acuity in logMAR and cycles/degree and assessed preterm and term infants separately.”  The authors state that this reduced the Cochrane reviews power to detect potential benefits of LCPUFA supplementation.

While this study demonstrates improvement during the first year of life, there is a scarcity of data beyond this time point.  Limitations of this review included heterogeneity in the study results, varying doses of LCPUFA supplementation, variable DHA/AA ratio supplied, and variability in maternal diets.

Related blog post:

Low levels of LCPUFA in Premature Infants … – gutsandgrowth

Low levels of LCPUFA in Premature Infants Associated with Intravenous Lipids

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Low levels of the long-chain polyunsaturated fatty acids (LCPUFA) docosahexanenoic acid (DHA) and arachidonic acid (ARA) in premature infants are correlated with an increased risk of developmental, respiratory, and infectious morbidities in premature infants.  A new report suggests that prolonged exposure to intravenous lipids exacerbates these low levels and could contribute to poor neurodevelopmental outcomes (J Pediatr 2013; 162: 56-61).

This study followed 26 extremely low birth weight premature infants with serial blood draws during the first two months of life using a prospective cohort design.  Infants who received more than 28 days of intravenous lipid emulsion had significantly decreased DHA levels compared to infants with shorter duration of parenteral lipid exposure; at 8 weeks, the DHA levels were 2.7 ± 0.6 compared with 4.2 ± 1.9 (all levels reported as g/100 g).  DHA levels at birth were 5.5 ± 1.4.

ARA levels decreased in a similar fashion in both groups, though values were mildly lower in the prolonged lipid group.  At 8 weeks, the ARA values were 9.4 ± 1.6 and 11.5 ± 2.5 respectively.  Thus, with a larger study group, this could be a significant finding as well.

These lower LCPUFA (especially DHA) levels may reflect a suboptimal intravenous lipid emulsion.  Alternatively, the underlying reason for the prolonged lipids, like sepsis and NEC , could result in these lower levels.  Perhaps attention to LCPUFA in parenteral formulations can improve neurodevelopmental outcomes in this vulnerable population.

Related blog entry:

Bone health in pediatrics

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Due to the survival of chronically ill children, exposure to skeletal toxic treatments, and wider availability of bone health measurement technology, osteoporosis in pediatrics has become a widespread problem.  A useful concise review is available (J Pediatr 2012; 161: 983-88).

One of the biggest problems is the limited pediatric evidence on which to base treatment decisions.

Specific points regarding osteoporosis and bone health:

  1. Bone accretion: most of one’s bone mass is reached by late adolescence or early adulthood
  2. Frequency of bone fractures: in the general population, 1/2 of boys and 1/3rd of girls have sustained a fracture by 16 years of age.  Thus, bone pathology should be suspected in those with unusual fractures.
  3. Pathological fractures: “meaningful” history of fracture history includes a lower extremity long bone fracture, 2 or more upper extremity long bone fractures and/or vertebral compression fracture.
  4. Testing: due to cost and precision, dual-energy x-ray absorptiometry (DXA) remains most widely used measurement tool. However, quantitative computed tomography (QCT) has some advantages.  It is less biased by bone size and directing generates a measurement of volumetric bone mineral density.
  5. Primary osteoporosis: osteogenesis imperfecta (OI), idiopathic juvenile osteoporosis (IJO), and osteoporosis-pseudoglioma syndrome (related to loss of function in low-density lipoprotein receptor-related protein 5 [LRP5]).
  6. Secondary osteoporosis: neuromuscular diseases, malabsorption syndromes, medication-induced (glucocorticoids, diuretics), chemotherapy, and radiation treatments.
  7. 1st line treatment: adequate nutrition –especially adequate calcium and vitamin D and exercise (especially weight-bearing exercise).  It is noted that with cystic fibrosis patients there has been a better response to vitamin D3 (cholecalciferol) than D2 (ergocalciferol); as a consequence, the CF Foundation recommends all CF patients receive vitamin D3.  With regard to weight-bearing exercise, the data are conflicting regarding its efficacy.
  8. 2nd line treatment: treat underlying disorder.  For example, with inflammatory bowel disease (IBD), treatment of chronic inflammation with infliximab has been shown to improve markers of bone formation.  Inflammation in IBD has been shown to play a more important role than glucocorticoid dosing in terms of predicting bone health.
  9. 3rd line treatment ??? a) “Currently, teriparatide is the only available treatment with anabolic actions on bone.” But, a black box warning has cautioned against its use in pediatric patients   b) bisphosphonates: pamidronate, aleondronate, and zoledronic acid. A review of the small pediatric studies, primarily in OI patients, have shown some improvement in fractures, skeletal pain, and mobility.  Optimal dose, frequency, and duration remain unknown.
  10. Safety of bisphosphonates: potential problems include ‘acute phase reaction,’ hypocalcemia, musculoskeletal pain, gastrointestinal side effects, and many other adverse reactions. Atypical fractures and jaw osteonecrosis have been reported in adults.

Related blog posts:

Ethanol locks -jump on the bandwagon

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http://ncp.sagepub.com/content/early/2012/12/10/0884533612468009.abstract

From Nutrition in Clinical Practice, published online before print, December 11, 2012, doi:10.1177/0884533612468009 (Thanks to Kipp Ellsworth for this link from his twitter feed):

“Our group of patients (n=14) showed a 73% reduction in CABSIs and a 77% reduction in catheter removal due to infection after ethanol lock therapy. In our patient population, weekly ethanol lock therapy for 2 hours is an effective technique to reduce CABSIs and catheter removal in long-term home PN patients.”

CABSIs =catheter-associated bloodstream infections

Another option for line locks

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A pediatric study from London with 19 patients demonstrates the utility of taurolidine line locks (JPGN 2012; 55: 403-7).

Taurolidine has broad antimicrobial activity against Gram-positive and Gram-negative bacteria in addition to antifungal properties.  Also, taurolidine prevents biofilm formation which can help minimize colonization of catheters.  It acts by binding to the cell walls of organisms; this results in the prevention of bacterial adhesion to biological surfaces. TauroLock™ | TauroLock™

15 of the 19 patients had a history of recurrent central catheter infections and 4 were started on the line locks empirically.  At the completion of the parenteral nutrition, 0.7 to 1 mL of the taurolidine solution was instilled and left for at least 12 hours.

Taurolidine-treated patients had 1.1 episodes per 100 catheter days of CVL infections; this compared with a rate of 8.6 episodes per 1000 catheter days for heparin control.  Furthermore, 74% (14) had no infections for up to 33 months after changing to taurolidine.  No reports of mulitresistant organisms or adverse effects were reported.  Taurolidine is nontoxic for humans and rapidly metabolized to taurine, carbon dioxide, and water.

To my knowledge, taurolidine is not available in the U.S.  Nevertheless, the data on line locks indicate that antimicrobial line locks are associated with reductions in catheter infections.

Related blog entries:

Additional reference: