Tag Archives: vitamin D deficiency

John Snow and Hepatology Potpouri

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If you mention the name “John Snow,” I bet most people would think about one of the characters from Game of Thrones.  However, a more important John Snow is referenced in a recent Hepatology review (Hepatology 2014; 60: 1124-25).  “In 1855, the physician and epidemiologist John Snow used the technique of medical geography to stem the cholera epidemic in London.  By mapping the number of choleras case and the local water supply, he found that the Broad Street pump station was responsible and after the pump handle was removed, incident cases declined.”

Hepatology 2014; 60: 1150-59, editorial 1124-25.  Using spatial (clustering) epidemiology, the authors show that parenteral antischistosomal therapy (PAT) alone cannot explain the high HCV prevalence in Egypt.  Other iatrogenic exposures and poor infection control are likely contributing factors.

Hepatology 2014; 60: 1222-30, editorial 1130.  In a prospective study (western Europe), the authors show that vitamin D (25-OH) levels were inversely associated with the risk of hepatocellular carcinoma (HCC).  What is remarkable about this study is the levels were obtained on average 6 years before HCC diagnosis.  Also, this study uses tertiles -comparing those in the top third to those in the lowest third.

Hepatology 2014; 60: 1399-1408.  More data showing injury from Herbals and dietary supplements.  Liver injury caused by bodybuilding herbal supplements (often anabolic steroids) were typically less severe than liver injury induced in non-bodybuilding herbals (predominantly middle-aged women). Table 3 identifies by name many of the herbal supplements/dietary supplements associated with death or liver transplantation.  “Contrary to popular belief, this study demonstrates that HDS products are not always safe.”

Why Adding Vitamin D May Not Help IBD

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Despite all of the accolades that vitamin D has received, the fact that low vitamin D is associated with worse outcomes, in a number of disease states, does not prove causality. A recent article indicates that vitamin D is likely more of a marker of disease activity than a mediator of disease activity in inflammatory bowel disease (IBD), and specifically Crohn’s disease (CD) (Inflamm Bowel Dis 2014; 20: 856-60).

Background: Binding sites for the vitamin D receptor (VDR) have been “identified in genes associated with CD, and vitamin D has been shown to enhance the production of interleukin-10 (IL-10) and induction of regulatory T-cells.”

Design:The authors prospectively collected samples of 37 CD patients; the mean age in those with active disease (n=20) was 34 years and it was 30 years in those with inactive disease. In 8 patients with active disease, vitamin D levels were measured at the time of active inflammation (day 0) and at 14 days after receiving infliximab (day 14).

  • Key finding in these 8 patients: Vitamin D (25-OH) was 23 ng/mL on day 0 and 40 ng/mL 2 weeks later.  Only 1 of these 8 patients was taking a vitamin D supplement.
  • Key finding in the entire cohort: in the active disease group mean vitamin D level was 27 ng/mL compared with 38 ng/mL in those in remission (P=0.02).

Take-home point: There is an inverse relationship between vitamin D levels and disease activity.  However, the early increases in vitamin D levels with clinical response to anti-TNF therapy suggests that a major mechanism of vitamin D deficiency is related to the burden of systemic inflammation.  Hence, repeat testing when patients are in remission may obviate the need for vitamin D supplementation in many patients.

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Explaining the Vitamin D Paradox

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For a long time, there has not been a satisfying explanation for the fact that blacks have higher bone mineral density but lower 25-hydroxy-vitamin D levels than whites.  New research (NEJM 2013; 369: 1991-2000, editorial 22047-48) helps explain this paradox.

This study examined a community cohort of 2085 individuals in the “Healthy Aging in Neighborhoods of Diversity across the Life Span” study.

Key Findings:

  • Blacks had higher bone mineral density and lower 25-hydroxy-vitamin D levels than whites
  • The calculated bioavailable levels of 25-hydroxy-vitamin D were similar to whites.

The editorial notes that the similar bioavailability is due to differences in the vitamin D-binding protein (aka GC-globulin).  “GC1F is the most abundant form in persons of African ancestry whereas GC1S is most abundant in European populations.”  Thus, it has been hypothesized that the vitamin D-binding protein in blacks has “increased affinity for vitamin D3, and thus able to transport vitamin D3 more efficiently from the skin to the liver for its metabolism to 25-hydroxy-vitamin D.”

Bottomline: This research in vitamin D metabolism may impact on how we determine vitamin D deficiency.  The measurement of vitamin D-binding protein may need to be incorporated into the assessment.

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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.

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