Issue: June 10, 2015
March 24, 2015
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Vitamin D deficiency linked to acute pain in children with sickle cell disease

Issue: June 10, 2015
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Vitamin D deficiency may be associated with vaso-occlusive complications in children with sickle cell disease, according to results of a cross-sectional study.

Patients with sickle cell disease experience high prevalence of vitamin D deficiency. However, data are limited with respect to the potential association between vitamin D deficiency and acute vaso-occlusive crisis, according to study background.

Margaret T. Lee, MD

Margaret T. Lee

Margaret T. Lee, MD, of the division of pediatric hematology, oncology and stem cell transplantation in the department of pediatrics at Columbia University Medical Center, and colleagues examined whether an association exists between vitamin D deficiency and acute pain and acute chest syndrome in children with sickle cell disease.

The analysis included 95 children with a median age of 10.6 years (range, 3-20 years). All children were treated at the Pediatric Hematology Clinic at Columbia University Medical Center.

The study included patients on hydroxyurea therapy. However, patients receiving chronic monthly transfusions — which can eliminate acute pain and acute chest syndrome — were excluded from the analysis.

Researchers collected serum 25-hydroxyvitamin D (25-[OH]D) between March 2009 and July 2010. The investigators collected patients’ histories of acute pain and acute chest syndrome within 2 years of obtaining 25-(OH)D levels.

Lee and colleagues used logistic regression to analyze the associations between 25-(OH)D levels and acute vaso-occlusive events.

They calculated ORs for the risk of pain and acute chest syndrome associated with vitamin D deficiency (25-[OH]D < 20 ng/mL).

The mean 25-(OH)D level was 18 ± 11 ng/mL. The lowest average occurred in spring (15.2 ± 11.1 ng/mL), and the highest occurred in summer (22.4 ± 8.9 ng/mL). However, researchers did not find an overall significant difference by season.

Researchers found that serum levels were lower in older children (> 10 years, 11.8 ± 6.6 ng/mL vs. < 10 years, 25.3 ± 11.6 ng/mL; P < .0001) and patients who received hydroxyurea therapy (11.9 ± 7.2 ng/mL vs. 19.7 ± 11.8 ng/mL; P = .005).

Results showed that 56 patients (59%) were vitamin D deficient (< 20 ng/mL), and 27 patients (28%) were severely deficient (< 10 ng/mL). Compared with patients with 25-(OH)D levels ≥ 20 ng/mL, vitamin D-deficient patients were older, predominantly female and experienced more pain.

Within the 2 years before researchers collected serum 25-(OH)D samples, 31 patients (33%) experienced at least one episode of pain and 29 (31%) had at least one episode of acute chest syndrome.

Serum 25-(OH)D was associated with pain (P = .0121), but researchers observed no significant association between serum 25-(OH)D and acute chest syndrome.

Of the patients who experienced pain, 74% (23/31) were vitamin D deficient, and 26% (8/31)  had 25-(OH)D levels ≥ 20 ng/mL (OR = 2.7; 95% CI, 1.05-6.94).

Patients aged older than 10 years demonstrated lower 25-OHD levels and more pain than those aged 10 years or younger.

“Our findings emphasize the high prevalence of vitamin D deficiency in sickle cell disease, and its potential association with acute vaso-occlusive complications,” Lee told HemOnc Today. “Patients with sickle cell disease have an underlying pro-inflammatory state and an increased susceptibility to infection. Both these pathologic mechanisms play critical roles in acute sickle vaso-occlusive complications, particularly in children.

“Vitamin D, through its immunoregulatory and antimicrobial functions, may help control these processes,” Lee said. “Correcting inadequate levels of vitamin D may offer a simple and low-cost intervention to help reduce acute vaso-occlusive complications in sickle cell disease.” – by Lauren Frisby

For more information:

Margaret T. Lee, MD, can be reached at Columbia University Medical Center, Division of Pediatric Hematology/Oncology/Stem Cell Transplantation, Children’s Hospital North, 10th Floor, Room 10-09A, 3959 Broadway, New York, NY 10032; email: ml653@cumc.columbia.edu.

Disclosure: The researchers report no relevant financial disclosures.