May 06, 2015
5 min read

Vitamin D levels may affect follicular lymphoma outcomes

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Low levels of serum vitamin D were associated with greater rates for mortality and disease progression in patients with follicular lymphoma, according to study results.

The association between poorer OS and low vitamin D levels did not reach statistical significance in one of the study cohorts; however, results from the overall population may be consistent enough to suggest that serum vitamin D may be a modifiable factor associated with outcomes in this setting, according to the researchers.

“There is a long history of evidence that vitamin D and sunlight might impact lymphoma risk, and recently there have been studies in other subtypes of lymphoma that vitamin D status can help predict lymphoma prognosis,” Jonathan W. Friedberg, MD, of the Wilmot Cancer Center at the University of Rochester School of Medicine and Dentistry, told HemOnc Today. “The study of follicular lymphoma is a particular area of interest because it is an indolent disease where you have time to study the effects of supplementation.”

Friedberg and colleagues evaluated data from previously untreated patients with newly diagnosed follicular lymphoma from SWOG (n = 183) clinical trials or the Lymphoma Study Association (LYSA) PRIMA trial (n = 240). A majority of both study cohorts were male (SWOG, 55%; LYSA, 53%) and aged 60 years or younger (SWOG, 71%; LYSA, 64%).

Patients in the SWOG cohort received CHOP chemotherapy plus rituximab (Rituxan, Genentech/Biogen Idec) or iodine-131 tositumomab (Bexxar, GlaxoSmithKline) between 1998 and 2008. Patients in the LYSA cohort received rituximab plus chemotherapy and were randomly assigned to rituximab maintenance or undergo observation.

Researchers measured 25-hydroxyvitamin D in baseline serum samples using a liquid chromatography-tandem mass spectrometry method. Vitamin D deficiency was defined as levels less than 20 ng/mL in the SWOG cohort and less than 10 ng/mL in the LYSA cohort.

PFS served as the study’s primary endpoint. Using these definitions, 15% of the SWOG cohort was vitamin D deficient (median serum 25-hydroxyvitamin D, 31 ng/mL) and 25% of the LYSA cohort was considered deficient (median serum 25-hydroxyvitamin D, 17 ng/mL).

After a median follow-up of 5.4 years in the SWOG cohort, 18% (n = 33) of the cohort had died and 44% (n = 81) had experienced progression. There was no association between vitamin D deficiency and cause of death or clinical response (OR for complete response = 1.14; 95% CI, 0.46-2.81). However, patients who were vitamin D deficient had significantly inferior PFS (HR = 2; P = .011) and OS (HR = 3.57; P = .003) compared with patients with higher vitamin D levels.

After a median follow-up of 6.6 years in the LYSA cohort, 10% (n = 25) had died and 47% (n = 112) experienced progression. There was no association between vitamin D deficiency and cause of death, and an equal proportion of patients who were and were not deficient demonstrated a clinical response to treatment.

Although patients with a vitamin D deficiency in the LYSA cohort demonstrated inferior PFS compared with patients with higher levels (HR = 1.66; P = .013) rates, the association between lower vitamin D and OS did not reach statistical significance (HR = 1.84).

Limitations to these data exist, Friedberg said.

“We were not able to define and appropriate threshold based on the differential characteristics of the European and American patient populations,” Friedberg said.

It is not clear at this point whether vitamin D supplementation is warranted, he added.

“In an era when we’re using different types of therapies, including novel oral agents and targeted therapies, there may be some data sets that allow us to do see if vitamin D is prognostic,” Friedberg said. “Ultimately, we will have to see how the community receives this to determine whether there will be energy to consider a trial of supplementation. It might be interesting to see if we can delay the time to treatment by giving vitamin D.” – by Cameron Kelsall

For more information:

Jonathan W. Friedberg, MD, can be reached at the James P. Wilmot Cancer Center at the University of Rochester School of Medicine and Dentistry, 601 Elmwood Ave., Box 704, Rochester, NY 14642; e-mail:

Disclosure: Friedberg reports a consulting role with Bayer, Kite Pharmaceuticals and Trubion and research funding from Genentech, Janssen Pharmaceuticals, Millennium Pharmaceuticals and Seattle Genetics. Please see the full study for a list of all other researchers’ relevant financial disclosures.