Pretreatment Vitamin D Deficiency Is Associated With Impaired Progression-Free and Overall Survival in Hodgkin Lymphoma
Journal of Clinical Oncology -DOI: 10.1200/JCO.19.00985
Sven Borchmann, MD1,2,3; Melita Cirillo, MD1,4; Helen Goergen, Dipl. Math1; Lydia Meder, PhD1,2; Stephanie Sasse, MD1; Stefanie Kreissl, MD1; ...
Yet again, a study found that Chemo works much better then there is a good level of vitamin D
- Lymphoid cancer deaths cut in half with 400 IU of vitamin D and 1 gram of Calcium (WHI) – RCT Nov 2017
- Lymphoma, leukemia etc, survival poor if low vitamin D – meta-analysis March 2015
- Cancer (colon, breast, lymph) survival about 2X better with high level vitamin D – meta-analysis July 2014
- Chemotherapy drugs often reduce Vitamin D levels, restoring levels helps– Aug 2018
- Vitamin D Insufficiency and Prognosis in Non-Hodgkins Lymphoma
Chemotherapy might be amplified by vitamin D has the following chart
Vitamin D deficiency is described as a modifiable risk factor for the incidence of and mortality in many common cancers; however, data in Hodgkin lymphoma (HL) are lacking.
PATIENTS AND METHODS
We thus performed a study measuring pretreatment vitamin D levels in prospectively treated patients with HL and correlated this with clinical outcomes. A total of 351 patients from the German Hodgkin Study Group clinical trials (HD7, HD8, and HD9) were included.
Fifty percent of patients were vitamin D deficient (< 30 nmol/L) before planned chemotherapy. Pretreatment vitamin D deficiency was more common in relapsed/refractory patients than matched relapse-free controls (median baseline vitamin D, 21.4 nmol/L v 35.5 nmol/L; proportion with vitamin D deficiency, 68% v 41%; P < .001). Vitamin D–deficient patients had
- impaired progression-free survival (10-year difference, 17.6%; 95% CI, 6.9% to 28.4%; hazard ratio, 2.13; 95% CI, 1.84 to 2.48; P < .001) and
- overall survival (10-year difference, 11.1%; 95% CI, 2.1% to 20.2%; hazard ratio, 1.82; 95% CI, 1.53 to 2.15; P < .001),
consistent across trials and treatment groups. We demonstrated that vitamin D status is an independent predictor of outcome and hypothesized that vitamin D status might be important for the chemosensitivity of HL.
We subsequently performed experiments supplementing physiologic doses of vitamin D (calcitriol) to cultured HL cell lines and demonstrated increased antiproliferative effects in combination with chemotherapy. In an HL-xenograft animal model, we showed that supplemental vitamin D (dietary supplement, cholecalciferol) improves the chemosensitivity of tumors by reducing the rate of tumor growth compared with vitamin D or chemotherapy alone.
On the basis of our clinical and preclinical findings, we encourage that vitamin D screening and replacement be incorporated into future randomized clinical trials to properly clarify the role of vitamin D replacement therapy in HL.