Meeting News CoveragePerspective

Low vitamin D levels predict stroke severity, worse outcomes

NASHVILLE, Tenn. — New data suggest that vitamin D may be a promising marker for cerebral ischemic vulnerability and a potential target for stroke prevention.

Researchers assessed whether low serum 25-hydroxyvitamin D, a marker of vitamin D status, was predictive of ischemic infarct volume and whether it was associated with worse outcomes.

Nils Henninger, MD

Nils Henninger

Nils Henninger, MD, assistant professor of neurology and psychiatry at the University of Massachusetts Medical School, conducted a retrospective analysis of 96 consecutive patients (median age, 73 years; 45% women) with acute ischemic stroke admitted to the University of Massachusetts Medical Center from January 2013 to January 2014. All patients had serum 25-hydroxyvitamin D levels drawn within 12 months of their stroke, and had their stroke size measured by MRI.

The researchers performed analyses to determine whether serum 25-hydroxyvitamin D levels were predictors of infarct volume and poor 90-day outcome, defined as modified Rankin scale score greater than 2.

Patients with insufficient serum 25-hydroxyvitamin D levels, defined as less than 30 ng/mL, had infarct sizes approximately twice as large as patients with normal levels (P = .01), and the effect was consistent regardless of whether the stroke was lacunar or nonlacunar, Henninger reported. However, the association was strong in patients who had vitamin D levels assessed within 2 weeks of stroke, and weaker in those who had it assessed earlier.

The researchers also found that the association of 25-hydroxyvitamin D with ischemic infarct volume was independent of other known predictors of the infarct extent (P < .001).

After adjustment, lower vitamin D, trichotomized as 30 ng/mL or more vs. 20 mg/nL to 29 mg/nL vs. less than 20 ng/mL, was associated with a poor 90-day outcome (OR = 9.46; 95% CI, 1.9-47.11). Poor 90-day outcomes occurred in approximately 50% of those with normal vitamin D levels and in approximately 65% of those with low vitamin D levels, Henninger said at a press conference.

Risk for poor 3-month outcome increased approximately twofold for each 10-ng/mL decrease in serum 25-hydroxyvitamin D level (OR = 2.11; 95% CI, 1-4.42).

“One way to think about this is that maybe vitamin D is associated with greater brain tissue damage after a stroke,” Henninger said. “In a situation where you have poor vitamin D status, the stroke being bigger might shift more people into the group with poor outcomes, but there also may be some independent effect.”

Henninger noted that this study was not designed to answer the question of the exact role of vitamin D. However, he said questions remain: “Is vitamin D the factor causing all the effects that we notice, or is it an innocent bystander, a sentinel or a biomarker?

“Our findings, if they are replicated in further studies, may be the impetus for more studies of patients at very high risk of developing stroke that you might then select for [vitamin D] supplementation.” – by Erik Swain

Reference:

Henninger N, et al. Abstract W MP62. Presented at: International Stroke Conference; Feb. 11-13, 2015; Nashville, Tenn.

Disclosure: Henninger reports no relevant financial disclosures.

NASHVILLE, Tenn. — New data suggest that vitamin D may be a promising marker for cerebral ischemic vulnerability and a potential target for stroke prevention.

Researchers assessed whether low serum 25-hydroxyvitamin D, a marker of vitamin D status, was predictive of ischemic infarct volume and whether it was associated with worse outcomes.

Nils Henninger, MD

Nils Henninger

Nils Henninger, MD, assistant professor of neurology and psychiatry at the University of Massachusetts Medical School, conducted a retrospective analysis of 96 consecutive patients (median age, 73 years; 45% women) with acute ischemic stroke admitted to the University of Massachusetts Medical Center from January 2013 to January 2014. All patients had serum 25-hydroxyvitamin D levels drawn within 12 months of their stroke, and had their stroke size measured by MRI.

The researchers performed analyses to determine whether serum 25-hydroxyvitamin D levels were predictors of infarct volume and poor 90-day outcome, defined as modified Rankin scale score greater than 2.

Patients with insufficient serum 25-hydroxyvitamin D levels, defined as less than 30 ng/mL, had infarct sizes approximately twice as large as patients with normal levels (P = .01), and the effect was consistent regardless of whether the stroke was lacunar or nonlacunar, Henninger reported. However, the association was strong in patients who had vitamin D levels assessed within 2 weeks of stroke, and weaker in those who had it assessed earlier.

The researchers also found that the association of 25-hydroxyvitamin D with ischemic infarct volume was independent of other known predictors of the infarct extent (P < .001).

After adjustment, lower vitamin D, trichotomized as 30 ng/mL or more vs. 20 mg/nL to 29 mg/nL vs. less than 20 ng/mL, was associated with a poor 90-day outcome (OR = 9.46; 95% CI, 1.9-47.11). Poor 90-day outcomes occurred in approximately 50% of those with normal vitamin D levels and in approximately 65% of those with low vitamin D levels, Henninger said at a press conference.

Risk for poor 3-month outcome increased approximately twofold for each 10-ng/mL decrease in serum 25-hydroxyvitamin D level (OR = 2.11; 95% CI, 1-4.42).

“One way to think about this is that maybe vitamin D is associated with greater brain tissue damage after a stroke,” Henninger said. “In a situation where you have poor vitamin D status, the stroke being bigger might shift more people into the group with poor outcomes, but there also may be some independent effect.”

Henninger noted that this study was not designed to answer the question of the exact role of vitamin D. However, he said questions remain: “Is vitamin D the factor causing all the effects that we notice, or is it an innocent bystander, a sentinel or a biomarker?

“Our findings, if they are replicated in further studies, may be the impetus for more studies of patients at very high risk of developing stroke that you might then select for [vitamin D] supplementation.” – by Erik Swain

Reference:

Henninger N, et al. Abstract W MP62. Presented at: International Stroke Conference; Feb. 11-13, 2015; Nashville, Tenn.

Disclosure: Henninger reports no relevant financial disclosures.

    Perspective
    Brian Silver

    Brian Silver

    This is an interesting study, but more research is needed before recommendations about supplementing vitamin D in stroke are made. We have a number of other examples, such as homocysteine and vitamin E, which looked promising in CVD, but did not pan out in randomized trials. I think a wait-and-see approach is appropriate. There is always the risk that people could take too much vitamin, which can be harmful.

    This study might generate questions from patients. The response that I would give is that just like any other study that comes out with preliminary results, we should not change our entire practice on the basis of it. If there is a clinical trial, patients should consider participating. 

    • Brian Silver, MD, FAHA
    • Director, Comprehensive Stroke Center Rhode Island Hospital, Providence, R.I.

    Disclosures: Silver reports no relevant financial disclosures.

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