Effect of Folate and Mecobalamin on Hip Fractures in Patients With Stroke

Only 8 years old. How incompetent is your stroke hospital if they haven't put this into place yet? Seems like a fireable offense for the hospital board of directors to enforce. Why would you even go to a hospital if they can't even read and apply research  to their areas of expertise? The following of Joint Commission standards is even more of a reason to never set foot in such a hospital. No innovation. But then I'm a stupid non-medical stroke survivor, they would have to be stupider than me to not see  where they can apply research to stroke protocols.
http://jama.jamanetwork.com/article.aspx?articleid=200453

ABSTRACT

ABSTRACT | METHODS | RESULTS | COMMENT | ARTICLE INFORMATION | REFERENCES

Context  Stroke increases the risk of subsequent hip fracture by 2 to 4 times. Hyperhomocysteinemia is a risk factor for both ischemic stroke and osteoporotic fractures in elderly men and women. Treatment with folate and mecobalamin (vitamin B₁₂) may improve hyperhomocysteinemia.
Objective  To investigate whether treatment with folate and vitamin B₁₂ reduces the incidence of hip fractures in patients with hemiplegia following stroke.
Design, Setting, and Patients  A double-blind, randomized controlled study of 628 consecutive patients aged 65 years or older with residual hemiplegia at least 1 year following first ischemic stroke, who were recruited from a single Japanese hospital from April 1, 2000, to May 31, 2001. Patients were assigned to daily oral treatment with 5 mg of folate and 1500 μg of mecobalamin, or double placebo; 559 completed the 2-year follow-up.
Main Outcome Measure  Incidence of hip fractures in the 2 patient groups during the 2-year follow-up.
Results  At baseline, patients in both groups had high levels of plasma homocysteine and low levels of serum cobalamin and serum folate. After 2 years, plasma homocysteine levels decreased by 38% in the treatment group and increased by 31% in the placebo group (P<.001). The number of hip fractures per 1000 patient-years was 10 and 43 for the treatment and placebo groups, respectively (P<.001). The adjusted relative risk, absolute risk reduction, and the number needed to treat for hip fractures in the treatment vs placebo groups were 0.20 (95% confidence interval [CI], 0.08-0.50), 7.1% (95% CI, 3.6%-10.8%), and 14 (95% CI, 9-28), respectively. No significant adverse effects were reported.
Conclusion  In this Japanese population with a high baseline fracture risk, combined treatment with folate and vitamin B₁₂ is safe and effective in reducing the risk of a hip fracture in elderly patients following stroke.

The risk of a hip fracture in patients after stroke is 2 to 4 times higher than that in age-matched healthy control patients.¹ These fractures usually occur relatively late after stroke onset and affect the paretic side of the body.^2- 5 Hip fractures are associated with more deaths, disabilities, and medical costs than all other osteoporosis-related fractures combined.⁶ We previously measured the bone mineral density (BMD) in patients with stroke in the second metacarpal bone and demonstrated a decrease in the bone mass in the hemiplegic limb that corresponded to the degree of palsy and vitamin D deficiency,⁷ which may explain why hip fractures in patients poststroke occur almost exclusively on the hemiplegic side of the body.

A close association between plasma homocysteine and risk of ischemic stroke has been reported,^8- 11 and plasma homocysteine levels are higher in patients with ischemic stroke in both acute^12- 13 and convalescent phases.^14- 17 In patients with homocysteinuria, a rare autosomal recessive biochemical abnormality, there is an increased prevalence of skeletal abnormalities,^18- 20 including osteoporosis, a primary risk factor for hip fracture. Thus, elevated plasma homocysteine concentrations may be associated with osteoporosis and increase the risk of a hip fracture. An increased homocysteine level appears to be a strong and independent risk factor for an osteoporotic fracture of the bones, including the hip, in older men and women.^21- 22

In the remethylation cycle, homocysteine is salvaged for methionine synthesis by the addition of a methyl group by methionine synthase.²³ Vitamin B₁₂ (cobalamin) is an essential cofactor for methionine synthase and N⁵-methyl-tetrahydrofolate serves as the methyl donor. Therefore, there are close relationships between plasma homocysteine and cobalamin and folate.^{8- 9,24- 26}

We previously demonstrated a reduction in plasma homocysteine levels by combination therapy with folate and vitamin B₁₂ in patients with ischemic stroke.²⁶ Our goal for this study was to investigate the efficacy of the combined therapy for decreasing the risk of fractures, particularly in the hip, in a 2-year trial in elderly patients with hemiplegia following ischemic stroke.