HOMOCYSTEINE AND BONE LOSS IN EPILEPSY
Abstract number :
3.186
Submission category :
Year :
2005
Submission ID :
5992
Source :
www.aesnet.org
Presentation date :
12/3/2005 12:00:00 AM
Published date :
Dec 2, 2005, 06:00 AM
Authors :
John O. Elliott, and Mercedes P. Jacobson
Elevated serum homocysteine (s-Hcy) is recognized as an independent risk factor in premature coronary disease and cognitive impairment. A recent study by van Meurs, et. al. found the risk of fracture was double in those with elevated s-Hcy. Epidemiological studies have found the incidence of fracture in epilepsy to be twice that of the normal population. Anti-epileptic drugs (AEDs) have been shown to increase s-Hcy by lowering blood folate levels. The literature suggests a homocysteine-associated disturbance in collagen cross-linking is involved in bone loss. The goal of this study was to see if there is a relationship between metabolic bone loss in epilepsy and homocysteine. Standard practice in our clinic is to address bone health and nutrition with all patients. We screened 405 patient charts seen in our clinic over the past 2 years. Data on 120 patients included: age, gender, seizure type, years on AEDs, s-Hcy, serum folic acid (s-FA), supplementation patterns and DEXA screening results was compiled. This was an adult epilepsy population: mean age: 44 years (SD = 14.1, range 17 to 81), there were 51 males and 69 females. Fifty were African American, 46 Caucasian, 20 Latino and 3 Asian/Other, average length of AED exposure: 26 years (SD = 14.8, range 2 to 64). DEXA results were found for 85 patients and homocysteine levels for 103 patients. Sixty-seven patients had complete records. Sixty-four subjects had abnormal DEXA results (osteopenia n = 35, osteoporosis n = 29). Normal DEXA results were found in 21 patients. There was a history of fracture in 22 subjects (18%). Mean homocysteine levels in micromol/L (SD) were 11.3 (7.6) for African Americans, 12.5 (8.3) Latinos, 9.4 (4.1) Caucasians and 6.8 (0.8) Asian/Other. Bivariate correlation analysis was performed. Bone loss status was not significantly correlated with s-Hcy (n = 67; Pearson[apos]s r = .11, p = .38). Surprisingly, length of years on AEDs was not correlated with an increased risk for bone loss (n = 85; Pearson[apos]s r = -.001, p = .99). As expected, body weight was inversely correlated with bone loss (n = 85; Pearson[apos]s r = -0.46, p = .000) and s-Hcy was inversely correlated with s-FA (n = 89; Pearson[apos]s r = -0.41, p = .000). Only four subjects had s-FA below the normal range of 5.4 ng/ml. This is the first study to look at s-Hcy and bone loss in epilepsy. Our data does not support a relationship, however; the use of a retrospective design may have prevented us from detecting an effect, since only 67 patients had completed both tests and half of the patients took multivitamins. In addition, this study included some older indivduals with diagnosis of epilepsy at mid-life. Our data supports previous studies, which found elevated s-Hcy in patients taking AEDs. Based on our data, elevated s-Hcy may also be related to ethnicity and/or related dietary habits. Six AEDs have known anti-folate mechanisms in pregnancy, cardiovascular protection and bone loss. Nutritional supplementation continues to be important in preventative epilepsy care.