Bone mass and turnover in women with epilepsy on antiepileptic drug monotherapy

Antiepileptic drugs, particularly cytochrome P450 enzyme inducers, are associated with disorders of bone metabolism. We studied premenopausal women with epilepsy receiving antiepileptic drug monotherapy (phenytoin, carbamazepine, valproate, and lamotrigine). Subjects completed exercise and nutrition questionnaires and bone mineral density studies. Serum was analyzed for indices of bone metabolism including calcium, 25-hydroxyvitamin D, parathyroid hormone, insulin growth factor I, insulin binding protein III, and bone formation markers, bone-specific alkaline phosphatase, and osteocalcin. Urine was analyzed for cross-linked N-telopeptide of type I collagen, a bone resorption marker. Calcium concentrations were significantly less in subjects receiving carbamazepine, phenytoin, and valproate than in those receiving lamotrigine (p = 0.008). Insulin growth factor-I was significantly reduced in subjects receiving phenytoin compared with those receiving lamotrigine (p = 0.017). Subjects receiving phenytoin had significantly greater levels of bone-specific alkaline phosphatase (p = 0.007). Our results demonstrate that phenytoin is associated with changes in bone metabolism and increased bone turnover. The lower calcium concentrations in subjects taking carbamazepine or valproate compared with those taking other antiepileptic drugs suggest that these antiepileptic drugs may have long-term effects. Subjects receiving lamotrigine had no significant reductions in calcium or increases in markers of bone turnover, suggesting this agent is less likely to have long-term adverse effects on bone.     

Carbamazepine and bone mineral metabolism

The status of bone mineral metabolism was studied in 21 epileptic out-patients receiving carbamazepine as the sole anticonvulsant drug. Hypocalcaemia was found in 3, hypophosphataemia in one and elevated serum alkaline phosphatase in 4 of the cases. Serum 25-hydroxyvitamin D values were significantly lower in the patients than in the controls. No statistically significant difference was observed in bone mineral density between the patients and controls. Histomorphometric analysis of the iliac crest cancellous bone did not reveal any statistically significant difference in the amount of trabecular bone or osteoid between the patients and controls, but the patients had an increased amount of trabecular resorption surfaces. An increased amount of osteoid, suggesting histological osteomalacia, was found in 2 of the 18 biopsies. We conclude that epileptic out-patients receiving carbamazepine therapy have vitamin D deficiency and may develop osteomalacic changes in their skeleton.     

Effect of carbamazepine and valproate on bone mineral density

The objective of this study was to examine the effect of carbamazepine and valproate monotherapy on bone mineral density in children. Femoral neck area bone mineral density was measured by dual-energy x-ray absorptiometry in 31 healthy children and 33 children with idiopathic epilepsy treated with either carbamazepine (n = 17) or valproate (n = 16) for more than 6 months. There were no significant differences between the control and study patients in age, height, weight, and physical activity. No patient had dietary restrictions or neurologic impairment. Serum levels (as mean +/- S.D.) of valproate and carbamazepine were 53.75 +/- 23.94 microg/mL and 6.26 +/- 2.00 microg/mL, respectively, and the duration of treatment for each drug was 24.38 +/- 10.58 months and 31.76 +/- 16.33 months, respectively. Calcium intake in the diet was similar in both the control and study groups. In the valproate-treated group, 25% of the patients were hypocalcemic, 6% had elevated alkaline phosphatase levels, and 50% were hypophosphatemic. In the carbamazepine-treated group, 17.6% of the patients were hypocalcemic and 35.3% were hypophosphatemic. Children treated with valproate had 31.9% reduction in bone mineral density at the femoral neck area (P < 0.05); the 20% reduction in bone mineral density in this anatomic location in carbamazepine-treated children was not significant. In conclusion, valproate monotherapy, but not carbamazepine therapy, significantly reduces femoral neck area bone mineral density in children with idiopathic epilepsy.     

Adverse effects of antiepileptic drugs on bone mineral density

The aim of this study is to determine the frequency of changes in biochemical markers of bone metabolism in children who are receiving valproic acid, carbamazepine, and oxcarbazepine. Thirty healthy children and 68 children with idiopathic epilepsy treated with either carbamazepine (n = 23), valproic acid (n = 31), or oxcarbazepine (n = 14) for more than 1 year were enrolled into the study. Blood samples were obtained in order to determine biochemical parameters (calcium, phosphorus, alkaline phosphates, parathormone, and 25-hydroxyvitamin D). Bone mineral density was measured with the dual-energy x-ray absorptiometry method. There were no significant differences in the serum concentrations of calcium, phosphorus, aspartate aminotransferase, alanine aminotransferase, and albumin levels between the four groups. However, serum alkaline phosphatase concentrations were higher in the patient group as compared with the control subjects. In patients receiving antiepileptic drugs, bone mineral density values were significantly lower than the healthy control group. In conclusion, long-term antiepileptic drug treatment either with valproic acid, carbamazepine, or with oxcarbazepine which has unknown effects on skeletal mineralization, induces a state of decreased bone mineral density.     

Effects of long-term combination treatment with valproate and atypical antipsychotics on bone mineral density and bone metabolism in premenopausal patients with bipolar disorder: a preliminary study

Objective

We investigated bone mineral density (BMD) and bone metabolism in female bipolar patients who were undergoing long-term treatment with valproate combined with a low-dose atypical antipsychotic.

Methods

Nineteen premenopausal women with bipolar disorder who were treated with valproate combined with atypical antipsycho-tics for at least 2 years were evaluated. The BMD was measured at lumbar spine and femur sites using dual-energy X-ray absorptiometry (DE-XA). The biochemical markers of bone turnover and circulating levels of gonadal hormones were assessed. Subjects with abnormal DEXA scans were compared to those with normal scans.

Results

Nine (47%) of nineteen subjects showed osteopenia or osteoporosis. The T-score for subjects with abnormal DEXA scans was -1.988. Decreased BMD was more prominent in the proximal femur than in the lumbar spine. Subjects with abnormal DEXA scans had high phosphorus and low testosterone levels relative to subjects with normal scans (p=0.008 and p=0.028, respectively). There was a significant negative correlation between phosphorus, osteocalcin, and femur neck BMD (p<0.05). However, multivariate analysis did not show a significant association between femur and lumbar BMD and biochemical markers of bone turnover.

Conclusion

Long-term treatment with valproate combined with low-dose atypical antipsychotics may adversely affect BMD in premenopausal women with bipolar disorder. A prospective, controlled-study with a larger population is warranted, and assessment of BMD and bone metabolism should be taken into consideration in long-term therapy with valproate and atypical antipsychotics.     

Alkaline phosphatase and its isoenzyme activity for the evaluation of bone metabolism in children receiving anticonvulsant monotherapy.

This study aimed to investigate whether carbamazepine, sodium valproate or phenobarbital as monotherapy in ambulatory epileptic children with adequate sun exposure have some effect on their bone metabolism based on the determination of total serum alkaline phosphatase (AP) levels and its bone isoenzyme activity. Blood samples were obtained from 118 epileptic children (37 on carbamazepine, 47 on sodium valproate and 34 on phenobarbital) and from corresponding healthy controls matched for age, gender and anthropometric parameters. AP and its liver, bone and intestinal isoenzyme levels, other common biochemical markers of bone and liver metabolism and drug levels were measured in the study participants. Patients on carbamazepine or phenobarbital had significantly elevated AP levels accompanied by increased bone and liver isoenzyme activity compared to controls. An increase of bone AP isoenzyme values, correlated with the duration of treatment ( r= 0.49, P= 0.002), was found in children on sodium valproate without, however, a concomitant significant elevation of total AP values. We conclude that children who receive antiepileptic drugs as monotherapy, even when residing in a Mediterranean country with adequate sunlight, may have their bone metabolism affected as indicated by the elevated levels of bone AP isoenzyme. This isoenzyme, but not total AP values, could therefore be used as a marker for the selection of patients who would be benefited by a thorough evaluation of their bone metabolism profile.     

Gender differences in bone mineral density in epilepsy

PURPOSE: Bone accrual in adolescence is a major determinant of peak bone mass and risk of osteoporotic fractures later in life. Postmenopausal women are at highest risk, although, both men and premenopausal women with epilepsy experience adverse bone effects. We examined gender differences in bone density in epilepsy. METHODS: Cross-sectional study examining age and gender-specific z-score total bone mineral density (z-BMD) in 108 ambulatory children with epilepsy between 6 and 18 years of age (61 females 12.8 +/- 3.6 years; 47 males 12.4 +/- 3.1 years) compared to 35 healthy controls who were first-degree cousins of patients (21 females 13.8 +/- 2.5 years and 14 males 11.7 +/- 2.5 years). RESULTS: Patients with epilepsy accrued lower z-BMD compared to controls (0.27 +/- 0.77 vs. 0.53 +/- 1.1, p < 0.05), and were reduced for both females (0.23 +/- 1.1 vs. 0.47 +/- 0.76; p = 0.14, NS) and males (0.3 +/- 1.1 vs. 0.8 +/- 0.5; p = 0.11, NS). Increasing duration of epilepsy was associated with lower BMD in males (correlation coefficient = 0.06; p = 0.05). Males with > or =6 years of epilepsy experienced the lowest z-BMD compared to controls (-0.89 +/- 0.80 vs. 0.62 +/- 0.80; p = 0.45). Fractures occurred in two females with epilepsy for > or =6 years and z-BMD of -1.5 and -2.7. CONCLUSIONS: BMD in both males and females with epilepsy is reduced. Young males with more chronic epilepsy (> or =6 years) had the lowest BMD. Age at onset of epilepsy, growth trends, and hormonal differences may underlie these gender differences. Lower bone accrual in adolescence may contribute to increased fracture risk for both men and women with epilepsy.     

The association between BsmI polymorphism and bone mineral density in young patients with epilepsy who are taking phenytoin

Purpose: This study sought to determine the association between BsmI polymorphism and bone mineral density, 25‐hydroxyvitamin D, and parathyroid hormone levels in patients with epilepsy. Methods: We recruited ambulatory young adults with epilepsy who were taking phenytoin. Data regarding demographics, basic laboratory studies, history of clinical epilepsy, parathyroid hormone, and vitamin D levels, as well as BsmI polymorphism of the vitamin D receptor (VDR) gene, were obtained. The bone mineral density (BMD) of the lumbar spine and left femur were measured using dual‐energy x‐ray absorptiometry. Key Findings: Ninety‐four patients were included in the study. BsmI polymorphism had a statistically significant lower T‐score of the lumbar spine and left femoral neck than patients with wild‐type VDR gene (p < 0.01 and p < 0.01, respectively). In addition, patients with BsmI polymorphism had a statistically significant lower z‐score of the lumbar spine and left femoral neck than patients with wild‐type VDR gene (p < 0.01 and p < 0.01, respectively). The 25‐hydroxyvitamin D level in patients with wild‐type genes was higher than in epileptic patients with BsmI polymorphism (p < 0.01 and p < 0.01, respectively). Parathyroid hormone level in patients with wild‐type VDR gene or patients having BsmI polymorphism was not correlated with BMD at either site. Significance: In patients with epilepsy taking phenytoin, having BsmI polymorphism was associated with lower BMD.     

抗癫痫药物四种对中青年绝经前女性骨代谢的影响

目的研究不同的常用抗癫痫药物对中青年女性骨代谢的影响。方法通过测量各组受试者的血清钙、25-羟基维生素D、碱性磷酸酶、甲状旁腺激素、胰岛素生长因子-1、胰岛素结合蛋白-3、骨密度等,分析长期单药服用不同抗癫痫药物如苯妥英钠(PHT)、卡马西平(CBZ)、丙戊酸钠(VPA)、左乙拉西坦(LEV)等对受试者骨代谢的影响。结果服用CBZ、PHT和VPA的受试者血清钙浓度低于服用LEV的受试者(P=0.002);服用PHT的受试者的ALP浓度显著高于服用CBZ、LEV和VPA的受试者(P=0.000);与LEV组相比,PHT组血清IGF-1水平降低(P=0.03);与LEV组相比,PHT组血清的IGFBP-3浓度显著降低(P=0.000)。结论抗癫痫药物会影响骨代谢,导致患者血清钙下降、骨量减低。LEV较其他抗癫痫药物对骨代谢的影响较小,但仍能造成患者碱性磷酸酶含量下降等。抗癫痫药物对中青年女性的骨代谢会产生一定影响,在临床用药过程中需监测相关指标。     

Evaluation of bone mineral density using digital image processing in children receiving anticonvulsants

Bone mineral density (BMD) increases rapidly in a biphasic manner in childhood. During and after adolescence, BMD correlates more closely with bone age than chronological age. Digital image processing (DIP) allows the rapid assessment of BMD and bone age on one X-ray film. Herein, using DIP methods, the effects of various anticonvulsants on chronological and bone age were evaluated in 98 epilepsy patients (age range, 3-15 years) with no intellectual or motor disorders or diseases affecting bone metabolism. All patients were taking one or a combination of the following anticonvulsants: valproate sodium (VPA); carbamazepine (CBZ); and phenobarbital (PB). Bone maturation scores for radius-ulnar-short bones (RUS) were calculated using Tanner-Whitehouse 2 methods. Bone age was determined based on standard Japanese bone-maturation scores. In each patient, Z-scores for chronological and bone ages were calculated by subtracting standard BMD for gender and age from each BMD, then dividing the result by the standard deviation. The Z-score for each drug in relation to the administration period was analyzed using the Mann-Whitney test. For chronological age, significant differences in BMD were observed regarding the administration periods in children taking multiple drugs, but not in children on VPA, CBZ, or PB monotherapy. For bone age, no significant differences in BMD were observed regarding the administration periods for all drugs. Children taking multiple drugs showed a significant negative correlation between administration period and Z-scores for BMD calculated based on chronological age (Spearman rank correlation: - 0.457, p = 0.008), but not bone age. Among children receiving long-term VPA administration, bone age was delayed approximately 1 year, and bone maturation may have been delayed. No delay in bone age was noted among children receiving long-term administration of multiple drugs, suggesting that these anticonvulsants do not influence bone maturity. These findings indicate that bone age should be considered when assessing BMD.     

长期应用托吡酯、丙戊酸钠对于血脂水平的影响

目的 观察长期应用托吡酯、丙戊酸钠单药治疗对癫痫患者血脂水平的影响。 方法 连续入组长期单药应用丙戊酸钠控制良好的癫痫患者28例、单药应用托吡酯控制良好的癫痫患者30例,并选取健康对照60例,观察各组间血脂代谢指标的差异。 结果 丙戊酸钠组血清脂蛋白（a）水平显著高于托吡酯组（P<0.001）及健康对照组（P=0.003）,而总胆固醇、低密度脂蛋白胆固醇、高密度脂蛋白胆固醇、甘油三酯水平较其他两组无明显差异。托吡酯组的总胆固醇、低密度脂蛋白胆固醇、高密度脂蛋白胆固醇、脂蛋白（a）、甘油三酯水平较对照组均未有显著差异。 结论 长期单药应用丙戊酸钠有可能增加癫痫患者脂蛋白（a）的水平,而长期单药应用托吡酯对于血脂水平影响并不明显。     

The bone mineral content alterations in pediatric patients medicated with levetiracetam,valproic acid,and carbamazepine

AimThe negative effect of antiepileptic drugs on bone health has been previously documented. However, which antiepileptic drug is safer in regard to bone health is still questionable. Our aims were to investigate the bone mineral density alterations in pediatric patients who receive antiepileptic medication for a minimum of two years and to compare the results of these drugs.Materials and methodsFifty-nine patients (32 males, 27 females; mean age: 8.6 ± 4.6 years) and a control group (13 males, 7 females; mean age: 7.6 ± 3.3 years) were included in the study. The patients were receiving necessarily the same antiepileptic drugs (AEDs) for at least two years, and none of the patients had mental retardation or cerebral palsy. The patients were divided into three groups: group 1 (patients receiving levetiracetam (LEV), n = 20), group 2 (patients receiving carbamazepine (CBZ), n = 11), and group 3 (patients receiving valproic acid (VPA), n = 28). Plasma calcium (Ca), phosphorus (P), parathyroid hormone (PTH), alkaline phosphatase (ALP), vitamin D levels, and bone mineral density (BMD) values of femur and vertebras (L1-4) and z-scores (comparative results of BMD values of the patients with the age- and gender-matched controls in device database) of the groups were compared.ResultsThe differences between P, PTH, ALP and age, Ca and BMD results, and vitamin D levels of the patients in all four groups was not statistically significant according to Kruskal–Wallis test (p > 0.05). The z-score levels of all the patient and control groups were also not statistically significantly different compared with each other.ConclusionIn contrast to previous reports in pediatric patients, our study has documented that there is not a considerable bone loss in patients receiving long-term AED medication. Although levetiracetam has been proposed as bone-protecting medication, we did not observe any difference between AEDs regarding bone mineral density after two years of treatment.     

Valproate-induced eosinophilia in children with epilepsy: role of interleukin-5

Interleukin-5 contributes both in eosinophilopoiesis and neural development. Serum interleukin-5 levels were measured with enzyme-linked immunosorbent assay technique in 68 children with epilepsy receiving sodium valproate monotherapy and compared with the levels of 60 healthy controls and 14 children with epilepsy receiving carbamazepine. Eosinophilia was observed in 35.3% of children receiving valproate. Interleukin-5 in valproate users was significantly higher compared with children receiving carbamazepine and controls. Valproate users who exhibited eosinophilia had higher interleukin-5 levels compared with those without eosinophilia. However, the interleukin-5 level was also elevated, although to a lesser degree, in children without eosinophilia. The majority of valproate responders had high interleukin-5 levels. A positive correlation between interleukin-5 levels and the eosinophil count was also noted. We postulate that valproate contributes to the pathogenesis of eosinophilia, probably inducing interleukin-5 production. The finding that serum interleukin-5 was significantly elevated in valproate responders and even in valproate users without eosinophilia suggests that the increase in interleukin-5 might represent one of valproate's antiepileptic mechanisms.     

Bone mineral density changes over a year in young females with schizophrenia: relationship to medication and endocrine variables

INTRODUCTION: Hyperprolactinaemia is associated with the use of potent dopamine-2 receptor blocking anti-psychotic agents in schizophrenia and with bone loss in the general population. Significantly higher rates of reduced bone mineral density (BMD) have been identified in young pre-menopausal females with schizophrenia receiving prolactin-raising anti-psychotics compared to those receiving prolactin-sparing anti-psychotics. This prospective study compared BMD alterations over a period of 1 year in patients maintained on either prolactin-raising (e.g. risperidone, amisulpride or depot anti-psychotics) or prolactin-sparing (olanzapine) anti-psychotics. The effects of specific interventions to improve BMD were also examined in the context of whether patients were receiving either prolactin-raising or anti-psychotics or Olanzapine. METHODS: Pre-menopausal females (n=38) with a diagnosis of schizophrenia, who had received exclusively either prolactin-raising (n=25) or prolactin-sparing (n=13) anti-psychotics during their treatment history, had clinical, endocrine and bone marker assessments performed at baseline and every 3 months for a period of 1 year. BMD was measured by DEXA scan at baseline and at 1-year follow-up. Patients from both groups either received specific interventions (n=16) or no interventions (n=16) to improve bone density. RESULTS: There was an overall gain in lumbar BMD values in the prolactin-sparing subgroup, compared to an overall loss in the prolactin-raising subgroup (p=0.02), for the groups that received no specific interventions to improve BMD. Within the group that received specific interventions, the subgroup receiving prolactin-sparing anti-psychotics had a significant increase in lumbar (p=0.01) and hip (p=0.01) BMD over time, whereas alterations in the prolactin-raising subgroup were not significant. DISCUSSION: Women taking prolactin-raising anti-psychotics and not receiving specific interventions to improve bone density had evidence of ongoing bone demineralisation over a year; whereas women taking prolactin-sparing anti-psychotics had a modest overall increase in BMD. Most clinical interventions appeared to be helpful, but were significantly more effective in those taking prolactin-sparing anti-psychotics.     

A 6-month longitudinal study of bone mineral density with antiepileptic drug monotherapy

Antiepileptic drugs (AEDs) can affect bone metabolism, but the exact mechanisms or differences in individual drugs are still unknown. The purpose of this study was to prospectively investigate the alterations in bone mineral density (BMD) and markers of bone metabolism induced by different AEDs in Koreans with epilepsy. Subjects included 33 drug-naïve, newly diagnosed patients with epilepsy aged between 18 and 50. BMD at right calcaneus and various markers for bone metabolism were measured before and after 6 months of AED monotherapy including carbamazepine, valproic acid, and lamotrigine. Carbamazepine caused a significant decrease in BMD, which was accompanied by a decrease in the level of vitamin D (25-OHD₃). BMD and vitamin D were not affected by 6 months of valproic acid or lamotrigine therapy. Interestingly, valproic acid and lamotrigine, but not carbamazepine, significantly increased osteocalcin, a marker of bone formation. All AEDs almost doubled the parathyroid hormone level, whereas urinary Pyrilinks, a marker of bone resorption, was not affected by those AEDs. These findings suggest that carbamazepine, a hepatic enzyme-inducing drug, decreases BMD.     

A comparative study of serum F protein and other liver function tests as an index of hepatocellular damage in epileptic patients

Gamma glutamyl transferase (GGT) and alkaline phosphatase (ALP) may not be sensitive indicators of hepatocellular damage in patients taking anticonvulsant drugs as raised levels may only reflect enzyme induction. Aspartate aminotransferase (AST) is a specific, but relatively insensitive marker of liver damage and has a poor correlation with liver histology. Serum F protein is found in high concentration in the liver and levels are not influenced by enzyme induction. We measured serum F protein levels in patients taking carbamazepine (CBZ) and phenytoin (PHT) as monotherapy and in patients receiving multiple drugs. We compared the results with patients taking sodium valproate (VPA). Serum F protein levels were elevated in 6%, 22% and 13% of patients receiving CBZ, PHT and VPA, respectively. Raised GGT levels were reported for both the CBZ (26%) and PHT (78%) groups. Raised ALP levels were observed in 16%, 25% and 4% of the CBZ, PHT and VPA groups, respectively. Raised levels of serum F protein in the VPA group and the absence of any associated increases in either GGT or AST may further support the suggestion that serum F protein is an indicator of hepatocellular dysfunction associated with anticonvulsant therapy. However, further correlation with liver histology is required.     

Reduced bone density and major hormones regulating calcium metabolism in anorexia nervosa.

Bone density of lumbar vertebrae (L2 to L4) and the whole body in 29 patients with anorexia nervosa were measured by dual photon absorptiometry, and the results were compared with those of 10 age-matched normal controls. The patients had significantly lower bone mineral density (BMD) in L3 and L2-4 than controls. However, there was no difference in whole-body BMD. L3 and L2-4 BMD was positively correlated with body weight and was negatively correlated with duration of illness and amenorrhea. Patients who had been more active 6 months before the time of the study had significantly higher L3 BMD than the less active patients. Most patients had an abnormally low serum estrogen level, whereas the mean serum levels of thyroid hormone (T3, T4), cortisol, calcitonin, parathyroid hormone and vitamin D were within the normal range. No correlation was found between L3 or L2-4 BMD and the levels of these hormones. These results suggest that severe weight loss, low physical activity, longer duration of amenorrhea and deficiency of estrogen contribute to bone loss in patients with anorexia nervosa, whereas calcium-regulating hormones such as parathyroid hormone, calcitonin and vitamin D are unlikely to be a primary contributor to bone loss.     

Bone metabolism markers and bone mineral density in children with neurofibromatosis type-1

Some experimental studies suggested that there may be a bone formation defect rather than a disorder in bone resorption in patients NF1. The aim of this study was to determine bone mineral density (BMD) with dual-energy X-ray absorptiometry (DEXA) and investigate specific bone formation and bone resorption and bone turnover markers in children with NF1. Thirty-two children and adolescents (16 boys, 16 girls; 16 prepubertal, 16 pubertal) with NF1 were recruited. Their age ranged from 3 to 17 years. They were compared with matched healthy children. Dual-energy X-ray absorptiometry were applied to 26 patients and 27 controls. Nine of 32 subjects with NF1 had a skeletal abnormality. BMD of the lumbar spine, and femoral neck in NF1 patients significantly decreased compared to that of healthy subjects. They were also significantly decreased in pubertal patients when compared to pubertal controls and in prepubertal patients when compared to prepubertal controls. Patients with skeletal abnormalities were found to have significantly lower level of osteocalcin when compared to patients without skeletal abnormality. Other biochemical markers did not exhibit any difference between the groups. In conclusion, our findings suggest that bone formation markers rather than DEXA could be good predictors of skeletal abnormalities among NF1 patients. However, in our study the number of the NF1 patients with skeletal abnormality and the number of bone formation markers studied were all limited. It is appropriate to perform larger studies with other bone formation markers beside osteocalcin.     

Lipid profile, apolipoproteins A and B in children with epilepsy

In this study, lipid profile was assessed, and the intimal wall thickness of both carotid arteries in children with idiopathic epilepsy was measured. The study comprised 22 children with idiopathic epilepsy on either carbamazepine or valproate. A profile including triglycerides, total cholesterol, low-density and high-density lipoproteins cholesterol, apolipoproteins AI and B, and Duplex estimation of intimal wall thickness of carotid arteries were performed. Patients on carbamazepine showed increase in total cholesterol, low-density and high-density lipoproteins cholesterol, and decrease in apolipoprotein AI levels compared with controls. Levels of total cholesterol, low-density lipoproteins cholesterol, and apolipoprotein AI were reduced in patients receiving valproate compared with controls, whereas total cholesterol, high-density lipoproteins cholesterol, and apolipoprotein AI were reduced compared with those receiving carbamazepine. Carotid arteries intimal wall thickness was not significantly changed in any of the studied groups. Although atherogenic ratios are not changed, the lowered apolipoprotein AI levels may suggest an increased risk for coronary heart disease.     

Accelerated bone remodeling in patients with poststroke hemiplegia.

A significant bone-mass reduction occurs on the hemiplegic side of stroke patients because of disuse and vitamin D deficiency. This may explain why hip fractures in poststroke patients occur almost exclusively on the hemiplegic side. To further evaluate this osteopenia, bone mineral density (BMD) in both second metacarpals was assessed in 61 patients and 28 control subjects. Serum concentrations of intact parathyroid hormone (PTH), osteocalcin (OC), tartrate-resistant acid phosphatase (TRAP), 25-hydroxyvitamin D (25-OHD), and calcium also were determined. The patients' BMD values were higher on the hemiplegic side than on the nonhemiplegic side. BMD on the hemiplegic side correlated positively with serum concentrations of PTH, OC and TRAP, which exceeded those in control subjects. Serum 25-OHD was low in patients, correlating negatively with BMD on the hemiplegic side. Serum PTH correlate positively with the levels of OC and TRAP and negatively with 25-OHD concentrations. The results indicate that skeletal remodeling is accelerated in patients with hemiplegia, with resorption predominating. We concluded that vitamin D deficiency and compensatory secondary hyperparathyroidism stimulating skeletal turnover is an important cause of osteopenia in the hemiplegic limbs of stroke patients. This osteopenia might be corrected by administration of etidronate to inhibit osteoclastic bone resorption together with a vitamin D supplement.