25-hydroxyvitamin-d-2 and Epilepsy

The objective of the study was to evaluate bone mass status (as measured by bone ultrasound) in patients on anticonvulsant therapy, and the influence that Vitamin D administration exerts over it.. We measured and compared the basal serum levels of 25(OH)D3, parathyroid hormone (PTH), and phalangeal bone ultrasound (Ad-SOS), in 30 adult patients who were taking anticonvulsant drugs, with a control group of similar age and sex. We then gave the patients a large oral dose of 3 mg (120.000 UI) of 25(OH)D3, and repeated the measurements after one month.. Basal 25(OH)D3 and Ad-SOS values were significantly lower, and PTH values significantly higher (P< 0.0001 in all), in the patient group. The low Ad-SOS values for the patients were independent of the treatment, but directly related to basal 25(OH)D3 levels (r = 0.45, P<0.01). There was a negative association between PTH and 25(OH)D3 (r = -0.64, P<0.0001), and no correlation between PTH y Ad-SOS (r = -0.20, p NS). After ingestion of the large dose of the vitamin D, the patient group registered a significant (P<0.0001) increase in 25(OH)D3 levels, their Ad-SOS values increased (P<0.0001) nearly to the mean basal value of the control group, and PTH decreased significantly (P<0.0001).. These findings justify the need to assure adequate vitamin D intake in patients being treated with anticonvulsants, independently of the treatment, age, sex, and activity status, in order to prevent osteomalacia.

Topics: 25-Hydroxyvitamin D 2; Adult; Aged; Anticonvulsants; Bone and Bones; Calcifediol; Carbamazepine; Epilepsy; Female; Fingers; Humans; Male; Middle Aged; Osteomalacia; Parathyroid Hormone; Phenytoin; Ultrasonography; Valproic Acid; Vitamin D

We examined the effect of short-term treatment with pharmacological doses of vitamin D2 or vitamin D3 on the serum concentration of 1,25(OH)2D metabolites in epileptic patients on chronic anticonvulsant drug therapy. Nine patients were studied before and after treatment with vitamin D2 4000 IU daily for 24 weeks and 10 before and after treatment with vitamin D3 in the same dose. Before treatment the serum concentrations of 1,25(OH)2D and 25(OH)D were significantly lower in epileptics than in normal subjects (P less than 0.01). Vitamin D2 treatment increased the serum concentration of 1,25(OH)2D2, but a corresponding decrease in 1,25(OH)2D3 resulted in an unchanged serum concentration of total 1,25(OH)2D. The serum concentration of 25(OH)D2 and 25(OH)D increased significantly, whereas there was a small decrease in 25(OH)D3. Vitamin D3 treatment did not change the serum concentration of 1,25(OH)2D3 whereas serum 25(OH)D3 increased significantly. The correlation between the serum ratio of 1,25(OH)2D2/1,25(OH)2D3 and 25(OH)D2/25(OH)D3 estimated on vitamin D2-treated epileptic patients and normal subjects was highly significant (P less than 0.01). The data indicate that the serum concentration of 1,25(OH)2D2 and 1,25(OH)2D3 are directly proportional to the amount of their precursors 25(OH)D2 and 25(OH)D3 and that the concentration of total 1,25(OH)2D is tightly regulated.

Topics: 25-Hydroxyvitamin D 2; Adult; Aged; Anticonvulsants; Calcifediol; Calcium; Cholecalciferol; Clinical Trials as Topic; Double-Blind Method; Epilepsy; Ergocalciferols; Female; Humans; Male; Middle Aged; Random Allocation

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.. 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.. 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..   In patients with epilepsy taking phenytoin, having BsmI polymorphism was associated with lower BMD.

Topics: 25-Hydroxyvitamin D 2; Absorptiometry, Photon; Adolescent; Adult; Anticonvulsants; Bone Density; Calcium; Cross-Sectional Studies; Demography; Deoxyribonucleases, Type II Site-Specific; DNA; Epilepsy; Female; Genotype; Humans; Male; Middle Aged; Parathyroid Hormone; Phenytoin; Polymorphism, Genetic; Real-Time Polymerase Chain Reaction; Receptors, Calcitriol; Spectrophotometry, Ultraviolet; Young Adult

The ketogenic diet (KD) is a high-fat, low-carbohydrate, and protein diet that effectively treats intractable epilepsy (IE).. The purpose of this study was to measure the change in bone mineral content (BMC) in children with IE treated with the KD for 15 mo.. Prepubertal children >or=5 y of age with IE were eligible. A 4:1 ketogenic diet was maintained for 15 mo, and whole-body and spine BMCs were measured with dual-energy X-ray absorptiometry. Z scores were generated by comparing the children with IE with a cohort of 847 healthy children. Other measurements included demographics, anthropometry, serum 25-hydroxyvitamin D (25-OHD), intact parathyroid hormone, electrolytes, and dietary intake. All measurements were performed at baseline and at 3, 6, 12, and 15 mo. Longitudinal mixed effects models were used to analyze change in BMC over time.. Twenty-five children (9 girls, 16 boys) with IE [age (x +/- SD): 7.3 +/- 1.9 y] participated. Growth and bone health status were suboptimal as were serum 25-OHD concentrations and dietary intake of calcium and vitamin D. Whole-body and spine BMC-for-age both declined by 0.6 z score/y and whole-body and spine BMC-for-height declined 0.7 z score/y and 0.4 z score/y, respectively. Height declined 0.5 z score/y. Body mass index (BMI; in kg/m(2)) z score, age, and ambulation were positive predictors of BMC, which declined sharply over 15 mo of KD treatment.. Bone health in children with IE was poor, particularly for younger nonambulatory children with low BMI status. The KD resulted in progressive loss of BMC. The mechanism is unclear. Further studies are needed.

Topics: 25-Hydroxyvitamin D 2; Absorptiometry, Photon; Body Mass Index; Bone and Bones; Bone Density; Calcium; Calcium, Dietary; Child; Diet, Ketogenic; Epilepsy; Female; Humans; Ketosis; Longitudinal Studies; Male; Nutritional Status; Osteoporosis; Vitamin D

The aim of this study was to describe vitamin D status in children with intractable epilepsy prescribed newer antiepileptic drugs (AEDs) before initiation of and during 15-month treatment with the ketogenic diet (KD).. Serum vitamin D (25-OHD and 1,25-OHD) and parathyroid hormone (PTH) were assessed in prepubertal children with intractable epilepsy before initiation of and during KD therapy. Three-day weighed dietary records including KD and vitamin and mineral supplementation were obtained at baseline and at 1 month.. Forty-five children (aged 5.1 +/- 2.7 years) were enrolled. Before KD therapy, 4% had deficient and 51% had insufficient serum 25-OHD levels. Vitamin D intake was less than recommended in 47%. Adequate vitamin D intake, fewer AEDs, and generalized seizures were associated with higher serum 25-OHD levels (p < 0.01). After 3 months on the KD, 25-OHD levels increased (p < 0.001), and PTH declined (p < 0.001). Over the next 12-month period, 25-OHD levels steadily declined (p < 0.001), and PTH did not significantly change.. Children with intractable epilepsy treated with newer AEDs had poor vitamin D status. Their status improved over the first 3 months of KD therapy with vitamin D supplementation and slowly declined thereafter.

Topics: 25-Hydroxyvitamin D 2; Adolescent; Anticonvulsants; Child; Child, Preschool; Dietary Fats; Dietary Supplements; Epilepsy; Female; Humans; Infant; Ketosis; Longitudinal Studies; Male; Nutritional Status; Parathyroid Hormone; Seasons; Vitamin D; Vitamin D Deficiency

Serum concentrations of vitamin D metabolites were measured before and during treatment with either vitamin D2 or vitamin D3, 4000 IU per day for 24 weeks, in 22 epileptic outpatients receiving phenobarbitone/phenytoin. The serum concentration of total 1,25(OH)2D did not change during the treatment period in any of the treatment groups. On the other hand, in the vitamin D2 group, serum 25(OH)D2, total 25(OH)D, and 24,25(OH)2D increased significantly during the trial, whereas serum concentrations of the vitamin D3 metabolites were unchanged. In the vitamin D3 group, serum concentrations of the vitamin D3 metabolites increased significantly, whereas the vitamin D3 metabolite levels remained unchanged. However, vitamin D3 treatment resulted in a 2-4-fold greater increase in serum concentrations compared to vitamin D2 treatment. Treatment with vitamin D2 and vitamin D3 in the same dose in IU results in considerably different serum concentrations of the vitamin D metabolites.

Topics: 24,25-Dihydroxyvitamin D 3; 25-Hydroxyvitamin D 2; Adult; Aged; Calcifediol; Calcium; Cholecalciferol; Dihydroxycholecalciferols; Epilepsy; Ergocalciferols; Female; Humans; Male; Middle Aged; Phenobarbital; Phenytoin

In a survey of 108 subjects with a history of epilepsy in a hospital for the mentally handicapped, administration of both phenobarbitone and phenytoin was associated with low serum calcium and plasma 25-hydroxyvitamin D (25-(OH)D) levels in female subjects only. Intake of phenytoin (as mg/kg body weight) in female subjects exceeded that in males by 22 per cent, whilst the intake of phenobarbitone was 37 per cent higher. The doses of phenobarbitone and phenytoin were each inversely related to plasma 25-(OH)D concentration, but anticonvulsant drug dosage did not correlate with the magnitude of the decline of plasma 25-(OH)D concentration in winter (November-February). No influence of sodium valproate was detected on serum calcium or on plasma 25-(OH)D levels. Limited exposure to ultraviolet irradiation (UVR) or oral administration of vitamin D restored plasma 25-(OH)D to normal levels and healed osteomalacia in a subject with tuberous sclerosis. In this subject, fit frequency declined in response to UVR and to a lesser extent in response to oral vitamin D, despite the attainment of similar levels of serum calcium and of plasma 25-(OH)D. Serum calcium levels in the other 108 subjects were lower in those experiencing the most frequent fits, but serum calcium could not be restored to levels found in subjects not receiving anticonvulsant drugs unless supraphysiological doses of vitamin D were given. Vitamin D deficiency in the epileptic population receiving drugs was assessed by the response of alkaline phosphatase to vitamin D administration. A consistent fall of serum alkaline phosphatase was found only if the initial level exceeded 175 per cent of the normal value established by reference to a population not receiving phenobarbitone or phenytoin. By this criterion five out of 45 subjects (11 per cent), aged nine to 36 years were vitamin D deficient.

Topics: 25-Hydroxyvitamin D 2; Adolescent; Adult; Alkaline Phosphatase; Anticonvulsants; Calcium; Child; Epilepsy; Ergocalciferols; Female; Humans; Male; Risk; Sex Factors; Vitamin D; Vitamin D Deficiency