cholecalciferol and Epilepsy

Topics: Anticonvulsants; Calcium; Carbamazepine; Cholecalciferol; Epilepsy; Ergocalciferols; Female; Humans; Reference Values; Vitamin D

Topics: Androsterone; Animals; Bone Diseases; Calcium; Cholecalciferol; Dihydroxycholecalciferols; Enzyme Induction; Epilepsy; Estradiol; Humans; Hydroxycholecalciferols; Microsomes, Liver; Osteoporosis; Phosphates; Progesterone; Rickets; Testosterone; Vitamin D

Topics: Adolescent; Adult; Aged; Alkaline Phosphatase; Anticonvulsants; Bone Diseases; Child; Child, Preschool; Cholecalciferol; Diagnosis, Differential; Epilepsy; Female; Humans; Hypocalcemia; Infant; Male; Middle Aged; Osteomalacia; Phosphates; Rickets; Time Factors; Vitamin D; Vitamin D Deficiency

Topics: Animals; Anticonvulsants; Bone Diseases; Calcium; Calcium Metabolism Disorders; Cholecalciferol; Enzyme Induction; Epilepsy; Humans; Intestinal Absorption; Liver; Phenobarbital; Phenytoin; Rats; Swine

Topics: Adolescent; Animals; Anticonvulsants; Biliary Tract; Bone Diseases; Calcium; Child; Cholecalciferol; Enzyme Induction; Epilepsy; Humans; Intestinal Absorption; Kidney; Liver; Metabolic Diseases; Phenobarbital; Phenytoin; Tritium; Vitamin D; Vitamin D Deficiency

Patients on long term anti-epileptic drug therapy are prone for Vitamin D deficiency for a myriad of reasons. The aim of this research was to study the effect of high dose vitamin D supplementation on vitamin D nutrition status of children newly started on anti-epileptic drug therapy.. This randomized controlled trial was conducted in a tertiary care Children's Hospital at New Delhi from November 2011 to March 2013. Eighty three children in the age group 5-10 years newly started on anti-epileptic drugs (AED) were randomized into two groups; group A - the intervention group, to whom 60,000 IU vitamin D3 was given orally/month under direct supervision along with AED for a period of 6 months, and group B- the control group, to whom AED without vitamin D3 was given. Serum 25(OH)D, ionized calcium (iCa), total calcium (tCa), inorganic phosphate (iP), alkaline phosphatase (ALP) and parathyroid hormone (PTH) levels were assayed at baseline and at the end of 6 months and were compared within and between the two groups.. The mean 25(OH)D in Group A was maintained at 6 months follow up [ 26 ng/ml, 95% CI 20-34 ng/ml] compared to baseline [25 ng/ml, 95% CI -19 to 33 ng/ml] [ p = 0.83]. In group B, there was a significant decrease in 25(OH)D levels at 6 months [13 ng/ml (95% CI 9 ng/ml-17 ng/ml)] compared to baseline [18 ng/ml (95% CI 13-24 ng/ml)] [p = 0.01]. At 6 months, mean serum 25(OH)D was significantly higher in group A as compared to group B (p = 0.005).. To conclude, oral administration of 60,000 IU vitamin D3/month is sufficient to maintain serum 25(OH)D level and prevent development of vitamin D deficiency in children newly started on AED over a period of 6 months. Non supplementation leads to the lowering of serum 25(OH)D in these children.. CTRI/2017/08/009234.

Topics: Alkaline Phosphatase; Anticonvulsants; Child; Child, Preschool; Cholecalciferol; Dietary Supplements; Epilepsy; Female; Humans; Male; Nutrition Therapy; Nutritional Status; Parathyroid Hormone; Phosphates; Treatment Outcome; Vitamin D; Vitamin D Deficiency

Vitamin D deficiency is highly prevalent among children with epilepsy. Lack of high-quality evidence led to variability among scientific societies recommendations. Therefore, we aim to determine the efficacy of different common doses used in the pediatric practice to maintain optimal 25-hydroxy vitamin D (25 [OH] vitamin D) level in children with epilepsy and normal baseline 25 (OH) vitamin D level over 6 months of supplementation.. This is a protocol for phase IV pragmatic randomized superiority controlled open-label trial at King Saud University Medical City in Riyadh. Children with epilepsy and receiving chronic antiepliptic medication and normal baseline 25 (OH) vitamin D level will be randomly assigned to receive Cholecalciferol 400 IU/day versus 1000 IU/day for 6 months. Our primary outcome is the proportion of children with vitamin D insufficiency (25 (OH) vitamin D level < 75nmol/L) at 6 months. Secondary outcomes include seizure treatment failure, seizure frequency, parathyroid hormone (PTH) levels, bone mineral density, and safety.. Our trial is set out to evaluate the efficacy of common different vitamin D maintenance doses on 25 (OH) vitamin D level, seizure control, and bone health for children with epilepsy. The results of our study will possibly help in shaping current vitamin D guidelines for vitamin D supplementation in children with epilepsy and provide a link between 25 (OH) vitamin D level and seizure control.

Topics: Adolescent; Bone Density; Child; Cholecalciferol; Clinical Protocols; Dietary Supplements; Epilepsy; Female; Humans; Male; Nutritional Status; Parathyroid Hormone; Treatment Outcome; Vitamin D; Vitamin D Deficiency; Vitamins

Vitamin D deficiency is common in children with neurodisabilities. Oral vitamin D3 may not be absorbed appropriately due to dysphagia and tube feeding. The aim of this study was to compare efficacy of vitamin D3 buccal spray with that of oral drops.. Twenty-four children with neurodisabilities (5-17 years) and vitamin D deficiency (25(OH)D ≤20 ng/mL) were randomized to receive vitamin D3 buccal spray 800 IU/daily (n = 12) or oral drops 750 IU/daily (n = 12) for 3 months during winter.. Both groups had a significant increase in 25(OH)D (z = 150; p < 0.0001). The differences between baseline and final parathyroid hormone measurements did not reach significance in both groups. Markers of bone formation and resorption did not change significantly in both groups. The satisfaction with the formulation was significantly higher in the patients using spray.. Vitamin D3 supplementation with buccal spray and oral drops are equally effective in short-term treatment of vitamin D deficiency in children with neurodisabilities. Buccal spray may be more acceptable by the patients.

Topics: Adolescent; Cerebral Palsy; Child; Child, Preschool; Cholecalciferol; Dietary Supplements; Drug Delivery Systems; Epilepsy; Female; Humans; Male; Treatment Outcome; Vitamin D Deficiency

The dose of vitamin D3 required to maintain normal serum 25-hydroxyvitamin D levels in epileptic patients was evaluated in a prospective study. Patients were divided into two groups, comprising 14 institutionalized and 18 non-institutionalized subjects; they were taking carbamazepine, phenytoin and phenobarbitone, alone or in combination. The study was divided into a dose titration stage and a further period of assessment on a fixed dose after attainment of normal serum 25-hydroxyvitamin D levels. Seventeen of the 18 non-institutionalized patients achieved normal levels over a period of 12 months; the remaining patient became normal after 15 months. The dose required to achieve normal levels ranged from 400 to 4000 IU/day; three patients required less than 2400 IU vitamin D3, 12 required 2400 IU and three required greater than 2400 IU. All institutionalized patients achieved normal levels over a period of 12 months; six patients required less than 2400 IU, six required 2400 IU and two required greater than 2400 IU vitamin D3. Raised alkaline phosphatase levels occurred in 11 patients, and reverted to normal in six patients during the initial return of 25-hydroxyvitamin D levels to normal. During the second 12 months, when patients were taking a fixed dose of vitamin D3, alkaline phosphatase increased in five patients who had achieved normal levels. During this phase normal 25-hydroxyvitamin D levels were not maintained in five patients. There was a significant seasonal variation of 25-hydroxyvitamin D levels institutionalized patients, being highest in June and lowest in December. Our findings show that while there was a wide range in the dose required to achieve normal serum 25-hydroxyvitamin D levels--between 400 and 4000 IU/day--78 per cent of patients responded to a dose of 2400 IU/day.

Topics: Adolescent; Adult; Alkaline Phosphatase; Anticonvulsants; Calcifediol; Calcium; Child; Cholecalciferol; Drug Administration Schedule; Epilepsy; Female; Humans; Male; Middle Aged; Osteomalacia; Prospective Studies; Risk Factors

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

Epileptic seizures are associated with the overproduction of free radicals in the brain leading to neuronal cell death. Therefore, reduction of oxidative stress may inhibit seizure- induced neuronal cell damage. The current study evaluated the effects of Vit D3 and melatonin and their combination on pentylenetetrazol (PTZ)-induced tonic-clonic seizures in mice.. Animals were divided into six groups. Group I was administered with normal saline (0.5 ml, intraperitoneally (i.p.)) on the 15th day of the experiment. Group II was injected with PTZ (60 mg/kg dissolved in 0.5 ml normal saline, i.p) on the 15th day. Groups III-IV were treated with diazepam (4 mg/kg/day), Vit D3 (6000 IU/kg/day), melatonin (20 mg/kg/day), and Vit D3 (6000 IU/kg/day)/melatonin (20 mg/kg/day), respectively, and were then injected with PTZ (60 mg/kg) on the 15th day of the experiment. Immediately after the injection of PTZ on the 15th day, mice were observed for a 30-min period to measure seizure latency and duration. For determination of oxidative stress markers, malondialdehyde (MDA) level and superoxide dismutase (SOD) activity were measured in mouse brains.. Treatment with Vit D3, melatonin, and Vit D3/melatonin significantly increased seizure latency and decreased seizure duration. The brain level of MDA was lower, and SOD activity was greater than in the PTZ group. Mice treated with Vit D3/melatonin had lower seizure duration than other treated groups.. The combination of Vit D3 and melatonin may reduce seizure frequency in epileptic patients; this effect may result from various mechanisms, including inhibition of oxidative stress.

Topics: Animals; Anticonvulsants; Cholecalciferol; Disease Models, Animal; Epilepsy; Melatonin; Mice; Pentylenetetrazole; Saline Solution; Seizures; Superoxide Dismutase

The epilepsy-related risk factors for vitamin D deficiency, particularly the use of enzyme-inducing antiepileptic drugs (EIAEDs), and how to treat vitamin D deficiency in patients with epilepsy remain unclear. Our aims were to explore risk factors and the influence of EAIEDs in vitamin D status and to determine the efficacy of a daily dose of oral cholecalciferol (vitamin D3) in epileptic patients with vitamin D deficiency. Clinical data were collected and 25-hydroxyvitamin D (25(OH)D) serum levels were measured. All patients with vitamin D deficiency (25(OH)D ≤20 ng/mL) or insufficiency (25(OH)D from 21-29 ng/mL) were treated with 6,670 IU/day cholecalciferol for eight weeks and 25(OH)D was then remeasured. Descriptive and inferential statistics were employed. A total of 92 patients (44.6% males), with mean age of 41.0±14.8 years, were included. Measurements of 25(OH)D revealed that 79.3% patients had abnormal levels: 56.5% were vitamin D deficient and 22.8% were vitamin D insufficient. The statistically significant risk factors for vitamin D deficiency identified were: number of AEDs, treatment with EIAEDs, low sun exposure, high body mass index (BMI) and a high frequency of epileptic seizures. After treatment, 25(OH)D mean level increased by 98.99% (regardless of EIAED use or being overweight). In our sample, more than half of the adults with epilepsy showed 25(OH)D deficiency. Patients on EIAEDs had lower 25(OH)D levels. A daily dose of 6,670 IU cholecalciferol successfully led to the correction of 25(OH)D levels. A higher dose in obese patients or in patients taking EIAEDs may not be warranted and this should be considered in future guidelines for routine vitamin D deficiency treatment.

Topics: Adult; Cholecalciferol; Epilepsy; Female; Humans; Male; Middle Aged; Portugal; Vitamin D; Vitamin D Deficiency; Vitamins

The association of antiseizure medication (ASM) and bone density abnormalities has long been recognized; however, there remains a lack of consensus on efficacy and optimal vitamin D dosing in patients receiving enzyme inducing and non-inducing ASMs. The objective was to explore the relationship between ASMs and vitamin D supplementation requirements in a population of adult patients with epilepsy.. Patients with a diagnosis of epilepsy receiving supplemental vitamin D were included in this retrospective chart review. All instances of 25-hydroxyvitamin D. There were 542 vitamin D levels evaluated from 172 unique patients. There was an 11.5 % higher absolute percent increase in patients who achieved a 25-OHD level over 30 ng/mL in the NIASM (p = 0.012). Patients on EIASMs were supplemented with an additional 508 units of vitamin D daily (95 %CI 136-878, p = 0.007). When adjusted for CKD, OTC vitamin D use, OTC multivitamin use, age, gender, and ethnicity, patients on EIASMs were supplemented with an additional 445 units of vitamin D (95 %CI -69 to 960, p = 0.089) compared to NIASM use.. Patients taking EIASMs had an increase in vitamin D deficiency and vitamin D supplementation suggesting that EIASMs impact vitamin D metabolism. Closer monitoring of vitamin D status in patients with epilepsy, especially those on EIASMs, is warranted. This evaluation suggests that for patients taking ASM, use of a lower dose OTC requires closer monitoring of vitamin D status in patients with epilepsy, especially those on EIASMs, is warranted. vitamin D agent may not be adequate.

Topics: Adult; Cholecalciferol; Dietary Supplements; Epilepsy; Female; Humans; Male; Middle Aged; Veterans; Vitamin D; Vitamin D Deficiency; Vitamins

Despite long use of antiepileptic drugs, it remains a challenge to achieve seizure control while reducing adverse effects and preventing cognitive impairment. Several lines of evidence suggest a role of vitamin D in epilepsy. So this study aimed to investigate the effect of vitamin D on epileptogenesis, cognitive dysfunction and antiepileptic activity of lamotrigine, in a rat model of chemical kindling. Rats were kindled by pentylenetetrazole injections every other day over four weeks, together with daily oral treatment by either vehicle, vitamin D, lamotrigine or combination of vitamin D and lamotrigine. The non-treated kindled rats developed generalized seizures and had poor cognitive performance in water maze, associated with prooxidative status; elevated malondialdehyde and nitric oxide with lowered glutathione levels; in brain tissues. Treatment with either vitamin D, lamotrigine or both leads to significant reduction of seizure activity score, improvement of cognitive performance, and amelioration of the disturbed oxidative stress biomarkers. These findings indicate that, vitamin D has anti-epileptic, cognitive improving and antioxidant effects, on its own and enhance the effects of lamotrigine, in a chronic model of epileptic seizures. Thus, vitamin D supplementation may be a useful addition to antiepileptic drugs improving seizure control and cognitive function in patients with epilepsy.

Topics: Animals; Anticonvulsants; Antioxidants; Cholecalciferol; Chronic Disease; Cognition; Disease Models, Animal; Drug Therapy, Combination; Epilepsy; Glutathione; Kindling, Neurologic; Lamotrigine; Male; Malondialdehyde; Maze Learning; Nitric Oxide; Nootropic Agents; Oxidative Stress; Pentylenetetrazole; Random Allocation; Rats, Wistar; Triazines

Children with epilepsy and intellectual disability have an increased risk of vitamin D deficiency. In this patient group, it is neither clear which factors are associated with the level of 25-hydroxyvitamin D nor what the therapeutic results are when Dutch guidelines are followed.. This retrospective study included 30 patients who, in October 2012, were residents of the children's wards of a tertiary epilepsy center in The Netherlands (Kempenhaeghe). From November 2012 onward they received cholecalciferol supplementation in doses that met or exceeded Dutch guidelines. At baseline, after 6, and 15 months, serum 25-hydroxyvitamin D concentration was measured.. At baseline, the vitamin D status in 11 (36.7%) residents was found to be deficient, in 10 (33.3%) to be insufficient and in 9 (30.0%) sufficient. Supplementation dose, diet, body mass index, intellectual disability, and mobility were significantly associated with baseline 25-hydroxyvitamin D concentrations. The mean 25-hydroxyvitamin D concentration increased significantly from 57.40 ± 22.00 nmol/L at baseline to 89.47 ± 26.77 nmol/L after 15 months (P < 0.001). In spite of supplementation ranging from 400 to 1200 IU/day, 64% of the residents in the deficient category and 30% of those with an insufficient level at baseline failed to attain a sufficient vitamin D status after 15 months.. Not all residents reached a sufficient vitamin D status after supplementation at least equal to the amount recommended by the Dutch guidelines. In a high-risk population, such as our residents, we advise monitoring 25-hydroxyvitamin D concentrations, adjusting supplementation accordingly and following patients to ensure they reach sufficiency.

Topics: Adolescent; Body Mass Index; Child; Child, Preschool; Cholecalciferol; Dietary Supplements; Epilepsy; Female; Follow-Up Studies; Humans; Intellectual Disability; Male; Retrospective Studies; Vitamin D; Vitamins; Young Adult

Topics: Anticonvulsants; Bone Density Conservation Agents; Carbamazepine; Cholecalciferol; Epilepsy; Humans; Male; Middle Aged; Muscular Diseases; Osteomalacia; Phenobarbital; Treatment Outcome

There is growing interest concerning the role of vitamin D in various medical conditions such as diabetes and oncological, cardiovascular and central nervous system disorders. Although vitamin D deficiency is known to be highly prevalent among epilepsy patients, only a single study, published nearly forty years ago, assessed the effect of vitamin D on seizure control. Here, we measured serum 25-hydroxy-vitamin D (25(OH)D) levels and normalized it by administration of vitamin D3 in 13 patients with pharmacoresistant epilepsy. To see if vitamin D3 has an impact on seizure frequency, we compared seizure numbers during a 90-day period before and after treatment onset. We found that seizure numbers significantly decreased upon vitamin D3 supplementation. Median seizure reduction was 40%. We conclude that the normalization of serum vitamin 25(OH)D level has an anticonvulsant effect.

Topics: Adult; Aged; Cholecalciferol; Epilepsy; Female; Humans; Male; Middle Aged; Pilot Projects; Treatment Outcome; Vitamin D; Vitamin D Deficiency; Vitamins; Young Adult

Topics: Adolescent; Adult; Age Factors; Anticonvulsants; Calcium; Child; Child, Preschool; Cholecalciferol; Electroencephalography; Epilepsy; Female; Humans; Hypocalcemia; Magnesium; Male; Middle Aged; Minerals; Phosphorus; Sex Factors; Time Factors

Dual energy X-ray absorptiometry (DEXA) is a non-invasive, rapid, accurate and highly reproducible method for the assessment of antiepileptic drug (AED)-induced osteopenia in epileptic children. In this study, we investigated bone mineral density (BMD) using DEXA in 56 epileptic children receiving long-term AED treatment for at least 2 years. All children received AED monotherapy or polytherapy plus a standard vitamin D3 supplement (400 U/day). BMD measurements were made from lumbar spine (L2-L4) regions. Age- and sex-specific BMD SD scores were calculated for each child. Osteopenia was defined as SD scores less than -1.5. There was no significant difference in mean BMD values between epileptic children receiving monotherapy or polytherapy. The results were also compared to the age- and sex-specific BMD SD scores obtained from healthy Turkish children. Only three patients (5%) receiving AED therapy had a BMD SD score less than -1.5. This rate is relatively lower than the rates of previous studies conducted on ambulatory children on long-term AED treatment without vitamin D3 supplementation.

Topics: Absorptiometry, Photon; Anticonvulsants; Bone Density; Bone Diseases, Metabolic; Child; Cholecalciferol; Cross-Sectional Studies; Drug Therapy, Combination; Epilepsy; Female; Humans; Male; Turkey

This study was conducted to determine if the adverse effects of anticonvulsant drug therapy and nonambulancy on bone status could be overcome with vitamin D therapy in severely handicapped individuals. Six male and five female gastrostomy fed, nonambulant, epileptic, profoundly mentally retarded individuals ranging in age from 7 to 17 years were given vitamin D therapy at a dosage of 4,000 IU/m2 body surface area/day for 6 months. Photon absorptiometry and biochemical indices of bone status were measured to follow the effects of therapy. Bone mineral content expressed as a percentage of normal improved by 11 percent (p less than 0.01), from 59.6 to 66.1 percent. Tartrate-resistant acid phosphatase, total alkaline phosphatase, and the bone isoenzyme activities declined 11 percent, 18 percent, and 11 percent respectively. These reductions were not statistically significant but they were consistent with the improvements observed by photon absorptiometry. The results of our study suggest that a conservative supplement of vitamin D will improve the bone status of severely disabled youths.

Topics: Adolescent; Anticonvulsants; Bone and Bones; Bone Diseases, Metabolic; Calcifediol; Child; Cholecalciferol; Epilepsy; Female; Humans; Institutionalization; Locomotion; Male; Minerals

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

Serum concentrations of vitamin D metabolites were measured in 30 epileptic outpatients on monotherapy with carbamazepine before and during treatment with either vitamin D2 or vitamin D3, 4000 IU per day for 24 weeks. Vitamin D2 treatment increased the serum concentration of 25OHD2, but a corresponding decrease in 25OHD3 resulted in an unchanged serum value of total 25OHD. Vitamin D3 treatment increased the serum concentration of 25OHD3. The resulting serum level of 25OHD was consequently twice the level of that in the D2-treated group. The serum concentrations of the dihydroxy metabolites showed a similar difference between the 2 treatment groups. We conclude that treatment with vitamins D2 and D3 in the same doses produces considerably different serum concentrations of vitamin D metabolites. If the present findings can be extrapolated to normal subjects, it is important to consider more carefully which D-vitamin should be used, both with regard to therapy and supplementation.

Topics: Adult; Aged; Carbamazepine; Cholecalciferol; Epilepsy; Ergocalciferols; Female; Humans; Male; Middle Aged

In 22 epileptic outpatients treated for at least 1 year with phenobarbitone/phenytoin the local and total bone mass, together with serum and urinary indices of calcium metabolism, were measured before and during treatment with either vitamin D2 or D3, 4,000 IU daily for 24 weeks. The results showed a distinct difference in the action of the two vitamins on bone metabolism during anti-convulsant treatment. The bone mass increased during treatment with vitamin D2, whereas the vitamin D3-treated patients showed unchanged values of bone mass, but an increased excretion rate of calcium, probably caused by increased intestinal calcium absorption. The data demonstrate that vitamins D2 and D3 (or their metabolites) have quantitative different effects in patients treated with phenobarbitone/phenytoin.

Topics: Adult; Alkaline Phosphatase; Bone and Bones; Calcium; Cholecalciferol; Double-Blind Method; Epilepsy; Ergocalciferols; Humans; Hydroxyproline; Middle Aged; Parathyroid Hormone; Phenobarbital; Phenytoin

Serum concentrations of the main vitamin D metabolites and of calcium, phosphate, and alkaline phosphatase were determined in each of the three trimesters of pregnancy and in simultaneously obtained maternal and cord blood at delivery in 22 epileptic women treated with diphenylhydantoin or carbamazepine alone or with a combination with one other drug. The results were compared with similarly obtained data from 22 normal pregnancies. Women in both groups received supplements of 400 IU vitamin D3 per day. All the women had 25-hydroxyvitamin D levels within the normal range for healthy adults (greater than 12 ng/ml) throughout pregnancy. The epileptic women had, however, significantly (p less than 0.05) lower median 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D levels and higher median 25,26-dihydroxyvitamin D values than the reference group. The 24,25-dihydroxyvitamin D concentrations did not differ significantly, but the median ratio of 24,25-dihydroxyvitamin D to 25-hydroxyvitamin D was higher in the epileptic women at the end of pregnancy (p = 0.05). The respective differences in cord serum concentrations reflected those of the mothers at delivery. Serum calcium tended to be lower during epileptic pregnancy, but none were hypocalcemic. The alkaline phosphatase and phosphate values did not consistently differ from those of the reference women. The median alkaline phosphatase level of cord serum was slightly higher in the epileptic group, but the calcium and phosphate levels were similar to the reference values. The various biochemical parameters of the carbamazepine-treated women tended to be intermediate between those of the healthy and diphenylhydantoin-treated groups. Antiepileptic drug therapy appears to affect vitamin D metabolism and calcium homeostasis during pregnancy. The derangements may not be of major clinical significance, however, in vitamin D-supplemented and normally functioning women on long-term low-dose therapy.

Topics: 24,25-Dihydroxyvitamin D 3; Adolescent; Adult; Alkaline Phosphatase; Anticonvulsants; Calcifediol; Calcitriol; Calcium; Carbamazepine; Cholecalciferol; Dihydroxycholecalciferols; Epilepsy; Female; Fetal Blood; Homeostasis; Humans; Phenytoin; Phosphates; Pregnancy; Pregnancy Complications; Vitamin D

In order to clarify whether carbamazepine causes disturbances in calcium and bone metabolism were examined the effect of vitamin D2 or D3 in 30 epileptic outpatients. They had been treated for at least 1 year with carbamazepine given as monotherapy. The local bone mineral in the forearms and the total bone mineral was measured before and during treatment with the vitamins (4000 IU/day) for 24 weeks. The bone mineral was not significantly different from controls before the study and it remained unchanged in both treatment groups during the study periods. Similarly, the biochemical indices of bone metabolism were virtually unchanged during the treatment period. We, thus, conclude that epileptic patients on carbamazepine monotherapy have normal bone metabolism.

Topics: Adult; Aged; Bone and Bones; Carbamazepine; Cholecalciferol; Epilepsy; Ergocalciferols; Female; Humans; Male; Middle Aged; Minerals; Osteomalacia; Vitamin D

The incidence of biochemical signs of vitamin D deficiency and the effects of vitamin D supplementation were investigated in 83 children and 95 adults on chronic antiepileptic therapy and 40 mentally retarded controls living under comparable conditions. Low 25-hydroxyvitamin D and serum calcium, and elevated immunoreactive parathyroid hormone and alkaline phosphatase was a common finding in all groups, but in patients on antiepileptic drugs, signs of vitamin D deficiency were recorded more frequently. Supplementation of 125 microgram or 250 microgram vitamin D3 per week for 9 months normalized the laboratory findings in most patients; the effect of 37.5 microgram/week only slightly exceeded the influences of season observed in the controls and in epileptic patients without vitamin D. It is suggested that a dose between 37.5 and 125 microgram vitamin D3/week might be most suitable to avoid biochemical signs of vitamin D deficiency in children and adults on antiepileptic drugs.

Topics: Adolescent; Adult; Aged; Alkaline Phosphatase; Anticonvulsants; Antigens; Calcium; Child; Cholecalciferol; Epilepsy; Female; Humans; Hydroxycholecalciferols; Male; Middle Aged; Parathyroid Hormone; Phosphates; Seasons; Vitamin D Deficiency

Parameters of mineral metabolism were examined in 6 patients with moderately severe anticonvulsant drug-induced osteomalacia. Compared to 15 matched controls, the patients exhibited significantly reduced serum calcium, inorganic phosphate, and 25-hydroxyvitamin D concentration, elevated serum alkaline phosphatase and immunoreactive parathyroid hormone (iPTH) concentration, reduced intestinal 47Ca absorption, reduced urinary calcium and increased urinary hydroxyproline excretion, and reduced forearm bone mass. Intestinal absorption of vitamin D3 was normal. Following 4 months of treatment with vitamin D3 (4000 units/day), serum 25-OHD concentration was increased to 3 times mean normal values and all parameters except serum iPTH, urinary calcium excretion, and forearm bone mass were returned to levels not significantly different from normal. Serum iPTH concentration was reduced by 39% (P less than 0.05); 24-h urinary calcium excretion rose by 98% (P less than 0.001), and forearm bone mass increased by 5.6% (P less than 0.05). It is concluded that moderate-dose vitamin D3 supplementation is effective in normalizing parameters of mineral metabolism in this disorder, despite evidence of resistance to the biologic effects of vitamin D.

Topics: Adult; Alkaline Phosphatase; Anticonvulsants; Bone and Bones; Calcium; Cholecalciferol; Epilepsy; Female; Humans; Hydroxycholecalciferols; Male; Osteomalacia; Parathyroid Hormone; Phosphates

Topics: Adult; Anticonvulsants; Calcium; Cholecalciferol; Creatinine; Epilepsy; Ergocalciferols; Female; Humans; Male; Middle Aged; Time Factors

In 54 epileptic outpatients treated for at least one year with anticonvulsants the bone mineral content (B.M.C.), an estimate of total body calcium, and serum calcium were measured before and during treatment with three doses of cholecalciferol (vitamin D3; 200, 100, and 50 mu-g daily) and 25-hydroxycholecalciferol (25-OHD3; 40, 20, and 10 mu-g daily) for 12 weeks. The results, when compared with the effects of calciferol (vitamin D2; 200, 100, and 50 mu-g daily) in 40 epileptic outpatients, showed different actions in anticonvulsant osteomalacia of vitamin D2 on the one hand and vitamin D3 and 25-OHD3 on the other. In the patients who received vitamin D2 an increase in B.M.C. was found whereas serum calcium was unchanged. The patients who received vitamin D3 or 25-OHD3 showed an increase in serum calcium but unchanged values of B.M.C. The results suggest that liver enzyme induction cannot alone explain anticonvulsant osteomalacia.

Topics: Anticonvulsants; Bone and Bones; Calcium; Cholecalciferol; Enzyme Induction; Epilepsy; Ergocalciferols; Humans; Hydroxycholecalciferols; Liver; Minerals; Osteomalacia

Topics: Alkaline Phosphatase; Bone and Bones; Calcium; Cholecalciferol; Epilepsy; Humans; Hydantoins; Hydroxylation; Osteomalacia; Time Factors; Vitamin D

Topics: Anticonvulsants; Child; Cholecalciferol; Epilepsy; Humans; Rickets

Calcium and folic acid absorption were studied in 28 adult male epileptics on chronic anticonvulsant therapy. In 16 patients on diphenylhydantoin alone, calcium absorption was abnormal in 9. In 12 patients on both diphenylhydantoin and phenobarbital, calcium absorption was abnormal in 3 patients. Folic acid (3H-PGA) absorption was normal in all but one patient, while serum folate (less than 6.4 ng/ml) was reduced in all patients. Hypocalcemia (less than 8.5 mg/100 ml) occurred in only 2 patients, while serum alkaline phosphatase was elevated in 7 patients. These findings support the proposal that rickets and osteomalacia reported in patients on chronic anticonvulsant therapy results from reduced calcium absorption. The effect of these drugs appears to be the acceleration of the metabolism of vitamin D and an increase in the excretion of polar metabolites. This may result in reduced levels of 25-hydroxycholecalciferol and 1,25-dihydroxycholecalciferol which are necessary for normal absorption of calcium. Since calcium absorption may be impaired secondary to a relative vitamin D deficiency, a supplemental increase in vitamin D intake by patients on anticonvulsant drugs is recommended.

Topics: Adult; Aged; Calcium; Cholecalciferol; Epilepsy; Folic Acid; Humans; Male; Middle Aged; Osteomalacia; Phenobarbital; Phenytoin; Rickets; Time Factors

Topics: Adolescent; Alkaline Phosphatase; Anticonvulsants; Calcium; Cholecalciferol; Diet; Enzyme Induction; Epilepsy; Female; gamma-Glutamyltransferase; Humans; Leucyl Aminopeptidase; Liver; Male; Nucleotidases; Phenobarbital; Phenytoin; Phosphates; Primidone; Radiography; Vitamin D Deficiency; Wrist

Topics: Animals; Anticonvulsants; Avitaminosis; Body Weight; Calcium; Calcium Radioisotopes; Cholecalciferol; Enzyme Induction; Epilepsy; Humans; Hypocalcemia; Intestinal Absorption; Liver; Long-Term Care; Mice; Osteomalacia; Phenobarbital; Phenytoin; Rats; Vitamin D

Topics: Anticonvulsants; Cholecalciferol; Epilepsy; Half-Life; Humans; Intestinal Absorption; Kidney; Liver; Osteoporosis

Topics: Age Factors; Alkaline Phosphatase; Animals; Anticonvulsants; Calcium; Cholecalciferol; Enzyme Induction; Epilepsy; Humans; Liver; Osteomalacia; Rats; Vitamin D

Topics: Adolescent; Adult; Anticonvulsants; Carbon Isotopes; Child; Cholecalciferol; Chromatography; Enzyme Induction; Epilepsy; Female; Humans; Hydantoins; Male; Middle Aged; Phenobarbital; Tritium; Vitamin D

Topics: Adult; Aged; Animals; Anticonvulsants; Cholecalciferol; Epilepsy; Female; Humans; Hydroxylation; Intestinal Absorption; Liver; Male; Middle Aged; Osteomalacia; Phenobarbital; Rats; Spectrum Analysis; Tritium

Plasma levels of 25-hydroxycholecalciferol (25-HCC) were measured by a specific competitive protein-binding assay. Mean levels in both normal London adults and adolescent schoolchildren were 16 ng/ml and the mean level in a group of epileptic patients on high-dosage anticonvulsant therapy was 5 ng/ml, (difference from normals P < 0.001). Two further epileptic patients, with well-marked anticonvulsant osteomalacia, were treated with small doses of 25-HCC during full metabolic balance studies; rapid healing followed administration of 25-HCC by mouth in doses of 10-45 mug daily, which is well below the effective dose range of calciferol in this condition. These findings provided further evidence that anticonvulsant osteomalacia results from hepatic enzyme induction which, by increasing the metabolism of cholecalciferol to inactive compounds, lowers 25-HCC levels in patients whose dietary vitamin D intake and exposure to sunlight are otherwise adequate. Results also indicated that under certain circumstances 25-HCC may have considerably stronger antirachitic potency in man than has hitherto been recognized.

Topics: Adolescent; Adult; Anticonvulsants; Binding, Competitive; Calcium; Child; Cholecalciferol; Diet; Enzyme Induction; Epilepsy; Female; Humans; Hydroxycholecalciferols; Liver; Male; Middle Aged; Osteomalacia; Phosphorus; Radioligand Assay; Rickets; Sunlight; Vitamin D

Topics: Adolescent; Adult; Anticonvulsants; Child; Child, Preschool; Cholecalciferol; Epilepsy; Hand; Humans; Leg; Osteoporosis; Radiography