cholecalciferol and Seizures

Calcium and phosphorus represent building material for bones. The supplier of these bone minerals is the hormone calcitriol, which originates from vitamin D, itself made by sunshine in human skin. Requirement for bone minerals is highest during phases of rapid growth, and no one grows faster than the foetus and the infant, making them particularly vulnerable. Deprivation of calcium, whether through low calcium intake or low vitamin D, leads to serious health consequences throughout life, such as hypocalcaemic seizures, dilated cardiomyopathy, skeletal myopathy, congenital and infantile rickets, and osteomalacia. These 5 conditions are often summarised as 'symptomatic vitamin D deficiency', are fully reversible but also fully preventable. However, the increasing prevalence of rickets and osteomalacia, and the deaths from hypocalcaemic cardiomyopathy, demand action from global health care providers. Clarification of medical and parental responsibilities is a prerequisite to deliver successful prevention programmes. The foetus and infant have the human right to be protected against harm, and vitamin D supplementation has the same public health priority as vaccinations.

Topics: Calcitriol; Calcium; Calcium, Dietary; Cardiomyopathy, Dilated; Cholecalciferol; Ergocalciferols; Female; Fetal Diseases; Humans; Infant; Infant, Newborn; Osteomalacia; Pregnancy; Pregnancy Complications; Rickets; Seizures; Vitamin D Deficiency; Vitamins

Hypomagnesemia with secondary hypocalcemia (HSH) is a genetic disorder arising from the body's impaired capacity to absorb and retain magnesium (Mg2+) consumed through diet. Consequently, Mg2+ levels in blood are significantly reduced, a condition referred to as hypomagnesemia. Insufficient levels of Mg2+ and calci-um (Ca2+) can lead to neurological complications that manifest during infancy, such as painful muscle spasms (tet-any) and seizures.. We reported a case of HSH involving a 10-year-old male patient from a Han Chinese family. He was admitted due to recurrent convulsions experienced over the past two years. The patient's initial episode occurred two years prior, when he collapsed without apparent cause and exhibited limb numbness, convulsions, and a disordered state of consciousness, accompanied by hypocalcemia. Cranial CT scans revealed multiple symmetrical calcifications in the basal ganglia, corona radiata, and cerebellar dentate nucleus.. During the hospital stay, the patient was administered the following treatments: Calcium Carbonate and Vitamin D3 Tablets (1.5 g of calcium carbonate and 125 IU of Vitamin D3 per tablet, 1 tablet/time) once daily, Calcitriol Soft Capsules (0.25 μg of calcitriol per capsule, 1 capsule/time) twice daily, Potassium Chloride Sustained-release Tablets (0.5 g of potassium chloride per tablet, 1 tablet/time) thrice daily, Potassium Aspartate and Mag-nesium Aspartate Tablets (158 mg of potassium aspartate and 140 mg of magnesium aspartate per tablet, 1 tablet/ time) thrice daily, and intravenous infusions of Magnesium Sulfate Injection (2.5 g/time) twice daily. After three days in the hospital, the patient's initial symptoms subsided, resulting in discharge with a prescription of ongoing oral medications including Calcium Carbonate and Vitamin D3 Tablets, Calcitriol Soft Capsules, and Potassium Aspartate and Magnesium Aspartate Tablets, with the same usage and dosage as the above three drugs. A month subsequent, the serum levels of Mg2+, Ca2+, potassium (K+), and phosphorus were 0.96 mmol/L, 2.52 mmol/L, 4.06 mmol/L, and 1.63 mmol/L, respectively.. Primary HSH is an uncommon manifestation of parathyroid hypoplasia, clinically characterized by low levels of Mg2+, Ca2+, and K+ in the blood. Our findings serve to enrich and consolidate the knowledge for future case studies and follow-up investigations.

Topics: Aspartic Acid; Calcitriol; Calcium; Calcium Carbonate; Child; Cholecalciferol; Humans; Hypocalcemia; Magnesium; Male; Potassium Chloride; Seizures; Tablets

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

Topics: Calcium Gluconate; Cholecalciferol; Humans; Hypocalcemia; Infant; Male; Rickets; Seizures

Nutritional rickets remains a significant public health issue for children worldwide. Although it has almost disappeared in industrialized countries following routine vitamin D supplementation, recent evidence suggests an increasing incidence, especially in young children. In addition to the classical clinical consequences on bone and the growth plate, rickets may also be associated with life-threatening neurological and cardiac complications in the most severe forms. Consequently, early screening and treatment are required. Here, we report the case of a 2-year-old child who presented with severe nutritional rickets associated with seizure and cardiomyopathy. Family screening revealed rickets in all the siblings. This case report emphasizes the importance of being aware of this disease, notably in population with sociocultural risk factors.

Topics: Bone Density Conservation Agents; Calcium Gluconate; Cardiomyopathies; Child, Preschool; Cholecalciferol; Humans; Male; Rickets; Seizures; Treatment Outcome

Topics: Biomarkers; Calcium; Cholecalciferol; Dietary Supplements; Female; Humans; Hyperparathyroidism, Primary; Hypocalcemia; Hypoparathyroidism; Infant, Newborn; Infant, Newborn, Diseases; Male; Pregnancy; Recurrence; Risk Factors; Seizures; Tetany; Time Factors; Treatment Outcome

From a theoretical point of view, cholecalciferol (vitamin D3) as a precursor of calcitriol, a representative of secosteroids, may have neuroprotective properties and affect seizure phenomena.. In the present study, interactions between cholecalciferol and three second generation antiepileptic drugs (oxcarbazepine, lamotrigine, and topiramate) were studied in the maximal electroshock test in mice. Effects of drugs on motor coordination, long-term memory and explorative behavior of animals were evaluated in the chimney test, passive-avoidance task and plus-maze test, respectively.. Cholecalciferol applied ip at doses of 37.5-75μg/kg significantly raised the electroconvulsive threshold. Cholecalciferol, administered at the subthreshold dose of 18.75μg, potentiated the anticonvulsant activity of oxcarbazepine and lamotrigine, but did not change their brain concentrations, therefore the revealed interactions seem to be pharmacodynamic. Furthermore, the action of cholecalciferol was not dependent on its conversion to calcitriol. The anticonvulsant effect of topiramate was enhanced by cholecalciferol applied at the higher dose of 37.5μg/kg, at which it also increased the brain level of topiramate. As regards adverse effects, cholecalciferol, antiepileptic drugs, and their combinations did not significantly impair motor coordination or long-term memory in mice. Moreover, cholecalciferol did not show either anxiolytic or anxiogenic properties.. Our findings show that cholecalciferol has not only its own anticonvulsant action but also enhances efficacy of certain antiepileptic drugs, at least in experimental conditions.

Topics: Animals; Anticonvulsants; Anxiety; Avoidance Learning; Cholecalciferol; Dose-Response Relationship, Drug; Electroshock; Exploratory Behavior; Fructose; Male; Maze Learning; Memory, Long-Term; Mice; Neuroprotective Agents; Seizures; Topiramate; Vitamins

Wilson's disease (WD) is not as rare as once believed, and has a wide range of presentations with equally wide range of age of onset. Sometimes the primary presentation might be unusual and may require a thorough investigation to avoid a misdiagnosis. Our case presented with uncontrolled seizures, severe hypokalemia, renal failure, and hypoparathyroidism. After being diagnosed as WD and treated for the same patient made a remarkable recovery.

Topics: Adolescent; Cholecalciferol; Hepatolenticular Degeneration; Humans; Hypocalcemia; Hypokalemia; Hypoparathyroidism; Renal Insufficiency; Seizures; Treatment Outcome; Vitamins; Zinc Acetate

The interactions between cholecalciferol, a precursor of the active form of Vitamin D(3), and conventional antiepileptic drugs (valproate, carbamazepine, phenytoin, and phenobarbital) were studied in the maximal electroshock test in mice. Vitamin D(3) applied i.p. at doses of 37.5 and 75 mug/kg, but not at 18.75 mug/kg, significantly raised the electroconvulsive threshold. Furthermore, cholecalciferol (at its highest subthreshold dose of 18.75 mug) potentiated the anticonvulsant activity of phenytoin and valproate. The action of carbamazepine and phenobarbital was also enhanced by Vitamin D(3), but when it was given at the higher dose of 37.5 mug/kg. Cholecalciferol, antiepileptic drugs, and their combinations did not produce significant adverse effects evaluated in the chimney test (motor coordination) and passive-avoidance task (long-term memory). Cholecalciferol did not significantly increase the brain concentrations of conventional antiepileptics, indicating a pharmacodynamic nature of revealed interactions. Our findings show that cholecalciferol may play an anticonvulsant role in the brain and can influence the efficacy of antiepileptic drugs, at least in experimental conditions.

Topics: Animals; Anticonvulsants; Avoidance Learning; Carbamazepine; Cholecalciferol; Disease Models, Animal; Dose-Response Relationship, Drug; Drug Synergism; Electroshock; Injections, Intraperitoneal; Male; Mental Recall; Mice; Motor Activity; Phenobarbital; Phenytoin; Seizures; Valproic Acid; Vitamins

Topics: Adolescent; Affective Symptoms; Age Factors; Cardiovascular Diseases; Child; Child, Preschool; Cholecalciferol; Depression; Erythropoiesis; Family; Female; Glomerulonephritis; Growth Disorders; Humans; Infant; Kidney Transplantation; Male; Renal Dialysis; Seizures; Terminal Care; Transplantation, Homologous; Uremia