Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vitamin D deficiency has re-emerged as a significant paediatric health issue, with complications including hypocalcaemic seizures, rickets, limb pain and fracture. A major risk factor for infants is maternal vitamin D deficiency. For older infants and children, risk factors include dark skin colour, cultural practices, prolonged breastfeeding, restricted sun exposure and certain medical conditions. To prevent vitamin D deficiency in infants, pregnant women, especially those who are dark-skinned or veiled, should be screened and treated for vitamin D deficiency, and breastfed infants of dark-skinned or veiled women should be supplemented with vitamin D for the first 12 months of life. Regular sunlight exposure can prevent vitamin D deficiency, but the safe exposure time for children is unknown. To prevent vitamin D deficiency, at-risk children should receive 400 IU vitamin D daily; if compliance is poor, an annual dose of 150,000 IU may be considered. Treatment of vitamin D deficiency involves giving ergocalciferol or cholecalciferol for 3 months (1000 IU/day if < 1 month of age; 3000 IU/day if 1-12 months of age; 5000 IU/day if > 12 months of age). High-dose bolus therapy (300,000-500,000 IU) should be considered for children over 12 months of age if compliance or absorption issues are suspected.
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PMID:Prevention and treatment of infant and childhood vitamin D deficiency in Australia and New Zealand: a consensus statement. 1694 23

Only one prospective, controlled study has compared the risk of accidental injury in persons with epilepsy to controls without seizures. A mildly increased risk in the epilepsy group was found, predominantly due to injuries that result directly from a seizure. With regard to injury type, this study found significantly higher rates of only head and soft tissue injury; however, most injuries were minor. Several retrospective, population-based studies have suggested increased rates of more serious injury types. Submersion injury has a high mortality; the risk of submersion in children with epilepsy is 7.5-13.9 fold higher than in the general population. The risk of fracture is elevated approximately twofold, either resulting directly from seizure-induced injury or predisposed by drug-induced reduction in bone mineral density. Burns due to seizures account for between 1.6% and 3.7% of burn unit admissions. The risk of motor vehicle accidents in drivers with epilepsy also appears increased, albeit marginally. Several factors predispose to a higher risk of injury among those with epilepsy. Seizures resulting in falls increase the risk of concussion and other injuries. Higher seizure frequency, lack of a prolonged seizure-free interval, comorbid attention deficit disorder, or cognitive handicap may also increase the risk of injury. While some restrictions are necessary to protect the safety of the person with epilepsy, undue limitations may further limit achievement of independence. Given the high morbidity and mortality of submersion injury, those with active epilepsy should bathe or swim only with supervision; however, showering is a reasonable option. Appropriate vitamin D and calcium supplementation and periodic measurement of bone mineral density in those at risk for osteopenia are recommended.
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PMID:Epilepsy-related injuries. 1704 32

The diagnosis of hypoparathyroidism with neurological findings occurring years after thyroid surgery is considered to be rare. The authors describe 3 cases of hypoparathyroidism associated to brain calcifications diagnosed many years after partial thyroidectomy. Two patients were admitted to Emergency Services presenting with seizures, without a previous diagnosis of hypoparathyroidism. The diagnosis was suspected adding the biochemical analysis to the scar on the neck. The CT, which was performed more than 20 years after surgery, showed large cerebral calcifications in both cases. The third patient did not have neurological symptoms, but presented basal and cerebellar calcifications that were demonstrated in the CT. All patients were treated with calcium and vitamin D with great improvement of clinical status. Adding to a case published previously, we count 4 cases from the same region. Thyroidectomies were very common in this region poor in dietary iodide. Since the clinical follow up was inadequate, we suspect that undetected cases similar to these may exist in the present moment.
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PMID:[Cerebral calcifications due to hypoparathyroidism: considerations about cases diagnosed many years after partial thyroidectomy]. 1722 Nov 23

This article reviews research on the use of diet, nutritional supplements, and hormones in the treatment of epilepsy. Potentially beneficial dietary interventions include identifying and treating blood glucose dysregulation, identifying and avoiding allergenic foods, and avoiding suspected triggering agents such as alcohol, aspartame, and monosodium glutamate. The ketogenic diet may be considered for severe, treatment-resistant cases. The Atkins diet (very low in carbohydrates) is a less restrictive type of ketogenic diet that may be effective in some cases. Nutrients that may reduce seizure frequency include vitamin B6, magnesium, vitamin E, manganese, taurine, dimethylglycine, and omega-3 fatty acids. Administration of thiamine may improve cognitive function in patients with epilepsy. Supplementation with folic acid, vitamin B6, biotin, vitamin D, and L-carnitine may be needed to prevent or treat deficiencies resulting from the use of anticonvulsant drugs. Vitamin K1 has been recommended near the end of pregnancy for women taking anticonvulsants. Melatonin may reduce seizure frequency in some cases, and progesterone may be useful for women with cyclic exacerbations of seizures. In most cases, nutritional therapy is not a substitute for anticonvulsant medications. However, in selected cases, depending on the effectiveness of the interventions, dosage reductions or discontinuation of medications may be possible.
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PMID:Natural approaches to epilepsy. 1739 65

Falls occur commonly in older persons and are the seventh leading cause of death. Falls are associated with functional deterioration and "fear of falling". Falls can be due to extrinsic factors such as poor lighting, throw rugs and other environmental hazards. Intrinsic causes of falls include physiological changes associated with aging, orthostatic hypotension, many medications, delirium, anemia, diabetes mellitus, Parkinson's disease, depression, cognitive impairment, syncope, partial complex seizures and vitamin D deficiency. Management of falls requires a multidisciplinary approach with a home assessment and modification where appropriate, a careful geriatric assessment, exercise programs focusing on balance, resistance and endurance exercise and adequate vitamin D replacement. All fallers should be assessed and treated for osteoporosis. The complexities of the causes and management of falls, make persons with frequent falls an ideal person to be referred for a geriatric consult.
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PMID:Falls--where do we stand? 1741 Aug 28

Published reports of studies on the long-term effects of anti-epileptic drugs (AED) on bone--its density, thickness, vitamin D metabolism and risk of fracture--have shown considerable methodological inadequacies (34). Despite these problems it has been clearly shown that patients with epilepsy who are on anti-epileptic drugs have a greater than normal risk of bone loss, abnormal mineralization and fractures. A patient on long-term treatment with AED has a two- to three-fold risk of sustaining a fracture. On average 50% of patients (ranging from 4-70% in different studies [18]) have an osteopathy (34). Type, dosage and duration of AED treatment determine the exact picture of the osteopathy--regardless of whether or not they are enzyme-inducing. Among the enzyme-inducing drugs, especially phenytoin, primidone, phenobarbital and carbamezapine have been investigated for their influence on vitamin D metabolism. Bone loss has also been noted even without evidence of vitamin D deficiency. Mixed forms of osteoporosis and osteomalacia occur particularly often and must be taken into account in any differentiated form of treatment. But the question remains unanswered whether current AEDs, such as lamotrigine, gabapentin or levetiracetam will cause little or no osteopathy. Comparable to the situation during long-term systemic administration of glucocorticoids, initial diagnosis, including the inexpensive dual-energy X-ray absorptiometry (DXA) and the serum concentration of 25-hydroxyvitamin D, must be obtained to determine whether initially there are any bone changes. In addition to a differentiated and clearly defined treatment of osteopathy in a patient with epilepsy, the aim must be to minimize the tendency towards seizures and their severity. The annual cost of adequate vitamin D substitution is about EUR 50, while biphosphonate treatment costs about EUR 500; the costs of vertebral or forearm fractures are about EUR 1000 and those of hip fracture about EUR 15,000. These figures exclude the costs of rehabilitation, nursing care and loss of earnings. Looked at in this way, the problem of AED-induced osteopathy has been underestimated. Yet it is actually preventable and--if already present--can be efficaciously and inexpensively treated when the new guidelines of the (German) Joint Organization of Osteology are followed. The prerequisite of rational treatment is a diagnostically clear distinction of osteoporosis and osteomalacia, but mixed forms are common. ("osteoporomalacia"). Further investigations of more recently developed AEDs (e.g. gabapentin, lamotrigine or levetiracetam) regarding their damaging action on bone during their long-term administration is essential. Systematic control of the state of bones in all patients on long-term treatment with AEDs is nowadays recommended without qualification, even though some study data are unsatisfactory or even lacking.
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PMID:[Antiepileptic drug-induced osteopathy. Subtypes, pathogenesis, prevention, early diagnosis and treatment]. 1758 32

Maternal vitamin D insufficiency is not uncommon. Infants born to mothers who are deficient in vitamin D and or calcium, usually due to cultural modifications in their diets or clothing habits, and in addition are breastfed, are at risk of developing vitamin D deficiency and hypocalcaemia. We present a case of neonatal hypocalcaemic seizures secondary to vitamin D deficiency. Rickets in children resulting from vitamin D deficiency is well documented. It is also becoming clear that there is a positive correlation between maternal vitamin D status during pregnancy and lactation and the development of rickets both in infancy and childhood. The correlation between maternal vitamin D, neonatal vitamin D and hypocalcaemia is not well documented.
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PMID:Maternal vitamin D deficiency associated with neonatal hypocalcaemic convulsions. 1788 Jun 94

Special treatment considerations are warranted in women with epilepsy, particularly those of childbearing age. Treatment guidelines generally recommend the use of antiepileptic drug (AED) monotherapy at the lowest dose possible during pregnancy. The UK Epilepsy and Pregnancy Register reported that the risk for major congenital malformations is higher with AED polytherapy than with monotherapy (6.0% vs 3.7%, respectively) and that valproate carries the highest individual risk. The AEDs that induce hepatic cytochrome CYP450 enzymes carry particular concern both before and after pregnancy. Hepatic enzyme inducers alter steroid metabolism in women receiving oral contraceptives, increase the risk for contraceptive failure, and interfere with calcium absorption and vitamin D metabolism, thus increasing the risk for osteoporosis and fractures. Vitamin K deficiency is another potential consequence of treatment with a hepatic enzyme-inducing AED, increasing the risk for coagulopathy and neonatal intraparenchymal and intracerebral hemorrhage during the first 24 hours of life. Supplemental vitamin K therapy during the last month of pregnancy is warranted. Preconceptional and gestational folate supplementation may also be warranted to prevent neural tube malformation related to AED treatment. Because AED pharmacokinetics may be altered during pregnancy, plasma AED concentrations should be measured before conception and monthly during pregnancy to prevent seizure breakthrough.
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PMID:Importance of monotherapy in women across the reproductive cycle. 1807 Nov 52

Diseases of the bone are becoming increasingly prevalent. Persons with epilepsy treated with antiepileptic drugs (AEDs) are at greater risk as evidenced by changes in bone turnover, osteoporosis, alterations in bone quality, and fracture. Biochemical indices of bone and mineral metabolism including calcium, vitamin D, parathyroid hormone, and bone turnover markers can be affected. AED exposure is a cause of secondary osteoporosis with decreased bone mineral density (BMD) secondary to poor bone accrual in children or accelerated bone loss in adults. Early reports described osteomalacia, a change in bone quality with increased unmineralized bone. Recent studies do not reveal osteomalacia, but there may be more subtle changes in bone quality. Multiple studies have found an increased risk of fractures in association with epilepsy and AED exposure. Cytochrome P450 enzyme inducing AEDs are most commonly associated with a negative impact on bone, but studies also suggest an effect of valproate. There is limited data regarding the newer AEDs. No single mechanism has emerged to explain all the changes in bone in association with epilepsy and AEDs. Although multiple therapies are available for the treatment of bone disease, there is limited study in persons with epilepsy. It is recommended that all persons obtain adequate amounts of calcium and vitamin D. In addition BMD screening is warranted for persons with long-term AED exposure particularly if they have other risk factors for bone disease.
Seizure 2008 Mar
PMID:Bone health in people with epilepsy: is it impaired and what are the risk factors? 1818 47

At Ataturk University Hospital, eight infants who presented with hypocalcaemic seizures were subsequently found to have rickets. Their mothers had osteomalacia. Neither mothers nor infants received vitamin D supplementation. Maternal vitamin D deficiency and non-supplementation in the infants were causes of rickets in these patients. It is recommended that neonatal hypocalcaemia may be due to maternal vitamin D deficiency and all unsupplemented vitamin D infants presenting with seizures should be investigated for rickets.
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PMID:Congenital rickets presenting with hypocalcaemic seizures. 1819 43


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