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)

For almost 40 years, diphenylhydantoin has been the preferred drug in the treatment of seizure disorders. Soon after the drug was introduced into clinical practice, gingival enlargement was noticed as a side effect and, despite much research effort, the etiology of this condition remains unknown. More recently, diphenylhydantoin-induced osteomalacia and the teratogenic effects of the drug have been reported. Recent advances in our knowledge of these conditions will be discussed and future directions for research will be outlined.
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PMID:Side effects of diphenylhydantoin: a review. 20 71

Anticonculsant drug-induced disorders in mineral and bone metabolism are apparently quite common. Current evidence indicates that these drugs derange bone metabolism, both through induction of increased hepatic catabolism of vitamin D and its biologically active products, as well as by direct effects on membrane cation transport systems. The significant clinical manifestions of the disorder include rickets with defective bone development, decreased bone mass with increased risk of pathological fracture and reductions in serum calcium levels which may predispose to increased seizure frequency. There is a broad range of clinical presentation with a number of factors -- drug dose, duration of therapy, vitamin D intake, amount of sunlight exposure, degree of physical activity and presence of other concurrent diseases -- which appear to determine the severity of the clinical manifestations. Current evidence indicates that appropriate vitamin D and calcium supplementation can significantly reduce the clinical manifestations of this disorder. All patients receiving chronic anticonvulsant drug therapy should be carefully evaluted for the presence of drug-induced osteomalacia and treated appropriately with vitamin D. This is especially important in those patients in whom the presence of multiple risk factors indicates an increased likelihood of deranged mineral metabolism.
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PMID:Bone complications of anticonvulsants. 78 46

The incidence of vertebral fractures in 87 epileptic outpatients was 16 per cent. The occurrence of vertebral fractures in epileptics was not correlated to age, state of osteomalacia or to type or number of epileptic seizures.
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PMID:Incidence of fractures of the vertebral spine in epileptic patients. 82 5

Individuals from the Asian sub-continent in the United Kingdom are at particular risk of developing osteomalacia. We report a Gujarati woman who developed osteomalacia whilst taking anticonvulsant drugs; withdrawal of anticonvulsant therapy was followed by a seizure complicated by femoral neck fracture. In patients with other risk factors for osteomalacia, as is the case for Asians living in Britain, anticonvulsant drugs should not be reduced or withdrawn until osteomalacia, which puts the skeleton at increased risk of fracture, and its associated hypocalcaemia, which reduces seizure threshold, have been sought and adequately treated.
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PMID:Osteomalacia should be sought and treated before withdrawal of anticonvulsant therapy in UK Asians. 157 Feb 56

A case of several severe fractures in one patient following epileptic seizures is reported. The patient suffered from epileptic osteomalacia and responded well to vitamin D treatment. The cause of anticonvulsant-induced osteomalacia and its treatment are discussed.
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PMID:Fractures caused by epileptic seizures and epileptic osteomalacia. 309 34

Relationship of antiepileptics to serum alkaline phosphatase (ALP), serum calcium (Ca) and inorganic phosphate (P) were studied in 172 epileptic patients treated with antiepileptics for clarifying the related factors to produce osteomalacia following antiepileptics administration. Laboratory findings of ALP, Ca, and P were compared with normal value and determined as abnormal by exceeding the normal limit (mean +2SD (ALP), mean-2SD (Ca, P)). The following results were obtained: 1) In the 172 patients, 20 cases (11.6%) showed abnormal value of ALP, 12 cases (7.0%) of Ca and 41 cases (23.8%) of P (Single abnormal groups). On the other hand, 47 cases (27.3%) were found abnormal in two or three of ALP, Ca and P (Combined abnormal group). The rest 52 cases (30.2%) of the patients showed all normal value (Normal group). 2) Abnormal value of ALP and/or Ca were observed mostly before 20 years of age. The patients with abnormal P were more distributed in age than others. 3) The earlier and/or the longer administration of antiepileptics is prone to produce the more abnormal value. 4) Acetazolamide, metharbital, primidone, carbamazepine and mephobarbital were more used in combined group than in normal group, and polypharmaceutical use of these antiepileptics was supposed to be related to the abnormality of ALP, Ca and P. There was no different use of diphenyl-hydantoin and phenobarbital in frequency and amount between combined group and normal group. 5) Mental retardation and epileptic personality changes were observed more frequently in combined abnormal group than in normal group. 6) No significant relations were observed between clinical seizure types, seizure frequencies and abnormal laboratory findings.
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PMID:[Changes in serum levels of alkaline phosphatase, calcium, and inorganic phosphate following antiepileptic therapy (author's transl)]. 732 19

Vitamin D is absolutely essential for the maintenance of a healthy skeleton. Without vitamin D, children develop rickets and adults exacerbate their osteoporosis and develop osteomalacia. Casual exposure to sunlight is the major source of vitamin D for most people. During exposure to sunlight, ultraviolet B photons photolyze cutaneous stores of 7-dehydrocholesterol to previtamin D3. Previtamin D3 undergoes a thermal isomerization to form vitamin D3. Increased skin pigmentation, changes in latitude, time of day, sunscreen use, and aging can have a marked influence on the cutaneous production of vitamin D3. Once vitamin D3 is formed in the skin or ingested in the diet, it must be hydroxylated in the liver and kidney to 1,25-dihydroxyvitamin D3 [1,25(OH)2D3]. It is now recognized that a wide variety of tissues and cells, both related to calcium metabolism and unrelated to calcium metabolism, are target sites for 1,25(OH)2D3. 1,25(OH)2D3 stimulates intestinal calcium absorption and mobilizes stem cells to mobilize calcium stores from bone. Noncalcemic tissues that possess receptors for 1,25(OH)2D3 respond to the hormone in a variety of ways. Of great interest is that 1,25(OH)2D3 is a potent antiproliferative and prodifferentiation mediator. As a result, 1,25(OH)2D3 and its analogs have wide clinical application in such diverse clinical disorders as rheumatoid and psoriatic arthritis; diabetes mellitus type I; hypertension; cardiac arrhythmias; seizure disorders; cancers of the breast, prostate, and colon; some leukemias and myeloproliferative disorders; chemotherapy-induced hair loss; and skin rejuvenation as well as skin diseases like psoriasis and ichthyosis.
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PMID:Noncalcemic actions of 1,25-dihydroxyvitamin D3 and clinical applications. 857 91

Bone loss leading to osteoporosis is common after the menopause and in the elderly but uncommon in normal young adults without predisposing factors. The risk factors usually associated with osteoporosis include a family history of osteoporosis or fractures, aging, prior diseases, sedentary lifestyle, low calcium intake, hypogonadism, vitamin D deficiency, smoking, and excessive alcohol consumption. However, the issue of drugs has to be considered in 'normal' individuals who present with osteoporosis or bone loss without predisposing genetic or other environmental factors. The list of drugs is extensive and includes, amongst others, glucocorticoids, thyroid hormone (excess), alcohol, medroxyprogesterone acetate, luteinizing hormone-releasing hormone agonists, anti-seizure medications, cyclosporine A, aluminium, lithium, and exchange resins. This paper reviews the pathophysiology and mechanisms of drug-induced bone loss, which includes osteoporosis and osteomalacia, and treatment concepts. Undoubtedly, physician awareness, appropriate investigation, careful prescribing, monitoring, and proper therapy for this eminently preventable side effect can preserve bone in the patients receiving bone-losing drugs.
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PMID:Drug-induced bone loss. 1109 67

Rickets usually occurs in the first two years of life and in puberty since metabolic demand is increased due to rapid growth in these two critical periods of life, when peak bone mass is achieved. Rickets remains one of the most prevalent pediatric diseases in developing countries. Although it is considered to have disappeared in developed countries, there is increasing evidence of widespread vitamin D deficiency among immigrants. There are many reports on rickets and osteomalacia in Asian infants, adolescents and pregnant women moving from India, Pakistan and Bangladesh to developed countries with a cooler climate. We describe three teenagers of Pakistani origin. Clinical presentation included limb pains, muscular weakness, knock-knees and seizures. In all three patients, biochemical findings included hypocalcemia, raised serum parathormone and alkaline phosphatase, and reduced 25-hydroxy vitamin D concentrations. After vitamin D treatment and dietary counseling, biochemical findings returned to normal and their symptoms improved. Given the recent increase in the number of immigrants to Spain, this forgotten disease will probably reappear.
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PMID:[Rickets in Asian immigrants during puberty]. 1219 51

Four noninstitutionalized patients, 4 months - 51 years old, presented out of 421 patients with epilepsy seen within a period of 2 years with serious symptoms of vitamin D deficiency secondary to chronic antiepileptic drug therapy. Presenting symptoms included exacerbation of seizure activity, status epilepticus, carpopedal spasms, fractures, osteomalacia, and rickets. All had low serum calcium and low vitamin D levels. Our experience supports the practice of screening patients on chronic antiepileptic drug therapy for vitamin D abnormalities.
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PMID:Symptomatic antiepileptic drug associated vitamin D deficiency in noninstitutionalized patients: an under-diagnosed disorder. 1529 60


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