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)

Acute renal failure secondary to interstitial nephritis caused by therapeutic ingestion of sodium diphenylhydantoins has been reported recently. The interference of sodium diphenylhydantoins on Vitamin D metabolism causing or aggravating ricketts has also been reported. This communication deals with an infant girl who was admitted to the hospital due to seizures. Four months before, she had convulsions and she was treated with diphenylhydantoins until admission. She was found to have renal failure and ricketts. Histological diagnosis of interstitial nephritis was established by means of percutaneous renal biopsy. Clinical and radiological improvement of ricketts was observed after dehydrotachysterol treatment. Clinical and biochemical alterations of renal failure slowly subsided. She had a clear-cut history of vitamin D defficiency ricketts. Seizures were due to hypocalcemia tetany but was erroneusly treated as "grand mal" epilepsy, with diphenylhydantoins. Interstitial nephritis complicated with acute renal failure was probably caused by diphenylhydantoins administration.
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PMID:[Renal failure and rickets]. 46 92

Small doses of vitamin D can probably prevent catastrophic skeletal demineralization in patients taking antiseizure medication. Moderate doses of vitamin D can reverse this degree of demineralization once it has occurred. Prophylactic vitamin D therapy was associated with a lowered incidence of seizure patients in the overall fracture census and a decrease in the number of in-hospital days for treatment of seizure patients with fractures. Vitamin D therapy should probably be used as a routine dietary supplement in all seizure patients at dosage levels of approximately 400 units daily. Much larger doses (50,000 units once or twice weekly) should be as necessary when these patients sustain fractures or other injuries.
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PMID:Vitamin D prophylaxis and the lowered incidence of fractures in anticonvulsant rickets and osteomalacia. 60 87

Vitamin D dependent rickets type II is an autosomal recessive disease caused by the vitamin D defective receptor. More than 200 patients with different types of lower limb deformities were detected in a rural area of the Cauca department in the southwest part of Colombia. Patients were well nourished and in good physical condition in spite of their deformities. None of them presented alopecia, myopathy, seizures or aminoaciduria. Serum analysis showed significantly lower serum calcium as compared to normal relatives, though in the normal low range, normal phosphorus, high alkaline phosphatase, normal 25-hydroxyvitamin D3 and high 1,25-dihydroxyvitamin D3, indicating target organ resistance. The cDNA analysis showed normal nucleotide sequence. We suggest that our patients represent a distinct form of receptor-positive resistance to vitamin D. This report is the first extensive study on this class of patients.
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PMID:Vitamin D dependent rickets type II and normal vitamin D receptor cDNA sequence. A cluster in a rural area of Cauca, Colombia, with more than 200 affected children. 758 52

Pregnanolone [5 beta-pregnan-3 alpha-ol-20-one (5 beta 3 alpha)] and allopregnanolone [5 alpha-pregnan-3 alpha-ol-20-one (5 alpha 3 alpha)] are neuroactive steroids that are reduced metabolites of progesterone. Both 5 beta 3 alpha and 5 alpha 3 alpha are potent positive modulators of the gamma-aminobutyric acid response that enhance the binding of [3H]flunitrazepam ([3H] FNZ) to the gamma-aminobutyric acid type A receptor. Chronic (48 hr) exposure of brain neurons in culture to 5 beta 3 alpha or 5 alpha 3 alpha abolishes potentiation of [3H]FNZ binding by these steroids. This uncoupling, or loss of allosteric interactions between steroid and benzodiazepine recognition sites, is dose dependent, stereospecific, and reversible. The number and affinity of [3H]FNZ binding sites are unaffected. In contrast, the steroids 5 beta-pregnan-3 beta-ol-20-one, beta-estradiol, testosterone, progesterone, deoxycorticosterone, and dexamethasone, which show little capacity to potentiate [3H]FNZ binding, are also much less effective in inducing uncoupling of steroid and benzodiazepine recognition sites. These results suggest a mechanism whereby neurons could become refractory to long term modulation by neuroactive steroids. The results are discussed in terms of their possible relevance to premenstrual anxiety and enhanced frequency of seizures in certain women.
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PMID:Gamma-aminobutyric acidA receptor regulation: chronic treatment with pregnanolone uncouples allosteric interactions between steroid and benzodiazepine recognition sites. 839 20

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

The effects of some neurosteroids on N-methyl-D-aspartic acid (NMDA)-induced seizures were examined in mice. Intraperitoneal (i.p.) administration of 5 alpha-pregnan-3 alpha-ol-20-one (5, 10 and 20 mg/kg). 5 beta-pregnan-3 alpha-ol-20-one (10 and 20 mg/kg), 5 alpha-pregnan-3 alpha-ol-11,20-dione (15 mg/kg), 5 alpha-androstan-3 alpha-ol-17-one (10 mg/kg) and dehydroepiandrosterone sulfate (25 mg/kg) significantly increased the dose of NMDA necessary to induce clonic convulsions in 50% of the tested animals (CD50). Furthermore, 5 alpha-pregnan-3 alpha-ol-20-one, 5 beta-pregnan-3 alpha-ol-20-one, 5 alpha-pregnan-3 alpha-ol-11,20-dione and 5 alpha-androstan-3 alpha-ol-17-one also protected the mice against NMDA-induced mortality. Importantly, it is only at the highest doses that neurosteroids impair motor performance of the animals, as estimated by a rotorod equilibrium procedure. The other neurosteroids tested, such as 5 alpha-pregnan-3 beta-ol-20-one (5-20 mg/kg), 5 alpha-pregnan-3 alpha,21-diol-20-one (10 and 15 mg/kg), 5 alpha-pregnan-3,20-dione (15 mg/kg) and pregnenolone sulfate (12.5-100 mg/kg) had no significant effects on the measured parameters. In another set of experiments, we evaluated the effects of neurosteroids on D-[3H]-aspartate release from rat hippocampal slices. None of the neurosteroids tested exerted a significant effect on basal D-[3H]-aspartate release. On the other hand, K(+)-stimulated D-[3H]-aspartate release was significantly attenuated by 5 alpha-pregnan-3 alpha-ol-20-one, 5 beta-pregnan-3 alpha-ol-20-one, alphaxalone, pregnenolone sulfate and dehydroepiandrosterone sulfate. The effect of 5 alpha-pregnan-3 alpha-ol-20-one was the most potent and was distinctly concentration-dependent, whereas the other compounds were effective only at the highest concentrations used. The above results indicate that some neurosteroids administered in non-sedative doses can protect mice against NMDA-induced seizures and mortality; furthermore, they inhibit D-[3H]-aspartate release in rat hippocampal slices.
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PMID:Protective effects of neurosteroids against NMDA-induced seizures and lethality in mice. 945 34

Vitamin D-deficient rickets is uncommon but becoming more prevalent in the pediatric population likely related to increases in breast-feeding. It should be considered in many clinical situations. We present 3 cases of rickets presenting acutely to the emergency department. Their presentations included a fracture concerning for child abuse, tetany, and hypocalcemic seizures. In all cases, laboratory and radiographic evaluations were consistent with the diagnosis of nutritional rickets and their symptoms were related to rickets resolved with appropriate treatment. Although uncommon, vitamin D-deficient rickets should be considered in children with the above presentations.
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PMID:Variable presentations of rickets in children in the emergency department. 1475 13

Although cases of Vitamin D-deficient Rickets have declined since the Industrial Revolution, certain populations remain at risk. Risk factors for developing vitamin D-deficient Rickets include breast-feeding without formula or vitamin supplementation, very dark skin and inadequate exposure to sunlight. We describe a case of Rickets in a breastfed infant with dark skin who presented with hypocalcemic seizures. The pathophysiology of Rickets is briefly described along with the emergency management of infants presenting with hypocalcemic seizure.
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PMID:Pediatric hypocalcemic seizures: a case of rickets. 1570 11

Here, we study the role of a neurosteroid hormone Vitamin D in epilepsy. To examine this problem, we used 1,25-dihydroxyvitamin D, an active form of Vitamin D, injected subcutaneously to NMRI mice (33 microg/20 microl) 40 min prior to seizures induced by systemic injection of pentylenenetrazole (PTZ, 70 mg/kg). Overall, compared to the vehicle-treated control animals (n=11 in each group), the Vitamin D-treated mice demonstrated reduced severity of PTZ-induced seizures (longer latency, shorter duration and lower mortality). In a separate experiment, we assessed the time-course of antiepileptic effects of 1,25-dihydroxyvitamin D. For this, we injected this compound (33 microg/20 microl) to NMRIx129S1 mice (n=11) 40 min, 3, 6, 12 and 24 h prior to seizures, showing that antiepileptic effects were short-term, almost disappearing 3h after administration. Our findings show that Vitamin D plays a direct anticonvulsant role in the brain and suggest that the Vitamin D endocrine system may represent a new target for the development of anticonvulsant drugs.
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PMID:Anticonvulsant effects of 1,25-dihydroxyvitamin D in chemically induced seizures in mice. 1614 Jan 75

Vitamin D is a neuroactive steroid hormone with multiple functions in the brain. Numerous clinical and experimental data link various Vitamin D-related dysfunctions to epilepsy. Here, we study the role of Vitamin D receptors (VDRs) in experimental epilepsy in mice. To examine this problem, we assessed the seizure profiles in VDR knockout mice following a systemic injection of pentylenetetrazole (70 mg/kg). Overall, compared to the wild-type (WT) 129S1 mice (n=10 in each group), the VDR knockout group significantly demonstrated shorter latencies to the onset, higher Racine scores and increased mortality rates. Our findings suggest that VDRs modulate seizure susceptibility in mice, and that the Vitamin D/VDR endocrine system may be involved in the pathogenesis of epilepsy.
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PMID:Increased severity of chemically induced seizures in mice with partially deleted Vitamin D receptor gene. 1625 71


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