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)

We report one case of amicrobic pustulosis cured with Dedrogyl (25-hydroxycholecalciferol), active metabolite of the vitamin D. The importance of our case stems from the physiopathologic study of this cure. The patient is a 16-year-old boy suffering from a hypoparathyroidism since his younger days. Consequently, he shows a hypocalcemia and convulsive seizures due to the hypoparathyroidism. Those seizures had been wrongly attributed to a primary epilepsy of a neurologic origin and a treatment with Phenobarbital had been instituted. In fact, they were side-effects of the hypoparathyroidism and the Phenobarbital had only aggravated the hypoparathyroidal hypocalcemia as a result of its effect on the metabolism of the vitamin D (deviation of this metabolism by enzyme induction at the level of the liver). The Dedrogyl (25-hydroxycholecalciferol) has restored a normal phospho-calcium balance and the hypocalcemia has disappeared as well as the convulsive seizures which, one year later, had not reappeared while they had previously been continual. And above all, standing back one year, we have recorded a complete cure of the amicrobic pustulosis on account of the Dedrogyl.
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PMID:[Amicrobic pustulosis hypoparathyroidism epilepsy: treatment by 25-hydroxycholecalciferol]. 723 92

Primary hypoparathyroidism was diagnosed in six dogs with profound hypocalcemia. Muscle tremors, tetany, generalized seizures, ataxia, and behavioral aberrations were the most common clinical signs. Lymphocytic parathyroiditis was found in four of five dogs that were biopsied. The serum concentration of immunoreactive parathyroid hormone was abnormally low in one dog in which it was measured. Treatment with vitamin D and calcium was successful in restoring and maintaining normal concentration of serum calcium in all six dogs. During treatment, large daily doses of vitamin D were required, dose response was unpredictable, serum calcium concentration fluctuated while treatment remained unchanged, and hypercalcemia occurred frequently.
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PMID:Primary hypoparathyroidism in the dog. 735 61

At the Aga Khan Hospital (AKUH), 65 infants presented with hypocalcaemic seizures, subsequently found to have rickets. Forty-six infants less than 6 months were totally or predominantly breast fed. In a subgroup of 15 mothers and their infants, we found very low plasma levels of 25(OH) vitamin D of < 5 micrograms/l and 7.5 +/- 3.3 micrograms/l, respectively. Neither mothers nor infants received vitamin D supplementation. Maternal vitamin D deficiency and non-supplementation in the infants were the likely causes of rickets in our patients. Prophylactic vitamin D 400 i.u. administered to infants up to 2 years and 800 i.u. to women in pregnancy and during lactation is recommended to prevent vitamin D deficiency.
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PMID:Vitamin D deficiency rickets in breast-fed infants presenting with hypocalcaemic seizures. 748 23

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

Clinical signs that included lethargy, inappetence, diarrhea, and vomiting and that progressed to seizures were observed in 40 feeder pigs that were approximately 70 days old. The pigs were fed ground red wheat and whole milk and were housed in a barn that did not allow exposure to direct sunlight. Analysis of samples of feed obtained from the farm indicated inadequate quantities of calcium and phosphorus as well as a low ratio of these 2 nutrients. Serum and tissue concentrations of vitamin A were less than normal. Low serum calcium concentrations, high serum phosphorus concentrations, and high alkaline phosphatase and creatine kinase activities were compatible with low vitamin D concentrations.
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PMID:Seizures and acute death attributable to hypovitaminosis A and suspected hypovitaminosis D in feeder pigs. 849 85

A 30 year-old, mentally retarded female presented with uncontrolled seizures. The diagnosis of pseudohypoparathyroidism was established on grounds of clinical, laboratory and radiological evaluation. Despite normalization of serum calcium levels with vitamin D treatment, the patient continued to suffer from frequent convulsions. The possible pathogenesis of the therapy-resistant seizures and the therapeutic approach are discussed.
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PMID:Therapy-resistant seizures in pseudohypoparathyroidism. A case report. 852 Nov 97

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

We describe a child with vitamin D dependent rickets type 1, who developed clinical signs of the disease at three months of age. The principal manifestations were hypocalcemia and seizure with EEG abnormalities. The circulating level of 1 alpha, 25 (OH)2D3 was low despite a normal level of 25 (OH)D3 and an adequate vitamin D supplementation. The patient responded to calcium gluconate infusions and pharmacologic doses of 1 alpha, 25 (OH)2D3 and a normalization of calcemia was obtained. After six months the therapy was progressively reduced to physiological dosage with optimal metabolic control. The patient is now 2.5 years old and receive a maintenance dose of calcitriol of 0.125 mcg/day. His clinical, biochemical and radiologic features are normal.
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PMID:[Vitamin D-dependent type-1 rickets: diagnosis and treatment of a further case]. 876 87

To assess the current picture of vitamin D deficiency, we reviewed all 17 cases of vitamin D-deficiency rikets seen in the referral clinic of a children's hospital in Toronto between 1988 and 1993. The diagnosis was made at 7 to 33 months of age. All the children were symptomatic all had biochemical and radiographic abnormalities, two suffered hypocalcemic seizures, and all had bowing of the extremities. Twelve of the children were born to parents who were recent immigrants to Canada. All were of Asian or African origin with dark skin. All the children had been exclusively breastfed with no vitamin D supplementation, and had had little or no sunlight exposure. All the patients responded to vitamin D therapy. We conclude that vitamin D-deficiency rickets remains an environmental/nutritional deficiency disease in this city and that efforts at prevention should target children with pigmented skin from families who are recent immigrants.
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PMID:Persistence of Vitamin D-deficiency rickets in Toronto in the 1990s. 909 96

Although nutritional rickets remains a problem primarily in developing countries, children in northern climates in developed countries may also be at risk. We reviewed the case histories of five children diagnosed in Alaska during 1993-96. Three of the children were black and two Alaska Native. Their ages ranged from 11 to 20 months and they presented during January, April, and September. All of the children were breast-fed but only two received their milk intake exclusively from breast milk. The presenting complaint included abnormal gait in two children and seizures, bowed legs, and growth delay in one child each. All five children demonstrated a decrease in their height-for-age percentile. The most common physical finding was a rachitic rosary which was present in four children. In Alaska, all black and Alaska Native children (and other more pigmented children) less than two years of age who receive all or part of their milk intake from breast milk should receive vitamin D supplementation regardless of the time of year.
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PMID:Nutritional rickets among breast-fed black and Alaska Native children. 947 10


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