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)

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

This study aimed to investigate the relationship between 25-hydroxyvitamin D [25(OH)D)] and parathyroid hormone (PTH) levels in adolescent females residing in a northern climate. Concern regarding vitamin D status in this population is due to limited sunlight exposure in northern latitudes, decreased outdoor recreational activities, as well as decreased conversion in black girls from increased skin pigmentation. In this cross-sectional analysis, serum samples were assayed for 25(OH)D using competitive protein binding (CPB) assay and PTH with immuno-radiometric (RIA) procedures. Four hundred postmenarcheal females (12-18 years) residing in northeastern Ohio were recruited. Subjects were excluded if they had a history of bone, kidney, or liver disease, or used medications that affect bone. The primary goal was to determine serum 25(OH)D concentrations in relation to circulating PTH levels in a population of adolescent girls. The Spearman correlation test was used to compare PTH and 25(OH)D. Fit multiple split models were run to determine change in slope of the regression line when 25(OH)D and PTH were plotted. Analysis of variance was determined using modeled means with differences by race and season in the final model. Unadjusted mean serum 25(OH)D and PTH levels were 55.0+/-30.4 nmol/l and 39.4+/-20.6 ng/l, respectively. Blacks had lower 25(OH)D and higher PTH compared with non-blacks (P<0.0001), especially during the winter months. Decreasing 25(OH)D was inversely correlated with PTH (r=-0.314) (P<0.0001), and at concentrations of 25(OH)D < or =90 nmol/l, an increase in PTH was observed. Adolescents are at risk for decreased serum 25(OH)D concentrations, especially black girls. We found that the widely used cutoff for vitamin D deficiency is associated with increasing PTH levels and is below the inflection point for a change in the slope of the regression line. Our results support the need for further research to establish optimal vitamin D status in adolescent girls.
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PMID:Low levels of 25-hydroxy vitamin D are associated with elevated parathyroid hormone in healthy adolescent females. 1517 48

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

We analyzed the characteristics of young infants diagnosed with vitamin D deficiency in early infancy at 2 medical centers in Turkey. In this retrospective, cross-sectional study, the clinical, biochemical, and radiographic findings of infants who were diagnosed with vitamin D deficiency at <3 mo of age between May 2001 and May 2003 were reviewed. A total of 42 infants (27 boys and 15 girls) were diagnosed with vitamin D deficiency in the first 3 mo of life during this 2-y period. The age of infants at diagnosis was 60 +/- 19 d (range 32-112 d). The majority (78.7%) presented with seizures. No skeletal deformities were detected clinically, and radiological findings were subtle. All infants had low serum calcium levels but serum phosphorous levels varied. Eight infants (19.0%) had low, 19 (45.3%) had normal, and 15 (35.7%) had elevated serum phosphorous levels. Serum 25-hydroxyvitamin D levels in those measured (29 infants and 15 mothers) were <37.5 nmol/L. Most infants (83%) were exclusively breast-fed without supplemental vitamin D, and none of the mothers were supplemented with vitamin D during pregnancy. All mothers had limited sunlight exposure and 33 of 42 mothers (78.6%) wore concealing clothing. The majority of young infants diagnosed with vitamin D deficiency present with seizures, have low dietary vitamin D intake, and mothers with poor vitamin D reserves. Evaluation of vitamin D status should be included into the workup of hypocalcemia in early infancy. Prevention of deficiency by supplementing pregnant women and infants who are exclusively breast-fed is essential.
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PMID:Vitamin D deficiency in early infancy. 1567 Dec 26

The case reports a neonate (twin 2 of a twin girl pregnancy) presenting with seizures due to hypocalcaemia. The presumptive cause of the hypocalcaemia was maternal hyperparathyroidism with concurrent vitamin D deficiency. The first twin remained free of hypocalcaemia and was vitamin D replete, despite similar exposure in the pregnancy and similar postnatal care.
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PMID:Maternal primary hyperparathyroidism: discordant outcomes in a twin pregnancy. 1648 95

This report is based on observations during the conduct of a study of hypocalcemia in infants and children. In a study of 50 cases, 13 exclusively breast fed infants manifesting with hypocalcemic seizures were confirmed to have vitamin D deficiency. None of the 13 infants had received vitamin D supplementation. All of them had biochemical evidence of hyperparathyroidism and low levels of 25 (OH) Vit D3 and promptly responded to therapy with vitamin D and calcium. All the mothers of these 13 infants had low levels of 25 (OH) Vit D3. Mothers of 5 infants had reported reduced exposure to sunlight due to religious reasons. This report emphasizes the need to supplement Vitamin D in exclusively breast fed infants and also to encourage exposure to sunlight in them and their mothers.
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PMID:Hypocalcemia due to vitamin D deficiency in exclusively breastfed infants. 1658 20

The epidemic scourge of rickets in the 19th century was caused by vitamin D deficiency due to inadequate sun exposure and resulted in growth retardation, muscle weakness, skeletal deformities, hypocalcemia, tetany, and seizures. The encouragement of sensible sun exposure and the fortification of milk with vitamin D resulted in almost complete eradication of the disease. Vitamin D (where D represents D2 or D3) is biologically inert and metabolized in the liver to 25-hydroxyvitamin D [25(OH)D], the major circulating form of vitamin D that is used to determine vitamin D status. 25(OH)D is activated in the kidneys to 1,25-dihydroxyvitamin D [1,25(OH)2D], which regulates calcium, phosphorus, and bone metabolism. Vitamin D deficiency has again become an epidemic in children, and rickets has become a global health issue. In addition to vitamin D deficiency, calcium deficiency and acquired and inherited disorders of vitamin D, calcium, and phosphorus metabolism cause rickets. This review summarizes the role of vitamin D in the prevention of rickets and its importance in the overall health and welfare of infants and children.
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PMID:Resurrection of vitamin D deficiency and rickets. 1688 50

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

Nutritional rickets and osteomalacia are reemerging in Western societies, particularly in young children and in adolescents of African or Asian descent. Hypocalcemic seizures resulting from vitamin D deficiency are rare in adolescents, whereas fractures caused by seizures without evidence of direct trauma have not yet been reported in this population. We present an unusual case of secondary bilateral femoral fractures caused by hypocalcemic seizures in a 17-year-old boy with primary vitamin D deficiency. We examine the epidemiology and the clinical presentation of rickets and osteomalacia in the adolescent population, the risk of secondary injuries in patients with seizures, and the evaluation and management of hypocalcemic seizures and primary vitamin D deficiency.
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PMID:Hypocalcemic seizures and secondary bilateral femoral fractures in an adolescent with primary vitamin D deficiency. 1707 97

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


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