Cases reported "Vitamin D Deficiency"

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1/6. First place winner. Recurrent febrile seizures: an unusual presentation of nutritional rickets.

    Nutritional rickets is a serious disease that is infrequently encountered in the united states today because of the fortification of infant formulas and dairy products with vitamin D. We report a case of undiagnosed nutritional rickets presenting with recurrent febrile seizures. Febrile seizures, a common and usually benign presenting complaint, are not among the symptoms generally known to be associated with rickets. Therefore, the disease was uncovered only after a careful history and physical examination prompted a more thorough investigation into an underlying cause for recurrent seizures. The diagnosis was subsequently confirmed by quantitative laboratory testing. We review the historical and cultural factors, symptoms, and physical findings suggestive of this potentially serious yet easily treatable disease.
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2/6. Loss of seizure control due to anticonvulsant-induced hypocalcemia.

    OBJECTIVE: To report a case of loss of seizure control due to hypocalcemia resulting from long-term treatment with phenytoin and phenobarbital. CASE SUMMARY: A 32-year-old mentally retarded man presented with a 12-month history of loss of seizure control, after being seizure-free for 5 years on a fixed regimen of phenobarbital and phenytoin. He had been institutionalized at the age of 10 years and had received anticonvulsant drugs since he was diagnosed with tonic-clonic epilepsy 20 years ago. On investigation, serum concentrations of the anticonvulsant drugs were within the therapeutic range, indicating adequate medication dosages. serum biochemistry was consistent with vitamin d deficiency: hypocalcemia, reduced 25-hydroxyvitamin D, increased alkaline phosphatase, and increased parathormone. Seizure control was regained after serum calcium had been normalized with administration of vitamin D and calcium. DISCUSSION: Antiepileptic drugs (AEDs) cause vitamin d deficiency through induction of hepatic microsomal enzymes that metabolize vitamin D. Institutionalized subjects are more vulnerable because of the added factors of multidrug therapy, poor diet, reduced exposure to sunlight, and physical inactivity. The resulting hypocalcemia can cause reactive seizures, thus offsetting the anticonvulsant action of the drugs. An objective causality assessment revealed that the adverse reactions of both phenobarbital and phenytoin were probable. CONCLUSIONS: Hypocalcemic seizures are uncommon and underdiagnosed complications of long-term therapy with AEDs. Loss of seizure control in a patient stabilized on AEDs is an indication to check the patient's calcium status. Proper treatment of this complication is vitamin D and calcium supplementation. Prophylactic supplementation with vitamin D is necessary in institutionalized patients treated with AEDs.
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3/6. risk of nutritional rickets among vegetarian children.

    Records of the dietary intake of 52 preschool vegetarian children seen from 1974 to 1976 revealed that macrobiotic vegetarian diets provided amounts of vitamin D, calcium, and phosphorus that were marginal as well as less than the amounts provided by other vegetarian diets. Vitamin D supplements were rarely given. Two subjects had roentgenographic evidence of rickets. The medical histories of 32 children on macrobiotic diets who were examined in 1977 more frequently included prior physical and roentgenographic findings indicative of rickets, whereas those of 17 other vegetarian children did not. Children in the former group were more likely to have elevated levels of serum alkaline phosphatase. Two additional cases of rickets in children consuming a macrobiotic diet confirmed by roentgenograms were brought to our attention during the study.
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4/6. vitamin d deficiency: a risk factor for osteomalacia in the aged.

    Deficiency of vitamin D is rare in the general population of the North American continent because of the availability of sunlight, vitamin D-fortified milk, and over-the-counter preparations containing the vitamin. Yet there are among the aged those who are at risk of developing a deficiency of the vitamin because of lack of exposure to sunlight and failure to ingest milk or vitamin supplements containing vitamin D. Four cases of vitamin D-deficiency osteomalacia are described, demonstrating the various findings in the patient history and the physical, radiologic, and laboratory evaluation. In all cases physiologic doses of the vitamin corrected the abnormality quickly and fully. vitamin d deficiency can be prevented prophylactically once the gerontologist is alert to the fact that some elderly people, who are easily identifiable by history alone, are likely to develop such deficiencies.
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5/6. Symptomatic vitamin a and D deficiencies in an eight-year-old with autism.

    An 8-year-old boy with autism developed a limp and periorbital swelling. He was found to have hypocalcemia and radiographic evidence of rickets. Ophthalmologic examination revealed xerophthalmia and corneal erosions. serum vitamin a was undetectable and serum 25-hydroxyvitamin D was decreased. Dietary history revealed a markedly altered intake consisting of only french fried potatoes and water for several years. All biochemical and physical abnormalities reversed with appropriate supplementation. The nutritional content of french fries is reviewed. Feeding dysfunction is an integral part of autism and closer attention should be paid to potential nutritional deficiencies.
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6/6. Early detection of infants with hypophosphatemic vitamin D resistant rickets (HDRR).

    The onset of physical signs in infants with hypophosphatemic vitamin D resistant rickets (HDRR) has generally been considered to be at the age of 12 months, but the time of appearance of hypophosphatemia and rachitic signs on radiographs remains unclear. We report a prospective study in three neonates whose mothers were HDRR. At birth, despite a low maternal serum inorganic phosphorus (Pi) level, the serum Pi level was normal together with a negligible renal Pi leak in one neonate. At age 3 months, their serum Pi levels, percentages of tubular reabsorption of Pi, and renal tubular maximal rates of Pi reabsorption in relation to the glomerular filtration rate were low except for one infant. Radiographically, their rickets were not apparent at birth but at age 3 months in all. A premature born infant, born at 28 weeks' gestation weighing 1240 g, was diagnosed as HDRR based on hypophosphatemia due to low renal tubular maximal rate of phosphorus reabsorption in relation to the glomerular filtration rate (TmP/GFR) and normal urine Ca excretion at age 5 months. They were initially treated with 1 alpha-hydroxyvitamin D3 (1 alpha OHD3) and later with 1 alpha OHD3 in combination with Pi, which results in healing of the rickets and a normal increase in height. Thus, early detection and treatment of patients born from mothers with HDRR before physical signs of bow-leg and short stature is possible, but the outcome of early treatment requires further study.
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