Cases reported "Hypocalcemia"

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1/24. Bilateral femoral neck fractures secondary to hypocalcemic seizures in a skeletally immature patient.

    We report the case of an 11-year-old, skeletally immature boy who sustained bilateral femoral neck fractures during seizure activity. These fractures were due to hypocalcemia. Although this condition is a rare complication of seizures, its early recognition and treatment are essential to minimize complications associated with the delayed treatment of intracapsular hip fractures.
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ranking = 1
keywords = femoral neck fracture, femoral neck, neck fracture, fracture, neck
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2/24. hypocalcemia due to spontaneous infarction of parathyroid adenoma and osteomalacia in a patient with primary hyperparathyroidism.

    A 49 year-old Japanese woman had subjected enlargement of a cervical tumor, and also suffered two bone fractures in 2 years. The cervical tumor had enlarged further in the month prior to admission, becoming warm and tender. Endocrinological examination revealed that the serum intact PTH concentration was remarkably high at 400 pg/mL despite the low serum calcium concentration, and that the serum vitamin Ds concentration was decreased. Bone roentgenograms revealed severe osteolytic changes compatible with osteitis fibrosa cystica and a pathologic fracture of the humerus. Under a diagnosis of primary hyperparathyroidism, parathyroidectomy was performed, followed by fixation surgery for the pathologic fracture. Histologically, the cervical tumor was a parathyroid chief-cell adenoma with massive necrosis, and the bone pathology by iliac bone biopsy revealed the existence of osteomalacia. She was treated with calcium, vitamins D and K2 and calcitonin after the surgery. This case is a rare condition manifesting hypocalcemia with catastrophic osteoporosis under the coexistence of spontaneous infarction of parathyroid adenoma with osteomalacia, suggesting that the clinical features of hyperparathyroidism are modified by both the autoparathyroidiectomy and the existence of osteomalacia due to vitamin d deficiency.
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ranking = 0.0016905116895796
keywords = fracture
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3/24. Fractures due to hypocalcemic convulsion.

    We report on two cases of patients in whom hypocalcemic seizures during hemodialysis led to right scapular body fracture in one and bilateral femoral neck fractures in the other.
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ranking = 0.20033810233792
keywords = femoral neck fracture, femoral neck, neck fracture, fracture, neck
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4/24. Renal magnesium wasting, hypomagnesemic hypocalcemia, hypocalciuria and osteopenia in a patient with glycogenosis type II.

    We describe a patient with late-onset glycogenosis type II with renal magnesium wasting, hypomagnesemic hypocalcemia, hypocalciuria and osteopenia. He was admitted to our hospital for evaluation of lower limb weakness and mild deterioration of liver function. serum magnesium and calcium were low with low-to-normal levels of PTH in the patient. Echocardiogram revealed marked concentric hypertrophy of the left ventricle. An x-ray film of his spine showed a thoracic (Th12) vertebral compression fracture. Bone mineral density of the lumbar spine L2-L4 showed a reduced value. kidney, liver and muscle biopsies were performed. These were found to have histologic features consistent with glycogenosis type II. In addition, accumulation of PAS-positive material in the cytoplasmic vacuoles of the tubular epithelium was present only in the distal tubules. An oral magnesium supplement was useful in helping to correct the hypomagnesemia, despite the presence of renal magnesium wasting in our patient. magnesium supplement was also sufficient to maintain normal serum calcium concentrations. However, the hypocalciuria persisted in our patient despite correction of hypomagnesemia. In conclusion, the consistent association between the glycogen accumulation in distal tubules, renal magnesium wasting, hypomagnesemic hypocalcemia and hypocalciuria, in the absence of other identifiable reasons, suggests a cause-and-result relationship. Also, the combination of renal magnesium wasting, hypomagnesemia and hypocalciuria is a picture similar to that of Gitelman's syndrome in our patient. The glycogen accumulation in distal tubules may cause renal magnesium wasting and hypocalciuria through tubular injury. Therefore, we may speculate that the present case has glycogenosis type II-associated Gitelman's-like syndrome.
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ranking = 0.00056350389652652
keywords = fracture
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5/24. Malignant infantile osteopetrosis initially presenting with neonatal hypocalcemia: case report.

    Autosomal recessive "malignant" osteopetrosis is a rare congenital disorder relating to bone resorption abnormalities. It is believed to arise due to the failure of osteoclasts to resorb immature bone. This leads to abnormal bone marrow cavity formation and, clinically, to the signs and symptoms of bone marrow failure. Impaired bone remodeling associated with dysregulated activity of osteoclasts for such a condition may typically result in bony narrowing of the cranial nerve foramina, which typically results in cranial nerve (especially optic nerve) compression. Abnormal remodeling of primary woven bone to lamellar bone results in "brittle" bone that is prone to fracture. Thus, fractures, visual impairment, and bone marrow failure are the classical features of this disease. We describe the case of a 23-day-old boy in whom neonatal hypocalcemia was present initially after birth. Malignant infantile osteopetrosis (MIO) was diagnosed for the patient at 4 months of age based on evidence of anemia, thrombocytopenia, leukoerythroblastosis, sclerotic bone, hepatosplenomegaly, and visual deficit from a bony encroachment by the cranial nerve foramina. Although only occasionally reported previously, MIO remains essentially unrecognized by clinicians as a cause of neonatal hypocalcemia, which often results in diagnostic confusion and delay. This is important in the context of curative hemopoietic stem cell transplantation where preservation of sight may depend upon early intervention.
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ranking = 0.001127007793053
keywords = fracture
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6/24. Fractures in biliary atresia misinterpreted as child abuse.

    Bone fractures in children without a history of injury are highly suspicious for child abuse. biliary atresia is a disorder associated with metabolic bone disease, and there are numerous reports of osteopenia, rickets, and/or fractures in this population. We report 3 cases of children with biliary atresia who had bony fractures as well as osteopenia whose caretakers were investigated for child abuse. Pediatricians should be aware of an increased incidence of fractures and overall prevalence of bone disease in this population.
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ranking = 0.0022540155861061
keywords = fracture
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7/24. Variable presentations of rickets in children in the emergency department.

    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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ranking = 0.00056350389652652
keywords = fracture
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8/24. celiac disease manifesting as isolated hypocalcemia.

    OBJECTIVE: To describe a patient who presented with hypocalcemia and hypocalciuria as the initial manifestations of celiac disease, despite a normal vitamin D status. methods: We review the diagnostic evaluation, treatment, and biochemical and bone mineral density responses of a patient with asymptomatic celiac disease, which was initially suggested because of a low serum calcium level that became attributable to isolated malabsorption of calcium. RESULTS: A 36-year-old woman presented with hypocalcemia in the presence of normal serum 25-hydroxyvitamin D and high serum 1,25-dihydroxyvitamin D levels. She had hypocalciuria and secondary hyperparathyroidism that were refractory to pharmacologic calcium and cholecalciferol supplementation. Fecal calcium excretion indicated malabsorption of calcium, and biopsy of the small intestine demonstrated pathologic changes characteristic of celiac disease. Bone mineral density, determined by dual-energy x-ray absorptiometry, was in the osteopenic range at the femoral neck. The initiation of a gluten-free diet resulted in correction of all biochemical abnormalities and a substantial increase in bone mineral density. CONCLUSION: Primary intestinal malabsorption of calcium without concomitant vitamin d deficiency is possible in celiac disease because of the preferential involvement of the proximal small intestine early in the disease process. Our patient had hypocalcemia caused by celiac disease and values for serum 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D that were normal and elevated, respectively. Correction was demonstrated after dietary gluten withdrawal.
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ranking = 0.026405358668579
keywords = femoral neck, neck
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9/24. Maternal and fetal outcome after long-term pamidronate treatment before conception: a report of two cases.

    The pregnancies of two women with osteogenesis imperfecta who received intravenous pamidronate before conception are reported. The mothers suffered no ill effects. One baby had transient asymptomatic hypocalcemia and one had bilateral talipes equinovarus. This report documents the pregnancy outcomes of two women with osteogenesis imperfecta (OI), types I and IV, who received intravenous pamidronate as part of an observational trial before conception. Pamidronate was not administered after conception. Other than hyperemesis in one woman, the pregnancies and deliveries were uneventful. Both babies inherited OI from their mothers. The baby with OI type IV also had bilateral talipes equinovarus. Biochemical evaluation of the mothers and babies at 24 h and/or 2 weeks postpartum was normal, apart from one baby with asymptomatic hypocalcemia at 24 h of age that had resolved when next measured on day 11 of life. No biochemistry was available on the second child until 13 days of age. Neither baby had skeletal modeling abnormalities consistent with in utero pamidronate exposure. The lumbar spine (L1-L4) areal BMD and anterior to posterior height ratios of lumbar vertebral bodies of both women remained constant during pregnancy. Both the mothers and babies remain well and free of fracture 14 and 16 months postpartum.
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ranking = 0.00056350389652652
keywords = fracture
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10/24. Cortical myoclonus due to hypocalcemia 12 years after thyroidectomy.

    Although seizures have been described in hypocalcemia, myoclonus has been rarely reported. We report the first case of a patient with hypocalcemic cortical myoclonus due to hypoparathyroidism following a previous thyroidectomy. The patient was an 84-year-old woman who presented with multifocal myoclonus, which was predominant in the upper extremities, neck, jaw, and facial muscles. Electrophysiological studies revealed enlarged somatosensory evoked potentials, cortical reflexes evoked by peripheral nerve stimulation, and a cerebral potential preceding myoclonic jerks determined by jerk-locked averaging. All these findings were consistent with cortical myoclonus. The myoclonic state disappeared as serum calcium level became normal. hypocalcemia should be considered in patients who had had a thyroidectomy, even if it was performed more than 10 years previously.
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ranking = 1.7679447451217E-5
keywords = neck
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