Cases reported "Hypocalcemia"

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1/62. Hypocalcemic tetany in a toddler with undiagnosed rickets.

    A 17-month-old black girl presented to the pediatric emergency department with sudden onset of her hands and feet "drawing up." A diagnosis of vitamin d deficiency rickets with tetany was made on a history of exclusive breast-feeding, low serum calcium, phosphorus, and 25-hydroxyvitamin D levels, and bone radiographs. Nutritional rickets should be considered in the differential diagnosis of acute hypocalcemia.
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2/62. Postoperative hypocalcemic tetany caused by fleet phospho-soda preparation in a patient taking alendronate sodium: report of a case.

    This case report describes a patient who was previously prescribed alendronate (Fosamax) and presented with postoperative hypophosphatemia and hypocalcemic tetany after bowel preparation with Fleet Phospho-Soda. This report suggests that patients taking bone metabolism regulators may not be able to respond appropriately to hypocalcemic stressors.
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3/62. Primary infantile hypomagnesaemia: outcome after 21 years and treatment with continuous nocturnal nasogastric magnesium infusion.

    Primary infantile hypomagnesaemia is an infrequent cause of neonatal hypocalcaemic seizures but one that responds well to magnesium supplementation. We describe a 22-year-old male, first reported at 4 months of age, who is currently free of neurological deficit but has suffered from intermittent hypomagnesaemic tetany and chronic diarrhoea due to large oral magnesium supplements. Hypothesizing that modest hypercalcaemia might prevent the tetany, we conducted a trial of 5 microg/day 1,25(OH)2D3 over 5 days. Despite the resultant increase in calcium, he developed tetany with the reduction of magnesium intake and decline of serum magnesium from 0.63 to 0.39 mmol/l (normal >0.65 mmol/l). After 1,25(OH)2D3 was stopped and the parenteral magnesium injections suspended, 33% of his usual oral supplement was given instead by continuous nasogastric infusion and serum magnesium rose to 0.60 mmol/l. This regimen was better tolerated because of decreased gastrointestinal side-effects and freedom from parenteral injections. We observed that 1,25(OH)2D3 supplements do not promote magnesium retention nor does the resultant hypercalcaemia prevent hypomagnesaemic tetany. CONCLUSION: Continuous nocturnal nasogastric infusion may be considered in lieu of parenteral therapy in primary infantile hypomagnesaemia.
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4/62. A novel activating mutation (C129S) in the calcium-sensing receptor gene in a Japanese family with autosomal dominant hypocalcemia.

    Autosomal dominant hypocalcemia can be caused by activating mutations of the calcium-sensing receptor (CaSR) gene. We experienced two patients (proband and her daughter) with hypocalcemia caused by a missense mutation of the CaSR gene. The proband, aged 25, showed hypocalcemia and hypoparathyroidism from infancy. She had been diagnosed as having idiopathic hypoparathyroidism and had been treated with calcitriol. She gave birth to a female infant at age 24 years. Her daughter was found to have hypocalcemia (Ca, 6.6mg/dl), without seizure or tetany, when she was 7 months old. dna analysis of their CaSR genes showed a novel heterozygous mutation at codon 129 (TGC-to-AGC) with substitution of cysteine for serine (C129S). Familial examination revealed that this mutation had occurred de-novo in the proband. Wild-type and niutant (C129S) CaSR cDNA were transfected into hek293 cells, and intracellular calcium concentrations were measured with a fluorescent calcium indicator. HEK cells transfected with the C129S mutant CaSR gene showed a larger increase in intracellular calcium concentration in response to the change in the extracellular calcium concentration than HEK cells transfected with the wild-type receptor. We conclude that the C129S mutation in the CaSR gene observed in these patients causes autosomal dominant hypocalcemia.
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5/62. Prolonged, symptomatic hypocalcemia with pamidronate administration and subclinical hypoparathyroidism.

    A 62-yr-old woman with thyroid carcinoma metastatic to bone, and a history of subclinical hypoparathyroidism was admitted to the hospital in hypocalcemic crisis 5 wk after receiving iv pamidronate. The patient had tetany and laryngospasm. An electrocardiogram showed junctional rhythm with QT segment prolongation. The patient had previously maintained a low-normal serum calcium on 500-750 mg of calcium carbonate and 600 IU of vitamin D daily. One week after pamidronate administration the patient's calcium and vitamin D supplementation were inadvertently discontinued. She continued to take daily intranasal calcitonin. At the time of her hospitalization for hypocalcemia, the patient's serum calcium was 4.3 mg/dL. The patient received aggressive calcium and vitamin D supplementation. However, her serum calcium remained below 6 mg/dL for a 2-wk period, and took another week to return to the normal range. In this article, we discuss the counterregulatory responses necessary to maintain calcium homeostasis following osteoclast inhibition by bisphosphonates. We also review the risk factors for hypocalcemia following bisphosphonate administration. Pamidronate and other bisphosphonates are becoming an integral part of the management of normocalcemic patients with malignant bone disease. Therefore, awareness of risk factors for hypocalcemia and familiarity with avenues available for protection from potentially catastrophic hypocalcemia are both crucial.
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6/62. Development of hungry bone syndrome after rapid lowering of PTH with intravenous maxacalcitol therapy in a patient with non-uremic secondary hyperparathyroidism.

    A 41 year-old woman complained of general bone pain and polyuria. She did not have Albright hereditary osteodystrophy. Laboratory examination revealed hypokalemia, hypocalcemia, and an elevation of serum intact PTH concentration. The patient was polyuric and relatively hypercalciuric, though her glomerular filtration rate (GFR) was normal. Neither urinary Pi nor cAMP excretion was remarkably promoted by an exogenous PTH load. An iliac bone biopsy revealed osteopenia, active osteoclastic bone resorption, fibrous transformation in bone marrow tissue, and severely disturbed calcification. Although the oral administration of alfacalcidol showed no effects, 3 weeks of intermittent intravenous injection of maxacalcitol therapy decreased the serum intact PTH concentration from 597 pg/ml to 40 pg/ml, and the bone pain was greatly relieved. However, plasma Ca concentration also decreased and symptoms of tetany appeared. pseudohypoparathyroidism type Ib was the most likely diagnosis in this patient. In conclusion, maxacalcitol therapy satisfactorily suppressed parathyroid function in a patient with secondary hyperparathyroidism without uremia. Appropriate Ca supplementation was required to perform it safely.
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7/62. 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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8/62. Transverse leukonychia in severe hypocalcemia.

    We report the case of a 26-year-old man with acral tetany and muscular cramps of the upper limbs associated with hypocalcemia caused by hypoparathyroidism and celiac disease. physical examination revealed a transverse leukonychia which disappeared after treatment with calcium lactogluconate, calcium carbonate and calcitriol. hypocalcemia may induce nail alterations with a double mechanism represented by angiospasm and disorganization of the hard keratin and of the integrin subunits.
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9/62. Hypocalcemic myopathy without tetany due to idiopathic hypoparathyroidism: case report.

    Myopathy due to idiopathic hypoparathyroidism is very unusual. We report on a 30 years-old man referred with complaints of sporadic muscle pain and mild global weakness for 10 years. His physical examination showed normal strength in distal muscle and slightly weakness in the pelvic and scapular girdles with no atrophy. Deep muscle reflexes were slightly hypoactive. Trousseau's and Chvostek's signs were absent. He had bilateral cataract and complex partial seizures. His laboratory tests showed decreased ionised and total calcium and parathyroid hormone and increased muscle enzymes. EMG and muscle biopsy was compatible with metabolic myopathy. After treatment with calcium and vitamin D supplementation he showed clinical, neurophysiological and laboratorial improvement. In conclusion: patients with muscle symptoms, even when non-specific and with normal neurological examination, should have serum calcium checked, as myopathy due to idiopathic hypoparathyroidism, even being rare, is treatable and easy to diagnose.
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10/62. Hypocalcemic generalised seizures as a manifestation of iatrogenic hypoparathyroidism months to years after thyroid surgery.

    Hypoparathyroidism is a relatively common side effect of a thyroidectomy and leads to hypocalcemia. Carpopedal spasm and tetany are typical manifestations and usually occur within weeks after surgery. The first signs can be less typical and include movement disorders such as chorea, as well as symptoms of increased intracranial pressure or epileptic seizures. We describe two cases with generalised tonic-clonic seizures as the first manifestation of postoperative hypoparathyroidism, appearing months and years after thyroidectomy. Iatrogenic hypoparathyroidism needs to be considered in the differential diagnosis of adult-onset, generalised, tonic-clonic seizures even if the thyroidectomy was performed years earlier.
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