Cases reported "Hypocalcemia"

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1/10. Primary hypomagnesemia in Thai infants: a case report with 7 years follow-up and review of literature.

    A female Thai baby born to non-consanguineous parents, presented with primary hypomagnesemia at 10 weeks of age, and suffered recurrent convulsions that responded to magnesium supplementation. She was found to have hypomagnesemia (Mg 0.35-1.02 mEq/L) and a low urinary magnesium excretion of less than 10 mg per day, or urinary Mg/Cr that ranged from 0.005-0.01 mg/mg. Intermittent hypomagnesemia and one episode of hypocalcemia with occasional convulsions developed, due to irregular consumption of oral magnesium sulfate, which had a bitter taste, caused frequent loose stools and black staining of the teeth. Better compliance after switching from magnesium sulfate to magnesium oxide resulted in an increased level of serum magnesium and the gradual disappearance of the black staining of the teeth and frequent loose stools. The patient required an oral elemental magnesium dosage of 15-30 mg/kg/day to maintain the serum magnesium level at between 1.02-1.33 mEq/L and keep her free from convulsions. The follow-up period was 7 years during which the patient showed normal physical growth and a mild degree of mental retardation.
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2/10. 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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3/10. 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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4/10. Severe hyperphosphatemia and hypocalcemia following the rectal administration of a phosphate-containing Fleet pediatric enema.

    BACKGROUND: Toxicity secondary to rectally administered hypertonic phosphate solution in patients with normal renal function is rarely reported in the literature. We report a case of electrolyte disturbance and seizure secondary to the rectal administration of 2 Fleet pediatric enemas. CASE REPORT: A 4-year-old white female with spinal muscular atrophy and chronic constipation was brought to the emergency department with complaints of lethargy and difficulty breathing following the administration of 2 Fleet pediatric enemas. In the emergency department, physical examination was significant for a depressed level of consciousness and shallow respirations. A basic metabolic profile was significant for a calcium of 3.3 mg/dL, phosphate of 23 mg/dL, and sodium of 153 mEq/L. Arterial blood gases revealed a pH of 7.24, Pco2 of 38 mm Hg, Po2 of 220 mm Hg. Electrocardiogram revealed a prolonged QT interval of 340 milliseconds with a corrected QT interval of 498 milliseconds. Sixteen hours postexposure, she experienced a generalized seizure unresponsive to multiple doses of lorazepam and responsive only to 100 mg of intravenous calcium chloride. Two days after presentation, the patient experienced complete resolution of symptoms. CONCLUSION: Osmotically acting hypertonic phosphate enemas can result in severe toxicity if retained. This is true even in patients without predisposing risk factors.
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5/10. A case of chromosome 22q11 deletion syndrome diagnosed in a 32-year-old man with hypoparathyroidism.

    Congenital hypoparathyroidism typically manifests with hypocalcemia with or without associated characteristic physical findings and is usually diagnosed during the neonatal period. This report describes an African-American male who was diagnosed at age 32 yr to have dysgenesis of the parathyroid glands due to chromosome 22 microdeletion. Symptomatic hypocalcemia did not develop until age 14 yr, a few weeks after initiation of anticonvulsant therapy for generalized tonic-clonic seizures. Because of the timing for onset of symptomatic hypocalcemia, it was presumed that the patient had anticonvulsant-induced hypocalcemia, and he carried that diagnosis for 18 yr. Chromosome 22q11 deletion syndrome was first suspected at age 32 yr, based on the findings of subtle dysmorphic facial features and a history of learning disability in a patient with PTH-deficient hypocalcemia. The diagnosis was confirmed by fluorescence in situ hybridization analysis.This case underscores the variable clinical presentation of this congenital form of hypoparathyroidism. Chromosome 22q11 microdeletions are relatively common, and the diagnosis should be considered even in adults with hypoparathyroidism because of the potential benefit of genetic counseling.
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6/10. Neonatal seizures and familial hypomagnesemia with secondary hypocalcemia.

    This report describes two female siblings suffering from hypomagnesemia with secondary hypocalcemia, diagnosed at the third and fifth week of age. They both presented with recurrent generalized convulsions. Because their serum calcium levels were low at the early stage, the diagnosis of late-onset neonatal hypocalcemia was mistakenly made. Their seizures did not respond to parenteral calcium initially, but were completely terminated after the administration of magnesium. The possible cause of hypomagnesemia in these two patients was the selective defect of magnesium absorption in the small intestine. Both patients continued to receive daily supplement of magnesium orally to the last follow-up appointment at the ages of 23 and 12 years, respectively. Despite having several generalized seizures before the correct diagnosis and proper treatment, normal physical and mental development was achieved in both patients.
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7/10. Accidental overdose of insufflated colchicine.

    An accidental overdose of colchicine by nasal insufflation occurred when the colchicine was mistaken for methamphetamine. colchicine insufflation is not believed to be a common practice among drug abusers; however, its physical appearance was similar enough to methamphetamine for it to be mistaken for that drug of abuse. In this case a 29-year-old White man presented to the emergency room 3 days after he 'snorted' approximately 200mg of colchicine powder. The colchicine was used as a 'root stimulator' in gardening by the patient's brother and stored in the same cabinet as the methamphetamine. Within 24 hours of exposure the patient began experiencing gastrointestinal distress and myalgia, which eventually prompted him to seek medical attention. The clinical course included hypocalcaemia (69 mg/L--day 5), hypophosphataemia (10 mg/L--day 5) and thrombocytopenia (19 X 10(3)/mm3 - day 8), all of which are consistent with colchicine toxicity. The patient improved with supportive care and electrolyte replacement, and was discharged after an 8-day hospitalisation.
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8/10. Unrecognized hypocalcaemia diagnosed 36 years after thyroidectomy.

    Hypoparathyroidism can present many years after thyroidectomy and symptoms may be non-specific. Hypocalcaemia may cause a variety of physical and mental symptoms and the diagnosis is easily overlooked with serious and potentially fatal consequences. patients with vague symptoms should always be asked about previous thyroid surgery and serum calcium should be measured.
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9/10. Two cases of pseudohypoparathyroidism in adolescent boys.

    pseudohypoparathyroidism (PHP) is characterized by end organ resistance to parathyroid hormone (PTH). PHP type Ia consists of Albright's osteodystrophy and resistance to PTH. In PHP type Ib physical appearance is normal and there is no response to PTH in U-cAMP excretion. In PHP type II both physical appearance and U-cAMP response to PTH infusion are normal. Two adolescent patients with severe hypocalcaemia were treated in our department. The first boy was admitted because of low back pain, latent tetany and recurrent collapsing, the second one due to Grand mal epilepsia. S-Ca concentrations were very low (1.1 and 1.03 mmol/l respectively), CT of the brain revealed multiple calcifications in basal ganglia and S-PTH concentrations were above upper reference level. Therefore the diagnosis of PHP was established. In the absence of skeletal malformations the most probable diagnosis is PHP Ib or II. Clinical state of the boys has dramatically improved after calcium and vitamin D supplementation.
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10/10. Hypocalcemic seizures in neonates.

    A case of a 2-week-old infant who presented to the emergency department (ED) with rapid eye blinking and jerking in the absence of physical abnormalities is presented. hypocalcemia and hypomagnesemia were detected. This case represents the common presentation, therapy, and outcome of neonatal hypocalcemia. It is of particular interest to ED physicians because most of the time the etiology of neonatal seizures can be diagnosed in the ED and appropriate therapy can be immediately instituted.
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