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Query: UMLS:C0036572 (seizures)
80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The case of a neonate is presented who had late onset seizure associated with hypocalcemia, hyperphosphatemia, and raised parathyroid hormone. The infant did not have any stigmata of pseudohypoparathyroidism. The hypocalcemia was initially resistant to calcium therapy, but responded to vitamin D analog therapy. The diagnosis of 'transient neonatal pseudohypoparathyroidism' was entertained, as the infant remained stable and seizure-free with normal serum biochemistry during 8 months of follow-up.
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PMID:Transient pseudohypoparathyroidism and neonatal seizure. 1133 28

Application of a sodium phosphate containing enema caused life-threatening metabolic disorders in a Dachshund and two cats. Clinical signs were characterised by dehydration and various neurological deficits including seizures. Most striking laboratory abnormalities were hypernatremia, hypocalcemia, hyperphosphatemia, and polycythemia. Despite intensive treatment the dog died, whereas the cats recovered completely. In face of possible severe and potentially fatal metabolic abnormalities sodium phosphate enemas, such as Practo-Clyss, should be used with caution or not at all in cats and small dogs.
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PMID:[Life threatening metabolic disorders after application of a sodium phosphate containing enema in the dog and cat]. 1140 50

Neonatal hypocalcemia (NH) is common in the neonatal period. Its cause falls into one of two clinical categories, early NH occurs in first 24-48 hours of life; late NH is observed at the end of the first week of life. NH due to congenital hypoparathyroidism, either permanent or transient, is rare. They both present with hypocalcemia, low levels of intact parathyroid hormones, and hyperphosphatemia. In this paper we report on four cases of neonatal hypocalcemia due to transient hypoparathyroidism. They are all full-term infants with normal birth weights, carried by nondiabetic mothers. The age of onset was 6 days old to 17 days old, there were three male and one female. Seizure was the major symptom except for case 2, who had a high pitch crying, irritability and opisthotonus. Laboratory data revealed calcium: 4.7 to 6.3 mg/dl, phosphorus: 6.8 to 9.2 mg/dl, and magnesium: 1.2 to 2.8 mg/dl. The intact parathyroid hormone levels were abnormally low in two cases (<13 pg/ml and 5.7 pg/ml), yet only subnormal in the other two (25.2 pg/ml and 22.2 pg/ml). Further studies on these four babies showed no evidence of Di George syndrome. Interestingly, two patients' mothers were found to have hyperparathvroidism. In conclusion, in case of neonatal hypocalcemia, measurements of calcium, phosphorus, and intact-PTH in neonates are required to recognize hypoparathyroidism. Pediatricians should always check maternal parathyroid status to rule out maternal hyperparathyroidism.
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PMID:Transient neonatal hypoparathyroidism: report of four cases. 1181 Dec 26

Abnormalities in serum phosphate levels are more prevalent in certain subsets of Emergency Department patients than in the general population. Patients with diabetic ketoacidosis, chronic obstructive pulmonary disease, alcoholism, malignancy, and renal failure are at increased risk. Multiple factors, including nutritional intake, medications, renal or intestinal excretion, and cellular redistribution, are potential etiologies. The clinical manifestations of mild hypophosphatemia or hyperphosphatemia are typically minor and nonspecific (myalgias, weakness, anorexia). When the imbalance is severe, critical complications may occur (tetany, seizures, coma, rhabdomyolysis, respiratory failure, ventricular tachycardia). Mild asymptomatic hypophosphatemia can be treated with oral phosphate supplementation (15 mg/kg daily) on an outpatient basis. Patients with severe or symptomatic hypophosphatemia should be treated with IV phosphate therapy (0.08-0.16 mg/kg over 6 h) and admitted for monitoring and subsequent serum electrolyte testing. Mild asymptomatic hyperphosphatemia is commonly managed in renal failure by limiting dietary intake and reducing absorption with phosphate-binding salts. Hemodialysis may be required for severe hyperphosphatemia with symptomatic hypocalcemia.
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PMID:Serum phosphate abnormalities in the emergency department. 1248 22

We report two sisters with a new syndrome of simplified gyral pattern, normal head circumference at birth but with subsequent development of microcephaly, intractable seizures, and early death. Dysmorphic features included coarse face, hypertrichosis, short nose, paranasal widening, long philtrum, short neck, upper limb micromelia, single transverse palmar lines, and clasp thumbs. The proband had repeated convulsions from shortly after birth and she required continuous artificial ventilation. Neurological examination showed absent sucking, rooting, Moro and grasping reflexes. MRI revealed a diffuse simplified gyral pattern with apparent agyria over the frontal lobes. Biochemical screening gave normal results. Her older sister had bilateral renal pelvic dilatation on prenatal ultrasound. She also developed severe convulsions on the first day of life, and she had to be artificially ventilated for 38 days. She had severe developmental retardation and neurological examination showed absence of spontaneous movements and Moro reflex, weak sucking reflex, and hypertonicity. CT scan of the brain showed a simplified gyral pattern. At 3 months, she developed hypocalcemia and hyperphosphatemia with normal levels of vitamin D and alkaline phosphatase, and parathyroid hormone level was low. Other biochemical tests gave normal results. She died at 5 months due to a massive aspiration event. Based on the unique clinical and radiological features found in our patients, we propose that this is a new syndrome.
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PMID:New syndrome of simplified gyral pattern, micromelia, dysmorphic features and early death. 1274 64

The problem of intracranial calcifications in children has not been widely discussed in the literature yet. The aim of this study is to emphasise different clinical aspects of intracranial calcifications found in subcortical nuclei and cerebellum in children with disturbed calcium metabolism. We report three different cases of hypoparathyroidism in children in whom similar radiological changes on computed tomography (CT) of the brain were found. An 11-year-old boy was referred to us after episode of tetany. We confirmed the diagnosis of idiopatic hypoparathyroidism (presence of Chvostek and Trousseau signs, hypocalcemia, hyperphosphatemia, low parathormone serum concentration). On brain CT small, symmetric calcifications in the subcortical nuclei and frontal lobes were imaged. A diagnosis of pseudohypoparathyroidism type Ib in 10-year-old girl was established on the basis of clinical symptoms (syncope with seizures, recurrent carpopedal spasms in the past) and laboratory investigations (hypocalcemia, hyperphosphatemia, high parathormone serum concentration). In 11-year-old girl autoimmune polyglandular syndrome type I was diagnosed (hypoparathyroidism with chronic mucocutaneous candidiasis and nail dystrophy from the age of 2). CT of the brain showed multiple irregular symmetric calcifications in cerebellar hemispheres, internal capsula and subcortical nuclei on the border of white and grey matter in both frontal lobes.
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PMID:[Association of brain computed tomography images of intracranial calcifications in three different cases of hypoparathyroidism]. 1550 18

Fosphenytoin is indicated for the treatment of generalized convulsions and seizures occurring during neurosurgery. Metabolites of fosphenytoin include phenytoin, phosphate, and formaldehyde. The drug monograph recommends caution in administering fosphenytoin to patients in whom phosphate restriction is necessary. Additionally, fosphenytoin has altered pharmacokinetics in end-stage renal disease patients. We report a 17-year old African-American male with end-stage renal disease who developed acute hyperphosphatemia to 3.9 mmol/L (12.1 mg/dL) following the intravenous administration of 1000 mg of fosphenytoin for an idiopathic complex partial seizure. To our knowledge, this is the first report of acute hyperphosphatemia due to fosphenytoin administration. Due to this risk of hyperphosphatemia, we recommend that fosphenytoin should be used with caution in the end-stage renal disease population.
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PMID:Hyperphosphatemia due to fosphenytoin in a pediatric ESRD patient. 1596 70

Hyperphosphatemia is a common serious complication of chronic renal diseases, which needs appropriate continuous treatment in order to avoid ominous side effects. Therefore, oral chelating agents able to avoid phosphate absorption by the gut are mandatory. In the past, Aluminium salts, and more recently Calcium and Magnesium salts, and a synthetic resin polyallylamine hydrochloride have been employed, but Aluminium was later abandoned, because it has been a silent killer of many uremic patients, due to subtle absorption eventually leading to toxicity on Central Nervous System and bone, with allucinations, seizures, dementia, and osteomalacia, bone pain, fracturing osteodystrophy, and death. Recently, a new chelating agent able to bind dietary phosphate, namely Lanthanum carbonate has been introduced, with a proven efficacy profile for short-term treatment. However, after careful examination of the very few scientific papers available to date, we strongly advise caution before adopting, at present, lanthanum carbonate as a phosphate binder in uremic patients. In fact, notwithstanding minimized, some data are worrying: first, Lanthanum ions are absorbed, though at a minimal extent, by human gut; 2) pharmacokinetic evaluations show a greater exposure to Lanthanum in uremic patients;3) Lanthanum concentration is increased tenfold in blood and fivefold in bone after short-term supplementation in uremic patients; 4) there is no proofs that Lanthanum cannot cross the blood brain barrier in uremic patients; 5)Lanthanum has many biological effects and is potentially highly toxic. The Aluminum story should serve as cautionary tale when considering the use of new metal ions.
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PMID:Blast from the past: the aluminum's ghost on the lanthanum salts. 1602 63

Klinefelter's syndrome is rarely associated with hypocalcemia, especially pseudohypoparathyroidism (PHP) type Ib. We describe a case of Klinefelter's syndrome associated with seizure, PHP type Ib and multiple endocrine dysfunctions. A 19-year-old Taiwanese male was admitted due to seizures with loss of consciousness. He had been diagnosed with Klinefelter's syndrome with seizure disorder and hypocalcemia 3 months previously. Physical examination revealed eunuchoidism but no osteodystrophy, while laboratory data revealed severe hypocalcemia, hyperphosphatemia, and elevated parathyroid hormone. Chromosomal study showed 47,XXY. Osteoporosis was found on chest and abdominal radiography. Dense calcification in the cerebrum and cerebellum was shown on brain computed tomography and magnetic resonance imaging. Elevation of the patient's serum calcium level was noted after vitamin D and calcium carbonate supplements were given. Klinefelter's syndrome is rarely associated with PHP type Ib; our patient's hypocalcemia improved after long-term aggressive treatment.
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PMID:Klinefelter's syndrome with seizure, pseudohypoparathyroidism type Ib and multiple endocrine dysfunctions. 1637 43

The case of a neonate is presented who had early onset seizure associated with hypocalcemia, hyperphosphatemia, and raised parathyroid hormone. The infant did not have any stigmata of pseudohypoparathyroidism. The hypocalcemia was initially resistant to calcium therapy, but responded to vitamin D analog therapy. The diagnosis of 'neonatal pseudohypoparathyroidism' was entertained; the infant remained stable and seizure-free with normal serum biochemistry during 3 months of follow-up.
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PMID:Neonatal pseudohypoparathyroidism. 1644 71


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