PURPOSE: To describe the clinical characteristics of full-term neonates with hypocalcemia and to suggest factors associated with neonatal hypocalcemia METHODS: The medical records of full-term neonates with hypocalcemia were reviewed. Hypocalcemia was defined as an ionized calcium (iCa) concentration of <4 mg/dL. Parathyroid hormone (PTH) insufficiency was defined as a serum PTH level of <60 pg/mL or a serum phosphorus level higher than the serum calcium level in the presence of hypocalcemia. RESULTS: Fifty-three neonates were enrolled. The median age at diagnosis of hypocalcemia was 3 days. In all the neonates, formula feeding predominance was observed. Thirty-eight neonates (69.8%) were compatible with PTH insufficiency. The number of formula-fed neonates was significantly higher than that of breast-fed patients among neonates with PTH insufficiency (P=0.017). Intact PTH was negatively correlated with serum phosphorus levels. Twelve out of 14 neonates (85.7%) had 25-hydroxy vitamin D (25OHD) levels <20 ng/mL and 9 neonates (64.3%) had 25OHD levels <10 ng/mL. Twenty-one neonates had hypocalcemic tetany. The serum calcium and iCa concentrations of neonates with tetany were 4.2-8.3 mg/dL and 1.85-3.88 mg/dL, respectively. Three neonates showed symptomatic hypocalcemia with calcium levels over 7.5 mg/dL. Among the 16 neonates who underwent electroencephalography (EEG), 12 had abnormalities, which normalized after 1-2 months. CONCLUSION: Formula milk feeding, PTH insufficiency and low serum vitamin D concentration are associated with the development of neonatal hypocalcemia. Symptoms such as tetany and QT interval prolongation can develop in relatively mild hypocalcemia. Moreover, transient neonatal hypocalcemia can cause transient EEG abnormalities.
Calcium ; Diagnosis ; Electroencephalography ; Humans ; Hypocalcemia* ; Infant, Newborn ; Medical Records ; Milk ; Parathyroid Hormone ; Phosphorus ; Tetany ; Vitamin D

Pseudohypoparathyroidism (PHP) is a group of genetic disorders in which the kidneys fail to respond to parathyroid hormone. Genetic defects in the GNAS complex locus lead to reduced Gsalpha (alpha-subunit of the heterotrimeric stimulatory G protein) activity in PHP type Ia patients. These patients exhibit characteristics of Albright hereditary osteodystrophy (AHO) and hypocalcemia, increased parathyroid hormone, and resistance to other Gsalpha protein-coupled hormones. AHO has a wide range of manifestations such as short stature, obesity, round face, subcutaneous ossification, and bone shortening in the hands and feet. In this study, we present the case of a 47-yr-old woman who was diagnosed with PHP type Ia with AHO. She showed tetany, dizziness, irritability to light, decreased visual acuity, cognitive impairment, and motor dysfunction. Direct sequencing identified a heterozygous missense mutation in exon 6 (c.466G>A, p.Asp156Asn) in GNAS1. To our knowledge, this case is the first report in Korea of PHP type Ia caused by a heterozygous missense mutation in exon 6 (c.466G>A, p.Asp156Asn) in GNAS1.
Dizziness ; Exons ; Female ; Foot ; Hand ; Humans ; Hypocalcemia ; Kidney ; Korea ; Mutation, Missense ; Obesity ; Parathyroid Hormone ; Pseudohypoparathyroidism* ; Tetany ; Visual Acuity

We report a case of acute suppurative thyroiditis complicated by idiopathic hypoparathyroidism. The patient was a 49-year-old female who visited our clinic with a painful goiter on the left lobe of the thyroid gland. She was hypocalcemic, which was accompanied unusually by acute suppurative thyroiditis. She also suffered from tetany of both hands and legs. She had undergone a right subtotal thyroidectomy at another hospital 23 years previously due to a benign thyroid nodule. Intact parathyroid hormone (PTH) levels were increased, but other laboratory findings were normal. No special treatment was administered for the acute suppurative thyroiditis, except antibiotics, to observe its natural course. Her PTH levels decreased and serum calcium returned to normal. The complication of acute suppurative thyroiditis suggested the possible involvement of idiopathic hypoparathyroidism.
Anti-Bacterial Agents ; Calcium ; Female ; Goiter ; Hand ; Humans ; Hypocalcemia* ; Hypoparathyroidism ; Leg ; Middle Aged ; Parathyroid Hormone ; Tetany ; Thyroid Gland ; Thyroid Nodule ; Thyroidectomy ; Thyroiditis, Suppurative*

Gitelman syndrome is a rare autosomal recessive hereditary salt-losing tubulopathy, that manifests as hypokalemic metabolic alkalosis, hypomagnesemia, and hypocalciuria. It is caused by mutations in the solute carrier family 12(sodium/chloride transporters), member 3 (SLC12A3) gene encoding the thiazide-sensitive sodium chloride cotransporter channel (NCCT) in the distal convoluted tubule of the kidney. It is associated with muscle weakness, cramps, tetany, vomiting, diarrhea, abdominal pain, and growth retardation. The incidence of growth retardation, the exact cause of which is unknown, is lower than that of Bartter syndrome. Herein, we discuss the case of an overweight 12.9-year-old girl of short stature presenting with hypokalemic metabolic alkalosis. The patient, on the basis of detection of a heterozygous mutation in the SLC12A3 gene and poor growth hormone (GH) responses in two provocative tests, was diagnosed with Gitelman syndrome combined with complete GH deficiency. GH treatment accompanied by magnesium oxide and potassium replacement was associated with a good clinical response.
Abdominal Pain ; Alkalosis ; Bartter Syndrome ; Diarrhea ; Gitelman Syndrome ; Growth Hormone ; Humans ; Incidence ; Kidney ; Magnesium Oxide ; Muscle Cramp ; Muscle Weakness ; Overweight ; Potassium ; Sodium Chloride Symporters ; Tetany ; Vomiting

The natural history of primary hyperparathyroidism, due to parathyroid adenoma, is unknown. Furthermore, spontaneous resolution of parathyroid necrosis or hemorrhage is rare and usually asymptomatic. Here, we report a case of parathyroid apoplexy of primary hyperparathyroidism, presenting as auditory hallucinations, accompanied with hypocalcemia. A 39-year-old man who was incidentally diagnosed with primary hyperparathyroidism, and waiting surgery for parathyroidectomy presented to psychiatric service with auditory hallucinations. He developed tetany, while taking psychiatric drugs. On a follow-up investigation, his serum calcium level fell from 11.8 to 5.8 mg/dL. His intact parathyroid hormone level also decreased from 1,017 pg/mL to 71.1 pg/mL. The parathyroid apoplexy was confirmed after a surgical removal of the infarcted adenoma. The auditory hallucinations disappeared, and serum calcium level was returned to within the normal range.
Adenoma ; Adult ; Calcium ; Follow-Up Studies ; Hallucinations ; Hemorrhage ; Humans ; Hyperparathyroidism, Primary ; Hypocalcemia ; Natural History ; Necrosis ; Parathyroid Hormone ; Parathyroid Neoplasms ; Parathyroidectomy ; Reference Values ; Stroke ; Tetany

Wilson's disease is an autosomal recessive disorder marked by disruptions in copper metabolism which leads to accumulation of copper in the liver, brain, cornea, and other tissues. Manifestations of this disease are more likely to be hepatic during early childhood and neurologic in adolescent. In addition, abnormalities that develop during disease progression may result in other manifestations such as hematologic, endocrine, or renal findings. Here we report a 13-year-old girl who presented with hypocalcemic tetany shortly after being diagnosed with Wilson's disease. Despite aggressive calcium, magnesium, and vitamin D replacement therapy, the hypocalcemia and hypomagnesemia did not promptly respond. Mineral levels in the blood took longer than 3 weeks to normalize. We speculate that a parathyroid insufficiency and disrupted vitamin D metabolism caused by copper accumulation and hepatic dysfunction resulted in hypocalcemic tetany.
Adolescent ; Brain ; Calcium ; Copper ; Cornea ; Disease Progression ; Hepatolenticular Degeneration ; Humans ; Hypocalcemia ; Hypoparathyroidism ; Liver ; Magnesium ; Tetany ; Vitamin D ; Vitamin D Deficiency

Dilated cardiomyopathy, which mostly has an idiopathic etiology or is caused by genetic inheritance or infection, can cause irreversible congestive heart failure. Hypocalcemia is a rare etiology of reversible dilated cardiomyopathy. Here we report the case of a two-month-old girl with congestive heart failure who was diagnosed as having dilated cardiomyopathy secondary to hypocalcemia. After calcium and vitamin D replacement therapy, the patient showed a rapid reduction in hypocalcemic tetany and a rapid recovery of left ventricular function. The cause of the hypocalcemia was vitamin D deficient rickets. She was exclusively breast-fed as an infant, and her mother had a vitamin D deficiency and was diagnosed with osteomalacia.
Calcium ; Cardiomyopathy, Dilated ; Heart Failure ; Humans ; Hypocalcemia ; Infant ; Mothers ; Osteomalacia ; Rickets ; Tetany ; Ventricular Function, Left ; Vitamin D ; Vitamin D Deficiency ; Vitamins ; Wills

A 65-year-old woman presented with acute pulmonary edema, generalized tetany, and paresthesia. She had severe hypocalcemia, a low intact parathyroid hormone level, and her echocardiogram revealed left ventricular dysfunction. She had no history of heart failure or thyroid surgery. The heart failure improved after calcium replacement and conventional heart failure management. She was diagnosed with hypocalcemia-induced heart failure caused by idiopathic hypoparathyroidism. Despite the crucial role of calcium in myocardial contractility, hypocalcemia is rarely reported as a cause of heart failure. In conclusion, plasma calcium should be measured in the initial workup of all patients with heart failure, and corrected if hypocalcemia is seen. Idiopathic hypoparathyroidism is a rare cause of reversible heart failure that should be considered in the etiologic assessment.
Aged ; Calcium ; Female ; Heart ; Heart Failure ; Humans ; Hypocalcemia ; Hypoparathyroidism ; Parathyroid Hormone ; Paresthesia ; Plasma ; Pulmonary Edema ; Tetany ; Thyroid Gland ; Ventricular Dysfunction, Left

Gitelman's syndrome is a rare autosomal recessive, inherited renal tubular disorder, first described by Gitelman et al. in 1966, and it is characterized by hypokalemic metabolic alkalosis, hypomagnesemia, salt wasting, normal to low blood pressure and rather low urinary calcium excretion rates with elevated plasma renin activity. This syndrome is caused by inactivating mutation in the SLC12A3 gene coding for the thiazide-sensitive sodium chloride cotransporter in the distal convoluted tubule. In most of the patients with Gitelman's syndrome, the disease manifests with transient episodes of muscular weakness and tetany in the adulthood. Herein, we report a case of Gitelman's syndrome atypically presented with chest pain and syncope.
Alkalosis ; Calcium ; Chest Pain* ; Clinical Coding ; Gitelman Syndrome* ; Humans ; Hypotension ; Muscle Weakness ; Plasma ; Renin ; Sodium Chloride Symporters ; Syncope* ; Tetany ; Thorax*

Hyperparathyroidism is a common finding in patients with chronic renal failure. Among the hyperparathyroidism, tertiary hyperparathyroidism, which is secreting parathyroid hormone autonomously in spite of hypercalcemia. Sometimes it requires surgical intervention due to not only symptomatic hypercalcemia, but also longstanding asymptomatic hypercalcemia. Hungry bone syndrome was known to be developed due to extensive re-mineralization of skeleton after parathyroidectomy. It is characteristic of persistent hypocalcemia, hypophosphatemia and often with tetany. The patient's condition improved without complication after the calcium chloride and calcium carbonate administration. We report a case of hungry bone syndrome developed after parathyroidectomy in patient with tertiary hyperparathyroidism and chronic renal failure.
Calcium Carbonate ; Calcium Chloride ; Humans ; Hypercalcemia ; Hyperparathyroidism* ; Hypocalcemia ; Hypophosphatemia ; Kidney Failure, Chronic ; Parathyroid Hormone ; Parathyroidectomy* ; Renal Dialysis* ; Skeleton ; Tetany