• Korean Journal of Head & Neck Oncology
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• v.15 no.1
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• pp.61-65
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• 1999

Introduction: The surgical treatment of Graves' disease has several advantage such as rapid and long lasting therapeutic effect, relatively low incidence of postoperative hypothyroidism and recurrence. Because of less frequent but serious postoperative complications, the operation have not been casually used for treatment of Graves' disease. Hypoclacemia, hoarseness and hematomas are common complications after operative treatment. However, the causative mechanisms of these complications have not been well explained. Objective: We aimed to analyze the risk factors affecting the occurance of complications in surgical treatment for Graves' disease and to evaluate what are the causative mechanisms of postoperative complications. Patients and Methods: From January 1985 to December 1998, a total of 668 surgically treated patients for Graves' disease were enrolled in this study. The incidence of postoperative complications were analyzed in relation to types of surgery, preoperaive preparation, specimen weight, bleeding amount and remnant weight. Results: Postoperative complication was developed in 108(16.2%) of 668 patients. The most common complication was transient hypocalcemia in 85 cases(12.7%). Other complications were: Hematoma in 9 cases(1.3%), transient hoarseness in 5 cases(0.7%), permanent hypocalcemia in 6 cases(0.9%), permanent hoarseness in 3 case(0.4%). The important etiologic factors affecting the occurance of complications were preoperative preparation, perioperative thyroid weight, and remnant thyroid weight. Since 1993, the incidence of complication was more decreased than that in before. Conclusion: To decrease the incidence of postoperative complications of Graves' disease, the patients should be selected carefully, sufficient preoperative preparation should be achieved, and the operation should be performed by well-experienced surgeons.

• Journal of Veterinary Clinics
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• v.26 no.6
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• pp.603-605
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• 2009

A 7-year-old intact female, Miniature Schnauzer dog was presented with an acute seizure episode and tremors. Fever and panting were noted when presented. Physical examination revealed apparent forelimb muscle rigidity, fasciculations and stiff gait. Characteristic laboratory findings in this dog were severe hypocalcemia with hyperphosphatemia. The low serum concentration of intact parathyroid hormone and ionized calcium levels were consistent with the diagnosis of primary hypoparathyroidism. In addition, there were increased urinary excretion of calcium and decreased urinary excretion of phosphorus in this case. Urgent treatment was initiated with 10% calcium gluconate. The dog remained healthy with vitamin D analogue and oral calcium supplementation. A transient hyperphosphatemia was controlled well with sevelamer hydrochloride. To the author's knowledge, this is the first case report describing the clinical and laboratory characteristic features of canine primary hypoparathyroidism and its clinical outcome in Korea.

• The Korean Journal of Pain
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• v.30 no.2
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• pp.86-92
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• 2017

Osteoblasts, originating from mesenchymal cells, make the receptor activator of the nuclear factor kappa B ligand (RANKL) and osteoprotegerin (OPG) in order to control differentiation of activated osteoclasts, originating from hematopoietic stem cells. When the RANKL binds to the RANK of the pre-osteoclasts or mature osteoclasts, bone resorption increases. On the contrary, when OPG binds to the RANK, bone resorption decreases. Denosumab (AMG 162), like OPG (a decoy receptor), binds to the RANKL, and reduces binding between the RANK and the RANKL resulting in inhibition of osteoclastogenesis and reduction of bone resorption. Bisphosphonates (BPs), which bind to the bone mineral and occupy the site of resorption performed by activated osteoclasts, are still the drugs of choice to prevent and treat osteoporosis. The merits of denosumab are reversibility targeting the RANKL, lack of adverse gastrointestinal events, improved adherence due to convenient biannual subcutaneous administration, and potential use with impaired renal function. The known adverse reactions are musculoskeletal pain, increased infections with adverse dermatologic reactions, osteonecrosis of the jaw, hypersensitivity reaction, and hypocalcemia. Treatment with 60 mg of denosumab reduces the bone resorption marker, serum type 1 C-telopeptide, by 3 days, with maximum reduction occurring by 1 month. The mean time to maximum denosumab concentration is 10 days with a mean half-life of 25.4 days. In conclusion, the convenient biannual subcutaneous administration of 60 mg of denosumab can be considered as a first-line treatment for osteoporosis in cases of low compliance with BPs due to gastrointestinal trouble and impaired renal function.

• Laboratory Medicine Online
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• v.7 no.2
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• pp.83-87
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• 2017

Pseudohypoparathyroidism (PHP) is a rare disorder caused by genetic and epigenetic aberrations in the GNAS complex locus resulting in impaired expression of stimulatory G protein ($Gs{\alpha}$). PHP type Ib (PHP-Ib) is characterized by hypocalcemia and hyperphosphatemia due to renal resistance to the parathyroid hormone, and is distinguished from PHP-Ia by the absence of osteodystrophic features. An 11-yr-old boy presented with poor oral intake and cramping lower limb pain after physical activity. Laboratory studies revealed hypocalcemia, hyperphosphatemia, and increased parathyroid hormone levels. The GNAS complex locus was evaluated using the methylation-specific multiplex ligation-dependent probe amplification (MS-MLPA) assay. Gain of methylation in the NESP55 domain and loss of methylation in the antisense (AS) transcript, XL, and A/B domains in the maternal allele were observed. Consequently, we present a case of PHP-Ib diagnosed using MS-MLPA.

• Endocrinology and Metabolism
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• v.33 no.4
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• pp.485-492
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• 2018

Background: Increasing evidence supports interplay between aldosterone and parathyroid hormone (PTH), which may aggravate cardiovascular complications in various heart diseases. Negative structural cardiovascular remodeling by primary aldosteronism (PA) is also suspected to be associated with changes in calcium levels. However, to date, few clinical studies have examined how changes in calcium and PTH levels influence cardiovascular outcomes in PA patients. Therefore, we investigated the impact of altered calcium homeostasis caused by excessive aldosterone on cardiovascular parameters in patients with PA. Methods: Forty-two patients (mean age $48.8{\pm}10.9$ years; 1:1, male:female) whose plasma aldosterone concentration/plasma renin activity ratio was more than 30 were selected among those who had visited Severance Hospital from 2010 to 2014. All patients underwent adrenal venous sampling with complete access to both adrenal veins. Results: The prevalence of unilateral adrenal adenoma (54.8%) was similar to that of bilateral adrenal hyperplasia. Mean serum corrected calcium level was $8.9{\pm}0.3mg/dL$ (range, 8.3 to 9.9). The corrected calcium level had a negative linear correlation with left ventricular end-diastolic diameter (LVEDD, ${\rho}=-0.424$, P=0.031). Moreover, multivariable regression analysis showed that the corrected calcium level was marginally associated with the LVEDD and corrected QT (QTc) interval (${\beta}=-0.366$, P=0.068 and ${\beta}=-0.252$, P=0.070, respectively). Conclusion: Aldosterone-mediated hypercalciuria and subsequent hypocalcemia may be partly involved in the development of cardiac remodeling as well as a prolonged QTc interval, in subjects with PA, thereby triggering deleterious effects on target organs additively.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.20 no.2
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• pp.44-49
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• 2020

Pseudohypoparathyroidism (PHP) is a disorder characterized by hypocalcemia and hyperphosphatemia due to end organ resistance to parathyroid hormone. PHP is caused by the deficiency of the α-subunit of the stimulatory G protein encoded by the GNAS gene, and this defect arises from genetic or imprinting disturbances. Sporadic PHP 1b shows two or more methylation defects of upstream of GNAS gene and some of them lead to loss of maternal GNAS imprints, therefore, only paternally derived GNAS gene is expressed. Here, we report a 10 year 9 month old boy presented with intermittent tetany who was finally diagnosed with PHP 1b caused by paternal uniparental disomy of chromosome 20q.

• Journal of Yeungnam Medical Science
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• v.14 no.1
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• pp.220-226
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• 1997

Idiopathic hypoparathyroidism is frequently associated with intracranial calcification and neuropsychiatric abnormalities. The most commonly recognized central nervous system manifestations of chronic hypoparathyroidism are seizure, alteration of mental function and extrapyramidal signs. We present a case of hypoparathyroidism, demonstrating extensive intracranial calcification, not only basal ganglia, but also outside the extrapyramidal system. An 58-year-old woman presented with 30 year history of seizure and memory disturbance. The physical examination and several laboratory studies disclosed normal. However hypocalcemia, hyperphosphatemia with hypocalciuria and decreased parathormone level were demonstrated. Clinical symptoms and signs showed improvement after supplementary calcium and Vit $D_3$ therapy.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.8
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• pp.3555-3560
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• 2012

The tumour lysis syndrome (TLS) is a group of metabolic abnormalities caused by rapid and unexpected release of cellular components into the circulation as a result of massive destruction of rapidly proliferating malignant cells. It usually develops in patients with hematologic malignancies like acute lymphoid leukemia, non-Hodgkin and Burkitt's lymphoma after initiation of chemotherapy or may, rarely, occur spontaneously. Though TLS is seldom observed in relation to solid tumours, there have been reports of connections with examples such as lung, liver, breast, gastric carcinomas. The clinical manifestations of TLS include hyperuricemia, hyperkalemia, hyperphosphatemia and hypocalcemia. These indications if untreated lead to life-threatening complications such as acute renal failure, cardiac arrhythmias, seizures, and eventually death due to multiorgan failure. Therefore early detection of TLS is of vital importance. This can be accomplished by identification of high risk patients, implementation of suitable prophylactic measures andmonitoring of the electrolyte levels in patients undergoing chemotherapy.

• Clinical and Experimental Pediatrics
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• v.57 no.1
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• pp.1-18
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• 2014

Channelopathies are a heterogeneous group of disorders resulting from the dysfunction of ion channels located in the membranes of all cells and many cellular organelles. These include diseases of the nervous system (e.g., generalized epilepsy with febrile seizures plus, familial hemiplegic migraine, episodic ataxia, and hyperkalemic and hypokalemic periodic paralysis), the cardiovascular system (e.g., long QT syndrome, short QT syndrome, Brugada syndrome, and catecholaminergic polymorphic ventricular tachycardia), the respiratory system (e.g., cystic fibrosis), the endocrine system (e.g., neonatal diabetes mellitus, familial hyperinsulinemic hypoglycemia, thyrotoxic hypokalemic periodic paralysis, and familial hyperaldosteronism), the urinary system (e.g., Bartter syndrome, nephrogenic diabetes insipidus, autosomal-dominant polycystic kidney disease, and hypomagnesemia with secondary hypocalcemia), and the immune system (e.g., myasthenia gravis, neuromyelitis optica, Isaac syndrome, and anti-NMDA [N-methyl-D-aspartate] receptor encephalitis). The field of channelopathies is expanding rapidly, as is the utility of molecular-genetic and electrophysiological studies. This review provides a brief overview and update of channelopathies, with a focus on recent advances in the pathophysiological mechanisms that may help clinicians better understand, diagnose, and develop treatments for these diseases.

• Journal of The Korean Society of Clinical Toxicology
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• v.5 no.2
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• pp.135-137
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• 2007

Hydrofluoric acid is a weak inorganic acid used for etching and as rust removals. Systemic toxicity after oral ingestion induces rapid development of hypocalcemia and hyperkalemia, leading to ventricular fibrillation and finally asystole. We report a case of intentional ingestion of hydrofluoric acid producing an altered mental state at the time of the patient's arrival in the emergency department. The patient died approximately 80 minutes after the exposure with asystol.