• Proceedings of the Korean Magnetic Resonance Society Conference
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• 2000.01a
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• pp.28-28
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• 2000

• Korean Journal of Clinical Pharmacy
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• v.23 no.2
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• pp.142-150
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• 2013

Background: Secondary hyperparathyroidism (SHPT) is common in patients with chronic kidney disease, affecting most of those who are receiving dialysis. Cinacalcet, a novel calcimimetic, targets the calcium-sensing receptor to lower PTH levels in dialysis patients. Objective: This study aimed to assess efficacy, safety and appropriateness of use of cinacalcet in dialysis patients. Method: This retrospective study was performed on total 24 cases with identified intact parathyroid hormone (iPTH), serum calcium and phosphorus levels before and 4 weeks after cinacalcet initiation at a teaching hospital from July 1st, 2011 to October 31st, 2012. Results: Cinacalcet decreased iPTH by 19% from baseline after 4weeks treatment and it was statistically significant (p<0.001). Cinacalcet also significantly decreased iPTH levels regardless of dialysis modality (hemodialysis group versus peritoneal dialysis group) and severity of SHPT (iPTH 300-800 pg/ml group versus iPTH >800 pg/ml group). Serum calcium, phosphorus and Ca x P levels were decreased without statistical significance. Gastrointestinal events, headache and hypocalcemia were the most common side effects. Monitoring for iPTH and serum calcium was not performed appropriately. 43.7% patients initiated cinacalcet therapy at serum calcium level< 9.0 mg/dl. Conclusion: In conclusion, cinacalcet lowers parathyroid hormone levels with no serious side effects. However, it is required to avoid cinacalcet treatment in patients with low serum calcium levels and monitor iPTH and serum calcium levels during cinacalcet administration.

• Clinical and Experimental Pediatrics
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• v.58 no.4
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• pp.148-153
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• 2015

The calcium sensing receptor (CaSR) plays an important role in calcium homeostasis. Activating mutations of CaSR cause autosomal dominant hypocalcemia by affecting parathyroid hormone secretion in parathyroid gland and calcium resorption in kidney. They can also cause a type 5 Bartter syndrome by inhibiting the apical potassium channel in the thick ascending limb of the loop of Henle in the kidney. This study presents a patient who had autosomal dominant hypocalcemia with Bartter syndrome due to an activating mutation Y829C in the transmembrane domain of the CaSR. Symptoms of hypocalcemia occurred 12 days after birth and medication was started immediately. Medullary nephrocalcinosis and basal ganglia calcification were found at 7 years old and at 17 years old. Three hypercalcemic episodes occurred, one at 14 years old and two at 17 years old. The Bartter syndrome was not severe while the serum calcium concentration was controlled, but during hypercalcemic periods, the symptoms of Bartter syndrome were aggravated.

• Journal of Nutrition and Health
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• v.29 no.7
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• pp.747-757
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• 1996

In this study, the serum level of 25-hydroxyvitamin D(25-(OH)D) was measured by high pressure liquid chromatography(HPLC), and factors affecting it were investigated in 72 young adults age ranging from 21 years to 39 years with normal bone density. The mean level of serum 25-(OH)D was 20.0$\pm$6.8ng/ml in males and 26.1$\pm$12.3ng/ml in females, which was significantly higher in females (p<0.01). The serum level of parathyroid hormone(PTH) showed a negative correlation with that of 25-(OH)D(p<0.05). Time spent outdoors in a day correlated positively with the serum level of 25-(OH)D(p<0.01). During the day, a specific time between 12:00 a.m. and 2:00 p.m. showed the most significant correlation with the level of 25-(OH)D(p<0.005). Among the nutrients studied, fat and vitamin D intake were positively correlated with the serum 25-(OH)D level. Stepwise multiple regression analysis showed that the serum level of 25-(OH)D could be fit by vitamin D intake(34.7% explained), serum PTH level (27.3% explained) and the time spent outdoors during the specific time(28.4% explained).1996)

• Journal of Nutrition and Health
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• v.29 no.9
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• pp.943-949
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• 1996

Bone mineral density depends largely on the status of dietary minerals such as Ca, P, Mg, and F and proteins, physical activities, parathyroid hormone(PTH), calcitonin(CT), and vitamin D. The decrease of bone density often results in bone fractures and osteoporosis which is prevalent among postmenopausal women. This study was intended to examine the role of parathyroid hormone, calcitonin and cholecaliferol in bone density of mice that were fed different dual photon energy beams. We have measured three major parts of the bone : whole body, head and femur. The results are summarized as follows : 1) Bone mineral density (BMD) was more increased by feeding high Ca diet compared to that of the low Ca diet. 2) Both PTH and Vit D3 enhanced BMD in all of the different Ca levels. 3) When the dietary Ca was deequate CT showed a synergistic effect with PTH in boosting bone density, while CT+Vit D3 showed a negative effect. 4) CT tended to inhibit the effect of increasing bone density by PTH and Vit D3 in medium and low Ca groups. 5) The effect of increasing bone density by PTH in the head of mouse increased when dietary Ca was lower : The increment of bone density by PTH in high, medium, and low Ca was 3%, 8%, 19%, respectively. 6) Femur bone density was affected significantly by dietary Ca levels than hormones. The above observations indicate that bone mineral density can be improved by high dietary Ca and hormone injections including PTH, CT and cholecalciferol, and thus proper dietary and hormonal treatment may be used in preventing bone fractures and osteoporosis.

• Clinical and Experimental Pediatrics
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• v.46 no.10
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• pp.1032-1035
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• 2003

In pseudohypoparathyroidism as reported by Albright in 1942, the parathyroid gland can normally synthesize and secrete parathyroid hormone(PTH). Pseudohypoparathyroidism has a similar biochemical finding with hypoparathyroidisms like hypocalcemia and hyperphosphatemia due to target tissue resistance to PTH. Administered PTH does not raise the serum levels of calcium and urinary phosphate. PTH activates G-protein in peripheral tissue and adenylate cyclase through a second messenger, cAMP. Pseudohypoparathyroidism produces hyperphosphatemia and hypocalcemia because of the resistance to PTH in peripheral tissue due to a defect of G-protein, although it releases PTH normally. According to the mechanism of resistance, pseudohypoparathyroidism is classified into types : Ia, Ib, Ic and psedopseudohypoparathyroism. Type Ia is accompanied by congenital growth retardation and abnormal bony development that shows mental retardation, obesity, low height, round face, short metacarpal bone and metatarsal bone, ectopic calcification, etc. We report a case of pseudohypoparathyroidism in a premature who shows hypocalcemia, hyperphosphatemia, elevation of serum PTH and 24 hr urinary basal c-AMP in biochemical tests without Albright's hereditary osteodystrophy at physical examination, accompanied by a spontaneous fracture in the femur.

• Journal of Veterinary Clinics
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• v.29 no.1
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• pp.98-102
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• 2012

A 1.5-year-old male Golden Retriever was presented with worsening lameness of two month duration. Abnomral findings of blood works and serum chemistry included anemia, thrombocytopenia, hypercalcemia and hyperglobulinemia. Radiography revealed osteolysis of polyostotic regions including right femur and tibia, bilateral ilium, and spinous processes from the 13th thoracic vertebra to 5th lumbar vertebra. Enlarged multiple lymph nodes and mixed echo pattern of muscular region ventral to vertebra were observed with ultrasonography. Because concentrations of both parathyroid hormone and parathyroid hormone related peptide were all within reference ranges, humoral hypercalcemia by tumor was ruled out and extensive osteolysis was considered as the cause of hypercalcemia. Based on radiographic and ultrasonographic study, lymphoma, multiple myeloma and osteomyelitis were included in differential diagnosis. Fungal serologic test was negative. Monoclonal gammopathy was not found on serum protein electrophoresis. Cytological and histopathological examinations of the lytic lesions revealed neoplastic lymphoid proliferation, and B cell type clonal expansion was detected by polymerase chain reaction for the antigen receptor gene rearrangement. The case was diagnosed as B cell lymphoma involving polyostotic regions.

• Preventive Nutrition and Food Science
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• v.1 no.1
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• pp.80-86
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• 1996

Parathyroid hormone(PTH) is known to stimulate bone resorption and to inhibit bone collagen synthesis. In contrast, as the evidence of stimulation of bone formation by PTH has recently been observed, the study on the role of PTH involved in osteoporosis draws remarkable attention. This study has dealt with the role of alkaline phoshatase(AP), a marker enzyme for bone formation and osteoblast action, Animals(BALS/cmice) were divided into three dietary groups(high and medium Ca and Ca-free) and hormones including PTH, calcitonin(CT), cholecalciferol(citamin D) were i.p. injected. AP in the serum and liver was measured using Sigma 221 alkaline buffer solutions containing 9mM of p-nitrophenyl phoshate. Enzume was reacted at 37$^{\circ}C$ for 10 minutes and the reaction was stopped by 1.8ml of 0.1N NaOH and measured at 410nm. We found that serum and liver AP activity was increased by low dietary Ac. Compared to the control, and serum Ap activity was enhanced by PTH and vitamin D regardless of the dietary Ca. On the other hand, liver AP activity was inhibited by OTH and vitamin D at all levels of dietary Ca. CT inhibited the action of PTH and vitamin D in the serum. But, the inhibition of PTH and vitamin D action by CT was not observed in the liver, unlike in the case of serum.

• Archives of Pharmacal Research
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• v.22 no.2
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• pp.119-123
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• 1999

Parathyroid hormone (PTH) treatment of bone and kidney-derived cells not only activates adenyly cyclase buy also increases intracellular free calcium, and translocates protein kinase C (PKC) from cytosol to plasma membranes. We have found that acute phorbol ester pretreatment significantly decreases PTH-induced calcium transients and the effect of phorbol ester was antagonized by staurosporine (ST). Although the major effect of ST in that study was the reversal of the action of phorbol ester, it appeared that ST may also have promoted the effect of PTH directly. To further investigate the observation, we examined the effect of ST on the intracellular calcium transients induced by PTH and $\alpha$-thrombin ($\alpha$-TH). For calcium transient experiments, UMR-106 cells were loaded with 2 mM fluo-acetoxymethylester for 30 min at room temperature. The cells were then washed and suspended in buffer containing 1 mM calcium. Fluorescence was detected at 530 nm, with excitation at 505 nm. ST alone did not cause calcium transients, but enhanced the transients elicited by PTH response. added 5 min before the hormone. Another protein kinase inhibitor H-7 likewise enhanced the calcium responses elicited by PTH, while genistein did not affect PTH response. Calcium transients elicited by $\alpha$-TH were also enhanced by ST. The results suggest that there might be tonically activated endogenous protein kinase(s) which inhibit calcium signaling of some calcemic agents.

• Journal of Korean Neurosurgical Society
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• v.61 no.4
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• pp.494-502
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• 2018

Objective : The loosening of pedicle screws (PS) is one of the frequent problems of spinal surgery in the patients with osteoporosis. Previous studies had revealed that intermittent injection of teriparatide could reduce PS loosening by improving bone mass and quality when their patients took parathyroid hormone for a considerable duration before surgery. However, although the teriparatide is usually used after spine surgery in most clinical situations, there was no report on the efficacy of teriparatide treatment started after spine surgery. The purpose of this retrospective study was to examine the efficacy of teriparatide treatment started immediately after lumbar spinal surgery to prevent pedicle screw loosening in patients with osteoporosis. Methods : We included 84 patients with osteoporosis and degenerative lumbar disease who underwent transforaminal interbody fusion and PS fixation and received parathyroid hormone or bisphosphonate (BP) postoperatively. They were divided into teriparatide group (daily injection of $20{\mu}g$ of teriparatide for 6 months, 33 patients, 172 screws) and BP group (weekly oral administration of 35 mg of risedronate, 51 patients, 262 screws). Both groups received calcium (500 mg/day) and cholecalciferol (1000 IU/day) together. The screw loosening was evaluated with simple radiographic exams at 6 and 12 months after the surgery. We counted the number of patients with PS loosening and the number of loosened PS, and compared them between the two groups. Clinical outcomes were evaluated using visual analog scale (VAS) and Oswestry disability index (ODI) preoperatively, and at 12 months after surgery. Results : There was no significant difference in the age, sex, diabetes, smoking, bone mineral density, body mass index, and the number of fusion levels between the two groups. The number of PS loosening within 6 months after surgery did not show a significant difference between the teriparatide group (6.9%, 12/172) and the BP group (6.8%, 18/272). However, during 6-12 months after surgery, it was significantly lower in the teriparatide group (2.3%, 4/172) than the BP group (9.2%, 24/272) (p<0.05). There was no significant difference in the number of patients showing PS loosening between the teriparatide and BP groups. The teriparatide group showed a significantly higher degree of improvement of the bone mineral density (T-score) than that of BP group (p<0.05). There was no significant difference in the pre- and post-operative VAS and ODI between the groups. Conclusion : Our data suggest that the teriparatide treatment starting immediately after lumbar spinal fusion surgery could reduce PS loosening compared to BP.