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Dive into the research topics where H.-Y. Son is active.

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Featured researches published by H.-Y. Son.


Clinical Endocrinology | 2010

The association of serum vitamin D level with presence of metabolic syndrome and hypertension in middle-aged Korean subjects.

Min-Hee Kim; Kang MooIl; Oh KiWon; Hyuk-Sang Kwon; Ji Hye Lee; Won-Chul Lee; Yoon KunHo; H.-Y. Son

Objective:  To examine the association of serum vitamin D level with metabolic syndrome (MetS) and hypertension (HTN) in middle‐aged Korean subjects.


Diabetic Medicine | 2007

Long-term effects of a structured intensive diabetes education programme (SIDEP) in patients with Type 2 diabetes mellitus—a 4-year follow-up study

S.-H. Ko; Kyuyoung Song; Sung-Rae Kim; Jong Min Lee; J.-S. Kim; J.-H. Shin; Yang Kyung Cho; Jong-Hyun Jeong; Kun-Ho Yoon; Bong-Yun Cha; H.-Y. Son; Yu-Bai Ahn

Aims  Patient education is a very important part of diabetes care. However, until now, little data has been presented about the long‐term effectiveness of structured intensive diabetes education programmes (SIDEP) for people with Type 2 diabetes mellitus.


Bone | 2000

The short-term changes of bone mineral metabolism following bone marrow transplantation

Moon-Won Kang; Won Young Lee; K.W Oh; Je-Ho Han; Ki-Ho Song; Bong-Yun Cha; Kyungji Lee; H.-Y. Son; S Kang; Chun Choo Kim

Organ transplantation is now the treatment of choice for many patients with life-threatening chronic diseases. A new set of side effects unique to these groups of patients has become recognized, and bone disease is one of these complications. However, little is known about the effects of myeloablative treatment followed by bone marrow transplantation (BMT) on bone mineral metabolism. We have prospectively investigated 31 patients undergoing BMT for hematologic diseases. Serum concentrations of calcium, phosphorus, creatinine, gonadotropins, sex hormones, and the biochemical markers of bone turnover were measured. The samples were collected before BMT and 1, 2, 3, 4, and 12 weeks, 6 months, and 1 year after BMT. Bone mineral density (BMD) was measured with dual-energy X-ray absorptiometry before BMT and 1 year after BMT. The serum carboxy-terminal cross-linked telopeptide of type I collagen increased progressively until 4 weeks after BMT. Thereafter, it began to decrease and reached basal values after 1 year. Serum osteocalcin decreased progressively until 3 weeks after BMT. After that, it increased and reached basal values after 3 months. No distinct differences were observed in the serum biochemical turnover markers between males and females, or between patients who received total body irradiation and those who did not. One year after BMT, lumbar spine BMD had decreased by 2.2%, and total proximal femoral BMD had decreased by 6.2%. Eighty-six percent of the women (12/14) went into a menopausal state immediately after BMT. This was caused by high gonadotropin levels and low estradiol levels. In contrast, gonadotropin levels and testosterone levels did not change significantly in the male patients after BMT. In conclusion, the rapid impairment of bone formation and the increase in bone resorption, as shown by the biochemical markers in this study, might play a role in post-BMT bone loss.


Osteoporosis International | 2002

The Role of Cytokines in the Changes in Bone Turnover Following Bone Marrow Transplantation

Won Young Lee; Moon-Won Kang; Eun-Sook Oh; Ki Won Oh; Ji-Youn Han; Bong-Yun Cha; Kyungji Lee; H.-Y. Son; Sung-Koo Kang; Chun-Choo Kim

Abstract: Osteoporosis is a common disease among patients undergoing transplantation and a loss of bone mass is usually detected after bone marrow transplantation (BMT), particularly during the immediate post-BMT period. Post-BMT bone loss is primarily related to gonadal dysfunction and immunosuppression. Cytokines, especially interleukin 6, play an important role in the pathogenesis of postmenopausal osteoporosis. However, the pathogenetic role of cytokines in post-BMT bone loss is unknown and data on the changes of cytokines in accordance with bone turnover markers are scarce. The aim of this study was to assess the relationship between bone turnover markers and cytokines, which are regularly sampled at peripheral blood and bone marrow before and after allogeneic BMT. This prospective study included two analyses. The first was a study of 46 BMT recipients (M/F 28/18), examining the relationship between bone turnover markers and serum cytokines that were measured before and at 1 week, 2 weeks, 3 weeks, 4 weeks and 3 months after BMT. Serum intact parathyroid hormone was measured before BMT and at 3 weeks after BMT and its relation to other cytokines and bone turnover markers was evaluated. The second analysis was a study of 14 (M/F 9/5) of 46 patients in whom bone marrow plasma cytokines [interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-α)] were measured at 3 weeks after BMT. The relationship between bone marrow plasma cytokines and bone turnover markers was studied because bone marrow is the microenvironment where the real changes in bone turnover occur. Serum type I collagen carboxyterminal telopeptide (ICTP), a bone resorption marker, increased progressively until 4 weeks (peak) after BMT and then decreased thereafter. Serum osteocalcin, a bone formation marker, decreased progressively until 3 weeks after BMT and then increased thereafter. Serum IL-6 increased until 2 weeks after BMT and declined thereafter. Serum TNF-a increased until 3 weeks after BMT and declined thereafter. There was a significant positive correlation between serum ICTP and bone marrow IL-6 levels at 3 weeks after BMT, when a marked change in bone metabolism occurs following BMT. However, a correlation between bone turnover markers and bone marrow TNF-aor peripheral blood cytokines was not found. At 3 months after BMT, there was a significant negative correlation between the mean daily steroid dose and the serum osteocalcin level (r=−0.43, p<0.05). The correlation between the mean daily steroid dose and serum ICTP was also significant (r= 0.41, p<0.05). Our data suggest that the progressive increase in bone resorption during the immediate post-BMT period is related to both steroid dose and the increase in bone marrow IL-6, which is a potent stimulator of bone resorption in vivo.


Diabetic Medicine | 2008

Cardiovascular autonomic dysfunction predicts acute ischaemic stroke in patients with Type 2 diabetes mellitus : a 7-year follow-up study

S.-H. Ko; Kyuyoung Song; S. A. Park; Sung-Rae Kim; Bong-Yun Cha; H.-Y. Son; Keon-Woong Moon; Ki-Dong Yoo; Jae-Hyung Cho; Kun-Ho Yoon; Yu-Bai Ahn

Aims  We investigated whether cardiovascular autonomic neuropathy (CAN) is associated with acute ischaemic stroke in patients with Type 2 diabetes.


Diabetic Medicine | 2005

Clinical characteristics of diabetic ketoacidosis in Korea over the past two decades

Seung-Hyun Ko; Won Young Lee; Jee-In Lee; Hyuk-Sang Kwon; Jong Min Lee; Sung-Rae Kim; Sung-Dae Moon; Ki-Ho Song; Ji-Youn Han; Yu-Bai Ahn; Soon-Jib Yoo; H.-Y. Son

Aims  The aim of this study was to investigate changes in the clinical characteristics of diabetic ketoacidosis (DKA) in Korea over the last two decades.


Frontiers in Bioscience | 2008

Loss of beta-cells with fibrotic islet destruction in type 2 diabetes mellitus.

Ji Won Kim; S.-H. Ko; Jongki Cho; Chenglin Sun; Ok Ki Hong; Seung Hwan Lee; J. H. Kim; Kyungji Lee; Hyuk-Sang Kwon; Jong Min Lee; Ki-Ho Song; H.-Y. Son; Kun-Ho Yoon

Recent morphologic analyses of human pancreases strongly suggest that a decreased beta-cell mass is observed from the early stages of diabetes and is caused by accelerated apoptosis of the beta-cells. In this article, we propose that fibrotic islet destruction might be one of the important pathogenic mechanisms of the limited capacity of beta-cell proliferation and accelerated apoptosis in diabetic patients. We have found that pancreatic stellate cells (PSCs) are involved in the progression of islet fibrosis in type 2 diabetes. High concentrations of glucose and insulin in islets contribute to PSC activation and proliferation through angiotensin II type 2 (ATII) signaling pathway, although the exact mechanisms remain to be confirmed. Angiotensin-converting enzyme inhibitors attenuate fibrotic islet destructions and that these have some beneficial effects on glucose tolerance. We suggest that PSCs might play a major role for the fibrotic islet destruction in patients with type 2 diabetes, and suppression of PSCs activation and proliferation might be one of the reasonable target to prevent and delay the progression of the type 2 diabetes mellitus.


Journal of Endocrinological Investigation | 2008

Subclinical Cushing’s syndrome associated with an adrenocortical oncocytoma

Se-Hoon Lee; Ki-Hyun Baek; Young Sun Lee; Jeongmin Lee; Moon-Won Kang; Bong-Yun Cha; Kyungji Lee; H.-Y. Son; S Kang

Oncocytoma is a neoplasm that can arise in several organs, and it has been more commonly described in the kidney, salivary gland and thyroid. Oncocytoma arising in the adrenal gland is a rare finding. Moreover, functioning adrenocortical oncocytoma is exceptionally rare. A 47-yr-old man was incidentally discovered to have a right adrenal mass. The patient had no clinical features suggestive of increased adrenal function. However, hormonal evaluation showed a disturbed cortisol circadian rhythm, supranormal urinary cortisol excretion, a low level of ACTH, and a lack of suppressibility of cortisol secretion after dexamethasone. Right adrenalectomy was performed, and this revealed a well-circumscribed dark-brown tumor that measured 2.4x2.2 cm. The tumor consisted almost exclusively of large eosinophilic and epitheloid cells whose cytoplasm was packed with eosinophilic granulations, which corresponded to the numerous mitochondria confirmed on electron microscopy. This is a rare case of subclinical Cushing’s syndrome that was caused by adrenocortical oncocytoma.


Diabetic Medicine | 1999

The effect of long-term glycaemic control on serum lipoprotein(a) levels in patients with Type 2 diabetes mellitus

Ki-Ho Song; Yu-Bai Ahn; Kun-Ho Yoon; Bong-Yun Cha; Kyungji Lee; H.-Y. Son; S Kang

Aims To examine whether long‐term glycaemic control affects lipoprotein(a) (Lp(a)) levels in patients with Type 2 diabetes mellitus.


International Journal of Laboratory Hematology | 2007

Pancytopenia and secondary myelofibrosis could be induced by primary hyperparathyroidism

Dong-Jun Lim; E. J. Oh; C.-W. Park; Hyuk-Sang Kwon; E.-J. Hong; Kun-Ho Yoon; Moon-Won Kang; Bong-Yun Cha; Kyungji Lee; H.-Y. Son; S Kang

Hyperparathyroidism may be a precipitating factor important to the development of myelofibrosis: however, there has been only a few reports regarding myelofibrosis secondary to primary hyperparathyroidism. Recently, a rare case of pancytopenia caused by myelofibrosis in a 41‐year‐old woman who complained of general weakness and arthralgia presented to our clinical service. The patient was diagnosed with primary hyperparathyroidism with pancytopenia. Bone marrow biopsy revealed myelofibrosis. Right parathyroidectomy was performed and a parathyroid adenoma was totally excised. After surgery, the CBC counts and other clinical abnormalities gradually improved without further intervention. We concluded that the pancytopenia was because of bone marrow fibrosis resulting from primary hyperparathyroidism. Therefore, physicians should consider myelofibrosis secondary to primary hyperparathyroidism as a cause of pancytopenia in hypercalcemic patients, even though it is rare.

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Bong-Yun Cha

Catholic University of Korea

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Kun-Ho Yoon

Catholic University of Korea

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Kyungji Lee

Catholic University of Korea

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S Kang

Catholic University of Korea

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Hyuk-Sang Kwon

Catholic University of Korea

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Ki-Ho Song

Catholic University of Korea

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Moon-Won Kang

Catholic University of Korea

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Sung-Rae Kim

Catholic University of Korea

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Yu-Bai Ahn

Catholic University of Korea

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