Pub Date : 2009-09-01DOI: 10.3803/JKES.2009.24.3.189
Se Kyung Park, Duk Su Kim, M. Roh, M. Song, C. Jung, J. Jung, H. Park, Y. Kim, J. Mok, Sang Jin Kim, C. Kim, Dong Won Kim, D. Byun, K. Suh, M. Yoo
Pheochromocytoma not only decreases insulin secretion but also increases insulin resistance. One third of patients with pheochromocytoma have diabetes mellitus and their clinical prognosis showed improvement after surgery. Until now, those patients whose prognosis for diabetes mellitus improved after the operation of pheochromocytoma had typical characteristics such as hypertension, palpitation, headache and elevated hormones such as Vanillylmandelic acid, metanephrine, epinephrine and norepinephrine. We present the case of a 75-year-old woman with asymptomatic adrenal incidentaloma identified as pheochromocytoma which exhibited normal biochemical test results, and after removal of the abdominal mass, her severe hyperglycemia improved.
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Pub Date : 2009-09-01DOI: 10.3803/JKES.2009.24.3.201
M. Yang, S. Han, Min-Seok Lee, Eun Kyung Kim, H. Kim, D. Kim, Yoon-Sok Chung, Tae Hee Lee, Jang-Hee Kim, K. Lee
Primary aldosteronism is a syndrome characterized by various clinical features that are due to excessive autonomous aldosterone secretion not sustained by the activation of the renin-angiotensin system. Aldosterone-producing adrenal adenoma is found in approximately 35% of the patients who suffer with primary aldosteronism. Laparoscopic adrenalectomy is the standard treatment for aldosterone-producing adrenal adenoma, and the result of this operation is normalization of the serum potassium and plasma aldosterone concentrations, as well as correcting the plasma renin activity in most cases. However, it is known that some of the patients with aldosterone-producing adrenal adenoma show transient hyperkalemia postoperatively due to the reversible suppression of the renin-aldosterone axis. We recently experienced the case of a 54-year-old woman with an aldosterone-producing adrenal adenoma, and she presented with severe hyperkalemia after unilateral adrenalectomy. Compared with the previously reported cases that showed transient suppression of the rennin-aldosterone axis for less than 7 months, our patient revealed a prolonged episode of hyperkalemia for 8 months postoperatively, and this required continuous mineralocorticoid replacement. (J Korean Endocr Soc 24:201~205, 2009) ꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏ
{"title":"A Case of Persistent Hyperkalemia After Unilateral Adrenalectomy for Aldosterone-Producing Adenoma","authors":"M. Yang, S. Han, Min-Seok Lee, Eun Kyung Kim, H. Kim, D. Kim, Yoon-Sok Chung, Tae Hee Lee, Jang-Hee Kim, K. Lee","doi":"10.3803/JKES.2009.24.3.201","DOIUrl":"https://doi.org/10.3803/JKES.2009.24.3.201","url":null,"abstract":"Primary aldosteronism is a syndrome characterized by various clinical features that are due to excessive autonomous aldosterone secretion not sustained by the activation of the renin-angiotensin system. Aldosterone-producing adrenal adenoma is found in approximately 35% of the patients who suffer with primary aldosteronism. Laparoscopic adrenalectomy is the standard treatment for aldosterone-producing adrenal adenoma, and the result of this operation is normalization of the serum potassium and plasma aldosterone concentrations, as well as correcting the plasma renin activity in most cases. However, it is known that some of the patients with aldosterone-producing adrenal adenoma show transient hyperkalemia postoperatively due to the reversible suppression of the renin-aldosterone axis. We recently experienced the case of a 54-year-old woman with an aldosterone-producing adrenal adenoma, and she presented with severe hyperkalemia after unilateral adrenalectomy. Compared with the previously reported cases that showed transient suppression of the rennin-aldosterone axis for less than 7 months, our patient revealed a prolonged episode of hyperkalemia for 8 months postoperatively, and this required continuous mineralocorticoid replacement. (J Korean Endocr Soc 24:201~205, 2009) ꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏ","PeriodicalId":119859,"journal":{"name":"Journal of Korean Endocrine Society","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2009-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"127229692","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2009-09-01DOI: 10.3803/JKES.2009.24.3.162
J. G. Kim
162 저혈당은 증상이 발현되는 시간에 따라서 공복 저혈당과 식후(반응성) 저혈당으로 분류가 되며 공복 저혈당의 원인으 로는 당뇨병 치료에 쓰이는 인슐린, 경구용 혈당강하제 등의 사용과 관련되어 흔하게 나타난다. 인슐린 길항호르몬인 성 장호르몬, 부신호르몬 등 부족과 관련된 저혈당, 그리고 음 주 후 발생되는 저혈당 등도 공복 저혈당의 빈번한 원인을 차지하고 있다. 한편 위의 원인들 외에 내인성 고인슐린혈증이 공복 저혈 당의 원인이 되기도 하는데 그 대표적인 질환들이 인슐린종 (insulinoma)과 인슐린자가면역 증후군(insulin autoimmune syndrome, 이하 IAS)이며 발생 빈도는 다른 공복 저혈당의 원인질환들에 비해 매우 드물다. IAS는 인슐린을 투여 받은 병력이 없는 환자에게서 인슐린자가항체가 나타나며 혈중 인슐린이 상승되어 있고 공복 저혈당을 특징으로 하는 질환 이다. 1972년 Hirata 등[1]이 처음 보고한 이래로 일본뿐만 아니라 우리나라에서도 내인성 고인슐린혈증에 의한 저혈당 의 흔한 원인으로 알려져 있으며, 일본에서 특히 서양인에 비해 IAS 환자가 많은 이유는 특정 HLA type 인구가 많은 것으로 DRB1*0406과 관련 있다고 하였다[2]. 인슐린종 역시 드문 질환으로서 90%가 양성 종양이며 매 년 25만 명 당 1명 정도 발생된다. 평균 발병 연령이 50대이 고 60%가 여성이나 다발성 내분비선종(1형)의 경우는 비교 적 젊은 나이에도 발생될 수 있다. 인슐린종의 크기는 직경 1~2 cm 정도가 거의 대부분으로 저혈당 증상을 호소하지 않으면 발견되기 어렵다. 임상적으로 혈당에 대한 반응이 둔 화되어 혈당이 심하게 떨어지지 않으면 증상을 유발하지 않 는다. Octreotide 스캔으로 과반수 환자에서 종양의 위치를 찾을 수 있으며 진단을 위해 동맥조영술을 할 수 있지만 위 음성, 위양성이 많아서 비침습적인 CT, MRI가 추천되며 45~75% 발견 가능하다. IAS는 고인슐린혈증, 공복 저혈당 증상과 함께 자가항체가 확인되면 쉽게 진단할 수 있으며 저혈당 원인이 되는 항체로 는 인슐린자가항체(insulin antibody) 또는 인슐린 수용체 항 체(insulin receptor antibody)가 있다. IAS의 발생에는 그레이 브스병이나 류마티스 관절염과 같은 자가면역 질환이 관련되 어 있다는 보고들[3,4]이 있으며, methimazole, penicillamine, procainamide 등 sulfhydryl기나 amide기를 포함하는 약제 들[4~7]과, captopril[8], imipenem[9], penicillin G[10], 그 리고 α-lipoic acid[11]를 복용한 환자에서 IAS의 발생이 보 고되고 있다. Ichihara 등[5]은 IAS 환자에게 포도당을 정주했을 때 혈 당이 일시적으로 상승하여 내당능장애 상태가 되었다가 이 후 저혈당이 발생됨을 관찰하였고, 이는 포도당 주사에 의해 고인슐린혈증이 유발 되지만 즉시 혈중 항체와 결합하여 유 리 인슐린이 오히려 줄어들어 고혈당이 유발 되고 그 이후 인슐린이 항체에서 유리되면 저혈당이 발생된다고 하였다. 박 등[12]이 보고한 증례도 IAS 환자에서 경구당부하검사를 했을 때 내당능장애를 보였고 이후 고인슐린혈증, 저혈당이 발생되었다. 정 등의 연구[13]에서 인슐린종과 IAS에서 당 화혈색소가 유의한 차이를 보이고 있으며(5.0% vs 5.6%, P < 0.05) IAS 환자에서 대조군의 당화혈색소 5.4% 보다 높 은 것으로 보아 상당수의 IAS 환자에서 내당능장애가 동반 된 것으로 판단된다. 일반적으로 저혈당이 시작되면 생리적으로 즉시 인슐린 분비가 차단된다[14]. 이후 인슐린 길항호르몬들이 순차적으 로 반응을 보이는데 그 중 글루카곤은 가장 빨리 그리고 가 장 중요한 역할을 담당한다[15]. 주로 해당작용 및 당신생을 촉진하게 되며 글루카곤의 반응이 적절하지 못한 경우에는 epinephrine이 다음으로 반응하며 당신생 외에도 인슐린 감 수성 조직에서 포도당의 이용을 제한하게 된다. 저혈당이 지 속되게 되면 성장호르몬과 코르티솔의 작용에 의해 포도당 의 이용이 줄어들고 당신생을 촉진시키게 된다. 내인성 고인슐린혈증에 의한 저혈당증에서의 포도당 길항호르몬 반응
162低血糖根据症状出现的时间分为空腹低血糖和饭后(反应性)低血糖，空腹低血糖的原因与糖尿病治疗用胰岛素、口服用血糖强化剂等的使用有关。胰岛素抗激素——生长激素、肾上腺激素等与不足相关的低血糖，还有饮后发生的低血糖等也是空腹低血糖频繁的原因之一。另外，内因性高胰岛素血症也可能是空腹低血糖的原因，其中最常见的疾病是胰岛素瘤(insulinoma)和胰岛素自体免疫综合征(insulin autoimmune syndrome，以下简称IAS)，与其他空腹低血糖疾病相比发生频率非常低。IAS是一种没有注射胰岛素病史的患者出现胰岛素自身抗体，血液中胰岛素上升，空腹低血糖为特征的疾病。1972年hirata等[1]第一次报告以来,不仅在日本,在我国也内源性胰岛素血症引起的低血糖的常见的原因是众所周知的,在日本,尤其是西方人相比,ias患者多的原因是将特定hla type人口众多有关drb1 * 0406”[2]。胰岛素瘤也是一种罕见的疾病，90%为良性肿瘤，每年每25万人中有1人发生胰岛素瘤。平均发病年龄为50多岁，60%为女性或多发性内分泌腺瘤(1型)在比较年轻的年龄也有可能发生。胰岛素种类的直径几乎为1~2厘米，如果不出现低血糖症状，就很难发现。在临床上，如果对血糖的反应钝化，血糖没有严重下降，就不会引发症状。Octreotide扫描可在过半数患者中找到肿瘤的位置，并可进行动脉造影诊断，但由于胃阴性、胃阳性较多，推荐非侵袭性CT、MRI，可发现45%至75%。IAS有高胰岛素血症、空腹低血糖症状，如果确认自身抗体，就很容易诊断，低血糖的原因有胰岛素自身抗体(insulin antibody)或胰岛素受体抗体(insulin receptor antibody)。IAS的发生与自身免疫疾病相关的报告[3,4]，包括甲基苯丙胺，penicillamine, procainamide等含有sulfhydryl或amide的药剂[4~7]，captopril[8]， imipenem[9]， penicillin G[10];服用格里戈α-lipoic acid[11]的患者中，IAS的发生正在增加。ichihara等[5]是ias给病人把葡萄糖郑州时血党暂时上升,我成了功能障碍状态,这后观察了随着低血糖的发生,这是被注射葡萄糖高胰岛素血症引发,但立刻和血液中的抗体结合胰岛素反而下降,诱发高血糖,此后胰岛素抗体的有利就发生了低血糖。朴等[12]报告的病例也在IAS患者口服嘱咐下检查时出现内糖功能障碍，此后发生高胰岛素血症，低血糖。在郑等人的研究[13]中，胰岛素瘤和IAS中糖化血红蛋白有显著差异(5.0% vs 5.6%， P < 0.05)， IAS患者中糖化血红蛋白高于对照组的5.4%，可见相当多的IAS患者同时出现了内糖功能障碍。通常低血糖开始后，生理上立即阻断胰岛素分泌[14]。此后胰岛素拮抗激素依次发生反应，其中胰高血糖素起着最快和最重要的作用[15]。如果胰高血糖素的反应不适当，epinephrine会其次反应，胰岛素感受性组织也会限制葡萄糖的使用。低血糖减慢，生长激素和皮质醇的作用会减少葡萄糖的利用，促进你的生命。内源性高胰岛素血症引起的低血糖症中葡萄糖吉抗激素的反应
{"title":"Glucose Counterregulatory Hormone Response During Hypoglycemia due to Endogenous Hyperinsulinemia","authors":"J. G. Kim","doi":"10.3803/JKES.2009.24.3.162","DOIUrl":"https://doi.org/10.3803/JKES.2009.24.3.162","url":null,"abstract":"162 저혈당은 증상이 발현되는 시간에 따라서 공복 저혈당과 식후(반응성) 저혈당으로 분류가 되며 공복 저혈당의 원인으 로는 당뇨병 치료에 쓰이는 인슐린, 경구용 혈당강하제 등의 사용과 관련되어 흔하게 나타난다. 인슐린 길항호르몬인 성 장호르몬, 부신호르몬 등 부족과 관련된 저혈당, 그리고 음 주 후 발생되는 저혈당 등도 공복 저혈당의 빈번한 원인을 차지하고 있다. 한편 위의 원인들 외에 내인성 고인슐린혈증이 공복 저혈 당의 원인이 되기도 하는데 그 대표적인 질환들이 인슐린종 (insulinoma)과 인슐린자가면역 증후군(insulin autoimmune syndrome, 이하 IAS)이며 발생 빈도는 다른 공복 저혈당의 원인질환들에 비해 매우 드물다. IAS는 인슐린을 투여 받은 병력이 없는 환자에게서 인슐린자가항체가 나타나며 혈중 인슐린이 상승되어 있고 공복 저혈당을 특징으로 하는 질환 이다. 1972년 Hirata 등[1]이 처음 보고한 이래로 일본뿐만 아니라 우리나라에서도 내인성 고인슐린혈증에 의한 저혈당 의 흔한 원인으로 알려져 있으며, 일본에서 특히 서양인에 비해 IAS 환자가 많은 이유는 특정 HLA type 인구가 많은 것으로 DRB1*0406과 관련 있다고 하였다[2]. 인슐린종 역시 드문 질환으로서 90%가 양성 종양이며 매 년 25만 명 당 1명 정도 발생된다. 평균 발병 연령이 50대이 고 60%가 여성이나 다발성 내분비선종(1형)의 경우는 비교 적 젊은 나이에도 발생될 수 있다. 인슐린종의 크기는 직경 1~2 cm 정도가 거의 대부분으로 저혈당 증상을 호소하지 않으면 발견되기 어렵다. 임상적으로 혈당에 대한 반응이 둔 화되어 혈당이 심하게 떨어지지 않으면 증상을 유발하지 않 는다. Octreotide 스캔으로 과반수 환자에서 종양의 위치를 찾을 수 있으며 진단을 위해 동맥조영술을 할 수 있지만 위 음성, 위양성이 많아서 비침습적인 CT, MRI가 추천되며 45~75% 발견 가능하다. IAS는 고인슐린혈증, 공복 저혈당 증상과 함께 자가항체가 확인되면 쉽게 진단할 수 있으며 저혈당 원인이 되는 항체로 는 인슐린자가항체(insulin antibody) 또는 인슐린 수용체 항 체(insulin receptor antibody)가 있다. IAS의 발생에는 그레이 브스병이나 류마티스 관절염과 같은 자가면역 질환이 관련되 어 있다는 보고들[3,4]이 있으며, methimazole, penicillamine, procainamide 등 sulfhydryl기나 amide기를 포함하는 약제 들[4~7]과, captopril[8], imipenem[9], penicillin G[10], 그 리고 α-lipoic acid[11]를 복용한 환자에서 IAS의 발생이 보 고되고 있다. Ichihara 등[5]은 IAS 환자에게 포도당을 정주했을 때 혈 당이 일시적으로 상승하여 내당능장애 상태가 되었다가 이 후 저혈당이 발생됨을 관찰하였고, 이는 포도당 주사에 의해 고인슐린혈증이 유발 되지만 즉시 혈중 항체와 결합하여 유 리 인슐린이 오히려 줄어들어 고혈당이 유발 되고 그 이후 인슐린이 항체에서 유리되면 저혈당이 발생된다고 하였다. 박 등[12]이 보고한 증례도 IAS 환자에서 경구당부하검사를 했을 때 내당능장애를 보였고 이후 고인슐린혈증, 저혈당이 발생되었다. 정 등의 연구[13]에서 인슐린종과 IAS에서 당 화혈색소가 유의한 차이를 보이고 있으며(5.0% vs 5.6%, P < 0.05) IAS 환자에서 대조군의 당화혈색소 5.4% 보다 높 은 것으로 보아 상당수의 IAS 환자에서 내당능장애가 동반 된 것으로 판단된다. 일반적으로 저혈당이 시작되면 생리적으로 즉시 인슐린 분비가 차단된다[14]. 이후 인슐린 길항호르몬들이 순차적으 로 반응을 보이는데 그 중 글루카곤은 가장 빨리 그리고 가 장 중요한 역할을 담당한다[15]. 주로 해당작용 및 당신생을 촉진하게 되며 글루카곤의 반응이 적절하지 못한 경우에는 epinephrine이 다음으로 반응하며 당신생 외에도 인슐린 감 수성 조직에서 포도당의 이용을 제한하게 된다. 저혈당이 지 속되게 되면 성장호르몬과 코르티솔의 작용에 의해 포도당 의 이용이 줄어들고 당신생을 촉진시키게 된다. 내인성 고인슐린혈증에 의한 저혈당증에서의 포도당 길항호르몬 반응","PeriodicalId":119859,"journal":{"name":"Journal of Korean Endocrine Society","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2009-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"131278884","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2009-09-01DOI: 10.3803/JKES.2009.24.3.165
J. Park, Ji In Lee, A. H. Tan, H. W. Jang, H. Shin, Y. Oh, J. Shin, J. H. Kim, J. S. Kim, Y. Son, S. Kim, J. Chung
Background: The outcomes of papillary thyroid carcinoma (PTC) variants have been described in a limited number of studies. The purpose of this study was to compare patient outcomes of PTC variants with those of patients with classic PTC. Methods: A single-institution retrospective analysis was performed to review 2,366 patients with classic PTC and 159 patients with PTC variants diagnosed between 1994 and 2004. PTC variant patients were divided into two groups, favorable (n = 119, 119 follicular variants including 14 encapsulated follicular variants) and aggressive (n = 40, including 13 diffuse sclerosing, 11 tall cell, six solid, six oncocytic, and four columnar cell variants). Results: Compared with classic PTC, the favorable and aggressive variants had a significantly larger tumor size (P < 0.001). The favorable variants had significantly lower rates of bilaterality, multifocality, extrathyroidal invasion, cervical lymph node metastasis, stage III and IV disease, and greater male to female ratio (P < 0.05). In particular, the encapsulated follicular variant showed no bilaterality, multifocality, extrathyroidal invasion, lymph node metastasis, and distant metastasis. However, the disease-specific survival and recurrence-free survival of patients with favorable PTC were not different from the patients with classic PTC. The aggressive variants had significantly higher rates of bilaterality and cervical lymph node metastasis compared to the classic PTC (P < 0.05). They had significantly reduced disease-specific survival and recurrence-free survival rates (P < 0.01). Conclusions: Knowledge of the nature of PTC variants, especially aggressive types, is important in predicting patient outcome and providing appropriate treatment. Further study is needed to better understand PTC variants. (J Korean Endocr Soc 24:165~173, 2009) ꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏ
{"title":"Clinical Differences between Classic Papillary Thyroid Carcinoma and Variants","authors":"J. Park, Ji In Lee, A. H. Tan, H. W. Jang, H. Shin, Y. Oh, J. Shin, J. H. Kim, J. S. Kim, Y. Son, S. Kim, J. Chung","doi":"10.3803/JKES.2009.24.3.165","DOIUrl":"https://doi.org/10.3803/JKES.2009.24.3.165","url":null,"abstract":"Background: The outcomes of papillary thyroid carcinoma (PTC) variants have been described in a limited number of studies. The purpose of this study was to compare patient outcomes of PTC variants with those of patients with classic PTC. Methods: A single-institution retrospective analysis was performed to review 2,366 patients with classic PTC and 159 patients with PTC variants diagnosed between 1994 and 2004. PTC variant patients were divided into two groups, favorable (n = 119, 119 follicular variants including 14 encapsulated follicular variants) and aggressive (n = 40, including 13 diffuse sclerosing, 11 tall cell, six solid, six oncocytic, and four columnar cell variants). Results: Compared with classic PTC, the favorable and aggressive variants had a significantly larger tumor size (P < 0.001). The favorable variants had significantly lower rates of bilaterality, multifocality, extrathyroidal invasion, cervical lymph node metastasis, stage III and IV disease, and greater male to female ratio (P < 0.05). In particular, the encapsulated follicular variant showed no bilaterality, multifocality, extrathyroidal invasion, lymph node metastasis, and distant metastasis. However, the disease-specific survival and recurrence-free survival of patients with favorable PTC were not different from the patients with classic PTC. The aggressive variants had significantly higher rates of bilaterality and cervical lymph node metastasis compared to the classic PTC (P < 0.05). They had significantly reduced disease-specific survival and recurrence-free survival rates (P < 0.01). Conclusions: Knowledge of the nature of PTC variants, especially aggressive types, is important in predicting patient outcome and providing appropriate treatment. Further study is needed to better understand PTC variants. (J Korean Endocr Soc 24:165~173, 2009) ꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏ","PeriodicalId":119859,"journal":{"name":"Journal of Korean Endocrine Society","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2009-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"122201738","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2009-09-01DOI: 10.3803/JKES.2009.24.3.212
Eun-Kyung Kim, Min Suk Lee, Yoon-Sok Chung, Kyu-sung Kwack, Ji-Hee Hong, Y. Won
Many studies have shown that patients taking antiepileptic drugs are at an increased risk for metabolic bone disease and low bone mineral density. Traditionally, this has been attributed to alterations in vitamin D metabolism by antiepileptic drugs which induce hepatic microsomal cytochrome P450 enzyme. However, there appear to be multiple mechanisms for antiepileptic drug-induced bone loss including lack of physical activity, reduced sunlight exposure, increased propensity for falling, and fractures associated with seizures or loss of consciousness. We experienced a case of antiepileptic drug-induced osteomalacia in a 63-year-old woman who had been on phenytoin for 8 years and was admitted with hypocalcemic seizures and multiple pathological fractures. This patient also had other risk factors for osteomalacia including reduced sunlight exposure, prolonged immobilization, and decreased dietary vitamin D intake. We discontinued phenytoin, and started calcium and vitamin D replacemen t. The patient's serum calcium and vitamin D level were normalized after treatment. Metabolic bone disease including osteomalacia should be considered in patients who are taking antiepileptic drugs especially those who are exposed to other risk factors. (J Korean Endocr Soc 24:212~216, 2009) ꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏ
{"title":"A Case of Osteomalacia with Multiple Fractures and Hypocalcemia Associated with Phenytoin Therapy","authors":"Eun-Kyung Kim, Min Suk Lee, Yoon-Sok Chung, Kyu-sung Kwack, Ji-Hee Hong, Y. Won","doi":"10.3803/JKES.2009.24.3.212","DOIUrl":"https://doi.org/10.3803/JKES.2009.24.3.212","url":null,"abstract":"Many studies have shown that patients taking antiepileptic drugs are at an increased risk for metabolic bone disease and low bone mineral density. Traditionally, this has been attributed to alterations in vitamin D metabolism by antiepileptic drugs which induce hepatic microsomal cytochrome P450 enzyme. However, there appear to be multiple mechanisms for antiepileptic drug-induced bone loss including lack of physical activity, reduced sunlight exposure, increased propensity for falling, and fractures associated with seizures or loss of consciousness. We experienced a case of antiepileptic drug-induced osteomalacia in a 63-year-old woman who had been on phenytoin for 8 years and was admitted with hypocalcemic seizures and multiple pathological fractures. This patient also had other risk factors for osteomalacia including reduced sunlight exposure, prolonged immobilization, and decreased dietary vitamin D intake. We discontinued phenytoin, and started calcium and vitamin D replacemen t. The patient's serum calcium and vitamin D level were normalized after treatment. Metabolic bone disease including osteomalacia should be considered in patients who are taking antiepileptic drugs especially those who are exposed to other risk factors. (J Korean Endocr Soc 24:212~216, 2009) ꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏ","PeriodicalId":119859,"journal":{"name":"Journal of Korean Endocrine Society","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2009-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"133519245","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2009-09-01DOI: 10.3803/JKES.2009.24.3.174
J. Chung, D. Cho, D. Chung, M. Chung
Background: In patients with hypoglycemia due to endogenous hyperinsulinemia such as insulinoma or insulin autoimmune syndrome, little is known about the counterregulatory hormone response to spontaneous hypoglycemia. We therefore compared hormone responses during spontaneous hypoglycemia due to endogenous hyperinsulinemia with those at the end of a 72-hour fast. Methods: We measured glucagon, epinephrine, cortisol, and growth hormone responses during spontaneous hypoglycemia in 8 patients with insulinoma and 18 patients with insulin autoimmune syndrome. We also assessed these responses in 13 normal control subjects who underwent a 72-hour fast. Results: In patients with insulinoma (median serum glucose level, 35.0 mg/dL), plasma glucagon levels (median, 42.9 vs. 76.2 pg/mL, respectively; P < 0.05) were lower than those in control subjects (serum glucose level, 62.5 mg/dL), whereas, there were no statistically significant differences in the other hormone responses between the two groups. In contrast, in the patients with insulin autoimmune syndrome (median serum glucose level, 34.5 mg/dL), plasma glucagon levels (median, 73.7 vs. 76.2 pg/mL, respectively) were lower than those in the control subjects, but there was no statistically significant difference between the two groups. There were no statistically significant differences in counterregulatory hormone responses during spontaneous hypoglycemia between patients with insulinoma and patients with insulin autoimmune syndrome. Conclusion: Our results suggest that defective glucagon secretion in patients with insulinoma rather than insulin autoimmune syndrome may contribute to hypoglycemia in addition to hyperinsulinemia. (J Korean
背景:在内源性高胰岛素血症(如胰岛素瘤或胰岛素自身免疫性综合征)引起的低血糖患者中，对自发性低血糖的反调节激素反应知之甚少。因此，我们比较了内源性高胰岛素血症引起的自发性低血糖和72小时禁食结束时的激素反应。方法:我们测量了8例胰岛素瘤患者和18例胰岛素自身免疫性综合征患者自发性低血糖时胰高血糖素、肾上腺素、皮质醇和生长激素的反应。我们还评估了13名进行72小时禁食的正常对照者的这些反应。结果:在胰岛素瘤患者(中位血清葡萄糖水平，35.0 mg/dL)，血浆胰高血糖素水平(中位，42.9 vs. 76.2 pg/mL;P < 0.05)均低于对照组(血清葡萄糖62.5 mg/dL)，而两组其他激素反应差异无统计学意义。相比之下，胰岛素自身免疫性综合征患者(血清葡萄糖水平中位数为34.5 mg/dL)，血浆胰高血糖素水平(中位数分别为73.7 vs 76.2 pg/mL)低于对照组，但两组间差异无统计学意义。胰岛素瘤患者与胰岛素自身免疫综合征患者自发性低血糖时的反调节激素反应无统计学差异。结论:我们的研究结果表明，除了高胰岛素血症外，胰岛素瘤患者胰高血糖素分泌缺陷可能导致低血糖，而不是胰岛素自身免疫性综合征。(J韩国
{"title":"Glucose Counterregulatory Hormone Response During Hypoglycemia due to Endogenous Hyperinsulinemia","authors":"J. Chung, D. Cho, D. Chung, M. Chung","doi":"10.3803/JKES.2009.24.3.174","DOIUrl":"https://doi.org/10.3803/JKES.2009.24.3.174","url":null,"abstract":"Background: In patients with hypoglycemia due to endogenous hyperinsulinemia such as insulinoma or insulin autoimmune syndrome, little is known about the counterregulatory hormone response to spontaneous hypoglycemia. We therefore compared hormone responses during spontaneous hypoglycemia due to endogenous hyperinsulinemia with those at the end of a 72-hour fast. Methods: We measured glucagon, epinephrine, cortisol, and growth hormone responses during spontaneous hypoglycemia in 8 patients with insulinoma and 18 patients with insulin autoimmune syndrome. We also assessed these responses in 13 normal control subjects who underwent a 72-hour fast. Results: In patients with insulinoma (median serum glucose level, 35.0 mg/dL), plasma glucagon levels (median, 42.9 vs. 76.2 pg/mL, respectively; P < 0.05) were lower than those in control subjects (serum glucose level, 62.5 mg/dL), whereas, there were no statistically significant differences in the other hormone responses between the two groups. In contrast, in the patients with insulin autoimmune syndrome (median serum glucose level, 34.5 mg/dL), plasma glucagon levels (median, 73.7 vs. 76.2 pg/mL, respectively) were lower than those in the control subjects, but there was no statistically significant difference between the two groups. There were no statistically significant differences in counterregulatory hormone responses during spontaneous hypoglycemia between patients with insulinoma and patients with insulin autoimmune syndrome. Conclusion: Our results suggest that defective glucagon secretion in patients with insulinoma rather than insulin autoimmune syndrome may contribute to hypoglycemia in addition to hyperinsulinemia. (J Korean","PeriodicalId":119859,"journal":{"name":"Journal of Korean Endocrine Society","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2009-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"128435677","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2009-09-01DOI: 10.3803/JKES.2009.24.3.181
Min Suk Lee, S. Han, Eun Kyung Kim, J. Hwang, Y. Chung, Se-Hyuk Kim, K. Cho, Nae-jung Rim, Ho Sung Kim
Background: The present study investigated the rates and the potential predictors of either new pituitary loss or recovery of hormonal function after transsphenoidal removal of a non-functioning pituitary adenoma. Methods: Patients who underwent transsphenoidal removal of a non-functioning pituitary adenoma from January 2003 to December 2007 at Ajou University Medical Center were included in this retrospective analysis. Patients were excluded if they had a history of previous pituitary tumor surgery, or did not have preoperative pituitary hormonal data. Results: Of 42 patients included in the analysis, 36 patients had hypopituitarism, 21 patients had "stalk compression" hyperprolactinemia, and 2 patients had normal pituitary function. At long term follow-up (longer than 6 months), 13 patients showed postoperative pituitary hormonal recovery in at least 1 hormonal axis, while 6 patients had developed postoperative hormonal loss in at least 1 hormonal axis. On analysis, neither preoperative serum prolactin level nor tumor size was related to postoperative pituitary hormonal changes. Conclusion: More than 1/3 of patients who underwent transsphenoidal surgery showed postoperative pituitary hormonal recovery. (J Korean Endocr Soc 24:181~188, 2009) ꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏ
{"title":"Pituitary Hormonal Changes after Transsphenoidal Tumor Removal in Non-Functioning Pituitary Adenoma","authors":"Min Suk Lee, S. Han, Eun Kyung Kim, J. Hwang, Y. Chung, Se-Hyuk Kim, K. Cho, Nae-jung Rim, Ho Sung Kim","doi":"10.3803/JKES.2009.24.3.181","DOIUrl":"https://doi.org/10.3803/JKES.2009.24.3.181","url":null,"abstract":"Background: The present study investigated the rates and the potential predictors of either new pituitary loss or recovery of hormonal function after transsphenoidal removal of a non-functioning pituitary adenoma. Methods: Patients who underwent transsphenoidal removal of a non-functioning pituitary adenoma from January 2003 to December 2007 at Ajou University Medical Center were included in this retrospective analysis. Patients were excluded if they had a history of previous pituitary tumor surgery, or did not have preoperative pituitary hormonal data. Results: Of 42 patients included in the analysis, 36 patients had hypopituitarism, 21 patients had \"stalk compression\" hyperprolactinemia, and 2 patients had normal pituitary function. At long term follow-up (longer than 6 months), 13 patients showed postoperative pituitary hormonal recovery in at least 1 hormonal axis, while 6 patients had developed postoperative hormonal loss in at least 1 hormonal axis. On analysis, neither preoperative serum prolactin level nor tumor size was related to postoperative pituitary hormonal changes. Conclusion: More than 1/3 of patients who underwent transsphenoidal surgery showed postoperative pituitary hormonal recovery. (J Korean Endocr Soc 24:181~188, 2009) ꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏ","PeriodicalId":119859,"journal":{"name":"Journal of Korean Endocrine Society","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2009-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"126003936","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2009-09-01DOI: 10.3803/JKES.2009.24.3.217
J. Chung, D. Cho, D. Chung, M. Chung
Intramural hematoma of the aorta is a variant of aortic dissection characterized by the absence of direct communication between the false lumen and the true lumen of the aorta. Primary aldosteronism, which is an uncommon cause of hypertension, may direct alter arterial structure through the pleiotropic effects of aldosterone as well as pressure-mediated indirect alterations. There have been several reported cases of aortic dissection in patients with primary aldosteronism, which suggests a causal relationship between the two diagnostic entities. However, intramural hematoma has not been described in a patient with primary aldosteronism. We describe a case of aortic intramural hematoma in a patient with primary aldosteronism and speculate about the causal relationship between these two entities. (J Korean Endocr Soc 24:217~220, 2009)
{"title":"Aortic Intramural Hematoma Associated with Primary Aldosteronism","authors":"J. Chung, D. Cho, D. Chung, M. Chung","doi":"10.3803/JKES.2009.24.3.217","DOIUrl":"https://doi.org/10.3803/JKES.2009.24.3.217","url":null,"abstract":"Intramural hematoma of the aorta is a variant of aortic dissection characterized by the absence of direct communication between the false lumen and the true lumen of the aorta. Primary aldosteronism, which is an uncommon cause of hypertension, may direct alter arterial structure through the pleiotropic effects of aldosterone as well as pressure-mediated indirect alterations. There have been several reported cases of aortic dissection in patients with primary aldosteronism, which suggests a causal relationship between the two diagnostic entities. However, intramural hematoma has not been described in a patient with primary aldosteronism. We describe a case of aortic intramural hematoma in a patient with primary aldosteronism and speculate about the causal relationship between these two entities. (J Korean Endocr Soc 24:217~220, 2009)","PeriodicalId":119859,"journal":{"name":"Journal of Korean Endocrine Society","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2009-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"128914116","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2009-06-01DOI: 10.3803/JKES.2009.24.2.93
H. Shin, H. W. Jang, Keun-Sook Kim, Ji In Lee, J. Park, S. Kim, Y. Min, Myung-Shik Lee, Moon-Kyu Lee, K. Kim, J. Chung
1 , ABSTRACT Background: Surgical excision is the only effective treatment of medullary thyroid carcinoma (MTC) and there is no certain treatment for recurrence or distant metastasis. Materials that influence MTC cell proliferation were recently reported. Presently, we evaluated the influence of dexamethasone, somatostatin, progesterone, estradiol-17-beta, forskolin and gastrin on MTC cell proliferation and calcitonin secretion. Methods: Genomic DNA was extracted and sequenced from untreated thyroid TT cells and cells treated with 10
{"title":"Search for Materials that Influence Human Medullary Thyroid Carcinoma Cell Proliferation","authors":"H. Shin, H. W. Jang, Keun-Sook Kim, Ji In Lee, J. Park, S. Kim, Y. Min, Myung-Shik Lee, Moon-Kyu Lee, K. Kim, J. Chung","doi":"10.3803/JKES.2009.24.2.93","DOIUrl":"https://doi.org/10.3803/JKES.2009.24.2.93","url":null,"abstract":"1 , ABSTRACT Background: Surgical excision is the only effective treatment of medullary thyroid carcinoma (MTC) and there is no certain treatment for recurrence or distant metastasis. Materials that influence MTC cell proliferation were recently reported. Presently, we evaluated the influence of dexamethasone, somatostatin, progesterone, estradiol-17-beta, forskolin and gastrin on MTC cell proliferation and calcitonin secretion. Methods: Genomic DNA was extracted and sequenced from untreated thyroid TT cells and cells treated with 10","PeriodicalId":119859,"journal":{"name":"Journal of Korean Endocrine Society","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2009-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"132970133","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2009-06-01DOI: 10.3803/JKES.2009.24.2.87
E. Jun, Hyun Sook Kim, H. Chung, J. Lee, S. Kim, E. Jung
Background: Thyroid hormones play an important role in the regulation of lipid and carbohydrate metabolism and the body mass index (BMI), which all affect non-alcoholic fatty liver disease (NAFLD). In a previous study, we demonstrated that free T4 was negatively associated with the BMI in euthyroid women. However, there is still uncertain as to whether the thyroid function within the normal range is associated with NAFLD and liver function abnormalities. We sought to evaluate the thyroid function (free T4, TSH) and its possible relationship with NAFLD in euthyroid women. Methods: A total of 835 euthyroid, non heavy alcoholics women who visit ed the Daegu Catholic University University Medical Centre for primary health screening from January 1, 2006 to December 31, 2006 participated in this cross-sectional study. The women who were not euthyroid or heavy alcoholics (> 70 g/week in women according to the DSM-IV), there was no known history of diabetes mellitus, the fasting blood glucose was more than 5.55 mmol/L and those who had viral hepatitis were excluded. Hepatic ultrasonography scanning was performed in all the participants by a single experienced radiologist. The TSH, free T4, BP, fasting glucose, serum liver enzymes (AST, ALT, GGT, T-bilirubin), lipid profiles [total-cholesterol, triglyceride (TG), HDL-C, LDL-C] and NAFLD were evaluated. Results: Euthyroid women with NAFLD had lower free T4 levels than did the euthyroid women without NAFLD. After adjustment for age and BMI, free T4 was negatively correlated with TG, but free T4 was positively correlated with the total serum bilirubin. Free T4 was not correlated with the serum AST, ALT and GGT. After adjustment for age, the BMI, the fasting glucose, the GGT and free T4, but not TSH, were significantly negatively correlated with NAFLD. Conclusion: We demonstrated a negative correlation between free T4 and NAFLD in euthyroid women. This finding suggests lower levels of free T4 is associated with NAFLD in euthyroid subjects. (J Korean
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