101秋季會

目 錄 理監事名單............................................................ 2 交通資訊................................................................ 3 會場圖.................................................................... 7 會長致詞................................................................ 8 理事長致詞............................................................ 9 程序表................................................................. 11 節目表................................................................. 12 特別演講摘要..................................................... 15 論文口頭發表摘要............................................. 23 論文壁報發表摘要............................................. 33 論文發表注意事項............................................. 45

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中華民國內分泌暨糖尿病學會 101年度秋季學術研討

中華民國內分泌學會 第十一屆理監事名單

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中華民國糖尿病學會 第十一屆理監事名單

理 事 長： 張慶忠

理 事 長： 莊立民

常務理事： 王佩文

常務理事： 許惠恒

黃天祥

陳榮福

理 事： 王治元

理 事： 杜思德

翁錦興

辛錫璋

陳思達

莊峻鍠

曾芬郁

黃禹堯

劉瑞川

葉振聲

蔡克嵩

裴 馰

鄧錦泉

蔡世澤

簡銘男

謝明家

常務監事： 林仁德

常務監事： 何橈通

監 事： 林宏達

監 事： 李洮俊

張天鈞

戴東原

秘 書 長： 陳沛隆

秘 書 長： 江怡德

副秘書長： 施翔蓉

副秘書長： 張恬君

林桓生

李弘元

交通資訊

交通資訊 會場：中國醫藥大學【立夫教學大樓】 B

1

國

際

會

議

廳

地址：40402台中市北區學士路91號

會場

中國醫藥大學校區分佈圖

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中華民國內分泌暨糖尿病學會 101年度秋季學術研討

學會免費接駁車（平和旅行社）  台北-台大醫院 台北集合地點：台大醫院-中山南路東址大廳 台北集合時間：9月1日（星期六）上午08:50 台北發車時間：9月1日（星期六）上午09:00 行駛路線：台大醫院→中國醫藥大學→台中金典酒店 導遊：高語婕小姐 電話：0932-044-483 王惠玲小姐 電話：0952-383-571 王昭富先生 電話：0927-830-988  林口-長庚醫院 林口集合地點：林口長庚醫學大樓 林口集合時間：9月1日（星期六）上午09:20 林口發車時間：9月1日（星期六）上午09:30 行駛路線：林口長庚醫院→中國醫藥大學→台中金典酒店 導遊：張奇旻先生 電話：0939-011-754  台中-高鐵烏日站 烏日站集合時間：9月1日（星期六）上午11:10 烏日站發車時間：9月1日（星期六）上午11:15 高 鐵 建 議 搭 乘：南下633列車 / 北上632列車 烏日站集合地點：高鐵烏日站2F大廳4B出口7-11便利商店前集合後，由導遊統一帶至 1F遊覽車上車處。 行駛路線：高鐵烏日站→中國醫藥大學→台中金典酒店 導遊：何玉珍小姐 電話：0955-991-174 李明賢小姐 電話：0920-778-930

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交通資訊

高鐵烏日站免費接駁車 （統聯客運）～需保留高鐵票根～ 上車地點：6 號出口13號月台 下車地點：學士路中國醫藥大學 （車程約40分鐘）

高 鐵 烏 日 站 發 車 時 刻 表 時 07 08 09 10 11 12

10 10 10 10 10

~ 分 35 45 30 45 30 45 30 45 30 45 30 45

55 55 55 55 55 55

時 13 14 15 16 17 18

10 10 10 10 10 10

~ 分 30 45 30 45 30 45 30 45 30 45 30 45

55 55 55 55 55 55

【自行開車】 1. 走國道 1 號 南下：由174.2K大雅交流道下，經中清路→大雅路左轉英才路，與學士路交叉 口，即可到達。 北上：由178.6K台中交流道下，經中港路左轉英才路，與學士路交叉口，即可到 達。 2. 走國道 3 號 南下：由176.1K沙鹿交流道下，經中清路→大雅路左轉英才路，與學士路交叉 口，即可到達。 北上：由209.0K中投交流道下，經中投快速道路→五權南路→五權路左轉學士 路，即可到達。

中國醫藥大學地理位置圖

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中華民國內分泌暨糖尿病學會 101年度秋季學術研討

【停車資訊】 本會補助會員，會議當日可在中國醫藥大學附設醫院院區內由竑穗興業有限公司經營之 「五權立體停車場」及「復建大樓停車場」享免費停車。免費停車卡，需在會場立夫教學 大樓1F報到處，向學會工作人員領取。於駛離停車場時，將此卡交予停車場收費人員即 可享免費停車。提醒開車前往的會員，週六看診病患人數仍多，復健大樓停車場車位易客 滿，建議可直接前往「五權立體停車場」停車。 (1) 五權立體停車場（平面車位）【竑穗興業有限公司】 台中市北區五權路499號---〈重症與預防醫學大樓附近〉 (2) 復建大樓停車場（機械式車位）【竑穗興業有限公司】 台中市北區學士路 91 號 ---〈兒童與復健醫療大樓附近〉 (3) 中正公園地下停車場（平面車位）【永耕建設股份有限公司】 ....（每小時40元）本停車場無停車優惠.... 台中市北區學士路108號【立夫醫療大樓】

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交通資訊

立夫教學大樓 平面圖

1樓

B1樓

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中華民國內分泌暨糖尿病學會 101年度秋季學術研討

會 長致 詞 各位內分泌暨糖尿病學會的會員朋友，大家好！ 首先謹代表中國醫藥大學附設醫院，歡迎各位先進，蒞臨參加 內分泌暨糖尿病學會舉辦的秋季研討會。本院成立於1985年，草創 之初，篳路藍縷，近十年來，在蔡董事長的領導之下，積極延攬海 內外優秀人才，邁向世界五百大。本院在內分泌外科方面，無論是 腦下垂體、甲狀腺、腎上腺或胰臟手術方面，成績有目共睹，今年 更引進達文西機器人手術，嘉惠病患。本院內分泌新陳代謝科，近 年來與中央研究院合作研究的第2型糖尿病易感基因，成績斐然，與 日韓及大陸合作的基因資料分析，今年刊登在Nature genetic。葛瑞 夫氏病的基因研究也有相當的成果；而糖尿病衛教中心除提供患者 全方位醫療照護外，2010 年通過衛生署生策會「國家品質標章」認 證，去年更榮獲國健局「傑出獎」。 台灣的醫療水準已獲國際肯定，期待各位會員代表在理事長的 領導之下，群策群力，精益求精，最後祝大會圓滿成功，各位會員 健康如意。

中國醫藥大學附設醫院 院長

周德陽

敬上

民國 101 年 9 月 1 日

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致詞

理 事長 致 詞 各位會員女士先生、各位來賓： 歡迎大家來台中市中國醫藥大學立夫教學大樓B1國際會議廳參 加中華民國內分泌暨糖尿病學會2012年秋季學術研討會。 秋季會為本兩會規模僅次於年會之學術研討會。本次秋季研討 會，很高興能獲得中國醫藥大學附設醫院內分泌新陳代謝科協辦。 節目有午餐專題演講1題，次發性代謝內分泌專題討論：高血脂症、 性腺低能症、副甲狀腺高能症與骨質疏鬆症等4子題，生長素不足症 專題演講2題，以及會員研究成果發表論文，內容精彩可期。將從會 員研究成果論文選出前三名，於晚宴頒發獎金。本次秋季會會後安 排會員日月潭九族文化村之旅，預祝各位旅遊愉快。 最後，感謝中國醫藥大學附設醫院周德陽院長、內分泌新陳代 謝科陳清助主任與張淳堆顧問，盡心盡力協辦。感謝各位演講者與 主持人用心準備學術節目；各位會員女士先生熱情參與。也感謝各 醫藥、生物科技及儀器產品公司贊助經費。祝福各位會員身體健 康，本次秋季會圓滿成功。

中華民國內分泌學會 理事長

敬上

民國 101 年 9 月 1 日

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中華民國內分泌暨糖尿病學會 101年度秋季學術研討

理事長致詞 各位會員女士先生大家好： 歡迎大家來到中國醫學大學附設醫院，參加本兩學會所共同舉辦 101年度秋季學術研討會！ 今年的秋季會安排有精彩的演講內容，包括了許多的內分泌與新 陳代謝異常的疾病，讓學員拓展新知也可溫故知新，此外陳清助主任 並準備「內分泌新陳代謝科醫療特色介紹」，其糖尿病衛教中心成立 於 1995 年，才第二年（1997）即獲得國民健康局評選為「糖尿病推廣 機構評級－中心級」。可見其對於糖尿病照護的卓越表現。長期且持 續的關心病友，使他們的生活質量上的改善，是最難能可貴。另外， 將臨床治療和教育緊密地聯繫起來，成為一個在醫院設施中獨特的綜 合服務項目，客製化的為每位病友提供最新且合適的治療，守護中台 灣民眾生命健康福祉。 台中地區為中部首善之區，為帶動中部經濟發展的火車頭，兼具 消費、文化以及大學城特色的魅力城市，其逢甲美食圈、綠園道、科 學博物館、美術館及巴洛克風格的台中火車站，更令人一再回味，二 天一夜的秋季研討會，歡迎所有會員及眷屬「敞開心、認真的學習、 盡興的遊覽」，也期勉各位會員平時在關懷病人、精進專業知識之 餘，也能適時的調整步伐，照顧自己的健康、多與家人相處。 感謝中國醫學大學附設醫院盡心盡力的協辦，各位會員的參與， 祝福各會員身體健康，本次秋季會圓滿成功。

中華民國糖尿病學會 理事長

敬上

民國 101 年 9 月 1 日

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程序表

中華民國內分泌暨糖尿病學會 101年度秋季學術研討會程序表 日期： 民國101年9月1日(星期六) 地點： 中國醫藥大學立夫教學大樓 協辦： 中 國 醫 藥 大 學 附 設 醫 院 時 間

主 題

12:00 ~ 1:00 pm

Lunch Special Lecture

1:00 pm 開始

報到

1:20 ~ 1:25 pm

中國醫藥大學附設醫院院長致歡迎詞

1:25 ~ 1:30 pm

中華民國內分泌學會理事長致開幕詞

1:30 ~ 1:55 pm

次發性高血脂症

1:55 ~ 2:20 pm

次發性性腺低能症

2:20 ~ 2:40 pm

Poster & Exhibits & Tea Break

2:40 ~ 3:05 pm

次發性副甲狀腺高能症

3:05 ~ 3:30 pm

次發性骨質疏鬆症

3:30 ~ 3:55 pm

兒童期之生長素不足症

3:55 ~ 4:15 pm

Poster & Exhibits & Tea Break

4:15 ~ 5:45 pm

會員研究成果發表論文投稿

5:45 ~ 5:55 pm

中國醫藥大學附設醫院內分泌新陳代謝科醫療特色簡介

5:55 ~ 6:00 pm

中華民國糖尿病學會理事長致閉幕詞

6:30 pm 開始

Welcome Dinner台中金典酒店

6: 35~ 7:00 pm

成人期之生長素不足症

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中華民國內分泌暨糖尿病學會 101年度秋季學術研討

中華民國內分泌暨糖尿病學會 101年度秋季學術研討會節目表 203教室

Lunch Special Lecture

Speaker

12:00~12:05 pm

Opening

杜思德

12:05~12:45 pm

Advantage and Benefit of Oral Incretin Based Therapy and Its Combination

Ken C. Chiu

12:45~12:55 pm

Discussion

杜思德

12:55~ 1:00 pm

Closing

杜思德

LS

B1國際會議廳

Special Lecture

Moderator

杜思德

Speaker

Moderator

1:30 ~ 1:55 pm SL1

次發性高血脂症

曾芬郁

林瑞祥 黃天祥

1:55 ~ 2:20 pm SL2

次發性性腺低能症

葉振聲

林仁德 黃建寧

2:40 ~ 3:05 pm SL3

次發性副甲狀腺高能症

蔡克嵩

辛錫璋 莊峻鍠

3:05 ~ 3:30 pm SL4

次發性骨質疏鬆症

陳榮福

林時逸 劉瑞川

3:30 ~ 3:55 pm SL5

兒童期之生長素不足症

蔡輔仁

林宏達 張淳堆

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節目表

B1國際會議廳

Oral Presentation

Speaker

Moderator

4:15~4:30 pm OP1

蛋白尿可獨立預測第二型糖尿 病病患的死亡率

沈峰志

江怡德

4:30~4:45 pm OP2

一位罹患第一型多發性內分泌 瘤的病人有罕見的胰臟腫瘤

洪逸芷

石光中

4:45~5:00 pm OP3

台灣老年第二型糖尿病病人總 死亡率及心血管疾病死亡率的 危險因子

黃怡欽

李洮俊

5:00~5:15 pm OP4

原發型高醛固酮症之血中脫氫 異雄固酮-硫酸鹽於女性患者之 表現

陳愛華

鄧錦泉

5:15~5:30 pm OP5

低血糖對第二型糖尿病腎功能 之影響

李宇力

黃禹堯

5:30~5:45 pm OP6

甲狀腺低下導致大量心包膜積 水：一案例報告

黃怡瓔

簡銘男

Speaker

Moderator

張天鈞

葉振聲

金典酒店11F 6:35~7:00 pm

SL6

Dinner Special Lecture 成人期之生長素不足症

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中華民國內分泌暨糖尿病學會 101年度秋季學術研討

1F大廳

Poster Presentation

First Author

1:00~6:00 pm PP1

臺灣糖尿病病人周邊動脈疾病危 險因子分析

周振凱

PP2

胰島母細胞增生以反覆飯後低血 糖表現-病例報告

杜業豐

Metformin 引起的乳酸中毒併呼吸 PP3 衰竭發生在一位30歲的第二型糖 尿病人

林彤沛

PP4 糖尿病酮酸中毒併發甲狀腺風暴

林毅欣

PP5

南部某醫學中心門診糖尿病人低 血糖原因分析及處理效益

梁綉鈴

PP6

副甲狀腺癌及副甲狀腺功能亢進 併發急性胰臟炎-病例報告

蔡政麟

某降糖保健食品對第二型糖尿病 PP7 人生化，發炎及凝血危險因子之 效應

陳世爵

降血脂藥物促發甲狀腺低下病人 肌炎、肢端無力一病例報告

葉乃誠

PP8

14

摘要

次發性高血脂症 Secondary Dyslipidemia 曾芬郁 台灣大學醫學院附設醫院內科部

Dyslipidemia may be caused by “non-lipid＂ disorders such as type 2 diabetes mellitus, (T2DM), hypothyroidism, cholestatic liver diseases, nephrotic syndrome, chronic renal failure, cigarette smoking, obesity, and drugs.

Patients with primary biliary cirrhosis and similar disorders may have marked hypercholesterolemia with accumulation of lipoprotein-X. Patients with nephrotic syndrome may have elevated serum levels of total cholesterol (CHOL), low-density lipoprotein (LDL-C), triglyceride (TG), lipoprotein(a), apo B, C-II, and E. Their levels of total low-density lipoprotein (HDL-C) are normal or reduced with decline in the HDL2 fraction. Patients with chronic renal disease may have elevated levels of LDL-C and TG; and low levels of HDL-C. Obese patients may have high CHOL, LDL-C, very low density lipoprotein (VLDL), and TG. Patients with hypothyroidism may have elevated levels of CHOL and TG. Patient with T2DM may have high TG, low HDL-C, larger VLDL, and smaller LDL. Their levels of VLDL, intermediate lipoprotein (IDL), and LDL may increase.

As an indicator of the severity of their primary disorder, secondary dyslipidemia may also play an important role in the cardiovascular outcomes. In clinical practice, possible underlying “non-lipid＂ etiology should be considered before treating patients with dyslipemia. Control of underlying disorders may lead to corrections of dyslipidemia.

15

中華民國內分泌暨糖尿病學會 101年度秋季學術研討

次發性性腺低能症 Secondary Hypogonadism 葉振聲 台北榮民總醫院新陳代謝科

Secondary (Hypogonadotropic hypogonadism) is a syndrome of a lack of secretion of pituitary gonadotrophin hormones: follicle stimulating hormone (FSH) and luteinizing hormone (LH), respectively. Generally, the hypothalamus releases gonadotropin-releasing hormone (GnRH) which stimulates the pituitary gland to release two trophic hormones, e.i., FSH and LH. These hormones stimulate the female ovaries and male testes to release sex hormones that lead to normal sexual development in puberty. Any change in this hormone release cascade may cause a lack of sex hormones and prevents normal sexual maturity. Failure of the hypothalamus is usually a result of Kallmann syndrome (KS). KS is an inherited form of hypogonadotropic hypogonadism that can occur with a loss of smell. The symptoms in females include absence of breasts and menstruation, in males, absence of enlargement of the testes and penis, deepening of the voice and facial hair may occur. In addition, inability to smell (anosmia), lack of characteristic at puberty, development may be absent or significantly delayed. The laboratory workup includes blood tests to measure basal hormone levels, FSH and LH responses to GnRH; MRI of the skull (to look for a lesion in the pituitary gland), olfactory bulb development.

The genetic testing includes KAL1 on Xp22.3 for the X-linked form and FGFR1 (fibroblast growth factor receptor 1, also known as KAL2) on 8p12 for the autosomal dominant form with incomplete penetrance. The KAL1 gene encodes a 680-amino-acid protein. The KAL2 gene, which spans 55 kb of genomic DNA, has 18 coding exons and dominant loss-of-function is a cause of KS. Depends on the cause of the problem, it may cover a broad spectrum of treatment such as injections of testosterone, slow-release testosterone skin patch, testosterone gels, estrogen and progesterone pills, injection of HMG and HCG or GnRH, etc. With proper hormone treatment, he or she can develop through puberty and fertility may be restored.

16

摘要

Reference: Jap TS, Chiu CY, Lirng JF and Won JGS, Identification of Two Novel Missense Mutations in the KAL1 Gene in Han Chinese Subjects with Kallmann Syndrome .

Journal of Endocrinological Investigation 2011, 34:53-59.

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中華民國內分泌暨糖尿病學會 101年度秋季學術研討

次發性副甲狀腺高能症 Secondary Hyperparathyroidism 蔡克嵩 台灣大學醫學院附設醫院內科部

Parathyroid glands have multiple physiological functions. Parathyroid hormone (PTH) helps to maintain stable levels of serum calcium, phosphate, and calcitriol and healthy skeletal system. The main stimulators of PTH thus are low calcium (Ca), high phosphate (P), inactivated calcium sensing receptors in parathyroid gland, low calcitriol levels, and through unknown mechanisms, osteomalacia of the bone.

Secondary hyperparathyroidism (2。HPT) in chronic renal diseases and uremia is caused mainly by hyperphosphatemia, and the associated hypocalcaemia. If unchecked, excessive PTH may aggravate hyperphosphatemia by releasing phosphate from the bones. Elevated FGF-23, a phosphatonin secreted by ostocytes, and low calcitriol levels also played roles. So the main component of treatment should be dietary phosphate restriction, phosphorus binders including calcium salts, calcimimetics which does not increase serum calcium level, active vitamin D analogues. The goal is to keep serum levels of phosphorus, calcium, CaxP product, and PTH levels in the desired levels. K/ DOQI and other guidelines are available for clinical uses.

Endocrinologists mainly see 2。HPT patients with relatively normal GFR. The patients may have hypocalcaemia due to bone hunger after parathyroid adenomectomy, severe osteoblastic bone metastasis and pseudohypoparathyroidism syndromes, Hypophosphatemic and other osteomalacia, tumoral calcinosis etc. They are difficult to diagnose accurately and usually needs special blood tests. The endocrinologists needs to combine the related biochemical parameters, make diagnosis cautiously, and treat the patients accordingly.

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摘要

次發性骨質疏鬆症 Secondary Cause Induced Osteoporosis 陳榮福 高雄長庚紀念醫院內科部新陳代謝科

There are many Endocrine/Hormonal Disorders can induce osteoporosis, such as Diabetes. People with diabetes have a higher risk of developing osteoporosis. While type 1 diabetes seems to cause the greatest amount of bone loss, people with both type 1 and type 2 diabetes have an increased risk of breaking bones.

Hyperparathyroidism is a condition in which the parathyroid glands produce too much parathyroid hormone (PTH) that causes bone loss. This condition is more common in women after menopause.

Hyperthyroidism can lead to weak muscles and fragile bones. Bone loss can also occur if a person takes too much thyroid hormone medicine for an underactive thyroid.

There could be many reasons for this, such as exercising too much or eating so little and very thin.

Other causes of irregular periods could include disorders of the ovaries or pituitary.

Loss of estrogen and extreme thinness can harm bones and affect other body systems.

In men, testosterone protects bone. Very low levels of testosterone suggest that there is an underlying disorder that needs to be evaluated.

Also many of the diseases and conditions that can cause bone loss directly/ indirectly are included as AIDS/HIV, ankylosing spondylitis, blood and bone marrow disorders, breast cancer, chronic obstructive pulmonary disease (COPD), including emphysema, Cushing's syndrome, depression, eating disorders, especially anorexia, gastrectomy, gastrointestinal bypass procedures, inflammatory bowel disease, including Crohn's disease and ulcerative colitis, kidney disease that is chronic and long lasting liver disease that is severe, including biliary cirrhosis, lupus, lymphoma and leukemia, malabsorption syndromes, including celiac disease, multiple myeloma, multiple sclerosis, organ transplants, Parkinson's disease, polio and post-polio syndrome, poor diet, including malnutrition, premature menopause, prostate cancer, rheumatoid arthritis, scoliosis, spinal cord injuries, stroke, thalassemia, weight loss etc.

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中華民國內分泌暨糖尿病學會 101年度秋季學術研討

兒童期之生長素不足症 Growth Hormone Deficiency in Children 蔡輔仁 中國醫藥大學附設醫院基因醫學部

很多原因會造成兒童的身材矮小，從家族遺傳、各種重大疾病乃至於內分泌 的障礙。我們今天把重點擺在生長素缺乏症的診斷及治療，有下列幾個方向要討 論（一）生長素的正常生理分泌（二）生長素的作用機轉（三）如何診斷生長素 缺乏症（四）目前健保體制下的治療原則（五）將來的研究方向。

20

摘要

成人期之生長素不足症 Growth Hormone Deficiency in Adults 張天鈞 台灣大學醫學院附設醫院內科部

人出生時約50公分，然後藉著長骨的生長板生長，使骨頭延長。女子到16 歲，男子18歲時epiphysis closure，就不再長高。1950年代，從人的屍體腦垂腺萃 取生長素，用來治療因生長素分泌不足的矮小。1985年，發現藥物可能被引起類 似狂牛症的普利子(prion)污染，使病人產生克賈氏症，因此禁用。李卓皓博士於 1966年定出生長素的胺基酸序列，因而於1977年John D Baxter得以率先cloning人 類生長素基因，因此可以用大腸桿菌，利用基因工程大量合成人類生長素。從此 以後除了可以治療因生長素不足引起的矮小，也可以考慮用來治療成年人的生長 素不足。生長素缺乏的成年人，生活品質問卷調查結果差異很大。在孩童時期就 生長素缺乏的人，到了大人以後，比較不容易觀察到生活品質受影響。成年人給 予生長素以後，生活品質的改善與開始時偏離正常的程度有關。而其改善，通常 在補充3個月內就會出現。早期的大型臨床試驗顯示病人可能出現胰島素抗性(13 ％)和第二型糖尿病(4％)。但現在劑量減少後，產生糖尿病的機會只有稍許增加 而已。視網膜病變是很少見的併發症，良性顱內高壓也是如此。至於腫瘤方面， 無確切的根據。生長素的治療也可能使血清free T4減少，cortisol減少，因此應定 期追蹤這些數值，必要時補充。診斷成年人生長素缺乏，由於生長素波動性釋 放，只取一次血比較不能代表實際值，取很多次又不實際，最好做刺激試驗。若 外表上，病人的脂肪增多、肌肉減少、活力減少、生活品質變差，這時可進一步 檢查確認。胰島素耐受試驗是黃金標準，但有些風險，特別是有癲癇或心臟血管 疾病的人。如果可能，合併GHRH和arginine做試驗，是最理想的，也比較不受老 化和肥胖之影響。但若下視丘異常的人，例如接受過電療，GHRH-arginine試驗可 能不準，因不會顯現異常。IGF-I和IGFBP-3，若低於正常值有幫忙，若正常，不 能排除生長素缺乏的診斷。若已經在用生長素，必須停用一個月後再評估，才會 準確。此外，若腦垂腺軸有三種以上出現不足，表示會出現生長素不足，並不一 定要做刺激試驗。在治療方面，大人的劑量若照小孩的算法，容易出現副作用， 年紀較大的人更是如此。<30歲，開始劑量每天0.4-0.5 mg。若30-60歲，開始劑量

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中華民國內分泌暨糖尿病學會 101年度秋季學術研討

每天0.3 mg，然後每1-2個月增加0.1-0.2 mg，直到臨床上有適當的效果，又沒有 副作用，而IGF-1值在正常範圍。此外可能需要6個月以上的治療才有明顯效果。 至於大於60歲，最好每天0.1-0.2 mg開始，且增加劑量的速度要更緩慢。在女人， 若是同時併用口服動情素，需要的生長素劑量較高，但若用藥膏則不需要。在維 持劑量已經達到後，每6個月要評估副作用、臨床效果及測量IGF-I值，每年要測 血脂肪及空腹血糖。如果最初的骨密度值不正常，每1-2年要再評估一次，以決 定是否要加上其它的治療方法。此外，評估生活品質也是一種監測的方法。如果 先前已補充甲狀腺素，在開始用生長素治療後，可能要調整劑量，腎上腺皮質類 固醇也是一樣。至於生長素要給多久仍不清楚。當然如果有效果，沒有理由要停 藥，如果治療一年以後沒有明顯的效果，則可以停掉生長素療法。總之，成年人 生長素缺乏症，值得補充生長素，但宜從低劑量開始，且視年齡而定，再依身體 脂肪、生活品質、IGF-1而做調整。長期的使用可以改善生活品質，減少心肌梗 塞，也不擔心腫瘤機會增加，因此值得使用。

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摘要

OP1

ALBUMINURIA INDEPENDENTLY PREDICTS ALL-CAUSE MORTALITY IN PATIENTS WITH TYPE 2 DIABETES 1

FENG-CHIH SHEN, 1I-CHIN HUANG, 1CHEN-KAI CHOU, 1MIN-SHIEN CHUNG, 1 RUE-TSUAN LIU 1 Division of Metabolism, Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Taiwan

OBJECTIVE Albuminuria is a major microvascular complication of diabetes. The aim of this study is to determine the relationship of albuminuria and all-cause mortality in patients with type 2 diabetes.

RESEARCH DESIGN AND METHODS A total of 1196 type 2 diabetic patients who visited the Metabolism clinic at Kaohsiung Chang Gung Memorial Hospital in 2004 were recruited and followed up for average 6.1 years. Information on survival or cause of death was recorded accorinding to the National Register of Deaths. Underlying causes of death were determined from death certificates coded according to the ninth revision of the International Classification of Diseases. Demographic, anthropometric, clinical, laboratory parameters and data on diabetes-associated microvascular complications were collected for analysis. Urinary

albumin excretion was determined to identify albuminuric status of subjects by measuring urinary albumin-to-creatinine ratio (UACR) in spot urine. Albuminuria is defined as presence of UACR greater than or equal to 30mg/g.

RESULTS One hundred and ninty eight deaths with known causes were registered during follow-up periods. The prevalences of microalbuminuria and macroalbuminuria at baseline were 25.8% and 14.7%, respectively. In univariate analysis, age (67.0± 11.4 vs. 60.3± 10.4, p<0.001), duration of diabetes (11.6± 7.2 vs. 8.9± 6.4, p<0.001), smoking history (39.6% vs. 28.2%, p=0.003), waist circumference (89.5± 10.2 vs. 87.3± 9.1, p=0.029), serum concentrations of creatinine (1.4± 1.1 vs. 1.0± 0.6, p<0.001), estimated glomerual filtration (eGFR) (73.2± 36.3 vs. 94.9± 38.6, p<0.001), triglyceride (162.7± 109.7 vs. 141.7± 97.6, p=0.014), HDL cholesterol (40.3± 13.2 vs. 44.6± 11.8, p<0.001) and the presence of albuminuria (68.7% vs.

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中華民國內分泌暨糖尿病學會 101年度秋季學術研討

34.9%, p<0.001) and retinopathy (45.1% vs. 30.0%, p<0.001) were significantly different between patienets with and without mortality. Multiple logistic regression analysis showed that older age [odds ratio (OR) 1.05 (95% CI: 1.03–1.08), p<0.001], higher serum creatinin [OR 1.70 (1.25–2.31), p=0.001], presence of albuminuria [OR 3.06 (95% CI: 2.00–4.71), p<0.001] and smoking history [OR 1.73 (95% CI: 1.14–2.60), p=0.011] were independent predictors for all-cause mortality. All-cause mortalities in the normoalbuminuria, microalbuminuria and macroalbuminuria groups were 13.8, 36.8 and 72.1/1,000 person-years (pyrs), respectively.

CONCLUSION Albuminuria is a useful predictor of all-cause mortality in patients with type 2 diabetes.

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摘要

OP2

UNUSUAL PANCREATIC TUMOR IN A PATIENT WITH MULTIPLE ENDOCRINE NEOPLASIA TYPE 1 1

YI-CHIH HUNG, 1,2TZU-YUAN WANG, 1,2CHING-CHU CHEN, 1,2CHWEN-TZUEI CHANG, 1,2 CHING-CHUNG CHANG 1 Division of Endocrinology and Metabolism, Department of Internal Medicine, China Medical University Hospital, Taichung, Taiwan, R.O.C 2 School of Chinese Medicine, College of Chinese Medicine, China Medical University, Taichung, Taiwan, R.O.C

A 46-year-old woman with history of acromegaly and nephrolithiasis presented for evaluation of left hip pain for 3 months.

She was diagnosed as having acromegaly in June, 2004 . She received two consecutive transsphenoidal adenomectomy in 2004 and 2005 with incomplete resections of a growth hormone (GH)-secreting pituitary adenoma. In 2009 she underwent gamma knife stereotactic radiosurgery because of persistent elevated GH level and symptoms of acromegaly. In Augest, 2011, she was admitted to our orthpedics department due to progressive left hip pain. Magnetic resonance imaging (MRI) of the pelvis showed multiple bone lesions in left acetabulum, bilateral iliac bones and bilateral pubic bones. Biopsy of the left acetabulum tumor revealed osteoclastoma. She received open reduction internal fixation because of pathologic fracture.

Hypercalcemia (Ca: 11.2 mg/dl) was noted during routine biochemistry examination and serum intact PTH were 2328.2 pg/mL (normal range:15-88), suggesting primary hyperparathyroidism.

She was transferred to endocrine department for further evaluation.

Thyroid ultrasonography revealed bilateral enlarged parathyroid glands and multinodular goiter with cystic degeneration in both lobes. Parathyroid scan revealed hyperfunctioning parathlyroid tissues in bilateral lower parathyroid glands. The diagnosis of MEN I was made.

Tracing back to her history, she had persistent watery diarrhea for about 3 years. An abdominal ultrasound was performed revealed a large retroperitoneal mass. Subsequent abdominal CT revealed a 10.4 cm × 7.4 cm tumor in the tail of the pancreas and a left adrenal tumor. She

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中華民國內分泌暨糖尿病學會 101年度秋季學術研討

underwent parathyroidectomy followed by subtoal pancreatectomy and splenectomy. Pathology of the parathyroid glands revealed chief cell hyperplasia. Immunohistochemical stain of the pancreatic tumor showed: Synaptophysin (+, diffuse), Chromogranin A (-), Ki-67(+,3%), Somatostatin (+, scattered, 2%), Insulin (-), Glucagon (-), Gastrin (-), Growth Hormone (-), Calcitonin (-), ACTH (-) and Vasoactive intestinal peptide (+, 25%). She was finally diagnosed as having VIPoma as a component of MEN I.

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摘要

OP3

RISK FACTORS FOR ALL CAUSE MORTALITY AND CARDIOVASCULAR DISEASE MORTALITY IN ELDERLY TYPE 2 DIABETIC PATIENTS IN TAIWAN 1

I-CHIN HUANG, 1CHEN-KAI CHOU, 1FENG-CHIH SHEN, 1RUE-TSUAN LIU 1 Division of Metabolism, Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Taiwan

Aim: To examine the effect of albuminuria and peripheral arterial disease (PAD) on the risk of all cause mortality and cardiovascular disease (CVD) mortality in elderly patients with type 2 diabetes.

Methods: A cross-sectional study was conducted among 579 type 2 diabetic patients aged ≥ 60 years who were regularly followed at the outpatient clinic of Dr. Rue-Tsuan Liu, Kaohsiung Chang Gung Memorial Hospital from March to August 2004. Diagnosis of PAD was by ankle-brachial index (ABI) <0.90 on either leg. Demographic, anthropometric, clinical data, diabetes-associated complications and laboratory parameters were obtained during this 6-month period. Deaths were verified by indexing to the National Register of Deaths till December 2010.

Underlying causes of death were determined from death certificates coded according to the ninth revision of the International Classification of Diseases.

Results: Of 579 type 2 diabetic patients aged ≥ 60 years (292 males, 287 females), mean age was 68.2 ± 6.6 years, duration of diabetes 10.5 ± 6.8 years, HbA1c 7.3 ± 1.4 %. With a total of 3500.4 person-years of follow-up, 116 patients died and the crude mortality rate was 33.1/1000 person-years. Cause of death ascribed to CVD was documented in 56 patients and the CVD mortality rate was 16.0/1000 person-years. Multiple Cox's regression analysis revealed that increasing age, creatinine level, albuminuria and PAD were independently associated with all cause mortality and CVD mortality. Patients with albuminuria and PAD had the highest risk for all cause mortality (OR: 8.2, p<0.001) and CVD mortality (OR: 10.7, p<0.001) than those without albuminuria and PAD.

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中華民國內分泌暨糖尿病學會 101年度秋季學術研討

Conclusion: Our study suggests that albuminuria and PAD are independent predictors of all cause mortality and CVD mortality in elderly type 2 diabetic patients. Patients with these two diabetic complications have the highest risk for mortality and should receive promptly comprehensive management.

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摘要

OP4

SERUM DEHYDROEPIANDROSTERONE SULFATE CONCENTRATION IS LOWER IN FEMALE WITH PRIMARY ALDOSTERONISM 1,2

AI-HUA CHEN, 2HUNG-YUAN LI, 2VIN-CENT WU, 2TIEN-SHANG HUANG 1 Department of Internal Medicine, Taipei Medical University Shuang Ho Hospital, Taipei, Taiwan 2 Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan

Short title: Serum DHEA-S decreased in female primary aldosteronism Objectives: To measure serum dehydroepiandrosterone sulfate (DHEA-S) concentration in both genders with primary aldosteronism Methods: The study enrolled 78 subjects with normal control, 46 subjects with essential hypertension and 85 subjects with primary aldosteronism from October 2007 to June 2011.

Subjects with primary aldosteronism were divided into three subtype groups: aldosteroneproducing adenoma (APA), bilateral idiopathic hyperplasia (IHA) and primary aldosteronism with negative imaging findings. Plasma aldosterone concentration (PAC) was measured by radioimmunoassay. Plasma renin activity (PRA) was measured as the generation of angiotensin-I in vitro by radioimmunoassay. Serum DHEA-S was measured by competitive chemiluminescent enzyme immunoassay. The tumor size was measured by radiology imaging in APA. Results: Female subjects with primary aldosteronism (N=49) had lower serum DHEA-S level compared with normal control and essential hypertension (P< 0.01). In subtype analysis, only female APA had lower serum DHEA-S level (P<0.01 compared with normal control, P<0.01 compared with subjects with essential hypertension). In APA, a significant correlation between tumor size and serum DHEA-S was found in female subjects (P<0.01).

Conclusions: Our data suggested that serum DHEA-S level is lower in female subjects with primary aldosteronism. In subtype groups, only female subjects with aldosteroneproducing adenoma had lower serum DHEA-S. There were no significant difference between subjects with bilateral essential hyperplasia, primary aldosteronism with negative imaging findings, normal control and essential hypertension in both genders. The serum DHEA-S level is negatively correlated with the size of aldosterone-producing adenoma.

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中華民國內分泌暨糖尿病學會 101年度秋季學術研討

OP5

THE EFFECT OF HYPOGLYCEMIA ON RENAL FUNCTION IN TYPE 2 DIABESTES 1

YU-LI LEE, 1SHYI-JANG SHIN, 1PI-JUNG HSIAO, 1KUN-DER LIN, 1WEI-WEN HUNG, 1 MEI-YUEH LEE, 1HSING-YI LIN, 1CHUN-WEI HO, 1PING-CHUAN CHOU 1 Division of Endocrine and Metabolism, Department of Internal Medicine, Kaohsiung Medical University Hospital, Taiwan, R.O.C.

Background: Hypoglycemia has been found to aggravate cardiovascular complication and increase mortality. However, whether hypoglycemia can affect the progression of diabetic nephropathy has been controversial. In the current study, we aimed to investigate the influence of hypoglycemia on renal function in type 2 diabetic patients.

Methods: Seventy-nine type 2 diabetic patients who were admitted in Endocrinology and Metabolism Ward with the major problem being hypoglycemia were recruited.The demographic and biochemical data were collected before admission and 1- 12 months after discharge.

Statistical analyses were performed using Student's t test, χ2 test ,Fisher's exact test, and the multiple linear regression .

Results: The mean value of increased creatinine concentration after the hypoglycemia event is 0.61 mg/dL and 1.01 mg/dL in patients with serum creatinine level ≦1.4 mg/dL and >1.4 mg/dL. 10% of patients with chronic kidney disease (CKD) stage I-II before hypoglycemia progressed to CKD III-IV, but none progressed to CKD V. However, 23.3% of patients with CKD III-IV progressed to CKD V(p<0.001). Multiple regression analysis also showed that impairment of renal function is an independent risk factor to predict the progression of renal dysfunction which is aggravated by hypoglycemia in type 2 diabetic patients.

Conclusion: In this study, we showed that hypoglycemia can significantly aggravate the severity of renal dysfunction in diabetic patients with CKD stage III-IV. These results indicate that we should pay more attention to the occurrence of hypoglycemia when we prescribe the regimen of strict glycemic control in diabetic patients with mild and moderated chronic kidney disease.

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摘要

OP6

HYPOTHYROIDISM WITH MASSIVE PERICARDIAL EFFUSION: A CASE REPORT 1

YI-YIN HUANG, 2CHUAN-JHONG CAI 1 Division of Endocrinology and Metabolism, 2Division of Cardivascular, Department of Internal Medicine, Tzuchi General Hospital Taichung Brach, Taiwan, R.O.C.

Abstract: We present a case of a 68 year-old female with massive pericardial effusion caused by postoperative hypothyroidism. The effusion was drainged and showed exudate, without other cause of pericardial effusion. Hypocellular bone marrow with pancytopenia was also noted. She was on levothyroxine replacement after subsequent thyroid function showed hypothyroidism and with improvement progressively.

Case: A 68-year-old female visited our emergency departement due to shortness of breath for 2 days. She has developed general weakness and bilateral lower leg edema since 3 months ago. She has past history of thyroidectomy for goiter at 50 decades. Post operative hypothyroidism was ever told but she has no thyroid hormone replacement nor any follow-up in the past years.

Her height was 150cm; weight, 51kg, with slowly movoment and husky voice. Vital signs were temperture, 36℃; blood pressure, 122/75mmHg; heart rate, 50bpm. Physical examination found facial edema, coarse hairs, periorbital edema, pale and thick lips. No goiter was palpable.

Threre was non-pitting edema but dry and exfoliations of skin of the extremities. Chest X-ray showed globular enlargement of the cardiac sihouette with “water bottle” configuration. EKG revaled sinus bradycardia with low voltage parrtern and first degree AV block. Cardioechography demonstated massive pericardial effusion. The effusin drained with pig tail was yellowish, 870ml at first day, 100ml at second day, 10ml on third day then it was removed.

The laboratoy revealed TSH 125.97 uIU/mL, Free T4 0.12 ng/dL, Anti-perosidase Ab 55.8 IU/mL, antithyroiglobulin Ab 1354.4 IU/mL. Blood white count 3440 /u:, Hb 9.9 g/dL, platelet 55000/uL, MCV 93.5fL, MCHC 36.0%, The biochemistry revealed Cr 0.8mg/dl, glucose 85mg/ dl. GPT 50IU/dL, GOT 85IU/L, Albumin 4.2 g/dL, LDH 651IU/L. TP 7.4 g/dL, The pericardial

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中華民國內分泌暨糖尿病學會 101年度秋季學術研討

fluid assay results were Glucose 119mg/dl. LDH 451.4 IU/L, total protein 7.2 g/dL, suggestive of an exudate. Besides there was negative finding in acid-fast stain, Gram's stain and bacterial culture, as well as lymphocyte 9%, Neutrophil 69% in cell count. Bone marrow aspiration for evaluation of pancytopenia showed hypocellurity and hypoplasia which associated with hypothyroidism was suspected. She was on eltroxin for replacement, from titration dose then followed up at OPD. Conculsion: Mild hypothyroidism was often asymptomatic and/or non-specific with unawareness. But It may be aggrivated with infection, diuretics, or stress.. Severe hypothyroidism causing pericadial effusion is not common. The amount of effusions accumulated is directly related to the duration and severity of the hypothyroidism.

Myocadial infartion, aortic dissection, or cardiac rupture should be rule out at first time. Thyroid function test should be performed in any unknown cause of pericardial effusion. Fluid biochemistry analysis, bacterial culture and cytological examination should be performed. Autoimmune disease is also considered if no other cause of pericardial effusion could be identified. The main treatment for hypothyroidism is replacement of levothyroxine.

Pericardiocentasis or cadiac window is necessory for survial if massive pericardial effusion or cardiac tamponade noted.

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摘要

PP1

ANALYSIS OF RISK FACTORS FOR PERIPHERAL ARTERIAL DISEASE IN TYPE 2 DIABETIC PATIENTS IN TAIWAN 1

CHEN-KAI CHOU, 1MIN-SHEN CHUNG, 1CHING-JUNG HSIEH, 1I-CHIN HUANG, 2 CHUNG-JHE LI, 1RUE-TSUAN LIU Divisions of 1Metabolism and 2Opthalmology Chang Gung Memorial Hospital-Kaohsiung Medical Center, Kaohsiung, Taiwan

Aims: Diagnosing peripheral arterial disease (PAD) and recognizing its associated risk factors in diabetes is important due to its association with high cardiovascular disease and limb loss risk. However, both traditional and nontraditional risk factors have seldom been analyzed in the large-sized diabetic cohort. The aim of this study was to examine the traditional and nontraditional risk factors for PAD in type 2 diabetic patients.

Methods: One thousand five hundred and forty type 2 diabetic subjects with mean age of 63.8 +/- 10.3 year and diabetes duration of 10.9 +/- 6.6 years were crosssectionally studied.

Diagnosis of PAD was by ankle-brachial index (ABI) <0.90 on either leg. The association between a wide range of traditional and nontraditional risk factors with PAD were analyzed.

Results: The overall prevalence of PAD as defined by ABI <0.90 using oscillometric pressure sensor method was 11.1% in type 2 diabetic patients. Multiple logistic regression analysis revealed older age, longer duration of diabetes, presence of albuminuria, history of cerebral vascular accident or coronary artery disease and wider pulse pressure were independent risk factors to distinguish those with and without PAD in diabetic patients.

Conclusions: We identified several important risk factors for PAD in type 2 diabetic individuals independently of numerous baseline confounding factors. Our results help pinpoint risk markers that might be useful for targeting ABI screening in type 2 diabetes.

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中華民國內分泌暨糖尿病學會 101年度秋季學術研討

PP2

NESIDIOBLASTOSIS PRESENTED WITH POSTPRANDIAL HYPOGLYCEMIA – A CASE REPORT 1

YE-FONG DU, 1HORNG-YIH OU, 2SHIH-MING HUANG, 1TA-JEN WU 1 Division of Endocrinology and Metabolism, Department of Internal Medicine, National Cheng Kung University Hospital, Tainan, Taiwan, R.O.C. 2 Division of General Surgery, Department of Surgery, National Cheng Kung University Hospital, Tainan, Taiwan, R.O.C.

A 34y/o women was in generally healthy condition until recently that she presented to our hospital due to recurrent episodes of drowsiness and general weakness, which usually occurred 1~2hr after meal, sometimes accompanied with chest tightness and cold sweating. She also experienced similar episodes at early morning after overnight fasting. Plasma glucose checked once at emergency department was 40mg/dl. Symptoms resolved after dextrose water infusion.

She refused admission initially, but was admitted on 2011/10/15 for 72 fasting test after recurrent episodes at least 4 times in a month.

After 72hr fasting, she did not have any discomfort, and the capillary blood glucose did not drop below 55mg/dl. The test ended up with inconclusive result. However, the hypoglycemia episodes recurred, mostly after midnight snacks. She had tried to eat chocolate to relieve the symptoms in vain. She was admitted again 2 weeks later.

This time, she received oral glucose tolerance test. The hypoglycemia episode was not induced after oral glucose load. She lost follow up after two inconclusive tests. However, the recurrent hypoglycemia episodes made her cognition declined. She was called back for mixed meal test and 72 fasting test again. Hypoglycemia with symptoms of dizziness and cold sweating was induced immediately post-prandially that persisted for 2 hours. Plasma glucose level dropped to 39mg/dl with simultaneously insulin level 65.72μU/ml and C-peptide 12.5ng/ ml. 72hr fasting test ended up at 51 hours when she presented cold sweating and concomitant plasma glucose 28mg/dl, C-peptide 3.5ng/ml with insulin level lost.

Abdominal MRI revealed nodular appearance of pancreatic body and tail without identified

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摘要

tumor, but tiny hapatic tumors in right hepatic lobe. Endoscopic ultrasound showed no space occupied lesion in the pancreas. Intra-arterial calcium stimulation test revealed 13-fold and 3-fold increase of insulin level at SA and GDA respectively during 30s~60s.

She received laparoscopic spleen preserving distal pancreatectomy on 2012/01/14.

Despite no tumor identified by intra-operative ultrasound, insulin level dropped significantly after distal pancreatectomy. Pathology report revealed islet cell hyperplasia, compatible with nesidioblastosis.

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中華民國內分泌暨糖尿病學會 101年度秋季學術研討

PP3

METFORMIN RELATED LACTIC ACIDOSIS WITH ACUTE RESPIRATORY FAILURE IN A 30 YEAR-OLD TYPE 2 DM PATIENT 1

TONG-PEI LIN, 1RONG-HSING CHEN, 1CHING-CHU CHEN, 1TZU-YUAN WANG, 1 CHWEN-TZUEI CHANG, 1CHING-CHVNG CHANG, 1WEI-LUN HUANG, 1 YI-CHIN HUNG 1 Division of Endocrinology and Metabolism, Department of Internal Medicine, China Medical University Hospital, Taichung, Taiwan, R.O.C.

Metformin, a dimethylbiguanide, is an oral antihyperglycemic drug. Metformin is considered to be first line treatment in overweight patients with type 2 diabetes and should be considered as a first line glucose lowering treatment in non-overweight patients with type 2 diabetes because of its other beneficial effects. The occurrence of metformin induced lactic acidosis is exceptional when the drug is used with caution. Clinical presentations of metforminassociated lactic acidosis are non-specific. Severe hypotension with reduced systemic vascular resistance and respiratory failure requiring mechanical ventilation has also been reported.

An aggressive treatment strategy for metformin-associated lactic acidosis is recommended.

Treatment for metformin associated lactic acidosis includes adequate supportive care, management of concurrent disease, correction of acidemia, acceleration of lactate metabolism, and elimination of the offending drug by renal excretion or dialysis.

Here, we report a case of 30 year-old male patient with a history of type 2 DM and mental retardation, referred from nursing home, was admitted via our ER due to conscious disturbance for hours. The patient has regular medication for psychiatric problems (clozapine, trihexyphenidyl HCl, tegol, valnon and gemfibrozil) and metformin(500) 1# BID for diabetes.

In recent one month, the patient suffered from several episodes of abdominal pain and visited the LMD, where only abnormal renal function was told.

In the early morning of admission day (June 19 2012), drowsy consciousness, shortness of breath and general malaise were told. No fever, seizure, nausea, vomiting, diarrhea, tarry stools

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摘要

or decreased urine output. He was sent to our ER immediately. As arriving our ER, the vital sign: BP: 86/50 mmHg, HR: 107/min, RR: 30/min, BT: 35.5℃, GCS: E4M4V2, Sat.O2: 100% (room air).

Physical examination: height: 160 cm, weight: 58.3 kg, BMI: 22.7. General appearance revealed acutely ill. Integument showed normal skin turgor. HEENT: pink conjunctiva and anicteric sclera. Neck is supple and no enlargement of thyroid. Chest: clear breathing sounds.

Heart: RHB and no murmur. Abd: hypoactive bowel sounds and no muscle guarding or rebound tenderness. Neurologic examination: muscle power: RUL/LUL: 4/4; RLL/LLL: 3/3.

The laboratory data: ABG: pH: 7.0, PCO2: 11 mmHg, PO2: 143 mmHg, HCO3-:3.0 mmol/ l, Anion gap: 28 meq/l. WBC: 12470/ul, RBC: 3.05x106/ul, Hb: 10.7 g/dl, Hct: 29%, MCV: 95.1 fl, platelet: 173k/ul, MCH: 35.1 pg, MCHC: 36.9 g/dl, segment: 89.6%, lymphocyte: 6.7%, monoctye: 3.1%, eosinophil: 0.2%, basophil: 0.4%, CRP: 0.23 mg/dl, GOT/GPT: 53/30 IU/l, BUN/Cr: 29/2.08 mg/dl, Ca/Mg/albumin: 8.0 mg/dl /3.0 mg/dl /3.6 g/dl, Na/K/Cl-:133 mmol/l /5.0 mmol/l / 102 mmol/l, CPK: 291 IU/l, CKMB: 4.0 ng/ml, troponinI: 0.03 ng/ml, GluAC: 102 mg/dl, LDH: 428 u/l, ammmonia: 136 N-ug/dl, blood osmolality: 331 mosm/kgH2O, uric acid: 13.3 mg/dl, blood amylase/lipase: 36/40 u/l, blood cortisol AM: 19.25 ug/dl, FT4/TSH: 0.85 ng/ dl /1.21 uIU/ml, urine diazepam: < 30 ng/ml, blood tegretol: 6.3 ug/ml, blood depakin (valproic acid): 13.4 ug/dl, lactate: 158.7 mg/dl, blood ketone body: 4.1 mmol/l, urine ketone: +3, CXR: presence of infiltration in peripheral region. EKG: sinus tachycardia. Brain CT: old infarct /brain injury in the right parietal lobe. Abdominal CT: No evidence of intraabdominal abscess. In the ER, massive NaHCO3 was given, central venous catheter was inserted and CVP level showed 21 cmH2O. Endotracheal tube was intubated. The ABG improved to pH:7.14, pCO2: 15 mmHg, pO2: 460 mmHg, HCO3: 5.1 mmol/L about 40 minutes later.

The ABG improved to pH: 7.47, pCO2: 16 mmHg, pO2: 358 mmHg, HCO3: 11.6 mmol/L about two hours later. Then he was admitted to the ICU in the same day. Lactate decreased to 32.9 mg/dl on June 20. Renal function improved to Cr: 1.5 mg/dl on June 19 and BUN/ Cr: 20/1.03 mg/dl on June 21. The patient's condition improved and he was transferred to the ward four days later after extubation. In the ward, glucagon stimulation test was performed for suspecting type 1 DM and C-peptide(0 minutes): 1.21 ng/ml, C-peptide(6 minutes): 16.4 ng/ml.

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中華民國內分泌暨糖尿病學會 101年度秋季學術研討

PP4

A CASE OF DIABETIC KETOACIDOSIS COMPLICATED WITH THYROID STORM/THYROTOXICOSIS 1

YI-HSIN LIN, 1SAI-MIN CHUANG 1 Division of Endocrinology and Metabolism, Department of Internal Medicine, Mackay Memorial Hospital, Taipei, Taiwan, R.O.C

A 43-year-old woman had type 2 diabetes mellitus for 2 years and Graves' disease for 3 years. She presented with sudden onset of loss of consciousness upon arrival at our hospital.

The diagnosis was severe diabetic ketoacidosis and acute respiratory failure. Her chest X-ray demonstrated acute pulmonary edema and cardiomegaly, which were differentiated by pulseinduced contour cardiac output monitoring with high cardiac index. We checked her thyroid function and assumed thyroid storm by including the diagnostic criteria from 1993 Bruch 's criteria and from 2008 Japan thyroid association. She recovered and underwent extubation in a short period of 3 days under intensive anti-thyroid drugs and heart failure treatment. We shared the experience of critical care of diabetic ketoacidosis and thyroid storm. Both of them have high mortality.

Key words: Diabetic ketoacidosis, thyroid storm, thyrotoxicosis

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摘要

PP5

CLINICAL ANALYSIS AND BENEFITS OF INTERVENTION FOR HYPOGLYCEMIA IN DIABETIC OUTPATIENTS IN A MEDICAL CENTER OF SOUTHERN TAIWAN 1

HSIU-LING LIANG, 1CHIA-LUN LEE, 1HSIU-CHU LIN, 1CHIN-WEI TSENG, 1 SHU-PING SUE 1 Kaohsiung Medical University Chung HO Memorial Hpspital Endocrinology and Metabolism

Introduction: Hypoglycemia is the most common endocrine emergency, but patients can prevent it. According to the study, early clinical intervention and diabetic education will prevent hypoglycemia; and improve glycemia control.

Purpose: To understand the causes and efficacy of 50 % glucose water treatment for diabetic outpatients with hypoglycemia.

Research objects and methods: For diabetic outpatients with capillary glucose lower than 50 mg/dl or 70 mg/dl were included in our study, then 30 grams or 15 grams of 50 % glucose water, respectively, were given orally. After 15 minutes, blood glucose monitoring performed again. If the patient's symptoms were released, certified diabetic educators would interview patients or their families and provide education leaflets to prevent the next episode of hypoglycemia. The content of interviews was based on the expert-recommended causes of hypoglycemia. If the blood glucose did not elevate to more than 70 mg/dl after two cycles of treatment, the patient was informed immediately to receive physician visit. One week later, certified diabetic educator gave telephone polling to these patients about the situation of hypoglycemia at home.

Results: Thirty-six diabetic outpatients were included, among which 17 (47.2 %) were male and 19 (52.8 %) were female. The mean age was 63.5 ± 15.4 years old, the mean BMI was 21 kg/m2, the mean glycosylated hemoglobin level was 7.2 ± 1.2 %, and 88.9 % were type2 diabetes. The sequence of treatment was oral medications and insulin (15 people, 41.6 %); oral medicine (13 persons, 36.3 %); insulin (7 persons, 19.4 %), and insulin pumps (1 person, 2.7 %).

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中華民國內分泌暨糖尿病學會 101年度秋季學術研討

There were 16.6 % of patients with glucose lower than 50 mg/dl (mean glucose level was 46.1 ± 5.1 mg/dl), and 83.3 % lower than 70 mg/dl (mean glucose level was 63.1 ± 25.3 mg/ dl). The mean glucose level of 36 patients was 59.5 ± 8.0 mg/dl. The causes of hypoglycemia listed in the order of frequency: 66.9 % were eating less than usual on the day to hospital; 13.8 % had no identified cause; 11.1 % were no oral intake after insulin injection; 5.5 % were adding medication dosage on their own; and 2.7 % had increased activity. Among the 36 patients, 5 refused to drink glucose water, 28 has their glucose level increased 38.8 ± 16.6 mg/dl after one cycle , and 3 had glucose level increased 36.3 ± 28.6 mg/dl after 2 cycles of 50 % glucose water treatment. Only one didn't need 50 % glucose water treatment by doctor's order. The average blood glucose level after treatment was 98.3± 17.0 mg/dl. According to the telephone polling, no further hypoglycemic episode occurred in one-week period of these patients.

Conclusions: Among the hypoglycemic episodes, blood glucose lower than 70 mg/dl happens frequently. The most common reason is eating less than usual on the day to hospital.

Most patients' blood glucose level can recover after one cycle of 50 % glucose water treatment.

Diabetic education training and appropriate treatment can help diabetic patients prevent hypoglycemia.

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摘要

PP6

PARATHYROID CARCINOMA AND HYPERPARATHYROIDISM COMPLICATED WITH ACUTE PANCREATITIS-A CASE REPORT 1

C-L TSAI, 1J-M CHEN, 2J-W HSU Division of Endocrinology and Metabolism, 1Department of Internal Medicine, 2Division of Gerenal Surgery, Tungs' Taichung MetroHarbor Hospital , Taiwan

This 50 y/o male patient with past history of hypertension and chronic alcohol use was referred to ER and admitted to ICU due to hypercalcemia, pancreatitis with pseudocyst formation and respiratory failure. He had ever been admitted in a local hospital for several weeks. Acute pancreatitis was impressed at first, and conservative treatment was given. But hypercalcemia, acute renal failure, hyperglycemia, anemia, jaundice, and neck tumor were also found there. After admission, percutaneous drainage for pseudocyst with abscess formation was arranged. Antibiotics for sepsis and hemodialysis for renal failure were ordered. But because of toxic sign and persistent abscess, open drainage, debridement and feeding jejunostomy was performed 2 weeks later.

For his hypercalcemia(13.7mg/dl), Intact PTH level up to 563.0 pg/mL (12-72) was found.

Neck ultrasound showed right lobe nodular goiter with some cystic change. Parathyroid scan revealed possible tumor of right thyroid gland or right parathyroid gland. After stable condition of pancreatitis, the right lobe with pyramidal of thyroid and right parathyroid was removed.

Then his calcium levels decreased to around 8.2mg/dl. His Intact PTH level decreased to 127 pg/mL. Pathological finding confirmed parathyroid carcinoma.

Parathyroid carcinoma is one of the rarest known malignancies that may occur sporadically or as a part of a genetic syndrome. It accounts for approximately 1% of patients with primary hyperparathyroidism. The majority (90%) of parathyroid cancer tumors are hormonally functional and hypersecrete parathyroid hormone (PTH). Thus, most patients exhibit strong symptomatology of hypercalcemia at presentation.

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中華民國內分泌暨糖尿病學會 101年度秋季學術研討

PP7

EFFECTS OF HYPOGLYCEMIC FORMULA ON BIOCHEMICAL, CHRONIC INFLAMMATION AND THROMBOGENIC RISK FACTORS IN TYPE 2 DIABETIC PATIENTS 1

SHIH-CHUEH CHEN, 3KUNG-CHI CHAN, 1CHIN-LIAN LAI, 2KUO-TING SUN, 3 PEI-CHI CHEN, 4SIMON HSIA 1 Section of Metabolism and Endocrinology, Department of Internal Medicine, Cheng Ching Hospital, Taichung, Taiwan 2 Department of Dentistry, China Medical University Hospital, Taichung, Taiwan 3 Department of Food and Nutrition, Providence University, Taichung, Taiwan 4 Institute of Biomedical Nutrition, Hung-Kuang University, Taichung, Taiwan

During the past 10 years, the prevalence of type 2 diabetes has increased dramatically in Taiwan. Hyperglycemia-induced oxidative damage plays an important role in the development of chronic complications in type 2 diabetic patients.

The purpose of this study was to investigate the effectiveness of a market-sold hypoglycemic formula (HF) on chronic inflammation and thrombogenic risk in type 2 diabetic patients.

Ninety type 2 DM patients were randomly assigned into four experimental groups in this double-blinded study: a placebo group, low HF group (LG), medium HF group (MG), and high HF group (HG). Before supplementation, plasma concentrations of triglyceride, cholesterol and hsCRP were significantly higher in patients with fasting plasma glucose ＞140 mg/dL than in those patients with＜140 mg/dL, together with lower AT-III activity, indicating a higher risk of macroangiopathy in these patients. After supplementation for 8 weeks, concentrations of fasting plasma glucose, HbA1c, insulin resistance (HOMA), MDA, inflammatory markers (hs-CRP and IL-6), von Willebrand factor (vWF), activity of coagulation factor VII (FVII), plasminogen activator inhibitor-1 (PAI-1) and anticoagulation factors (antithrombin III, AT-III and protein c, PC) were measured.

The results of this study showed that the concentration of fasting glucose was decreased

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摘要

in the HF groups, and HbA1c was decreased and the insulin level increased in the HG group.

MDA was decreased in the HF groups. Activity of PC was elevated by supplementing HG. Concentrations of hs-CRP, vWF and PAI-1 all tended to be decreased by HF supplementation.

In conclusion, supplementing high dosage HF may have the beneficial effects of decreasing fasting glucose and oxidative stress, ameliorating chronic inflammation and abnormal blood coagulation, and hence decreasing thrombogenic risk in type 2 diabetic patients.

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中華民國內分泌暨糖尿病學會 101年度秋季學術研討

PP8

HYPOLIPIDEMIC AGENTS INDUCE MYOSITIS, LIMBS WEAKNESS IN A HYPOTHYROIDISM PATIENT– A CASE REPORT 1

NAI-CHENG YEH, 1CHWEN-YI YANG, 1KAI-JEN TIEN, 1FENG-CHIEH YEN, 1 SHANG-YU LEE, 1CHIEN-WEN CHOU 1 Division of Endocrinology and Metabolism, Department of Internal Medicine, Chi Mei Medical Center

Myalgia is one of clinical symptoms of hypothyroidism. Muscle injury is also a common complication of hypolipidemic agents. It is less common to seen in patients with use fibrates than whom with statins. We present a 30-year-old male denied any underlying disease.

Hyperlipidemia was occasional found in routine health exam. Myositis, rhabdomyolytis, and even more limbs weakness were complained after fibrates use. He then was admitted and thyroid function was surveyed after clinical features suspected. Hypothyroidism was diagnosed with high TSH level up to 85.43 μIU/ml. Microsomal antibodies was also shown with high titers.

Hashimoto thyroiditis was impressed. Other autoimmune disorders including type 1 diabetes mellitus were not discovered after series survey.

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中華民國內分泌暨糖尿病學會 101年度秋季學術研討

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中華民國內分泌暨糖尿病學會 101年度秋季學術研討

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