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Ki Soo Kim  (Kim KS) 11 Articles
A Case of Ectopic ACTH Syndrome Caused by Thymic Carcinoid Tumor and Localized by PET.
Jong Chul Won, Sung Kwan Hong, Hyun Ju Lee, Sang Ook Kim, Yun Hee Jeong, Dae Hyuk Moon, Dong Kwan Kim, Kyung Yub Kong, Jae Sung Lee, Ki Soo Kim
J Korean Endocr Soc. 1999;14(4):771-778.   Published online January 1, 2001
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Ectopic ACTH syndrome is frequently caused by lung cancer and uncommonly by other tumors such as thymic carcinoid. For its treatment, early diagnosis and complete resection is irresponsible, but some cases are remained unlocalized in spite of all diagnostic modalities. Here we report a case of ectopic ACTH syndrome which was localized by PET but could not be localized by conventional technique. A tumor at thymic area was ACTH secreting thymic carcinoid which was operated but couldnt resect completly. Glucocorticoid hypersecretion was persisted with chemotherapy, radiotherapy, and ketoconazole treatment. Patient died of sepsis after 12 months of diagnosis.
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A Case of Isolated ACTH Deficiency with Rapid Deterioration.
Sung Kwan Hong, Eun Joo Lee, Ki Soo Kim, Chul Ryong Lee, Hyung Joo Park, Hun Ho Song, Young Soo Lee
J Korean Endocr Soc. 1999;14(2):396-400.   Published online January 1, 2001
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Isolated ACTH deficiency is a rare disorder, and usually characterized by its chronic course. The 59 year-old woman patient who had been healthy until 2 months ago, admitted because of abdomial pain, general weakness and loss of weight about 12kg for 2 months. She looked a little pallor but color of skin was not remarkable. Blood pressure, serum electrolyte, and glucose on admission were within normal range. Serum calcium was elevated with the value of 12.6mg/dL, which was normalized after hydration. Cortisol response to RI induced hypoglycemia did not show any response. Anterior pituitary hormone except ACTH showed normal response during combined pituitary hormone stimulation test. These clinical and laboratory finding reveals that isolated ACTH deficiency was developed in a short term period. There were no abnormalities in sellar MRI except pineal cyst. Her complaints were disappeared dramatically after hydroccetisone replacement at 4th. hospital day. Here we report a case of isolated ACTH deficiency, which was rapidly developed, with hypercalcemia, abdominal pain, and loss of weight about 12kg for 2 months.
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A Comparison Technetium-99m and Iodine-123 Scan in Thyroid Hot Nodules.
Eun Sook Kim, Seok Jun Hong, Young Ki Song, Jin Sook Ryu, Dae Hyuk Moon, Ki Soo Kim
J Korean Endocr Soc. 1999;14(2):339-345.   Published online January 1, 2001
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BACKGROUND
Pertechnetate ( Tc) has been widely employed for thyroid imaging. While pertechnetate and radioiodide have usually similar results in identifying thyroid nodules, occasionally differences have been noted. We intended to observe that the thyroid nodules which appeared to be hot on pertechnetate and to compare them with the images by radioiodide. METHODS: 'I scan was performed to thirty-eight cases (mean age: 48.9 +/- 13.2) presenting as hot nodule on Tc scan. Thyroid function test and pathologic diagnosis were obtained in all patients. RESULTS: Of the 38 patients, 24 had euthyroidism, 13 had hyperthyroidism, and 1 had hypothyroidism. Thirty patients had adenomatous goiter, 4 papillary carcinoma, 3 Hashimotos thyroiditis, and 1 had HQrthle cell tumor. 28 of 38 patients showed similar images, but the remaining 10 patients(26.3%) revealed discordant images on Tc and 131I scan. Among the concordant cases, 23 had adenomatous goiter, 3 had papillary carcinoma, and 2 had Hashimotos thyroiditis. Among the discordant cases, 7 had adenomatous goiter, 1 had papillary carcinoma, 1 had Hashimotos thyroiditis, and 1 had HQrthle cell tumor. The incidence of malignancy was 10.7% of concordant cases, and 20% of discordant cases and was revealed statistically insignificant (p>0.05). CONCLUSION: We observed higher incidence of malignancy in patients presenting hot nodules on 99mTc scan than ever reported. Fine needle aspiration should be performed to all patients with hot nodules and the 'I scan would not be recommended for further diagnostic study.
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Effect of Radioactive Iodine Therapy in Patients with Scan-Negative, Thyroglobulin-Positive Thyroid Cancer.
Eun Sook Kim, Seok Jun Hong, Jin Yub Kim, Young Ki Song, Jin Sook Ryu, Dae Hyuk Moon, Ki Soo Kim, Sang Wook Kim
J Korean Endocr Soc. 1999;14(2):330-338.   Published online January 1, 2001
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BACKGROUND
After total thyroidectomy the presence of detectable serum thyroglobulin(Tg) concentration is an index of residual or metastatic thyroid tissue and is usually well correlated with positive I whole body scan. However, it is not rare to find a patient with detectable serum Tg levels but without any uptake on I whole-body scan. At present it is not certain how to manage such patients. We performed whole body scan after administration of therapeutic dose of 131I to evaluate the usefulness of radioactive iodine therapy in the above setting. METHODS: Fifteen patients (4 males and 11 females, ranging in age from 17 to 74 years) were studied. They had been previously treated with total thyroidectomy for papillary thyroid cancer followed by therapy with 131I for ablation of their thyroid residue. Tg levels were determined by immunoradiometric assay method. 131I (100-200 mCi) therapy was administered and whole body scan was performed. 99mTc MIBI scans were taken in 9 patients. Follow up data of Tg were available in 12 patients at time interval of 6 12 months from the first study and treatment. RESULTS: Tg(on) levels of these patients were in a range of 2.2210 ng/mL (mean 36.1 +/- 59.1 ng/mL) and Tg(off) levels were 17.3 1,592 ng/mL (mean 197.3 +/- 400.3 ng/mL). After radioiodide therapy, Tg(on) levels were in 1.48.5 ng/mL (mean 11.0 +/- 13.5 ng/mL), Tg (off) were 11.9 478.0 ng/mL (mean 159.3 +/- 159.8 ng/mL). The Tg (on) levels were decreased significantly after RAI therapy, but Tg (off) levels had no significant difference, In 8 of the 15 patients (53.3%), posttreatment whole body scan showed definite positive uptakes which were not evident in pretreatment diagnostic scan. There were local recurrence in 3 cases, regional lymph node metastasis in 4 cases, and lung in I case. Diffuse hepatic uptake was definitely seen in 7 cases. The MIBI scan showed abnorml uptakes in 4 of 9 cases. CONCLUSION: The therapeutic usefulness of 100 to 200 mCi of 131I treatment in patients with 131I scan-negative and Tg-positive was unclear. And the MIBI scan was only partially effective. Further studies with other diagnostic and therapeutic approachs are required to evaluate the exact lesions and to improve prognosis.
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A Case of Multiple Endocrine Neoplasia Type I Presented with Secondary Amenorrhea and Osteoporosis.
Sang Bum Hong, Seok Jun Hong, Young Ki Song, Ki Soo Kim, Sang Wook Kim, Ki Ub Lee, Min Kyu Kim, Seung Mo Hong, Duck Jong Han
J Korean Endocr Soc. 1998;13(4):684-689.   Published online January 1, 2001
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AbstractAbstract PDF
MEN type 1 is characterized primarily by the presence of functioning and nonfunctioning tumors or hyperplasia of the pituitary gland, parathyroid glands, and pancreatic islet cells. Pancreatic islet tumors in MEN type 1 produce different kinds of hormone which were pancreatic polypeptide, gastrin, glucagon, insulin and so on. To date, ten cases had been reported in Korea. We report another case with MEN type 1 having prolatin-secreating pituitary adenoma, parathyroid hyperplasia and insulinoma. A 36-year-old woman was admitted because of long-standing amenorrhea and recently diagnosed osteoporosis. Otherwise, she had been in good health except experiencing one episode of loss of consciousness after skipped meal. The blood chemistries were normal except hypercalcemia and hypophosphatemia. Hormonal studies revealed elevated levels of intact PTH and prolactin and decreased value of estradiol with low LH and FSH. The neck CT revealed 1 cm-sized nodule at posterior portion of right thyroid gland and 99mTc-sestamibi sintigraphy showed a increased uptake in left lower and right lower parathyroid glands. The sella MRI showed 0.7 cm-sized enhanced lesion in the left pituitary gland. The ratio of immunoreactive insulin to glucose was elevated and 3-4 pancreatic masses of variable size were identified by endoscopic ultrasonography and angiography. Subtotal parathyroidectomy and pyrolus-preserving pancreaticoduodenectomy with spleen-preserving distal pancreatectomy was done. Postoperative she had been doing well with normocalcemia and normoglycemia. Transsphenoidal adenonectomy was done 5 months later. Histologic examination of removed tissues revealed a single insulinoma, prathyroid hyperplasia and prolactin-secreating pituitary adenoma.
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A Case of Somatostatinoma which Manifested as Insulinoma when Metastasized to the Liver.
Joong Yeol Park, Byung Doo Lee, Kyung Soo Ko, Kyung Yub Gong, Ki Soo Kim, Sung Jo Bang, Jae Hwan Lee, Yoon Ey Chung, Sang Wook Kim, Hye Je Cho, Ki Ub Lee
J Korean Endocr Soc. 1998;13(4):670-676.   Published online January 1, 2001
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We report a case of somatostatinoma, which manifested as insulinoma after liver metastasis. A 74-year-old man suffered from diabetes mellitus and jaundice. The abdominal CT scan of this patient showed a mass in the pancreas head, which obstructed biliary duct. He underwent Whipples procedure. Immunohistochemical staining of postoperative specimen disclosed that this tumor was strongly positive for somatostatin. After 4 months, follow up CT scan showed multiple metastatic lesions in the liver. We performed transarterial chemoinfusion two times, but the response was disappointing. After 2 months, he suffered from altered mentality, which was relieved by intake of sugar. Biochemical laboratory findings and immunohistochemical staining of liver biopsy disclosed that the metastatic lesion in this patient was insulinoma. We performed embolization of hepatic artery with gelform. The biochemical response was dramatic, but he died of septic shock, which was caused by gas forming liver abscess. In summary, we report a case of somatostatinoma which manifested as insulinoma after metastasis to the liver.
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Concurrent Medullay and Papillary Carcinoma of the Thyroid.
Seok Jun Hong, Kyung Yub Gong, Young Ki Song, Jin Sook Ryu, Ki Soo Kim, Jung Hee Lee
J Korean Endocr Soc. 1998;13(4):634-639.   Published online January 1, 2001
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The origins of medullary carcinoma and papillary carcinoma of thyroid are embryologically different. We report a case of simultaneous occurrence of medullary carcinoma and papillary carcinoma of the thyroid in the same thyroid gland. In this case, the occurrence of the two tumors may be a coincidence, does not have embryological or genetical significance.
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A Case of Adult Fanconi Syndrome and Osteomalacia associated with x-Light Chain Monoclonal Gammopathy.
Chul Hee Kim, Hong Kyu Kim, Shi Jung Chung, Juog Min Ko, Soo Kil Park, Woo Kun Kim, Ki Soo Kim
J Korean Endocr Soc. 1998;13(1):99-107.   Published online January 1, 2001
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The Fanconi syndrome is a complex tubulopathy, which is characterized by urinary hyperexcretion of amino acids of all classes, phosphate, glucose, bicarbonate, calkium, potassium, and otherions, and proteins with molecular weights under 50,000 daltons. This metabolic disease leads to hypophospatemia, hypokalemia, growth failure, metabolic acidasis, and rickets/osteomalacia. Fanconi syndrome may be inherited or acqulred. Most cases of adult Fanconi syndrome are acquired, and the acquired syndrome is associated with thermal burns, exposure to heavy metals or drugs, vitmnin D deficiency, renal transplantation, or light chain deposition. The most common cause of adult Fanconi syndrome is multiple myeloma. We ribe here a case of adult Fanconi syndrome and osteomalacia associated with x-light chain monoclonal gammopathy. A 47-year-old woman presented with multiple bane pain and proximal muscle weakness for 2 years. Laboratory findmgs showed hypophosphatemia, mild hypocalcemia, marked elevation of serum alkaline phosphatase, metabolic acidosis, low 25-OH- vitamm D level and secondary hyperparathyroidism. Urinary excretion of protein, uric acid, phosphate, and glucose was mcreased, and tubular reabsorption of phosphate was decreased to 50%. Protein immunofixation electrophoresis of serum and urine showed x-light chain type monoclonal gammopathy. Bone marrow examination was normal except moderate elevation of plasma cell component(8.8%). The skeletal radiography showed fractures of both lower ribs and pseudofracture in right femoral lesser trochanter. We treated the patient with calcium, 1.25-(OH)2-vitamin D, phosphorus, bicarbonate, and potassium, and her clinical symptoms were gradually relieved.
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A Case of Polyglandular Autoimmune Syndrome.
Chul Hee Kim, Hong Kyu Kim, Joong Yeol Park, Young Ki Song, Ki Soo Kim, Kyo Sang Yoo
J Korean Endocr Soc. 1997;12(4):672-676.   Published online January 1, 2001
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The polyglandular autoimmune syndrome is constellation of multiple endocrine insufficiencies often associated with diseases of nonendocrine organs occurring in individual patients and their families. In 1980, Neufeld classified this syndrome into three major types. Type II is characterized by adrenocortical insufficiency, autoimmune thyroiditis, and insulin-dependent diabetes mellitus. We experienced a case characterized by adrenocortical insufficiency, autoimmune thyroiditis, and ovarian failure and report with the review of the literature. A 38-year-old woman visited our clinic because of progressing brown colored pigmentation of skin and mucosa which is developed a year ago. Nine years ago prior to visit, amenorrhea was developed after right oophrectomy. Three years ago, she revealed feature of hyperthyroidism such as palpitation, loss of body weight (8kg/1-2years), heat intolerance, and sweating, so received antithyroid therapy for 14 months. Brown colored pigmentation of skin and mucosa, especially scar and gingiva, has been progressively aggravated during last year. She had no past or family history of other endocrine disease. Diffuse pigmentation of skin, loss of axillary and pubic hair, and diffuse enlargement of both thyroid glands were shown on physical examination. Blood cell count, serum chemistry and blood sugar test were all within normal range. Basal hormone levels were T3-uptake 29.7% (30~40), T3 153 ng/dL (85~185), T4 7.5ug/dL (5.5~11.5), TSH 2.4 IU (0.34~3.5), anti-TG antibody <100 U/mL (0~100), anti-microsome antibody <50 U/mL (0~100), TBII (thyrotropin binding inhibiting immunoglobulin) 2.2% ( (-15)~15), ACTH 989 pg/mL (0~37), cortisol 0.1 ug/dL (5~25), renin 7.1ng/mL/hr (1~2.5), aldosterone 81.0pg/mL (50~194), LH 115.2 mIU/mL (0.6~16.8), FSH 122 mIU/mL (1.6~19.0), and estradiol <10.0pg/mL (30~120). In ACTH stimulation test, levels of basal cortisol, 30 minutes, and 60 minutes were <0.1, <0.1, and <0.1 g/dL respectively. And, in glucagon stimulation test, levels of basal C-peptide, 5 minutes, 10 minutes, and 15 minutes were 0.9, 5,1, 6.3, and 5.5 ng/dL respectively. Thyroid scan showed diffuse enlargement of bilateral thyroid glands and pelvic ultrasonogram showed atrophy of left ovary. We administered corticosteroid, estrogen, and progesterone which were deficient to the patient, and has followed up the clinical course of the patient.
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Effects of Thyroid Hormone on Preduction of Interleukin-6 and Interleukin-11 in Human Bone Marrow Stromal Cells.
Chul Hee Kim, Dong Kwan Kim, Hong Kyu Kim, Young Ki Song, Ki Soo Kim
J Korean Endocr Soc. 1997;12(4):557-564.   Published online January 1, 2001
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BACKGROUND
It is well known that excessive thyroid hormone in the body is associated with bone loss. However, the mechanism by which thyroid hormone affects bone cell metabolism remains unclear. It has been shown that thyroid hormones stimulate osteoclastic bone resorption indirectly via some unknown mediators secreted by osteoblasts, This study was undertaken to determine if interleukin-6 (IL-6) or interleukin-11 (IL-l1) could be the mediator (s) of thyroid hormone-induced bone loss. METHODS: We treated primary cultured human bone rnarrow stromal cells with 3,5,3-triiodo-thyronine (T) and measured basal and interleukin-l (IL-1)-stimulated IL-6/IL-ll production. We also investigated the possible modulating effect of 17B-estradiol (17B-E2.) on thyroid hormone action. RESULTS: T3 at 10 (-12) ~ 10 (-8) M concentration, significantly increased the basal IL-6 production in a dose-dependent manner, and also potentiated the stimulatory effect of IL-1 on IL-6 production. However, T failed to elicit a detectable effect on basal or IL-1-stimulated IL-11 production. Treat#ment with l7B-E2. inhibited IL-1-stimulated IL-6 production, but the effects of T3 on IL-6 production were not affected by 17/B-E. CONCLUSION: These results suggest that thyroid hormone may increase bone resorption by increasing basal IL-6 production and potentiating IL-1-induced IL-6 production from osteoblast-lineage cells, and these effects were independent of estrogen status.
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Anticardiolipin Antibody in Graves' Disease.
Young Ki Song, Ki Soo Kim, Jung Hee Lee
J Korean Endocr Soc. 1997;12(4):528-532.   Published online January 1, 2001
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BACKGROUND
S: Antiphospholipid antibodies which are frquently found in systemic lupus erythematosus and primary antiphospholipid syndrome are associated with recurrent abortions and thromboembolism. In this study the authors investigated whether antiphospholipid antibodies are found in Graves disease, a representative organ-specific autoimmune disease and what is the clinical implication of the antiphospholipid antibodies if they appear in Graves disease. METHODS: Anticardiolipin antibody and lupus anticoagulant activity were measured in 57 untreated hyperthyroid Graves patients. 42 euthyroid patients with thyroid nodules served as controls. RESULTS: Eight of the 57 patients with Graves disease had anticardiolipin antibody which was significantly more frequent than in control group. Six of the eight patients who had anticardiolipin antibody had IgM type antibody and two had IgG type antibody. All their antibody activity declined with several months of antithyroid drug therapy and finally disappeared when the patients became euthyroid. Presence of anticardiolipin antibody had no relationship with clinical events such as spontaneous abrtion and thromboembolism. CONCLUSION: Anticardiolipin antibody is frequently found in patients with Graves disease. They seem to appear as an epiphenomenon of autoimmunity and they seem not to have any clinical implications.
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