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Case Report
- A Case of Drug Induced Nephrogenic Diabetes Insipidus and Hyperprolactinemia in Schizophrenia Simultaneously.
- Ho Yoel Ryu, Mi Young Lee, Yeon Lee, Jang Hyun Koh, Mi Jin Kim, Young Goo Shin, Choon Hee Chung
- J Korean Endocr Soc. 2005;20(4):407-412. Published online August 1, 2005
- DOI: https://doi.org/10.3803/jkes.2005.20.4.407
- 2,717 View
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Abstract
PDF - In schizophrenia, when treatment using antipsychotics fails, lithium, which is known as an antimanic drug, can also be administered. It is reported that 12~20% of patients taking lithium develop nephrogenic diabetes lactotrophs. Hyperprolactinemia is induced by typical antipsychotics, as they block the dopamine-2 receptors of latotrophs in the pituitary gland. Therefore, atypical antipsychotics for decreasing the side effect, such as hyperprolactinemia, can be used. However, hyperprolactinemia can be induced by risperidone, one of the atypical antipsychotics. Here, a case of drug induced nephrogenic diabetes insipidus and simultaneous hyperprolactinemia, which occurred in a patient with schizophrenia, is reported.
Original Article
- Effect of LiCl on Iodine Kinetics in Thyroid Cancer Cell Lines Transduced by Recombinant Adenovirus Containing Sodium Iodide Symporter(NIS) Gene.
- Won Bae Kim, Ja Young Song, Sung Min Han, Jeong Seok Yeo, Heui ran Lee, Young Kee Shong, Dae Hyuk Moon
- J Korean Endocr Soc. 2003;18(2):166-176. Published online April 1, 2003
- 1,358 View
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Abstract
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- BACKGROUND
Lithium is known to increase the retention of iodide in the thyroid gland, or in well differentiated thyroid cancer tissue. The effects of lithium on the function of the sodium iodide symporter (NIS) protein, especially when the lithium is increased in the retention of iodide in NIS-producing cells, the effect of lithium, on the kinetics of undifferentiated thyroid cancer cells transduced by a recombinant adenovirus containing the NIS gene, were checked. METHOD: Human NIS cDNA was inserted into pAxCAwt, a recombinant adenoviral cosmid vector, where the E1 & E2 genes have been deleted, making Rad-hNIS, which was propagated in 293 cells. The iodide uptake was evaluated by the 125I uptake assay in the undifferentiated thyroid cancer cells, ARO, FRO and NPA, following the infection with Rad-hNIS (1 or 10 MOI) in the presence, or absence, of LiCl at optimized concentrations. The iodide efflux was evaluated by the 125I efflux assay, for 1 hour, in the same cells expressing the NIS in the presence, or absence, of LiCl. Similar experiments were performed in the normal thyroid cell line, FRTL-5, cultured in 6H5 media. RESULTS: LiCl, at concentrations over 1.0mM, caused a significant decrease in the cell viability, as evaluated by trypan blue dye exclusion, in a dose dependent manner. When infected with Rad-hNIS, the iodide uptake was not affected by the LiCl in the ARO or NPA cells. However, LiCl(0.1and 1.0mM) increased the iodide uptake by 50 to 100%(vs. control) in the Rad-hNIS transduced FRO cells. In the Rad-hNIS transduced FRO cells, the iodide was released rapidly from the cells, with only 20.7+/-4.8% of the iodide uptake remaining at 1 hour, which was no different in the presence of LiCl (24.5+/-7.9%). The iodide efflux was not affected by the LiCl in the FRTL-5 cells cultured in the presence of TSH. CONCLUSION: These results suggest that the lithium-induced iodide retention in the thyroid gland, or in well differentiated thyroid cancer tissue, is not caused by the effect of the lithium on the NIS function, or the function of proteins or channels, involved in iodide transport via cell membranes. Although the iodide uptake can be markedly increased by the expression of NIS, with the transduction of Rad-hNIS, in undifferentiated thyroid cancer cells, the iodide taken up is rapidly released from the cells. A method for inducing the iodide retention in the cell should be elucidated in order to render the NIS gene therapy effective.
Case Reports
- A Case of Thyrotoxicosis During Lithium Therapy.
- Young Sik Choi, Yo Han Park, Joon Chul Pyun, Dal Soo Park, Chul Hee Lee, Hyo KYun Chung, Hyun Joo Kim, Soo Yeol Ahn, Jin Sook Jun, Yong Chang Oh
- J Korean Endocr Soc. 1998;13(4):629-633. Published online January 1, 2001
- 1,377 View
- 23 Download
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Abstract
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- Lithium has been established as a drug useful for the treatment of manic depressive disorder. It is now well recognized that long-term administration of this drug is associated with various antithyroid effects such as goiter, and subclinical and overt hypothyroidism. However, it has been associated less commonly with thyrotoxicosis. Recently we experienced a case of thyroitoxicosis during lithium therapy. A 24-year-old man treated with lithium carbonate 900 mg-1,200 mg/day for manic-depressive illness for four weeks. He then complained of nervousness, palpitation, tremor, heat intolerance, and sweating. Neck pain was not noted. At that time the results of thyroid function test were consistent with hyperthyroidism: T3 568.8 ng/dL, TSH 0.01 mU/mL, FT4 6.0 ng/dL, but 24 hr radioiodine uptake was 0.3%. We suspected this case as lithium induced thyrotoxicosis and discontinued lithium administration. After discontinuation of lithium thyrotoxic symptoms were subsided. One month later, thyroid hormon levels became normalized: T 100.2 ng/dL, TSH 0.06 mU/mL, FT4 0.97 ng/dL and 24hr radioiodine uptake was 16%. We report this case with review of literatures.
- Four Cases of Newly Developing Goiter During Lithium Carbonate Therapy.
- Kwan Woo Lee, Young Goo Shin, Sung Keun Lee, Sung Kyu Lee, Yun Suk Chung, Hyun Man Kim
- J Korean Endocr Soc. 1997;12(4):621-626. Published online January 1, 2001
- 1,094 View
- 19 Download
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Abstract
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- Since 1949, lithium has been widely used for treatment of manic depressive disorder. It has also been used for agranulocytosis after anticaneer chemotherapy and partially for hyperthyroidism. But it is well known that the long term administration of this drug is associated wih various antithyroid effects such as hypothyroidism, simple goiter, nodules and even thyrotoxicosis. Although the exact mechanism for leading hypothyroidism or goiter is still unknown, the incidence of lithium-induced hypothyroidism is 1-37% during lithium atment. We had an experience of newly developing goiter with or without hypothyroidism during lithium treatment in 4 MDP patients. Among our patients, the duration of lithium administration was from 0.7 months to 11 years, and the development of thyroid abnormality was impossible to predict. They were treated with thyroxine while lithium was discontinued causing favorable outcome. We suggest that routine thyroid function test include thyroid autoimmune antibody screening in patients planning to undergo lithium treatment.
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