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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
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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
- New Mutation Site in Vasopressin V2 Receptor Gene in a Family with Congenital Nephrogenic Diabetes Incipidus.
- Soon Hee Lee, Chang Hoon Choi, See Hyung Park, Young Sun Choi, Jeong Gook Kim, Seung Woo Ha, Bo Wan Kim
- J Korean Endocr Soc. 2000;15(1):97-106. Published online January 1, 2001
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Abstract
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- BACKGROUND
Congenital nephrogenic diabetes insipidus (NDI) is a rare inherited disorder, in which two different hereditary forms, X-linked and autosomal recessive traits, have been identified. The X-linked recessive form, mostly (>90%) congenital NDI, has been known to be caused by mutation of the arginine-vasopressin receptor 2 (AVPR2) gene. AVPR2 mutation sites are different in ethnic groups and recently 72 different mutation sites have been reported among AVPR2 gene. This study aimed to analyze AVPR2 gene in selected members in a Korean family with NDI and provided a report of the existence of a new mutation site in AVPR2 gene. METHODS: Three-generation maternal pedigree of the index patient (21-year old male, patient I) and his younger brother (19-year old male, patient II) with NDI was collected. Genomic DNA was obtained from patient I, II, III (index patient's male maternal cousin with NDI), index patient's mother, three maternal aunts, one female maternal cousin and, for control, one healthy male volunteer. Three coding exons of AVPR2 gene were amplified by PCR using 4 pairs of oligonucleotide primers. After direct sequencing of amplified PCR products, the sequence was compared with whole squence of normal AVPR2 gene and identification of a new site of mutation in this gene was done. RESULTS: 1) all three male patients had transversion of G to C at position 1033 of the AVPR2 gene, resulting in a subsequent change of amino acid from glycine to cysteine in codon 201. 2) Two small peaks of G and T, the result of direct sequencing in five female members in this family, would suggest that they are carriers of G to N transversion. CONCLUSION: These results can demonstrate the significant functional correlation of the mutation in AVPR2 gene sequence with clinical NDI, and suggest the clinical utility of direct mutation testing for congenital NDI in family.
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