新生儿严重甲状旁腺功能亢进症继发于一种新的纯合CASR基因突变。

Q3 Medicine Clinical Cases in Mineral and Bone Metabolism Pub Date : 2017-09-01 Epub Date: 2017-12-27 DOI:10.11138/ccmbm/2017.14.3.354
Noman Ahmad, Mona Bahasan, Balgees Abdulhadi Abdullah Al-Ghamdi, Halah Faleh Al-Enizi, Ali Saeed Al-Zahrani
{"title":"新生儿严重甲状旁腺功能亢进症继发于一种新的纯合CASR基因突变。","authors":"Noman Ahmad,&nbsp;Mona Bahasan,&nbsp;Balgees Abdulhadi Abdullah Al-Ghamdi,&nbsp;Halah Faleh Al-Enizi,&nbsp;Ali Saeed Al-Zahrani","doi":"10.11138/ccmbm/2017.14.3.354","DOIUrl":null,"url":null,"abstract":"<p><p>Neonatal severe hyperparathyroidism (NSHPT) is a rare autosomal recessive disease. Children present within the first 6 months of life and more commonly in the first few weeks. Common presentation is poor feeding, polyuria, dehydration, lethargy, failure to thrive, hypotonia, gastrointestinal dysmotility, osteopenia and symptoms of respiratory distress due to a poorly developed chest cage. We present a case of a 2-month old girl with severe hypercalcemia and hyperparathyroidism. She was found to have a novel homozygous mutation in the acceptor splicing site of intron 4 (c.1378 -2A>G) of the calcium sensing receptor gene (<i>CASR</i>). This mutation causes frame shift deletion of exon 5 and insensitivity of CASR to calcium. The patient was treated with intravenous fluids, fruosemide, calcitonin, intravenous pamidronate and oral cinacalcet. She did not respond to medical treatment. Parathyroid gland imaging including ultrasound, MRI and sestamibi nuclear scan were not helpful in localizing the glands. Her symptoms resolved following total parathyroidectomy. She is being treated with alfacalcidiol and calcium supplements to maintain normal serum calcium and phosphate. She achieved her normal developmental milestones.</p>","PeriodicalId":47230,"journal":{"name":"Clinical Cases in Mineral and Bone Metabolism","volume":"14 3","pages":"354-358"},"PeriodicalIF":0.0000,"publicationDate":"2017-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5762229/pdf/354-358.pdf","citationCount":"9","resultStr":"{\"title\":\"Neonatal severe hyperparathyroidism secondary to a novel homozygous <i>CASR</i> gene mutation.\",\"authors\":\"Noman Ahmad,&nbsp;Mona Bahasan,&nbsp;Balgees Abdulhadi Abdullah Al-Ghamdi,&nbsp;Halah Faleh Al-Enizi,&nbsp;Ali Saeed Al-Zahrani\",\"doi\":\"10.11138/ccmbm/2017.14.3.354\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Neonatal severe hyperparathyroidism (NSHPT) is a rare autosomal recessive disease. Children present within the first 6 months of life and more commonly in the first few weeks. Common presentation is poor feeding, polyuria, dehydration, lethargy, failure to thrive, hypotonia, gastrointestinal dysmotility, osteopenia and symptoms of respiratory distress due to a poorly developed chest cage. We present a case of a 2-month old girl with severe hypercalcemia and hyperparathyroidism. She was found to have a novel homozygous mutation in the acceptor splicing site of intron 4 (c.1378 -2A>G) of the calcium sensing receptor gene (<i>CASR</i>). This mutation causes frame shift deletion of exon 5 and insensitivity of CASR to calcium. The patient was treated with intravenous fluids, fruosemide, calcitonin, intravenous pamidronate and oral cinacalcet. She did not respond to medical treatment. Parathyroid gland imaging including ultrasound, MRI and sestamibi nuclear scan were not helpful in localizing the glands. Her symptoms resolved following total parathyroidectomy. She is being treated with alfacalcidiol and calcium supplements to maintain normal serum calcium and phosphate. She achieved her normal developmental milestones.</p>\",\"PeriodicalId\":47230,\"journal\":{\"name\":\"Clinical Cases in Mineral and Bone Metabolism\",\"volume\":\"14 3\",\"pages\":\"354-358\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2017-09-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5762229/pdf/354-358.pdf\",\"citationCount\":\"9\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Clinical Cases in Mineral and Bone Metabolism\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.11138/ccmbm/2017.14.3.354\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2017/12/27 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q3\",\"JCRName\":\"Medicine\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinical Cases in Mineral and Bone Metabolism","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.11138/ccmbm/2017.14.3.354","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2017/12/27 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 9

摘要

新生儿严重甲状旁腺功能亢进是一种罕见的常染色体隐性遗传病。儿童在生命的前6个月内出现,更常见的是在最初的几周内。常见的表现是摄食不良、多尿、脱水、嗜睡、发育不良、张力低下、胃肠运动障碍、骨质减少以及由于胸廓发育不良引起的呼吸窘迫症状。我们提出一个2个月大的女孩与严重的高钙血症和甲状旁腺功能亢进。她在钙敏感受体基因(CASR)的4内含子受体剪接位点(c.1378 -2A>G)发现了一个新的纯合突变。这种突变导致外显子5的移框缺失和CASR对钙的不敏感。患者给予静脉输液、氟索塞米、降钙素、静脉注射帕米膦酸盐和口服西那卡塞。她对药物治疗没有反应。甲状旁腺影像学包括超声、MRI和核扫描对腺体的定位没有帮助。她的症状在全甲状旁腺切除术后消失。她正在接受alfacalcidiol和钙补充剂治疗,以维持正常的血清钙和磷酸盐。她达到了正常的发育阶段。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

摘要图片

摘要图片

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
Neonatal severe hyperparathyroidism secondary to a novel homozygous CASR gene mutation.

Neonatal severe hyperparathyroidism (NSHPT) is a rare autosomal recessive disease. Children present within the first 6 months of life and more commonly in the first few weeks. Common presentation is poor feeding, polyuria, dehydration, lethargy, failure to thrive, hypotonia, gastrointestinal dysmotility, osteopenia and symptoms of respiratory distress due to a poorly developed chest cage. We present a case of a 2-month old girl with severe hypercalcemia and hyperparathyroidism. She was found to have a novel homozygous mutation in the acceptor splicing site of intron 4 (c.1378 -2A>G) of the calcium sensing receptor gene (CASR). This mutation causes frame shift deletion of exon 5 and insensitivity of CASR to calcium. The patient was treated with intravenous fluids, fruosemide, calcitonin, intravenous pamidronate and oral cinacalcet. She did not respond to medical treatment. Parathyroid gland imaging including ultrasound, MRI and sestamibi nuclear scan were not helpful in localizing the glands. Her symptoms resolved following total parathyroidectomy. She is being treated with alfacalcidiol and calcium supplements to maintain normal serum calcium and phosphate. She achieved her normal developmental milestones.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Clinical Cases in Mineral and Bone Metabolism
Clinical Cases in Mineral and Bone Metabolism ENDOCRINOLOGY & METABOLISM-
CiteScore
2.60
自引率
0.00%
发文量
0
期刊介绍: The Journal encourages the submission of case reports and clinical vignettes that provide new and exciting insights into the pathophysiology and characteristics of disorders related to skeletal function and mineral metabolism and/or highlight pratical diagnostic and /or therapeutic considerations.
期刊最新文献
From the Editor-in-Chief. Hypothyrodism as a risk factor of periodontitis and its relation with vitamin D deficiency: mini-review of literature and a case report. Atypical femur fractures: a distinctive tract of adult hypophosphatasia. Surgical treatment of neglected hip fracture in children with cerebral palsy: case report and review of the literature. Pitfalls in interpreting interventional studies for osteoporosis.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1