一名患有多结节性甲状腺肿和慢性肾脏病的患者的甲状旁腺癌病例报告:诊断和治疗中的困难(实践观察)

© А.А. Аверкина, Р.А. Золотарева, И.В. Ким, Е.В. Бондаренко, А.Ю. Абросимов, М.В. Дегтярев, Е.О. Мамедова, Ж.Е. Белая, Л.Я. Рожинская, Anastasia A. Averkina, Radmila A. Zolotareva, Ilya V. Kim, Ekaterina V. Bondarenko, A.Yu. Abrosimov, Mikhail V. Degtyarev, E. Mamedova, Zhanna E. Belaya, L. Rozhinskaya
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摘要

我们要介绍的是一个临床病例,患者患有病因复杂的慢性肾病和多结节性甲状腺肿,甲状旁腺癌位置不典型,导致严重的原发性甲状旁腺功能亢进。患者S.现年59岁,因 "慢性肾小管间质性肾炎伴肾硬化"、慢性肾脏病(CKD)G3-4导致的继发性甲状旁腺功能亢进、骨质疏松症和多结节甲状腺瘤在三级转诊医院接受了长期随访。2021年7月,她被转诊到内分泌研究中心,以明确诊断,因为尽管接受了西那卡西酮治疗,但她的甲状旁腺激素(PTH)水平仍然极高。经检查,诊断出原发性甲状旁腺功能亢进症、左侧甲状旁腺病变、多结节性甲状腺肿伴亚临床甲状腺毒症和维生素D缺乏症。在切除左侧甲状旁腺病灶(组织学证实为甲状旁腺癌)和左侧甲状旁腺半切除术后,出现了低钙血症("饥饿骨综合征"),但甲状旁腺激素水平仍保持升高。术后3-18个月,没有获得原发性甲状旁腺功能亢进症复发的数据。PTH的持续中度升高被认为是继发性甲状旁腺功能亢进症(CKD)和低钙血症。使用抗骨质吸收药物地诺单抗、维生素D及其活性代谢产物、钙制剂和甲状旁腺切除术对骨质疏松症进行综合治疗,可显著提高骨质密度(BMD),且术后18个月未再发生骨折。对于透析前患有慢性肾脏病且PTH水平较高的患者,有必要对原发性甲状旁腺功能亢进症(PHPT)和继发性甲状旁腺功能亢进症(SHPT)进行鉴别诊断。原发性甲状旁腺功能亢进症的严重表现可怀疑为甲状旁腺癌。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Parathyroid carcinoma case-report in a patient with multinodular goiter and chronic kidney disease: difficulties in diagnosis and treatment (observation from practice)
We would like to present a clinical case of severe primary hyperparathyroidism due to a parathyroid carcinoma of atypical location in a patient with chronic kidney disease of complex etiology and multinodular goiter. Patient S., 59 years old, was followed-up for a long time in tertiary referral hospitals for “chronic tubulointerstitial nephritis with nephrosclerosis”, secondary hyperparathyroidism due to chronic kidney disease (CKD) G3–4, osteoporosis, and a multinodular euthyroid colloid goiter. In July 2021 she was referred to the Endocrinology Research Centre in order to clarify the diagnosis because of the persistence of an extremely high level of parathyroid hormone (PTH) despite cinacalcet treatment. During examination, primary hyperparathyroidism, a left parathyroid gland lesion, multinodular goiter with subclinical thyrotoxicosis, and vitamin D deficiency were diagnosed. After the removal of the left parathyroid gland lesion (histologically confirmed parathyroid carcinoma) and a left-sided hemithyroidectomy, hypocalcemia («hungry bone syndrome») developed, but the level of parathyroid hormone remained elevated. After 3–18 months after surgery, no data for relapse of primary hyperparathyroidism was obtained. The persistent moderate increase in PTH was regarded as secondary hyperparathyroidism in CKD and hypocalcemia. Complex therapy of osteoporosis with the antiresorptive drug denosumab, vitamin D and its active metabolite, calcium preparations, and parathyroidectomy led to a significant increase in bone mineral density (BMD) and no repeated fractures 18 months after surgery.Conclusion. In patients with pre-dialysis CKD and high PTH levels, it is necessary to make a differential diagnosis between primary (PHPT) and secondary hyperparathyroidism (SHPT). Severe manifestations of primary hyperparathyroidism can be suspicious for parathyroid carcinoma.
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