Iacobone Maurizio, Carnaille Bruno, Palazzo F Fausto, Vriens Menno
Endocrine Surgery Unit, Department of Surgery, Oncology and Gastroenterology, University of Padua, Via Giustiniani 2, 35128, Padova, Italy.
Department of Endocrine Surgery, Université de Lille, Lille, France.
Langenbecks Arch Surg. 2015 Dec;400(8):867-86. doi: 10.1007/s00423-015-1342-7. Epub 2015 Oct 8.
Hereditary hyperparathyroidism has been reported to occur in 5-10 % of cases of primary hyperparathyroidism in the context of multiple endocrine neoplasia (MEN) types 1, 2A and 4; hyperparathyroidism-jaw tumour (HPT-JT); familial isolated hyperparathyroidism (FIHPT); familial hypocalciuric hypercalcaemia (FHH); neonatal severe hyperparathyroidism (NSHPT) and autosomal dominant moderate hyperparathyroidism (ADMH). This paper aims to review the controversies in the main genetic, clinical and pathological features and surgical management of hereditary hyperparathyroidism.
A peer review literature analysis on hereditary hyperparathyroidism was carried out and analyzed in an evidence-based perspective. Results were discussed at the 2015 Workshop of the European Society of Endocrine Surgeons devoted to hyperparathyroidism due to multiple gland disease.
Literature reports scarcity of prospective randomized studies; thus, a low level of evidence may be achieved.
Hereditary hyperparathyroidism typically presents at an earlier age than the sporadic variants. Gene penetrance and expressivity varies. Parathyroid multiple gland involvement is common, but in some variants, it may occur metachronously often with long disease-free intervals, simulating a single-gland involvement. Bilateral neck exploration with subtotal parathyroidectomy or total parathyroidectomy + autotransplantation should be performed, especially in MEN 1, in order to decrease the persistent and recurrent hyperparathyroidism rates; in some variants (MEN 2A, HPT-JT), limited parathyroidectomy can achieve long-term normocalcemia. In FHH, surgery is contraindicated; in NSHPT, urgent total parathyroidectomy is required. In FIHPT, MEN 4 and ADMH, a tailored case-specific approach is recommended.
据报道,遗传性甲状旁腺功能亢进症发生于5% - 10%的原发性甲状旁腺功能亢进症病例中,这些病例与1型、2A型和4型多发性内分泌腺瘤病(MEN)、甲状旁腺功能亢进-颌骨肿瘤综合征(HPT-JT)、家族性孤立性甲状旁腺功能亢进症(FIHPT)、家族性低钙血症性高钙血症(FHH)、新生儿重症甲状旁腺功能亢进症(NSHPT)以及常染色体显性中度甲状旁腺功能亢进症(ADMH)相关。本文旨在综述遗传性甲状旁腺功能亢进症主要的遗传、临床和病理特征以及外科治疗方面的争议。
对遗传性甲状旁腺功能亢进症进行了同行评议文献分析,并从循证角度进行分析。结果在2015年欧洲内分泌外科医生协会关于多腺体疾病所致甲状旁腺功能亢进症的研讨会上进行了讨论。
文献报道前瞻性随机研究较少;因此,证据水平可能较低。
遗传性甲状旁腺功能亢进症通常比散发性病例发病年龄更早。基因的外显率和表达性各不相同。甲状旁腺多腺体受累很常见,但在某些类型中,可能会异时发生,且通常有较长的无病间期,类似单腺体受累。应进行双侧颈部探查并施行甲状旁腺次全切除术或甲状旁腺全切除术 + 自体移植,尤其是对于MEN 1型患者,以降低持续性和复发性甲状旁腺功能亢进症的发生率;在某些类型(MEN 2A型、HPT-JT)中,有限的甲状旁腺切除术可实现长期血钙正常。对于FHH,手术禁忌;对于NSHPT,需要紧急施行甲状旁腺全切除术。对于FIHPT、MEN 4型和ADMH,建议采用针对具体病例的个体化方法。