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遗传性综合征中的甲状旁腺功能亢进症:特殊表现与特殊管理

Hyperparathyroidism in hereditary syndromes: special expressions and special managements.

作者信息

Marx Stephen J, Simonds William F, Agarwal Sunita K, Burns A Lee, Weinstein Lee S, Cochran Craig, Skarulis Monica C, Spiegel Allen M, Libutti Steven K, Alexander H Richard, Chen Clara C, Chang Richard, Chandrasekharappa Settara C, Collins Francis S

机构信息

Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892-1802, USA.

出版信息

J Bone Miner Res. 2002 Nov;17 Suppl 2:N37-43.

Abstract

Hyperparathyroidism (HPT) in its hereditary variants assumes special forms, has special associations, and requires special managements. Familial hypocalciuric hypercalcemia (FHH or FBHH) and neonatal severe primary hyperparathyroidism (NSHPT) reflect heterozygous or homozygous mutations, respectively, in the calcium-sensing receptor. FHH and NSHPT represent the mildest and severest variants of HPT. Both cause hypercalcemia from birth and atypical HPT that always and uniquely persists after subtotal parathyroidectomy. Their HPT is likely polyclonal and nonneoplastic. In contrast, mono- or oligo-clonal parathyroid neoplasia underlays most other HPT variants: multiple endocrine neoplasia type 1 (MEN1), multiple endocrine neoplasia type 2A (MEN2A), and hyperparathyroidism-jaw tumor syndrome (HPT-JT). Familial-isolated HPT combines several diagnoses, including occult forms of the above syndromes. Each neoplastic variant has tumors in multiple parathyroids and a delayed, but still early age of onset for HPT (average age, 25-35 years). Each justifies special and similar approaches to parathyroidectomy: typically, identification of four glands, subtotal parathyroidectomy, rapid intraoperative parathyroid hormone (PTH) assays, and parathyroid cryopreservation. Outcomes of parathyroidectomy remain suboptimal in each. Each syndrome of parathyroid neoplasia associates with characteristic cancer(s): enteropancreatic neuroendocrine or foregut carcinoid tissues (MEN1), thyroidal C cells (MEN2A), or parathyroid (HPT-JT). HPT has promoted gene discovery more through its rare hereditary variants than through common adenoma; the main genes causing four of six hereditary variants are known. The RET mutation test became essential in management of MEN2A. The MEN1 test is less urgent, because it rarely guides a major patient benefit. The CASR test, perhaps least urgent, has largely been unavailable. Further progress in molecular genetics will enhance understandings, diagnosis, and therapy of HPT.

摘要

遗传性甲状旁腺功能亢进症(HPT)有其特殊的形式、特殊的关联因素,且需要特殊的管理方式。家族性低钙血症性高钙血症(FHH或FBHH)和新生儿重症原发性甲状旁腺功能亢进症(NSHPT)分别反映了钙敏感受体的杂合或纯合突变。FHH和NSHPT分别代表HPT最轻微和最严重的变异形式。二者均自出生起即导致高钙血症,且在次全甲状旁腺切除术后总是会独特地持续存在非典型HPT。它们的HPT可能是多克隆性且非肿瘤性的。相比之下,大多数其他HPT变异形式的基础是单克隆或寡克隆甲状旁腺肿瘤形成:1型多发性内分泌腺瘤病(MEN1)、2A型多发性内分泌腺瘤病(MEN2A)以及甲状旁腺功能亢进-颌骨肿瘤综合征(HPT-JT)。家族性孤立性HPT合并了多种诊断,包括上述综合征的隐匿形式。每种肿瘤性变异形式在多个甲状旁腺中都有肿瘤,且HPT发病年龄延迟但仍较早(平均年龄25 - 35岁)。每种情况都需要采取特殊且相似的甲状旁腺切除术方法:通常包括识别四个甲状旁腺、次全甲状旁腺切除术、术中快速甲状旁腺激素(PTH)检测以及甲状旁腺冷冻保存。在每种情况下,甲状旁腺切除术的效果仍不尽人意。每种甲状旁腺肿瘤综合征都与特定的癌症相关:肠胰神经内分泌或前肠类癌组织(MEN1)、甲状腺C细胞(MEN2A)或甲状旁腺(HPT-JT)。与常见腺瘤相比,HPT通过其罕见的遗传变异形式在基因发现方面起到了更大的推动作用;导致六种遗传变异形式中的四种的主要基因已为人所知。RET突变检测在MEN2A的管理中变得至关重要。MEN1检测的紧迫性较低,因为它很少能为患者带来重大益处。CASR检测可能是最不紧急的,而且在很大程度上无法进行。分子遗传学的进一步进展将增进对HPT的理解、诊断和治疗。

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