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Clinical Implications of the New WHO Classification 2017 for Pituitary Tumors
Experimental and Clinical Endocrinology & Diabetes ( IF 1.6 ) Pub Date : 2021-03-09 , DOI: 10.1055/a-1310-7900
Wolfgang Saeger 1 , Arend Koch 2
Affiliation  

According to the WHO classification 2017 of Pituitary Tumors adenomas are classified not only by structure and immunostaining for pituitary hormones but also by expression of the pituitary transcription factors Pit-1, T-pit and SF-1. By these factors, three cell lineages can be identified: Pit-1 for the GH-, Prolactin- and TSH-cell lineage, T-pit for the ACTH-cell lineage, and SF-1 for the gonadotrophic cell lineage. By this principle, all GH and/or Prolactin producing and all TSH producing adenomas must be positive for Pit-1, all corticotrophic adenomas for T-pit, and all gonadotrophic for SF-1. In adenomas without expression of pituitary hormones immunostainings for the transcription factors have to be examined. If these are also negative the criteria for an endocrine inactive null cell adenoma are fulfilled. If one transcription factor is positive the corresponding cell lineage indicates a potential hormonal activity of the adenoma. So Pit-1 expressing hormone-negative adenomas can account for acromegaly, hyperprolactinemia, or TSH hyperfunction. T-pit positive hormone negative adenomas can induce Cushing’s disease, and SF-1 positive hormone negative tumors indicate gonadotrophic adenomas. Instead of the deleted atypical adenoma of the WHO classification of 2004 now (WHO classification 2017) criteria exist for the identification of aggressive adenomas with a conceivably worse prognosis. Some adenoma subtypes are described as aggressive “per se” without necessity of increased morphological signs of proliferation. All other adenoma subtypes must also be designated as aggressive if they show signs of increased proliferation (mitoses, Ki-67 index>3–5%, clinically rapid tumor growth) and invasion. By these criteria about one third of pituitary adenoma belong to the group of aggressive adenomas with potentially worse prognosis. The very rare pituitary carcinoma (0.1 % of pituitary tumors) is defined only by metastases. Many of them develop after several recurrences of Prolactin or ACTH secreting adenomas. The correlation of clinical findings and histological classification of pituitary adenomas is very important since every discrepancy has to be discussed between clinicians and pathologists. Based on data of the German Registry of Pituitary Tumors a table for examinations of correlations is shown in this review.

中文翻译:

新的 WHO 分类 2017 对垂体瘤的临床意义

根据 WHO 2017 年垂体瘤分类,腺瘤不仅根据垂体激素的结构和免疫染色进行分类,还根据垂体转录因子 Pit-1、T-pit 和 SF-1 的表达进行分类。通过这些因素,可以确定三个细胞谱系:用于 GH、催乳素和 TSH 细胞谱系的 Pit-1,用于 ACTH 细胞谱系的 T-pit,以及用于促性腺激素细胞谱系的 SF-1。根据这一原则,所有产生 GH 和/或催乳素和所有产生 TSH 的腺瘤必须对 Pit-1、所有促肾上腺皮质腺瘤对 T-pit 呈阳性,对 SF-1 来说所有促性腺激素腺瘤都必须呈阳性。在没有垂体激素表达的腺瘤中,必须检查转录因子的免疫染色。如果这些也为阴性,则满足内分泌无活性空细胞腺瘤的标准。如果一个转录因子为阳性,则相应的细胞谱系表明腺瘤的潜在激素活性。因此,表达 Pit-1 的激素阴性腺瘤可以解释肢端肥大症、高催乳素血症或 TSH 功能亢进。T-pit阳性激素阴性腺瘤可诱发库欣病,SF-1阳性激素阴性肿瘤提示促性腺激素腺瘤。现在,不同于 2004 年 WHO 分类中删除的非典型腺瘤(WHO 分类 2017),存在用于识别预后可能更差的侵袭性腺瘤的标准。一些腺瘤亚型被描述为具有侵袭性的“本身”,而无需增加增殖的形态学迹象。如果所有其他腺瘤亚型显示增殖增加的迹象(有丝分裂,Ki-67 指数>3-5%,临床上快速的肿瘤生长)和侵袭。根据这些标准,大约三分之一的垂体腺瘤属于侵袭性腺瘤,预后可能较差。非常罕见的垂体癌(占垂体肿瘤的 0.1%)仅由转移定义。他们中的许多人在催乳素或促肾上腺皮质激素分泌腺瘤的几次复发后发展。临床发现与垂体腺瘤的组织学分类的相关性非常重要,因为临床医生和病理学家之间必须讨论每个差异。本综述根据德国垂体肿瘤登记处的数据显示了相关性检查表。非常罕见的垂体癌(占垂体肿瘤的 0.1%)仅由转移定义。他们中的许多人在催乳素或促肾上腺皮质激素分泌腺瘤的几次复发后发展。临床发现与垂体腺瘤组织学分类的相关性非常重要,因为临床医生和病理学家之间必须讨论每个差异。本综述根据德国垂体肿瘤登记处的数据显示了相关性检查表。非常罕见的垂体癌(占垂体肿瘤的 0.1%)仅由转移定义。他们中的许多人在催乳素或促肾上腺皮质激素分泌腺瘤的几次复发后发展。临床发现与垂体腺瘤的组织学分类的相关性非常重要,因为临床医生和病理学家之间必须讨论每个差异。本综述根据德国垂体肿瘤登记处的数据显示了相关性检查表。
更新日期:2021-03-10
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