[Pathology and pathogenesis of pituitary corticotroph adenoma].
[Pathology and pathogenesis of pituitary corticotroph adenoma].
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垂体促肾上腺皮质激素腺瘤的病理及发病机制[J].
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发表时间：
2002
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通讯作者：
J. Trouillas
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作者：
J. Trouillas
促肾上腺皮质激素细胞腺瘤是一种由腺垂体细胞组成的良性肿瘤，肿瘤转移和异位腺瘤也有报道。在我们的病理系列中，这种类型的腺瘤的频率为13%（1970年至2001年间切除了250/1863个肿瘤）。通常，促肾上腺皮质激素腺瘤合成源自POMC成熟的肽：ACTH、β-内啡肽和ssLPH。在绝大多数情况下，ACTH诱导皮质机能亢进，具有库欣病的临床和生物学体征。然而，一些肿瘤的病理学家确定为促肾上腺皮质激素腺瘤是不相关的临床症状的皮质功能亢进（20%的促肾上腺皮质激素腺瘤在我们的系列）。促皮质激素腺瘤是一种嗜碱性或嫌色细胞肿瘤，由皮质醇调节的细胞组成。这可以解释80%的病例中这种类型的腺瘤体积小的原因。相比之下，合成高重量POMC的“沉默”腺瘤或大腺瘤是侵袭性侵袭性肿瘤。神经外科手术适用于治疗促肾上腺皮质激素腺瘤。复发的原因是肿瘤切除不完全。可能需要进行围手术期研究以发现微腺瘤。在某些情况下，必须切除整个垂体并连续切片，才能发现小于2 mm的肿瘤。我们认为，促肾上腺皮质激素细胞增生诱导库欣病的存在仍有待证实（我们从未观察到一例）。肿瘤的垂体起源基于其单克隆性。肿瘤发生的一般机制是已知的，但涉及的具体因素和侵袭性的标志物仍有待发现。
Corticotroph adenoma is a benign tumor composed of adenohypophyseal cells; carcinoma with metastasis and ectopic adenoma have also been reported. In our pathological series, the frequency of this type of adenoma is 13% (250/1863 tumors removed between 1970 and 2001). Usually, corticotroph adenomas synthesize peptides derived from POMC maturation: ACTH, ss-endorphine, and ssLPH. In the great majority of cases, ACTH induces hypercorticism with clinical and biological signs of Cushing's disease. However, some tumors the pathologist identifies as corticotroph adenomas are not associated with clinical signs of hypercorticism (20% of the corticotroph adenomas in our series). Corticotroph adenoma is a basophilic or chromophobe tumor composed of cells which remain regulated by cortisol. This may explain the small size of this type of adenoma in 80% of the cases. In contrast, "silent" adenomas or macroadenonas which synthesize high-weight POMC are aggressive invasive tumors. Neurosurgery is indicated for the treatment of corticotroph adenoma. Recurrence is explained by incomplete removeal of the tumor. Peroperative studies may be necessary to find microadenomas. In some cases, the whole pituitary must be removed and cut in serial sections to find a tumor measuring<2 mm. In our opinion, the existence of corticotroph hyperplasia inducing Cushing's disease remains to be proven (we have never observed one). The pituitary origin of the tumor is based on its monoclonality. The general mechanism of tumorigenesis is known, but the specific factors involved and markers of aggressiveness remain to be discovered.