Hori A, Schmidt D, Kuebber S
Institute of Neuropathology, Med. Hochschule Hannover, Hannover, Germany.
Microsc Res Tech. 1999 Jul 1;46(1):59-68. doi: 10.1002/(SICI)1097-0029(19990701)46:1<59::AID-JEMT6>3.0.CO;2-S.
Developmentally pathological conditions of the anterior pituitary cells include failed separation of the primary pituitary gland into sellar and pharyngeal ones, ectopic migration into the subarachnoid space, and basophil invasion into the posterior lobe although the last is a physiological phenomenon with pathological potentiality in certain circumstances. Pituitary primordium appears at about 4 weeks of gestation. One of the causes of the pituitary gland agenesis may be a formation of the primary hypothalamic ganglionic hamartoma just at the time of occurrence of the pituitary primordium, as analyzed in cases of Pallister-Hall syndrome. A double pituitary in a single individual is a rare malformation. Its pathogenesis is considered as a result of notochordal anomaly. In the 8th gestational week, the primary pituitary gland separates into sellar and pharyngeal parts. The disturbance of this histogenesis results in a rare pituitary malformation, a "pharyngosellar pituitary." Despite the failed separation in this case, differentiation of the pituitary cells proceeds and the hormone production of this malformed pituitary gland can be displayed immunohistochemically. In this case, the distribution of the different hormone producing cells was atypical, particularly in those of gonadotropic hormones and ACTH. Life-long existence of the pharyngeal pituitary is a normal anatomical state in humans. Cell differentiation (hormone production) in the pharyngeal pituitary occurs about 4-10 weeks later than in the sellar pituitary. In pharyngeal pituitary, all kinds of adenohypophyseal hormones are produced. Extracranial pituitary adenomas (with intact sellar pituitary), exclusively found in the nasopharynx, sphenoid sinus, and clivus, may occur from the pharyngeal pituitary while another tumorigenesis can develop from the residual tissue fragment in the craniopharyngeal canal. The "overshoot" of the adenohypophyseal cell migration in the distal part of the sellar pituitary is frequently observed in the leptomeninges of the peri-infundibular or peri-hypothalamic region as ectopic pituitary cell clusters that are apparently independent of the pars tuberalis. It is suggested that these cells, frequently found in "normal" individuals, may be one of the possible origins of the intracranial ectopic pituitary adenomas. However, the reason why a majority of the reported intracranial ectopic pituitary tumors are ACTH-adenomas remains unexplained, since the ectopic cells, found in "normal" individuals, consist of fairly different hormone-producing cells. A further enigmatic phenomenon is a "basophil invasion." ACTH-positive cells invade from the pars intermedia into the posterior lobe of the pituitary. This invasion increases in intensity and frequency according to increase in age. However, the invasion of ACTH cells is observed as early as in the fetal life. The invasive cells display occasionally cell atypia as well as mitotic activity. The origin of extremely rare pituitary adenomas inside the posterior lobe can be explained by the existence and proliferative activity of basophil invasion.
垂体前叶细胞的发育性病理状况包括原始垂体未能分离为蝶鞍部和咽部垂体、异位迁移至蛛网膜下腔以及嗜碱性细胞侵入后叶，不过最后一种情况虽是一种生理现象，但在某些情况下具有病理潜能。垂体原基约在妊娠4周时出现。垂体发育不全的原因之一可能是恰好在垂体原基出现时原发性下丘脑神经节错构瘤的形成，如在帕利斯特 - 霍尔综合征病例中所分析的那样。单个个体出现双垂体是一种罕见的畸形。其发病机制被认为是脊索异常的结果。在妊娠第8周，原始垂体分离为蝶鞍部和咽部。这种组织发生的紊乱会导致一种罕见的垂体畸形，即“咽蝶垂体”。尽管在这种情况下分离失败，但垂体细胞的分化仍会进行，并且这种畸形垂体的激素产生可以通过免疫组织化学显示出来。在这种情况下，不同激素产生细胞的分布是不典型的，特别是促性腺激素和促肾上腺皮质激素的细胞。咽部垂体终身存在是人类的一种正常解剖状态。咽部垂体中的细胞分化（激素产生）比蝶鞍部垂体大约晚4 - 10周。在咽部垂体中会产生各种腺垂体激素。颅外垂体腺瘤（蝶鞍部垂体完整）仅在鼻咽部、蝶窦和斜坡中发现，可能起源于咽部垂体，而另一种肿瘤发生可能源于颅咽管中的残留组织碎片。在蝶鞍部垂体远端腺垂体细胞迁移的“过度延伸”在漏斗周围或下丘脑周围区域的软脑膜中经常观察到，表现为异位垂体细胞簇，这些细胞簇显然与结节部无关。有人认为，这些在“正常”个体中经常发现的细胞可能是颅内异位垂体腺瘤的可能起源之一。然而，大多数报道的颅内异位垂体肿瘤是促肾上腺皮质激素腺瘤的原因仍未得到解释，因为在“正常”个体中发现的异位细胞由相当不同的激素产生细胞组成。另一个神秘现象是“嗜碱性细胞侵入”。促肾上腺皮质激素阳性细胞从中间部侵入垂体后叶。这种侵入的强度和频率会随着年龄的增长而增加。然而，促肾上腺皮质激素细胞的侵入早在胎儿期就可观察到。侵入细胞偶尔会表现出细胞异型性以及有丝分裂活性。后叶内极其罕见的垂体腺瘤的起源可以通过嗜碱性细胞侵入的存在和增殖活性来解释。
