原发性甲状腺功能减退症与垂体增生:附7例报告

原发性甲状腺功能减退症是由于甲状腺本身病变所致甲状腺激素（thyroid hormone,TH）分泌减少而引发的一组内分泌疾病。由于TH分泌减少，可反馈性地引起促甲状腺激素（thyroid-stimulating hormone,TSH）分泌增加和垂体TSH细胞增生，临床上易误诊为垂体瘤。我院自1999年6月至2005年10月共收治7例原发性甲状腺功能减退症伴反应性垂体增生患者，现报告如下：     

原发性甲状腺功能减退致垂体增生的诊断与治疗

目的探讨原发性甲状腺功能减退致垂体增生的诊断和治疗原则。方法回顾性分析3例原发性甲状腺功能减退致垂体增生患者的临床资料。对3例原发性甲状腺功能减退患者行垂体及靶腺功能和影像学检查,并在左旋甲状腺素替代治疗l～3个月后行内分泌功能及MRI复查。结果3例均为原发性甲状腺功能减退症,MRI示垂体明显增大,信号强化均匀。左旋甲状腺素替代治疗3个月后甲状腺功能减退症状消失;MRI示垂体大小恢复正常2例,明显缩小1例;血浆甲状腺素、促甲状腺素和泌乳素水平恢复正常。结论原发性甲状腺功能减退病人可以伴有垂体增生;努力提高对其垂体增生MRI表现的认识,及时诊断,并首选甲状腺素替代治疗效果好。     

原发性甲状腺功能减退致反应性垂体增生的诊断和处理

目的探讨原发性甲状腺功能减退致垂体反应性增生的诊断和处理原则。方法回顾性分析5例确诊病人的临床资料。结果均为原发性甲状腺功能减退症,MRI示垂体占位,直径1.2~2.1 cm。经甲状腺素替代治疗,2~4个月后MRI示垂体恢复正常4例,垂体占位明显缩小1例;血浆甲状腺素水平、促甲状腺素(TSH)和泌乳素(PRL)水平恢复正常。结论原发性甲状腺功能减退病人可以伴有垂体占位,首选激素替代治疗,而不宜行垂体手术。     

原发性甲状腺功能减退致垂体增生四例报告及文献复习

目的 探讨原发性甲状腺功能减退致垂体增生的诊断和处理原则.方法 结合文献回顾性分析4例原发性甲状腺功能减退致垂体增生的临床资料.结果 4例均表现为促甲状腺激素(TSH)及催乳素(PRL)增高,FT3及FT4减少,MRI示垂体增大,甲状腺素替代治疗2-4个月后,垂体恢复正常,TSH及PRL水平亦恢复正常.结论 原发性甲状腺功能减退致垂体增生具有影像学特征,结合临床可明确诊断.治疗首选甲状腺素实验性替代治疗,而不宜行手术治疗.     

原发性甲状腺功能减退致垂体增生的诊断和治疗

目的 探讨原发性甲状腺功能减退致垂体增生的诊断和治疗.方法 回顾性总结3例原发性甲状腺功能减退患者的临床表现、影像学表现、内分泌检查资料.结果 根据临床表现、影像学表现、内分泌检查可明确诊断原发性甲状腺功能减退合并垂体增生;甲状腺素替代治疗5～8个月,甲状腺功能减退症状消失,血清促甲状腺激素和三碘甲状腺原氨酸、四碘甲状腺原氨酸、泌乳素水平正常,垂体大小恢复正常.结论 原发性甲状腺功能减退导致的垂体增生,不应该简单考虑垂体瘤予以手术治疗.甲状腺素替代治疗是治疗原发性甲状腺功能减退致垂体增生的有效手段.     

原发性甲状腺功能减退致垂体增生1例报告

垂体腺瘤与垂体增生均表现为垂体增大,垂体腺瘤多采取手术治疗,而垂体增生则不宜手术治疗,垂体增生临床少见,影像表现与垂体瘤不易鉴别,易误诊而造成不良后果。现将1例原发性甲状腺功能减退导致垂体增生报告如下。     

儿童甲状腺功能减退导致垂体增生四例报告及文献复习

目的 探讨儿童甲状腺功能减退导致垂体增生的临床特点、发病机制和治疗。方法 报告4例儿童继发于甲状腺功能减退的垂体增生病例，并结合文献进行分析。结果 4例儿童均表现为TSH和PRL增高及FT3，和FT4的减少、垂体增大。CT和MRI冠状扫描显示垂体高度1．6～2．3cm，3例服用甲状腺素后垂体肿物消失及内分泌紊乱恢复正常；另1例手术行肿物大部切除，病理报告“垂体细胞瘤样增生”，服用甲状腺素及强的松，3个月后复查MRI显示为部分性空蝶鞍。结论 当患儿有TSH和PRL增高伴垂体增大时，首先应考虑为“垂体增生”，仅服用甲状腺素治疗即可获得痊愈。     

儿童及青少年原发性甲状腺功能减退导致垂体增生的诊断与治疗

目的探讨原发性甲状腺功能减退所致垂体增生患者的临床特征、影像学特征、诊断及治疗。方法回顾性分析14例18岁以下儿童及青少年原发性甲状腺功能减退所致垂体增生患者的临床资料,包括内分泌学检查、影像学检查及治疗结果。结果头部MRI检查显示14患者垂体均存在不同程度增大,信号均匀,增强后均匀强化。14例患者血清三碘甲状腺原氨酸和四碘甲状腺原氨酸水平均正常,14例患者血清促甲状腺激素水平均升高,9例患者血清催乳素水平升高。14例患者经甲状腺素替代治疗后随访12个月,头部MRI显示增大的垂体均恢复到正常范围内,内分泌学检查均恢复正常。结论MRI检查可有效诊断原发性甲状腺功能减退导致的垂体增生,确诊应结合临床表现、内分泌检查以及甲状腺素替代治疗结果,正确诊断可避免不必要手术治疗。     

原发性甲状腺功能减退致垂体增生的诊断和治疗(附3例报告)

目的探讨原发性甲状腺功能减退致垂体增生的诊断和治疗。方法回顾性总结3例原发性甲状腺功能减退患者的临床表现、影像学表现、内分泌检查资料。结果根据临床表现、影像学表现、内分泌检查可明确诊断原发性甲状腺功能减退合并垂体增生;甲状腺素替代治疗5～8个月,甲状腺功能减退症状消失,血清促甲状腺激素和三碘甲状腺原氨酸、四碘甲状腺原氨酸、泌乳素水平正常,垂体大小恢复正常。结论原发性甲状腺功能减退导致的垂体增生,不应该简单考虑垂体瘤予以手术治疗。甲状腺素替代治疗是治疗原发性甲状腺功能减退致垂体增生的有效手段。     

继发于原发性甲状腺功能减退的垂体TSH腺瘤

继发于甲状腺功能减退症的垂体促甲状腺(TSH)腺瘤少见。国内文献仅有内分泌科零星报道,迄今未见有外科手术证实的报告。本文将我们在2年多来所遇到的2 例病人,结合文献作一报道。 临床资料 病例1,男性,37岁,2年来无明显诱因出现双下肢、颜面部非凹陷性水肿、乏力、多睡、行动迟缓、皮肤粗糙变硬、记忆力下降和性功能减退。2年来体重增加20kg。甲状     

Biopsy proven pituitary sarcoidosis presenting as a possible adenoma

Sarcoidosis is a well-recognized systemic granulomatous process which involves the central nervous system in 5–15% of patients. One of the more frequent sites of central nervous system involvement is the pituitary and hypothalamic region. Involvement of the sellar region by sarcoidosis is overall an infrequent occurrence, comprising less than 1% of all intrasellar lesions. Patients typically present with an infiltrative lesion on imaging studies and clinically with symptoms related to diabetes insipidus or hyperprolactinemia. This report describes a 38-year-old woman who initially presented with a variety of symptoms including headaches, light sensitivity, nausea and vomiting, acute visual changes, cold intolerance, amenorrhea, decreased libido, fatigue and galactorrhea. She had an elevated serum prolactin level and evidence of oligoclonal bands in the cerebrospinal fluid. Imaging studies discovered a 1.8 cm mass involving the pituitary gland and compressing the optic chiasm. The lesion was excised and microscopically was marked by a chronic inflammatory cell infiltrate and scattered nonnecrotizing granulomas. Stains and microbiologic cultures failed to demonstrate microorganisms. There was no evidence of other organ involvement on postoperative imaging. She was treated with prednisone with improvement of symptoms and subsequently required methotrexate to treat left eye pain and blurred vision, 29 months after her surgery. Achieving treatment control in patients with pituitary and hypothalamic improvement in sarcoidosis still remains a challenge.     

Idiopathic prolactin cell hyperplasia of the pituitary mimicking prolactin cell adenoma: a morphological study including immunocytochemistry,electron microscopy,and in situ hybridization

Summary Prolactin cell adenoma is the most frequently found lesion in surgically removed pituitaries of patients with hyperprolactinemia. However, in several instances, instead of prolactin cell adenoma, other lesions are encountered by morphological investigation. We report here the morphological findings in a patient with hyperprolactinemia who underwent transsphenoidal pituitary surgery for suspected prolactin cell adenoma. A morphological diagnosis of tumor could not be confirmed and massive diffuse prolactin cell hyperplasia was identified. The aim of this publication is to describe the lesion by histology, immunocytochemistry, electron microscopy, and in situ hybridization and to call attention to primary prolactin cell hyperplasia which can mimic prolactin cell adenoma.     

Primary hypothyroidism in a child simulating a prolactin-secreting adenoma

Objects  To report a case of primary hypothyroidism associated to hyperprolactinemia mimicking a prolactin secreting adenoma. Materials and methods  A girl (10 years and 10 months old) was evaluated for hyperprolactinemia (prolactin: 317 ng/mL [1.9–25]). Diagnostic evaluation demonstrated free thyroxine (F-T4): 0.22 ng/dL (0.75–1.80) and thyroid-stimulating hormone (TSH): 135 UI/mL (0.3–5.0). Pituitary magnetic resonance imaging (MRI) showed an intrasellar and suprasellar mass measuring 1.9 × 1.7 × 1.7 cm, impinging on the optic chiasm. Due to the possibility of a pseudoprolactinoma caused by hyperplasia of the TSH and prolactin-producing cells, she was treated for the primary hypothyroidism with levothyroxine. After 2 months, F-T4, TSH, and prolactin returned to normal values. A new pituitary MRI, 8 months later, demonstrated a complete resolution of the pituitary mass confirming the initial suspicion of thyrotroph hyperplasia. Conclusion  This paper illustrates the importance of thyroid function investigation in patients with hyperprolactinemia and possible prolactinoma in order to avoid unnecessary surgery.     

Mammosomatotroph adenoma of the pituitary associated with gigantism and hyperprolactinemia. A morphological study including immunoelectron microscopy

Summary A 29-year old giantess with growth hormone excess and hyperprolactinemia underwent transsphenoidal surgery to remove her pituitary tumor. Electron microscopy revealed a mammosomatotroph adenoma composed of one cell type. Immunoelectron microscopy, using the immunogold technique, demonstrated predominantly growth hormone or prolactin or a varying mixture of both growth hormone and prolactin in the adenoma cells. The presence of growth hormone and prolactin was found not only in the cytoplasm of the same adenoma cells but also in the same secretory granules. In the nontumorous adenohypophysis, somatotrophs and lactotrophs showed ultrastructural signs of hyperactivity. This finding is in contrast with the presence of suppressed somatotrophs and lactotrophs seen in nontumorous portions of adult pituitaries harboring growth hormone or prolactin-secreting adenomas. Our morphological study reinforces the view that growth hormone-producing pituitary tumors, originating in childhood, are different from those of the adult gland.Supported in part by Grant MT-6349 of the Medical Research Council of Canada     

垂体转移性肺非典型类癌

目的报道1例垂体转移性肺非典型类癌患者的临床资料,总结此类肿瘤的临床病理学特征及诊断与鉴别诊断要点。方法与结果女性患者,81岁,临床表现为头痛,突然失明;头部MRI提示鞍区占位性病变。遂行经鼻蝶入路鞍区占位性病变切除术,术中可见肿瘤位于鞍内,呈灰红色,直径约2 cm,质地柔软,血运不丰富,无包膜,边界欠清晰,沿边缘手术全切除肿瘤。组织学形态观察,肿瘤组织由形态较单一、大小较一致的小圆形细胞构成,呈巢片状弥漫性分布,可见核分裂象和灶性坏死。免疫组织化学染色,肿瘤细胞弥漫性表达突触素、CD56,部分表达甲状腺转录因子-1、广谱细胞角蛋白、P53,不表达生长激素、泌乳素、促肾上腺皮质激素、卵泡刺激素、促甲状腺激素、黄体生成素、S-100蛋白、甲状腺球蛋白、降钙素,Ki-67抗原标记指数约为33%。结论垂体转移瘤临床少见,垂体转移性肺非典型类癌更为罕见,明确诊断依靠临床病史、组织学形态和免疫表型。     

Immunohistochemistry of folliculo-stellate cells in normal human adenohypophyses and in pituitary adenomas

Summary Presence and distribution of S-100 protein (S-100), neuron-specific enolase (NSE), cytokeratin polypeptides, glial fibrillary acidic protein (GFAP), vimentin, actin, lysozyme and pituitary hormones (prolactin, hGH, ACTH, -FSH, -LH, -TSH, alpha subunit) in folliculo-stellate cells (FSC) were studied in seven normal human pituitary glands and 28 pituitary adenomas using peroxidase-antiperoxidase and the avidin-biotin immunohistochemical techniques. Approximately 5% of the cells of the adenohypophysis were agranular, non-hormon-producing FSC most of which showed a conspicuous and strong reaction with S-100 antibodies but some were, in addition, GFAP- and vimentin-positive. In contrast to endocrine cells (EC), FSC were not decorated by antibodies to NSE or cytokeratins. In addition to supportive functions, these cells, due to their close special relationship to EC, seem to have transport and other metabolic functions yet to be elucidated. By their S-100 reactivity and their distribution FSC are comparable to glial cells of the central and schwann and satellite cells of the peripheral nervous system (PNS) as well as to supportive cells in neuroendocrine organs and related tumors (e.g., pheochromocytomas, paragangliomas, carcinoids). With one exception, S-100 reactive FSC were not found in pituitary adenomas. The immunohistochemical demonstration of S-100 protein in pituitary tissue is, therefore, a reliable aid in the discrimination between adenomas and normal pituitary tissue, particularly in small and poorly preserved specimens. In one adenoma FSC were found in addition to ACTH-producing tumor cells. This seems to be an extremely rare event suggesting a combination tumor.Supported in part by Fonds zur Förderung der wissenschaftlichen Forschung (no. 4708) to H. Denk     

Masked hyperprolactinemia: tumor-derived factors inhibiting prolactin secretion caused by pituitary-stalk damage

Tumor-induced secondary hyperprolactinemia in patients with non-prolactin (PRL)-secreting pituitary tumors has traditionally been ascribed to pituitary stalk damage. We conducted a retrospective analysis of secondary hyperprolactinemia in 106 patients who underwent surgery for non-PRL-secreting pituitary adenoma. The incidence of hyperprolactinemia was evaluated, and pituitary-stalk damage was assessed radiographically using MRI (size of tumor and extension type) and endocrinologically by monitoring hormonal function using a provocation test. The effect of a tumor-derived intrasellar factor, leukemia inhibitory factor (LIF), on hyperprolactinemia was also investigated. Hyperprolactinemia was observed in 31 of the 106 (29.2%) patients. It was not correlated with either physical stalk compression or endocrinological dysfunction. However, LIF expression was negatively correlated with the incidence of secondary hyperprolactinemia (p<0.01). Although secondary hyperprolactinemia might be caused by pituitary stalk damage, it is possible that LIF masks the effect.