Thyroid-stimulating hormone pituitary adenomas and hyperthyroidism

Six cases of hyperthyroidism secondary to thyroid-stimulating hormone (TSH)-hypersecreting pituitary adenomas are presented (five females and one male). Hyperthyroidism presenting with diffuse goiter was associated with hyperprolactinemia in three cases. Elevation of triiodothyronine (T3) and thyroxine (T4) plasma levels was associated with TSH levels ranging between 2 and 2,000 microU/mL. Polytomography and computed tomography scanning with coronal views revealed four invasive and two enclosed tumors. Two patients underwent transfrontal operations, four underwent transsphenoidal operations, and one underwent both. Two cases of enclosed adenoma were cured primarily by a transsphenoidal approach without additional pituitary deficit. In four cases of invasive adenomas, operations and radiation therapy resulted in three failures and one cure. In cases presenting with hyperthyroidism and detectable TSH, early neuroradiological studies are indicated, as biological cure can be achieved by the transsphenoidal approach. Early treatment is also advocated because of the tendency for these tumors to become invasive (four out of six tumors).     

Two cases of TSH-secreting pituitary adenoma; endocrinological, diagnostic and therapeutic approach to the disease

Two cases of TSH-secreting pituitary adenoma were reported. Endocrinological and immunohistochemical features of these cases were described and problems in diagnosis and treatment of the rare disease are discussed. [case 1] A 28 year-old woman suffered from hyperthyroidism with a relatively high value of serum TSH (T3; 350 ng/dl, T4; 10.0 micrograms/dl, TSH; 24.5 microU/ml). She was treated with antithyroid drug and then underwent subtotal thyroidectomy. Although the levels of serum T3 and T4 were lowered to within normal range, the level of serum TSH still remained high. One month later, she developed frontal headache, amenorrhea and bitemporal hemianopsia. A CT scan showed an enhanced mass in the sellar and suprasellar region. Preoperative endocrinological studies showed elevated values of TSH (47 microU/ml) and its alpha-subunit (9.0 ng/ml). The levels of both T3 (190 ng/dl) and T4 (10.0 micrograms/dl) were near the upper normal limit. Serum TSH was suppressed by administration of exogenous T3, but did not respond to exogenous TRH, l-Dopa nor bromocriptine. Under the diagnosis of TSH-secreting pituitary adenoma, the patient was operated on by craniotomy and received local radiation therapy (50 Gy). In 1990, 12 years after the treatment, she is well and endocrinologically normal. Immunohistochemical study revealed that most tumor cells were positive for TSH. [case 2] A 28 year-old woman visited our hospital for examination of hyperthyroidism. Serum level of TSH was detectable (4.5 microU/ml). A CT scan performed at that time disclosed no pituitary tumor. Thyroid function was normalized by antithyroid drug, but the level of TSH was still high and progressively increased.(ABSTRACT TRUNCATED AT 250 WORDS)     

Pituitary adenomas and dyspituitarism.

Recent studies of the structure and function of pituitary adenomas reveal that the majority are functional and that the commonest type is a prolactin secreting adenoma. Studies of hypothalamic-pituitary function provide evidence to suggest that the adenoma develops following prolonged hypothalamic stimulation of the pituitary gland, and that the clinical dyspituitarism is due to the hypothalamic-pituitary dysfunction and not to pituitary destruction by the adenoma. Pituitary adenomas may be classified into those due to a basic neuroendocrine dysfunction (prolactin secreting, acromegaly, Cushing's disease) and those arising secondary to end-organ failure (TSH and FSH secreting). The former group have APUD characteristics and may form part of a pluriglandular syndrome of apudomas. The persistence of a basic neuroendocrine dysfunction following the surgical removal of an adenoma explains the frequent recurrence of symptoms in patients and indicates a need for continued surveillance and long-term therapy.     

促甲状腺激素型垂体腺瘤的临床诊疗特点

目的 研究促甲状腺激素(TSH)型垂体腺瘤的临床诊断和治疗特点.方法 回顾性分析2001年1月至2008年12月收治的19例TSH型垂体腺瘤患者的临床资料.男性14例,女性5例;年龄20～70岁,平均40.5岁;病程1～228个月,平均55个月.15例患者因甲状腺功能亢进(甲亢)症状就诊,其中12例被误诊为原发性甲亢并口服抗甲亢药物治疗,另3例入院后很快确诊.4例患者因头痛和视力视野障碍等肿瘤占位效应就诊.在12例误诊患者中,2例行131I放射性核素治疗,1例行甲状腺大部分切除.所有患者均行经蝶垂体腺瘤切除术.结果 病理均为垂体腺瘤,免疫组化TSH阳性17例,阴性2例,生长激素阳性2例,泌乳素阳性1例,促肾上腺皮质激素阳性1例.术后MRI显示肿瘤全切除15例,肿瘤残留4例.随访时间6个月～7年,平均3.6年.术后3个月内甲状腺激素水平各项均正常13例,其中2例3个月后复查TSH再次升高,但MRI未见肿瘤复发,行垂体放疗后甲状腺各项激素均正常.手术治愈率11/19,手术加放疗治愈率13/19.结论 对合并TSH升高的甲亢患者的筛查是提高TSH型垂体腺瘤的早期诊断的关键.治疗采用以手术治疗为主,垂体放疗和生长抑素为辅的治疗方法.     

促甲状腺激素型垂体腺瘤的临床诊疗特点

目的 研究促甲状腺激素(TSH)型垂体腺瘤的临床诊断和治疗特点.方法 回顾性分析2001年1月至2008年12月收治的19例TSH型垂体腺瘤患者的临床资料.男性14例,女性5例;年龄20～70岁,平均40.5岁;病程1～228个月,平均55个月.15例患者因甲状腺功能亢进(甲亢)症状就诊,其中12例被误诊为原发性甲亢并口服抗甲亢药物治疗,另3例入院后很快确诊.4例患者因头痛和视力视野障碍等肿瘤占位效应就诊.在12例误诊患者中,2例行131I放射性核素治疗,1例行甲状腺大部分切除.所有患者均行经蝶垂体腺瘤切除术.结果 病理均为垂体腺瘤,免疫组化TSH阳性17例,阴性2例,生长激素阳性2例,泌乳素阳性1例,促肾上腺皮质激素阳性1例.术后MRI显示肿瘤全切除15例,肿瘤残留4例.随访时间6个月～7年,平均3.6年.术后3个月内甲状腺激素水平各项均正常13例,其中2例3个月后复查TSH再次升高,但MRI未见肿瘤复发,行垂体放疗后甲状腺各项激素均正常.手术治愈率11/19,手术加放疗治愈率13/19.结论 对合并TSH升高的甲亢患者的筛查是提高TSH型垂体腺瘤的早期诊断的关键.治疗采用以手术治疗为主,垂体放疗和生长抑素为辅的治疗方法.     

促甲状腺激素型垂体腺瘤的临床诊疗特点

目的 研究促甲状腺激素(TSH)型垂体腺瘤的临床诊断和治疗特点.方法 回顾性分析2001年1月至2008年12月收治的19例TSH型垂体腺瘤患者的临床资料.男性14例,女性5例;年龄20～70岁,平均40.5岁;病程1～228个月,平均55个月.15例患者因甲状腺功能亢进(甲亢)症状就诊,其中12例被误诊为原发性甲亢并口服抗甲亢药物治疗,另3例入院后很快确诊.4例患者因头痛和视力视野障碍等肿瘤占位效应就诊.在12例误诊患者中,2例行131I放射性核素治疗,1例行甲状腺大部分切除.所有患者均行经蝶垂体腺瘤切除术.结果 病理均为垂体腺瘤,免疫组化TSH阳性17例,阴性2例,生长激素阳性2例,泌乳素阳性1例,促肾上腺皮质激素阳性1例.术后MRI显示肿瘤全切除15例,肿瘤残留4例.随访时间6个月～7年,平均3.6年.术后3个月内甲状腺激素水平各项均正常13例,其中2例3个月后复查TSH再次升高,但MRI未见肿瘤复发,行垂体放疗后甲状腺各项激素均正常.手术治愈率11/19,手术加放疗治愈率13/19.结论 对合并TSH升高的甲亢患者的筛查是提高TSH型垂体腺瘤的早期诊断的关键.治疗采用以手术治疗为主,垂体放疗和生长抑素为辅的治疗方法.     

促甲状腺激素型垂体腺瘤的临床诊疗特点

目的 研究促甲状腺激素(TSH)型垂体腺瘤的临床诊断和治疗特点.方法 回顾性分析2001年1月至2008年12月收治的19例TSH型垂体腺瘤患者的临床资料.男性14例,女性5例;年龄20～70岁,平均40.5岁;病程1～228个月,平均55个月.15例患者因甲状腺功能亢进(甲亢)症状就诊,其中12例被误诊为原发性甲亢并口服抗甲亢药物治疗,另3例入院后很快确诊.4例患者因头痛和视力视野障碍等肿瘤占位效应就诊.在12例误诊患者中,2例行131I放射性核素治疗,1例行甲状腺大部分切除.所有患者均行经蝶垂体腺瘤切除术.结果 病理均为垂体腺瘤,免疫组化TSH阳性17例,阴性2例,生长激素阳性2例,泌乳素阳性1例,促肾上腺皮质激素阳性1例.术后MRI显示肿瘤全切除15例,肿瘤残留4例.随访时间6个月～7年,平均3.6年.术后3个月内甲状腺激素水平各项均正常13例,其中2例3个月后复查TSH再次升高,但MRI未见肿瘤复发,行垂体放疗后甲状腺各项激素均正常.手术治愈率11/19,手术加放疗治愈率13/19.结论 对合并TSH升高的甲亢患者的筛查是提高TSH型垂体腺瘤的早期诊断的关键.治疗采用以手术治疗为主,垂体放疗和生长抑素为辅的治疗方法.

Abstract：

Objective To study the clinical characteristics, diagnosis and surgical effects of thyroid-stimulating hormone pituitary adenomas (TSH-omas). Methods The clinical data of 19 patients (14 female and 5 male) with TSH-omas were analyzed retrospectively in this study from January 2001 to December 2008. The patients ranged from 20 to 70 years old ( average 40. 5 years old) and had disease histories from 1 to 228 months (average 55 months). Among these patients, 15 of them complained of thyrotoxicosis symptoms, while the other 4 patients' symptoms were associated with headache and/or visual disturbance caused by the tumor mass effect. Initially, 12 of the 15 patients with thyrotoxicosis symptoms were misdiagnosed with Grave's disease. As a result 2 of them received 131Iodine, and one received subtotal thyroidectomy. All of these patients underwent transsphenoidal microsurgery. Results Average follow-up period was 3. 6 years (6 months-7 years). Pathological analysis of the surgical specimen showed pituitary adenoma in all patients, immunohistostains were positive for TSH in 17 cases, negative for TSH in 2,positive for growth hormone in 2, positive for prolactin in 1, and positive for adrenocorticotrophic hormone in 1. Postoperative MRI revealed that the tumors in 15 patients were removed totally, though 4 patients still had residual tumors. The thyroid hormone level tests suggested that 13 patients could be considered normal 3 months after their tumors were removed, though 2 of patients with normal postoperative MRI and thyroid hormones showed increased levels of TSH. For these 2 patients, tumors did not recur and their thyroid hormone levels returned to normal after pituitary radiotherapy. The cure rate was 11/19 after surgery and 13/19 after surgery plus pituitary radiotherapy. Conclusions The screening test for hyperthyroidism patients with high TSH levels is a key point to improve the accuracy rate in early diagnoses of TSH-omas. The transsphenoidal microsurgery is first choice to treat TSH-omas, while pituitary radiotherapy and somatostatin analogs are beneficially adjunctive therapies.     

Endocrinological evaluation of sellar and suprasellar tumor cases (the seventh report)--endcrinological study on four cases of pituitary adenoma with intratumoral hemorrhage (author's transl)]

Four cases of pituitary adenoma with intratumoral hemorrhage were studied endocrinologically. 1) It would be suggested that ACTH and TSH secretion of these cases was strongly impaired but LH, FSH and PRL secretion was fairly preserved immediately after hemorrhagic episode. 2) Two of these four cases revealed normal TSH secretion and normal thyroid function following the period of excessive TSH secretion and impaired thyroid function.     

PITUITARY ADENOMAS AND DYSPITUITARISM

Recent studies of the structure and function of pituitary adenomas reveal that the majority are functional and that the commonest type is a prolactin secreting adenoma. Studies of hypothalamic-pituitary function provide evidence to suggest that the adenoma develops following prolonged hypothalamic stimulation of the pituitary gland, and that the clinical dyspituitarism is due to the hypothalamic-pituitary dysfunction and not to pituitary destruction by the adenoma. Pituitary adenomas may be classified into those due to a basic neuroendocrine dysfunction (prolactin secreting, acromegaly, Cushing's disease) and those arising secondary to end-organ failure (TSH and FSH secreting). The former group have APUD characteristics and may form part of a pluriglandular syndrome of apudomas. The persistence of a basic neuroendocrine dysfunction following the surgical removal of an adenoma explains the frequent recurrence of symptoms in patients and indicates a need for continued surveillance and long-term therapy.     

TSH-Secreting Pituitary Adenoma: Current Management and Review

The neurosurgical literature contains little information about the current management of patients with thyroid-stimulating hormone (TSH)-secreting pituitary adenomas or about the usefulness of the somatostatin analogue octreotide in such cases. While TSH-secreting pituitary adenomas are rare, our review and illustrative case demonstrate the effectiveness of pretreating patients with octreotide therapy not only to reduce tumor size prior to surgical resection but also to increase the possibility of clinical remission.A 52-year-old male presented with signs and symptoms of hyperthyroidism and elevated TSH, thyroxine, and triiodothyronine. Magnetic resonance imaging revealed a pituitary macroadenoma with extension into the suprasellar cistern. The patient was treated with octreotide for 6 months prior to surgery. Approximately 3 months after initiation of octreotide therapy, the patient exhibited excellent biochemical and clinical response. Tumor shrinkage of nearly 50% was associated with resolution of suprasellar extension and optic nerve compression. Subsequent transsphenoidal surgery for resection of residual adenoma was followed by symptomatic and hormonal remission without the need for reinstitution of octreotide therapy.Pretreatment with octreotide for TSH-secreting pituitary adenomas has a beneficial effect on disease symptoms and reduces tumor mass. We suggest that patients with these rare tumors can be managed with a combination of octreotide therapy and subsequent surgical removal of residual tumor. Although this combination treatment helps to facilitate clinical remission, only short-term follow-up has been reported and thus the optimal management of these patients remains to be determined.     

Intrasellar small TSH secreting pituitary adenomas, 2 case reports

Thyroid-stimulating hormone (TSH)-secreting pituitary adenoma accounts for 1% of pituitary adenoma and often manifests as invasive macroadenoma. If the TSH value is not high enough to cause clinical symptoms presenting as inappropriate secretion of TSH, the tumor may be missed or misdiagnosed as Graves disease. Some of these patients receive inadequate treatment with the antithyroid agent, radioiodine treatment, and thyroidectomy. This tumor is also known as a tough and firm tumor because of the significant interstitial fibrosis. We report two cases of TSH-secreting pituitary adenomas which were comparatively small. Although a tough and difficult operation was expected, actual tumor dissection was easy and gross total removal was achieved within less than 3 hours. We discuss the relationship between the intraoperative findings and histopathology, as well as the ultrastructure and endocrinology.     

TSH-Secreting Pituitary Adenoma: Current Management and Review

The neurosurgical literature contains little information about the current management of patients with thyroid-stimulating hormone (TSH)-secreting pituitary adenomas or about the usefulness of the somatostatin analogue octreotide in such cases. While TSH-secreting pituitary adenomas are rare, our review and illustrative case demonstrate the effectiveness of pretreating patients with octreotide therapy not only to reduce tumor size prior to surgical resection but also to increase the possibility of clinical remission.

A 52-year-old male presented with signs and symptoms of hyperthyroidism and elevated TSH, thyroxine, and triiodothyronine. Magnetic resonance imaging revealed a pituitary macroadenoma with extension into the suprasellar cistern. The patient was treated with octreotide for 6 months prior to surgery. Approximately 3 months after initiation of octreotide therapy, the patient exhibited excellent biochemical and clinical response. Tumor shrinkage of nearly 50% was associated with resolution of suprasellar extension and optic nerve compression. Subsequent transsphenoidal surgery for resection of residual adenoma was followed by symptomatic and hormonal remission without the need for reinstitution of octreotide therapy.

Pretreatment with octreotide for TSH-secreting pituitary adenomas has a beneficial effect on disease symptoms and reduces tumor mass. We suggest that patients with these rare tumors can be managed with a combination of octreotide therapy and subsequent surgical removal of residual tumor. Although this combination treatment helps to facilitate clinical remission, only short-term follow-up has been reported and thus the optimal management of these patients remains to be determined.

     

Plurihormonal pituitary adenoma with concomitant adrenocorticotropic hormone (ACTH) and growth hormone (GH) secretion: a report of two cases and review of the literature

Plurihormonal pituitary adenomas are tumours that show immunoreactivity for more than one hormone that cannot be explained by normal adenohypophysial cytodifferentiation. The most common combinations in these adenomas include growth hormone (GH), prolactin (PRL) and one or more glycoprotein hormone sub-units (β-TSH, β-FSH, β-LH and αSU). The authors report two cases of a plurihormonal pituitary adenoma expressing the rare combination of ACTH and GH. They both underwent successful transphenoidal hypophysectomy (TSH). Long-term post-operative follow-up revealed no evidence of tumour recurrence. Due to the multiple secretions and plurihormonal characteristics clinical diagnosis of composite pituitary adenomas can be difficult. The authors discuss the diagnosis and management of composite pituitary adenomas and review the literature regarding this rare phenomenon.     

Pituitary adenoma and concomitant Rathke’s cleft cyst

Summary Although pituitary adenomas and Rathke’s cleft cysts have a shared ancestry, they rarely occur simultaneously. Only 32 reports involving a pituitary adenoma and a concomitant Rathke’s cleft cyst were identified upon review of the literature. Most initial presenting complaints include hormonal symptoms, visual disturbances, and headache. Next to growth hormone, Prolactin was the most commonly hypersecreted pituitary hormone. Rathke’s cleft cysts show variable position, size, and signal intensity on magnetic resonance imaging (MRI). Here, we report a patient with a growth hormone- secreting pituitary adenoma associated with a Rathke’s cleft cyst. The mass contained two different signal intensities on MRI. The lesion was successfully removed assisted by intraoperative MRI, when the presence of both lesions was confirmed. When a non-enhancing cyst-like structure is demonstrated on imaging in a patient with a pituitary adenoma, the possibility of a coexisting Rathke’s cleft cyst should be considered.     

Thyrotropin-secreting pituitary adenomas

TSH-secreting pituitary adenomas represent 0.5 to 1% of all pituitary adenomas. They are recognized with increasing frequency due to the measurement of TSH level in patients with hyperthyroidism, the ultra sensitive TSH assays and the improvement in pituitary imaging. Patients present mild or moderate signs of hyperthyroidism. Hormonal evaluation shows increased free thyroid hormone concentration with detectable, normal or increased serum TSH level, raising the differential diagnosis with pituitary resistance to thyroid hormone syndrome. Magnetic resonance imaging reveals pituitary adenomas in most patients. Transphenoidal surgery remains the treatment of choice in patients with TSH-secreting pituitary microadenomas, while long-acting somatostatin analogs seem to be an alternative medical treatment to surgery in patients with macroadenomas or invasive pituitary tumors.     

Accreditation in Belgium: a 10 Years’ Experience

Purpose : Toxic adenoma is one of the main causes of hyperthyroidism. We investigated the efficacy of surgery in the treatment of toxic adenoma.

Methods : Serum thyroid stimulating hormone (TSH) measurement, ultrasound and scintigraphy of the thyroid were made for diagnostic purpose. The safety of surgery was evaluated by postoperative clinical course of patients. The efficacy of surgery was determined by the function of the remaining thyroid tissue.

Results : The incidence of hyperthyroidism was 53% in surgically treated patients with nodular goitre in our iodine deficient region. The cause of thyrotoxicosis was toxic adenoma in 15 patients (14%). Suppressed serum TSH levels indicated the hyperthyroidism in all of 15 patients. Solitary solid adenoma was found by ultrasonographic examination, and solitary autonomous hot nodule by thyroid scintigraphy. Surgical treatment consisted of unilateral total lobectomy. It was the primary treatment in 13 patients. Two patients had surgery as secondary treatment after unsuccessful primary radioactive iodine application. The early postoperative clinical course of all patients was uneventful. Thirteen patients who had surgery as primary treatment had normal thyroid function postoperatively contrary to other two patients who became hypothyroid after having unsuccessful radioiodine therapy, and surgery as the secondary treatment. Conclusions : The incidence of hyperthyroidism and toxic adenoma is high in our surgically treated patients with nodular goitre. The diagnosis of toxic adenoma is not difficult by serum TSH measurements, and ultrasound and nuclear imaging of the thyroid. Surgery is effective and safe, and the treatment of choice for patients with toxic adenoma in order to control radically the hyperthyroidism and to achieve the goal of providing the euthyroid status.     

A case of pleomorphic TSH-producing pituitary adenoma with calcification

We reported a rare case of pleomorphic TSH-producing pituitary adenoma with calcification and reviewed the literature. A 25-year-old female was admitted to our hospital with a complaint of anterior neck swelling. An endocrinological examination demonstrated elevated serum levels of free triiodothyronine (FT3: 5.6 pg/ml), free thyroxin (FT4: 2.2 ng/dl), TSH (5.85 microIU/ml), and TSH a-subunit (5.9 ng/ml), whereas a physical examination revealed no goiter. CT scan showed a suprasellar isodensity mass with dense calcification. Contrast-enhanced T1-weighted images revealed a less enhancing tumor extending from the left upper portion of pituitary fossa into suprasellar cistern. The patient underwent gross total removal of the tumor via the right pterional approach. Microscopically, medium-sized to enlarged tumor cells with marked pleomorphism and prominent calcification were observed.The tumor cells displayed positive reaction for TSH (beta-subunit). The MIB-1 index averaged 2.9%. The histological diagnosis was a pleomorphic TSH-producing pituitary adenoma. Postoperatively, the serum levels of FT3, FT4, TSH, and TSH alpha-subunit decreased to normal range. Follow-up MR images showed no evidence of recurrent tumor 3 years after the resection. All of six patients with densely calcified TSH-producing pituitary adenoma, previously reported in the literature, remained well without tumor recurrence. We suggest that this type of TSH-producing pituitary adenoma may be associated with favorable prognosis despite histologically pleomorphic appearance.     

Propofol pharmacokinetics in a patient with TSH producing pituitary adenoma

We investigated propofol pharmacokinetics in a patient with secondary hyperthyroidism caused by thyroid stimulating hormone (TSH) producing pituitary adenoma. Laboratory data indicated thyrotoxic state with elevated TSH, FT3 and FT4 levels. General anesthesia was maintained with a doubled propofol infusion rate (8-10 mg.kg-1.hr-1) compared to our standard procedure. During 370 min of infusion, propofol concentrations in arterial blood were kept within optimal ranges (2-4 micrograms.ml-1). Although the clearance of propofol was high (2.8 l.min-1) because of the thyrotoxic state, the patient showed delayed recovery from anesthesia. The half-life of blood propofol after the termination of infusion exceeded 30 minutes (normal: 10-15 minutes). We conclude that the delayed recovery was due to the accumulation of propofol in the adipose tissue during long-term infusion in spite of the increased propofol clearance.     

Thyroid-stimulating hormone pituitary adenomas

OBJECT: Thyroid-stimulating hormone (TSH)-secreting pituitary adenomas are rare, representing < 2% of all pituitary adenomas. METHODS: The authors conducted a retrospective analysis of patients with TSH-secreting or clinically silent TSH-immunostaining pituitary tumors among all pituitary adenomas followed at their institution between 1987 and 2003. Patient records, including clinical, imaging, and pathological and surgical characteristics were reviewed. Twenty-one patients (6 women and 15 men; mean age 46 years, range 26-73 years) were identified. Of these, 10 patients had a history of clinical hyperthyroidism, of whom 7 had undergone ablative thyroid procedures (thyroid surgery/(131)I ablation) prior to the diagnosis of pituitary adenoma. Ten patients had elevated TSH preoperatively. Seven patients presented with headache, and 8 presented with visual field defects. All patients underwent imaging, of which 19 were available for imaging review. Sixteen patients had macroadenomas. RESULTS: Of the 21 patients, 18 underwent transsphenoidal surgery at the authors' institution, 2 patients underwent transsphenoidal surgery at another facility, and 1 was treated medically. Patients with TSH-secreting tumors were defined as in remission after surgery if they had no residual adenoma on imaging and had biochemical evidence of hypo-or euthyroidism. Patients with TSH-immunostaining tumors were considered in remission if they had no residual tumor. Of these 18 patients, 9 (50%) were in remission following surgery. Seven patients had residual tumor; 2 of these patients underwent further transsphenoidal resection, 1 underwent a craniotomy, and 4 underwent postoperative radiation therapy (2 conventional radiation therapy, 1 Gamma Knife surgery, and 1 had both types of radiation treatment). Two patients had persistently elevated TSH levels despite the lack of evidence of residual tumor. On pathological analysis and immunostaining of the surgical specimen, 17 patients had samples that stained positively for TSH, 8 for alpha-subunit, 10 for growth hormone, 7 for prolactin, 2 for adrenocorticotrophic hormone, and 1 for follicle-stimulating hormone/luteinizing hormone. Eleven patients (61%) ultimately required thyroid hormone replacement therapy, and 5 (24%) required additional pituitary hormone replacement. Of these, 2 patients required treatment for new anterior pituitary dysfunction as a complication of surgery, and 2 patients with preoperative partial anterior pituitary dysfunction developed complete panhypopituitarism. One patient had transient diabetes insipidus. The remainder had no change in pituitary function from their preoperative state. CONCLUSIONS: Thyroid-stimulating hormone-secreting pituitary lesions are often delayed in diagnosis, are frequently macroadenomas and plurihormonal in terms of their pathological characteristics, have a heterogeneous clinical picture, and are difficult to treat. An experienced team approach will optimize results in the management of these uncommon lesions.     

Perioperative management of patients undergoing transsphenoidal pituitary surgery

Pituitary adenomas often present with the symptoms of hormonal hypersecretion, and although medical therapy is available for most hyperfunctioning states, it is not curative. As a result, transsphenoidal pituitary surgery has become a commonly performed neurosurgical procedure with unique challenges for the anesthesiologist due to the distinct medical comorbidities associated with various adenomas. Any type of pituitary tumor may also produce hypopituitarism and local mass effects secondary to the expanding intrasellar mass. Here we review the perioperative concerns surrounding surgery to remove adenomas and decompress the sellar space. Special attention is given to Cushing's disease (hypercortisolism secondary to an adrenocorticotropic hormone-secreting adenoma), acromegaly (secondary to a growth hormone-secreting adenoma), and hyperthyroidism in the setting of thyrotropic adenomas. Operative risks, including bleeding, diabetes insipidus, the syndrome of inappropriate antidiuretic hormone secretion, and hypopituitarism, are addressed in detail. Understanding preoperative assessment, intraoperative management, potential complications, their management, and strategies for avoidance are fundamental to successful perioperative patient care and avoidance of morbidity and mortality.