新生儿先天性甲状腺功能减退症筛查中TSH切值的探讨

新生儿筛查中发现,TSH水平与先天性甲状腺功能减退症(CH)检出率呈直线正相关.当TSH切值点分别为9、10、15和20 mU/L时,CH阳性检测敏感度分别 99.77%、96.80%、81.25%和71.88%.TSH>9 mU/L是较好的切点.     

术前TSH水平与甲状腺结节良恶性关系

目的：探讨血清促甲状腺激素（TSH）浓度与甲状腺结节良恶性的关系。 方法：回顾性分析近3年间收治的421例甲状腺结节患者的临床资料,其中结节性甲状腺肿347例,甲状腺癌74例。比较良恶性甲状腺结节患者血清TSH浓度差异,并分析TSH浓度与甲状腺结节的恶性风险以及甲状腺癌不同病理类型与血清TSH浓度的关系。 结果：甲状腺癌患者血清TSH浓度明显高于结节性甲状腺肿患者[（2.57±3.32）mIU/L vs. （1.67±2.90）mIU/L]（P<0.05）;甲状腺结节的恶性风险随血清TSH浓度的升高而逐渐升高,当TSH>5 mIU/L时,恶性率为50.0%;甲状腺癌不同病理类型间血清TSH浓度无统计学差异（P>0.05）。 结论：甲状腺结节恶性风险随血清TSH浓度的升高而增加,术前血清TSH测定可以作为甲状腺结节良恶性判断的一个辅助性指标。     

影响血清甲状腺球蛋白水平因素的流行病学研究

目的 研究不同因素对≥14周岁人群血清甲状腺球蛋白(TG)水平的影响。方法 选择碘缺乏、碘充足和碘过量的3个农村社区,测定3地区甲状腺球蛋白抗体(TGAb)阴性的3335例居民的血清TG、促甲状腺激素(TSH)水平和甲状腺体积(B超法)。结果 在尿碘中位数(MUI)80—650μg/L人群中,血清TG浓度呈现一个V型变化,即碘缺乏和碘过量状态都可以导致血清TG的升高;血清TSH浓度与血清TC浓度也呈现V型的关系,即血清TSH低于0．3mU／L时,血清TG显著升高;血清TSH高于4．8mU／L时,血清TG也显著升高;甲状腺的体积与血清TG的水平呈现明显正相关的关系;女性的血清TG浓度显著高于男性;年龄对血清TG的影响仅发生在碘缺乏地区,50岁以上人群的血清TG水平显著增高。结论 性别、碘摄入量、血清TSH浓度和甲状腺体积因素影响血清TG浓度。     

肿瘤坏死因子对鼠甲状腺细胞钙离子的作用

目的　观察 Ｔ Ｎ Ｆα对甲状腺细胞肌醇脂质／ 钙离子（ Ｉｎｓ／ Ｃａ２ ＋ ） 系统的作用。方法　利用激光扫描共聚焦显微镜（ Ｌ Ｓ Ｃ Ｍ） 观察 Ｔ Ｎ Ｆα对鼠甲状腺 Ｆ Ｒ Ｔ Ｌ５ 细胞内 Ｃａ２ ＋ 的影响。实验前细胞以不含 Ｔ Ｓ Ｈ 的５ Ｈ（５ 种激素） 培养液培养３ 天，将待测细胞以 Ｆｌｕｏ３ 负载，分别加入不同浓度的 Ｔ Ｎ Ｆα，以 Ｌ Ｓ Ｃ Ｍ 扫描（４８８ｎｍ ） 测定细胞内 Ｃａ２ ＋ ，观察 Ｔ Ｎ Ｆα的作用。结果　１ ． Ｔ Ｎ Ｆα可降低 Ｆ Ｒ Ｔ Ｌ５ 细胞内基础的 Ｃａ２ ＋ 水平，其效应随 Ｔ Ｎ Ｆα浓度的增加而增强。２ ． Ｔ Ｎ Ｆα可抑制 Ｔ Ｓ Ｈ 刺激甲状腺 Ｆ Ｒ Ｔ Ｌ５ 细胞 Ｃａ２ ＋ 升高的效应。结论　 Ｔ Ｎ Ｆα可以通过抑制甲状腺细胞 Ｉｎｓ／ Ｃａ２ ＋ 系统发挥其抑制效应。     

Gender-dependent dissociation between oxytocin but not ACTH, cortisol or TSH responses to m-chlorophenylpiperazine in healthy subjects

m-chlorophenylpiperazine (m-CPP), a serotonin (5-HT) agonist with some selectivity for the 5-HT_2C receptor subtype, which is widely used to examine 5-HT receptor function in human subjects, has been found to induce oxytocin and thyrotropin (TSH) responses in rodents. This study examined whether m-CPP had any effect on plasma oxytocin, TSH and aldosterone concentration in healthy volunteers using a double-blind, placebo-controlled crossover design. Plasma adrenocorticorticotropic hormone (ACTH) and cortisol responses, two generally accepted markers of m-CPP-induced 5-HT receptor activation, were measured in parallel. Male subjects (n = 7) received placebo, 0.25 and 0.5 mg/kg oral m-CPP. In female subjects (n = 5), the effects of placebo and 0.25 mg/kg m-CPP were studied. After placebo, given in the morning, ACTH, cortisol, TSH and aldosterone concentrations decreased over time. m-CPP 0.25 mg/kg avoided decreases in ACTH, cortisol and TSH concentrations; these responses were significant. At the dose of 0.5 mg/kg, m-CPP caused increase in ACTH, cortisol, TSH and aldosterone concentrations. Significant plasma oxytocin responses were found in female subjects only; thus this effect of m-CPP was statistically significantly gender dependent. Other responses to m-CPP were similar in male and female subjects. The present results suggest that there are clear differences, including dose and gender-dependent dissociations, among the 5-HT receptor agonist m-CPP-induced neuroendocrine responses. Received: 6 June 1997/Final version: 27 October 1997     

Thyrotropin releasing hormone (TRH): Restoration of oxotremorine tremor in mice

Summary Both TRH and quipazine (2.5–25 mg/kg) were found to restore and to intensify the oxotremorine-induced tremor in mice when injected i.p. 60 min after oxotremorine 0.5 mg/kg s.c. This phenomenon does not seem to be due to an increase in body temperature or muscle tone. Also other dopaminergic drugs, e.g. amphetamine, methylphenidate, nomifensine and apomorphine had a significant but lesser effect than TRH or quipazine. Haloperidol and methysergide both antagonized the effect of quipazine but not that of TRH. Neither propranolol, phenoxybenzamine, alpha-methyl-p-tyrosine, nor p-chlorophenylalanine inhibited the activity of TRH or quipazine. The restoration of oxotremorine-induced tremor could be prevented by atropine but not by methylatropine.It is concluded that quipazine exerts its effect by direct stimulation of serotoninergic and dopaminergic receptors, whereas TRH receptors may represent separate entities and TRH may function as a neurotransmitter or neuromodulator.Parts of this paper were presented at the Sixth International Congress of Pharmacology (IUPHAR), Helsinki, July 20–25, 1975     

The effects of peptides on the stimulus properties of ethanol

Male Sprague-Dawley rats were trained to discriminate ethanol (2 g/kg, PO: EtOH) from saline (10 ml/kg, PO: SAL) in a two-bar positively reinforced operant task on a VI 15 sec schedule. After the rats reached criterion performance (greater than 90% correct responses on the appropriate lever), thyrotropin releasing hormone (pyroGlu-His-Pro-NH2: TRH), a metabolite of TRH (His-Pro diketopiperazine: HP), and a structural analog of TRH (HPCA-His-ThiaPro-NH2: OHT) were tested for their ability to antagonize the EtOH cue. These peptides were chosen for their reported ability to reverse ethanol-induced narcosis. However, at doses that did not disrupt performance, TRH, HP, and OHT did not affect the stimulus properties of ethanol at any dose tested, nor did they change the stimulus properties of saline. Naloxone and ACTH(1-10)-NH2 were also tested as ethanol antagonists of the training dose. Pretreatment with either of these compounds failed to alter ethanol-appropriate responding. In addition, (DA1a2-Met5)-enkephalin-ol, (DAla2-Met(O)5)-enkephalin-ol, substance P, delta sleep-inducing peptide, and bombesin were tested for their ability to elicit ethanol appropriate responding. The EtOH cue generalized to none of these peptides.     

Effects of thyrotropin releasing hormone on hypothalamic thermosensitive neurons of the rat

The actions of thyrotropin releasing hormone (TRH) were tested on the firing rat of temperature-sensitive and temperature-insensitive neurons in the rat preoptic/anterior area of the hypothalamus (POA). Iontophoretic application of TRH resulted in inhibition of the firing rate of temperature-insensitive, warm-sensitive and cold-sensitive neurons. The inhibitory response of cold sensitive neurons in TRH was relatively mild, however, and 2 of 6 of these neurons inhibited by TRH also displayed rebound increases in discharge rate following cessation of TRH application. These results parallel the hyperthermic effects of microinjected TRH and lend further support of the hypothesis that TRH acts as a neurotransmitter or neuromodulator in the POA portion of the CNS thermoregulatory network.     

Comparison of thyrotropin-releasing hormone with melanocyte-stimulating-hormone-release-inhibiting factor as pentobarbital antagonists in monkeys

Thyrotropin-releasing hormone (TRH), 0.1 mg/kg, i.m., significantly counteracted pentobarbital narcosis in six monkeys, but melanocyte-stimulating-hormone-release-inhibiting factor (MIF), 0.1 mg/kg i.m., did not. Earlier dose-response studies in unanesthetized monkeys had shown that this dose of MIF stimulated motor activity; this dose of TRH had shown no stimulant effect, but a higher dose depressed activity. Thus, an MIF dose that stimulates unanesthetized monkeys does not reverse pentobarbital narcosis; a TRH dose that by itself is neither stimulant nor depressant does partially reverse pentobarbital narcosis.     

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.