原发性甲状腺功能减退症合并垂体增生32例临床分析

目的 通过对原发性甲状腺功能减退症(甲减)合并垂体增生的临床和影像学资料的分析,了解其临床特点及甲状腺激素替代治疗后的影像学变化.方法 分析华山医院1999至2008年门诊和住院的32例甲减合并垂体增生的患者的临床表现、激素水平、影像学检查以及治疗后随访结果.结果 32例患者多为青少年,病程在半年～8年之间,除甲减的表现外,影像学上可见垂体饱满或弥漫性增大.甲状腺素替代治疗后,1～6个月后垂体可缩小至正常.结论 青少年的原发性甲减易伴垂体增生,原发性甲减所致的垂体增生在充分的甲状腺素替代治疗后可完全逆转.

Abstract：

Objective To improve the recognition of pituitary hyperplasia secondary to primary hypothyroidism by analyzing clinical and imaging data. Methods The clinical features, hormone data,imaging findings, and treatment were reviewed in 32 patients with pituitary hyperplasia secondary to primary hypothyroidism in Huashan Hospital from 1999 to 2008. Results Thirty-two patients, most juvenile,presented clinical and imaging features suggestive of functional primary pituitary adenoma. The dose of levothyroxine was increased to maintain the thyrotropin concentration at normal values. Following adequate thyroxine replacement, pituitary hyperplasia regressed on average within 6 months. Conclusions Pituitary hyperplasia secondary to primary hypothyroidism seems to be quite prevalent in children and adolescents.Complete regression will be achieved with thyroxine replacement therapy.     

不同甲状腺功能状态血清胃促生长素水平的变化

探讨不同甲状腺功能状态下血清胃促生长素水平的变化及其与体重指数、腰臀比、甲状腺功能、血糖、胰岛素及胰岛素抵抗的关系.初诊甲状腺功能亢进症(甲亢)患者50例及甲状腺功能减退症(甲减)患者30例,测定其治疗前及甲状腺功能恢复正常后空腹血清胃促生长素、胰岛紊、血糖、游离三碘甲状腺原氨酸(FT_3)、游离甲状腺素(FT_4)和促甲状腺激素(TSH)水平,同时测量身高、体重、腰围、臀围,计算体重指数、腰臀比、稳态模型评估的胰岛素抵抗指数(HOMA-IR)等,以健康对照者30例为对照.甲亢患者治疗前血清胃促生长素水平低于正常对照组[(63.2±9.6)ng/L对(80.9±13.9)ng/L,P<0.01],经多元逐步回归分析提示HOMA-IR是胃促生长素的独立影响因素(r=-0.314,P=0.027).甲状腺功能减退症患者,治疗前后胃促生长素水平和正常对照组比较均无明显差异(均P0.05).本研究提示,在不同甲状腺功能状态下,胰岛素抵抗可能是胃促生长素水平改变的重要影响因素.     

131I治疗甲状腺机能亢进症的230例疗效分析

随访观察131I治疗甲亢的疗效,分析影响因素。230例甲亢患者服用131I,每例患者均于治疗后1.5、3、6、12个月或者更长时间随访,均复查FT3、FT4及TSH。结果显示,临床治愈181例（78.6%）,好转22例（9.5%）,早发甲减23例（10.0%）,迟发甲减4例（1.7%）。所有甲减患者均用甲状腺素替代治疗,其中12例恢复正常,另15例需要终身替代治疗。结论：根据患者年龄、病程、ATD应用情况、甲状腺大小及形状、甲状腺激素水平等因素决定治疗剂量。治疗后需密切随访观察,警惕甲减的发生。对早发甲减应及时替代治疗,降低永久性甲减的发生率。     

甲状腺功能异常患者心肌酶变化的分析

为了解原发性甲状腺功能减退症（甲减）患者和甲状腺功能亢进（甲亢）患者心肌酶的变化,检测了20例原发性甲减患者、27例甲亢患者以及30例健康体检者（对照组）的空腹血清天门冬酸氨基转移酶（AST）、肌酸激酶（CK）及其同工酶（CK-MB）、乳酸脱氢酶（LDH）及其同工酶（HBDH）、FT3、FT4、TSH、总胆固醇（Tch）。结果显示,原发性甲减患者AST、CK、CK-MB、LDH、HBDH及Tch均明显高于对照组（P分别〈0.01、0.01、0.01、0.01、0.05、0.01）;TSH和FT4与心肌酶、Tch均无相关性;FT3与CK、CK-MB负相关（r=-0.53,-0.47,P均〈0.05）,与Tch呈负相关（r=-0.504,P〈0.05）;甲亢患者血清CK-MB明显高于对照组（P〈0.01）,且血清FT4与CK-MB呈显著正相关（r=0.462,P〈0.01）。结论：原发性甲减患者和甲亢患者常伴心肌酶升高,其中甲减者FT3水平与CK、CK-MB、Tch升高关系更密切。     

Postprandial lipemia as a risk factor for cardiovascular disease in patients with hypothyroidism

Postprandial lipoprotein metabolism is suggested to play a role in the pathogenesis of atherosclerosis. In this study, we investigated postprandial lipemia and its relationship to cardiovascular risk factors in patients with overt and subclinical hypothyroidism. Twentynine female patients with TSH levels greater than 5 μIU/mL and 12 euthyroid control female subjects were included in the study. Fifteen patients had subclinical hypothyroidism and 14 had overt hypothyroidism. All subjects underwent an oral lipid tolerance test. If triglyceride levels increased by 80% or more, subjects were considered postprandial lipemia positive. Control, overt hypothyroid, and subclinical hypothyroid groups were not statistically different with respect to anthropometric measurements, fasting blood C-reactive protein, uric acid, homocysteine, glucose, insulin, lipoprotein (a), apolipoprotein B levels, and homeostasis model assessment index. Fasting triglyceride levels correlated positively with TSH levels. Postprandial lipemia frequency was higher in overt hypothyroid subjects than in the control group. The subclinical hypothyroid group did not differ from the hypothyroid group with respect to postprandial lipemia frequency. In subjects with TSH levels higher than 5 μIU/mL, PPL risk was increased sevenfold. The results of this study show that postprandial triglyceride metabolism is affected in hypothyroidism.     

Thyroid dysfunction in patients with systemic lupus erythematosus (SLE): relation to disease activity

We examined the prevalence of thyroid dysfunction and the production of anti-thyroid antibodies (ATA) in patients with systemic lupus erythematosus (SLE) and assessed the association between ATA production and SLE disease activity status. Seventy-seven patients who met the American College of Rheumatology classification criteria for SLE participated in the study. Fifty-two individuals served as a control group. Demographic, clinical information and SLE disease activity (SLEDAI) status were collected from all patients. The sera of all participants were tested for free thyroxine (FT4), thyroid-stimulating hormone (TSH), anti-thyroglobulin (ATg) and anti-thyroid peroxidase (TPO). A SLEDAI score of > or =6 was considered clinically significant. The results of the thyroid function tests and ATA were compared between the study group and the control group. ATA levels were compared between the patients with a SLEDAI score of > or =6 to those with a SLEDAI score of <6. Hypothyroidism was detected in 11.6% of SLE patients compared to 1.9% in the control group. None of the patients or controls had evidence of hyperthyroidism. No statistically significant difference was observed in the levels of ATg or TPO between the study group and the control group. No correlation was found between ATA levels and the degree of the disease activity. Among the different variables tested in this study, hypothyroidism was the only significant abnormal finding in SLE patients. No association was found between the SLEDAI score and the prevalence of ATA production. Larger controlled, longitudinal studies are necessary to confirm these findings and elucidate the role played by ATA in the pathogenesis of thyroid dysfunction in SLE patients.     

慢性淋巴细胞性甲状腺炎

慢件淋巴细胞件甲状腺炎于1912年由日本学者首先报道,属于最常见的自身免疫性甲状腺疾病,也是甲状腺功能减退(甲减)最主要的病因,好发于中老年女性.患者起病隐匿,常无特征性的临床表现,容易漏诊.本病诊断尚缺乏国际统一标准,主要依靠一些非特异性的症状与体征,尤其是甲状腺肿大、甲状腺功能减退,并结合相应的辅助检查.如甲状腺自身抗体阳性,且滴度较高,对诊断意义更大.甲状腺穿刺细胞学检查不作为常规项目,但对诊断困难者具有确诊价值.伴有甲减者,需要常规采用替代治疗,尤其是甲状腺肿大明显者、孕妇以及儿童可以给予左旋甲状腺素替代治疗,但仅有亚临床甲减者,或甲状腺功能正常而甲状腺自身抗体阳性的患者是否需要治疗尚存在争议.     

Increased thrombin-activatable fibrinolysis inhibitor and decreased tissue factor pathway inhibitor in patients with hypothyroidism

Various abnormalities of coagulation–fibrinolytic system have been reported in patients with thyroid dysfunction. Several studies indicate that coagulation and fibrinolytic system is disturbed in the patients with hypothyroidism. Also, the influence of hypothyroidism on hemostasis is controversial; both hypocoagulable and hypercoagulable states have been reported. The levels of plasma thrombin-activatable fibrinolysis inhibitor (TAFI) antigen and tissue factor pathway inhibitor (TFPI) have been investigated only once in patients with hypothyroidism. Therefore, the main purpose of this study was to evaluate the profile of coagulation and fibrinolytic parameters including TAFI and TFPI in patients with hypothyroidism. Fifteen patients with untreated hypothyroidism and 15 age-matched healthy controls were included in the study. Factors V(FV), VII (FVII), VIII (FVIII) activities, von Willebrand factor (vWF), protein C, protein S, thrombomodulin (TM), TFPI, and TAFI were measured. The relationships between serum thyroid hormones and these hemostatic parameters were examined. Compared with the control subjects, FVII activity, and TM Ag and TAFI Ag levels were significantly increased in patients with hypothyroidism, whereas FV, FVIII, vWF, protein C and protein S activities, and TFPI Ag levels were significantly decreased. We did not find any significant correlation between serum thyroid hormones and the hemostatic parameters that we measured. In conclusion, we found some important differences in the hemostatic parameters between the patients with hypothyroidism and healthy controls. Increased FVII, TM, and TAFI and decreased FV, FVIII, vWF, protein C, protein S, and TFPI in these patients represent a potential hypercoagulable and hypofibrinolytic state, possible endothelial dysfunction, which might augment the risk for atherosclerotic and atherothrombotic complications. Thus, disturbances of the hemostatic system may contribute to the excess mortality due to cardiovascular disease seen in patients with hypothyroidism.     

Rhabdomyolyse sévère révélant une myopathie hypothyroïdienne d’origine auto-immune: À propos de deux cas

While muscular manifestations are common of hypothyroidism, hypothyroid myopathy is most often limited to myalgia, muscular stiffness and cramps with, in some patients, elevated levels of muscle enzymes. We report two cases of rhabdomyolysis related to hypothyroid myopathy. One of the patients developed acute renal failure. Thyroid hormone replacement therapy improved thyroid and renal function with involution of rhabdomyolysis. Hypothyroidism appears to be an authentic cause of rhabdomyolysis and should be carefully ruled out in all patients with elevated serum levels of muscle enzymes.     

Consequences of combined maternal, fetal and persistent postnatal hypothyroidism on the development of auditory function in Tshrhyt mutant mice

Tshrhyt/hyt mutant mice express a point mutation in the gene encoding the thyrotropin receptor, and affected animals are congenitally hypothyroid and profoundly deaf as a consequence when the condition is untreated. In this investigation, a previously unrecognized developmental stage was identified in the hypothyroid, mutant progeny of hypothyroid dams by tracking developmental changes in the auditory brainstem response (ABR). ABR thresholds develop rapidly in normal, euthyroid animals, decreasing as much as 80 dB between P12 (postnatal day 12) and P15, with mature sensitivity being gradually acquired by P18. In contrast, Tshrhyt/hyt mutant mice remained profoundly deaf on P24 and although thresholds improved by approximately 30 dB by P60, residual frequency-dependent deficits of 20-70 dB were observed in animals exhibiting end-stage disease. The rate of threshold improvement in mutant mice was approximately ten times slower than in normal mice. While ABR wave latencies and interpeak intervals decreased early in postnatal life, values decreased over a delayed and protracted time period, reaching adult values well after those of controls attained maturity. As with normal mice, slopes of wave I latency-intensity curves were significantly steeper in immature animals than those observed in adults and decreased during development, but failed to achieve normal adult values and remained significantly steeper than those for controls. Findings reported here suggest that passive aspects of electromechanical transduction achieve maturity in Tshrhyt/hyt progeny of Tshrhyt/hyt mice and that development, limited as it may be, occurs most prominently in the basal half of the cochlea.