奥氮平单药或联合用药治疗后甲状腺激素水平的变化

目的探讨精神疾病患者接受奥氮平单药或与其他非典型抗精神病药物联合用药治疗后,甲状腺激素水平的变化,并比较两种治疗方案之间的差异。方法回顾44例接受奥氮平治疗的住院精神疾病患者的病例,其中24例接受单药治疗,20例接受多药联合治疗,比较治疗前后甲状腺激素水平的差异。结果治疗后,单药组中游离四碘甲状腺原氨酸(FT4)、总四碘甲状腺原氨酸(TT4)血清水平降低,促甲状腺激素(TSH)水平升高,与治疗前比较差异有统计学意义(相对于基线变化值的中位数:FT4:-2.86 pmol/L,P<0.001;TT4:-22.09 nmol/L,P=0.002;TSH:0.97 mIU/L,P<0.001)。联合用药组中游离三碘甲状腺原氨酸(FT3)、总三碘甲状腺原氨酸(TT3)、FT4和TT4的血清水平均降低,TSH血清水平升高,与治疗前相比,差异有统计学意义(相对于基线变化值的中位数:FT3:-0.34 pmol/L,P=0.022;TT3:-0.17 nmol/L,P=0.049;FT4:-1.28 pmol/L,P=0.001;TT4:-12.31 nmol/L,P=0.028;TSH:1.59 mIU/L,P=0.012)。两组患者亚临床甲状腺激素功能减退的发生率分别为4.2%、20.0%,两组比较差异无统计学意义(P=0.242)。结论为了避免甲状腺激素水平异常引起其他的疾病,应关注接受奥氮平治疗的精神疾病患者的甲状腺激素水平。     

糖尿病肾病伴发甲状腺功能低下40例的临床分析

目的探讨糖尿病肾病伴发甲状腺功能低下临床特征及治疗。方法选取益阳市中心医院肾脏内分泌科住院的40例糖尿病肾病伴发甲状腺功能低患者,随机分为A、B两组,A组给予胰岛素+肾病治疗+甲状腺素,B组给予胰岛素+肾病治疗,观察治疗前后两组甲状腺功能[血清甲状腺素(TT4)、游离血清甲状腺素(FT4)、三碘甲状腺原氨酸(TT3)、游离三碘甲状腺原氨酸(FT3)],血浆白蛋白、24h尿蛋白、TSH,尿素氮(BUN)、血肌酐(Cr)。并对结果数据进行统计学分析。结果分别比较两组治疗前后各项指标,血清TT4、TT3、FT4水平明显提高,血清TSH水平降低(P<0.05)。比较治疗后两组间血清TT4、TT3、FT4、TSH水平差异无统计学意义(P>0.05)。结论糖尿病肾病伴甲状腺功能低下患者应以治疗糖尿病和肾病为主,监测甲状腺功能利于估计病情,判断预后。     

2型糖尿病患者甲状腺激素水平变化分析

目的 分析2型糖尿病患者甲状腺激素水平变化,探讨甲状腺激素水平评估2型糖尿病患者疾病严重程度及预后的临床价值。方法 选取我院收治的2型糖尿病患者80例,所有患者均排除甲状腺功能异常,设为观察组。另选择同期行健康体检对的健康人80例设为对照组。观察组患者根据糖尿病病情严重程度分为轻症亚组(43例)和重症亚组(37例)。观察组患者均由同一组分泌内科医师制定治疗方案。采集所有受试者入组时及观察组患者治疗3个月后的空腹外周静脉血,检测血清甲状腺激素五项指标：三碘甲状腺原氨酸(TT3)、总甲状腺素(TT4)、游离三碘甲状腺原氨酸(FT3)、游离甲状腺素(FT4)、促甲状腺激素(TSH)水平。观察比较分组、分亚组、亚组治疗前后血清甲状腺激素五项指标。结果 观察组患者血清TT3、TT4、FT3、FT4及TSH水平均低于对照组受试者,轻症亚组患者血清TT3、TT4、FT3、FT4及TSH均高于重症亚组患者(P<0.05);治疗后,轻症亚组患者和重症亚组患者血清TT3、TT4、FT3、FT4及TSH均较治疗前上升,且重症患者上升幅度较轻者亚组患者上升幅度高(P<0.05)。结论 2型糖尿病患...     

内科危重病患者血清甲状腺激素水平的监测及预后评估

目的探讨危重患者甲状腺功能的变化。方法186例内科危重住院患者作为观察组,同期健康体检者186例作为对照组,观察正常甲状腺病态综合征(euthyroid sick syndrome,ESS)发生情况,对比观察组与对照组、观察组中存活组与病死组治疗前后甲状腺激素检查结果,ESS者治疗前后甲状腺激素检查结果,ESS与死亡的关系。结果186例内科危重病患者中发生ESS78例,发生率41.93%(78/186);观察组入院时TT3、FT3低于对照组,TT4、FT4、TSH两组比较无显著性差异(P>0.05);观察组中存活组和病死组比较TSH无显著性差异外、病死组TT3、FT3、TT4、FT4均低于存活组(P<0.05);原发病治疗好转后,甲状腺激素可恢复或接近正常;发生ESS病死率30.77%高于未发生变化的病死率13.9%。结论血清甲状腺激素水平的变化反映了危重住院患者的全身状态和严重程度,动态检测血清中甲状腺激素水平可以观察肺心病的发展和转归。     

甲状腺功能异常与脑出血急性期出血部位的相关性分析

目的分析甲状腺功能异常与脑出血急性期出血部位的相关性。方法收集2012年3月-2014年5月该院神经内科就诊的急性脑出血患者220例,其中丘脑出血患者57例,非丘脑出血患者163例。分别检测所有患者甲状腺激素水平,并统计各组甲状腺功能异常患者数,计算甲状腺功能异常与脑出血部位的相关性。结果脑出血患者初诊时FT3、FT4、TT3、TT4及TSH均相近,差异均无统计学意义(P>0.05)。出血24h检测,丘脑出血组血清FT3和TT3水平均低于非丘脑出血组,差异均有统计学意义(P<0.05)。而2组患者血清FT4、TT4及TSH水平相差不大,差异无统计学意义(P>0.05)。丘脑出血组甲状腺功能异常发生率为73.68%高于非丘脑出血组的34.97%,差异有统计学意义(P<0.05)。经相关系数检测比较,R值2.107,95%可信区间1.372~2.512,故存在显著相关性(P<0.05)。结论甲状腺功能异常与脑出血急性期出血部位存在相关性,丘脑出血患者更易出现甲状腺功能异常。     

原发性高血压病人血清甲状腺激素水平的改变

目的 研究原发性高血压病人血清甲状腺激素水平的改变。方法 用放射免疫分析法测定38例高血压病人和20例健康对照者的血清甲状腺激素水平。结果 原发性高血压病人的血TT3、FT3值明显低于正常人,rT3值明显高于正常人,而TT4、FT4、TSH水平与正常组相比差异无显著意义;血TT3、FT3值的和rT3值的升高与高血压病的严重程度有关而与病程无关。结论 原发性高血压常伴有低血清TT3、FT3水平,且随着高血压病情的加重而逐渐降低。     

甲状腺功能正常的2型糖尿病患者血清甲状腺激素水平与糖尿病视网膜病变的关系

目的 探讨甲状腺功能正常的2型糖尿病(T2DM)患者血清甲状腺激素(TH)水平与糖尿病视网膜病变(DR)的关系。方法 回顾分析2019年6月至2020年8月住院治疗的T2DM患者785例,分为DR组(n=119)和非DR组(NDR组,n=666)。将其游离三碘甲状腺原氨酸(FT3)、游离甲状腺素(FT4)、促甲状腺激素(TSH)、FT3/FT4从低到高进行五分位分组(Q1、Q2、Q3、Q4、Q5),比较不同甲状腺激素水平对DR患病率的影响。将样本人群的糖化血红蛋白(HbA1c)分为A组(<7.0%)和B组(≥7.0%),比较2组间FT3、FT4、TSH水平以及FT3/FT4。结果 DR组患者的年龄、糖尿病病程、胱抑素-C、尿微量白蛋白与尿肌酐比值(UACR)明显高于NDR组,差异有统计学意义(P<0.05);DR组的空腹C肽、FT3水平、FT3/FT4、eGFR明显低于NDR组,差异有统计学意义(P<0.05)。FT3-Q1组的DR患病率明显高于Q2-Q5组,差异均有统计学意义(P<0.05),而将FT3-Q2-Q5的DR患病率两两间比较,差异无统计学意义(P&...     

花都地区孕妇早中晚期甲状腺功能变化研究

目的研究花都地区孕妇早中晚期甲状腺功能变化。方法选择广州市花都区的孕妇作为观察组,进一步分为早期妊娠组、中期妊娠组、晚期妊娠组,选择非孕妇女作为对照组,检测甲状腺功能指标三碘甲状腺原氨酸(TT3)、总甲状腺素(TT4)、游离三碘甲状腺原氨酸(FT3)、游离甲状腺素(FT4)及促甲状腺激素(TSH)的水平。结果早期妊娠组孕妇的甲状腺功能指标TT3、TT4、FT3、FT4与对照组的差异无统计学意义(P0.05),TSH水平低于对照组、差异有统计学意义(P0.05);中期妊娠组和晚期妊娠组TT3、TT4、FT3、FT4水平均低于对照组,TSH水平高于对照组、差异有统计学意义(P0.05)。结论妊娠早期孕妇甲状腺功能无明显变化,妊娠中晚期时甲状腺激素水平显著降低,需要在临床中采取检查措施以及时发现、进而保证胎儿的正常发育。     

甲状腺功能指标TSH、FT3、FT4及血清脂联素水平与妊娠期高血压的相关性分析

目的探讨甲状腺功能指标促甲状腺激素（TSH）、游离三碘甲状腺原氨酸（FT3）、游离甲状腺素（FT4）和血清脂联素水平与妊娠期高血压的相关性。方法收集该院妊娠期高血压疾病患者280例,其中妊娠高血压70例,轻度子痫前期70例,重度子痫前期70例,子痫70例,分别作为A、B、C、D组。同期收集正常妊娠的健康志愿者70例作为对照组,于分娩当日清晨抽取空腹肘静脉血5ml,测定各组孕妇甲状腺功能指标TSH、FT3、FT4和血清脂联素水平,并进行比较分析。结果甲状腺功能指标FT3、FT4均从对照组、A组到D组依次降低,TSH从对照组、A组到D组依次升高,且A、B、C、D组各项指标与对照组比较,差异均有统计学意义（P〈0.05）。对照组血清脂联素水平最高,从A组到D组血清脂联素水平依次降低,A、B、C、D组与对照组比较,差异均有统计学意义（P〈0.05）。结论妊娠期高血压疾病患者甲状腺功能指标FT3、FT4及血清脂联素水平显著低于健康孕妇,并随着妊娠期高血压的加重降低;TSH水平高于健康孕妇,并随着妊娠期高血压的加重而升高。     

NSCLC 患者化疗前后血清甲状腺激素水平的变化及临床意义

目的：分析非小细胞肺癌（non-small cell lung cancer,NSCLC）患者血清甲状腺激素水平化疗前后的变化及临床意义。方法选取住院治疗的 NSCLC 患者60例,同时选取同期体检健康志愿者共60例作为正常对照组,对比 NSCLC 患者化疗前和正常对照组甲状腺功能,对比 NSCLC 患者化疗前不同分化程度、临床分期的甲状腺功能,对比 NSCLC 患者化疗前和化疗后有效/无效患者的甲状腺功能。结果 NSCLC 患者化疗前的游离三碘甲状腺原氨酸（FT3）、游离甲状腺素（FT4）、总三碘甲状腺原氨酸（ TT3）、总甲状腺素（ TT4）显著低于正常对照组,促甲状腺激素（TSH）显著高于正常对照组（ P ﹤0.01）。低分化组化疗前的 FT3、FT4、TT3、TT4显著低于中、高分化组,TSH 显著高于中、高分化组（ P ﹤0.05）;Ⅲb ~Ⅳ期组化疗前的 FT3、FT4、TT3、TT4显著低于Ⅱb ~Ⅲa 期组,TSH 显著高于Ⅱb ~Ⅲa 期组（ P ﹤0.01）。化疗后有效的 NSCLC 患者 FT3、FT4、TT3、TT4较化疗前显著升高,TSH 显著降低（ P ﹤0.05）;化疗后无效的 NSCLC 患者 FT3、FT4、TT3、TT4较化疗前和化疗后有效患者降低,TSH 显著升高（ P ﹤0.05）。结论在 NSCLC 患者中,化疗前后的甲状腺激素水平具有一定差异,可以用于判断病情和评价化疗疗效。     

地塞米松治疗桥本甲状腺炎的临床价值

目的 观察口服左旋甲状腺素钠（1evothyroxine，LT）联合甲状腺内注射地塞米松磷酸钠（DX）治疗亚临床甲状腺功能减退（SCH）的桥本甲状腺炎（HT）的疗效。方法80例伴SCH的HT患者随机分为LT组40例和DX组40例。两组于治疗前及治疗后测定游离甲状腺素（FT4）、游离三碘甲状腺原氨酸（FT3）、高敏促甲状腺激素（sTSH）、抗甲状腺球蛋白抗体（TGAb）、抗甲状腺过氧化物酶抗体（TPOAb）、皮质醇（Cortisol）、促肾上腺皮质激素（ACTH）等含量。结果两组治疗后FT3、FT4含量较治疗前升高（t=2．123，P〈0．05；t=2．210，P〈0．05），sTSH含量较治疗前下降（t=2．183，P〈0．05）。两组治疗后血清TPOAb、TGAb水平较治疗前下降（t=2．198，P〈0．05；t=2．230，P〈0．05）。DX组sTSH含量下降更明显。两组治疗后甲状腺体积较治疗前缩小，DX组缩小更明显。颈部外观积分及压迫症状均下降，DX组积分下降更明显。DX组在缩小甲状腺肿、降低甲状腺自身抗体滴度及改善颈部外观、压迫症状等方面均优于LT组。结论口服LT联合甲状腺内注射DX治疗HT患者明显优于单用LT。     

肝硬化病人下丘脑-垂体-甲状腺轴的功能变化及临床意义

目的 探讨不同级别肝硬化(LC)病人下丘脑-垂体-甲状腺轴的变化及临床意义.方法 91例LC病人按Child-Turcotte-Pugh(CTP)计分评级分为三组:LC-A组25例,LC-B组35例,LC-C组31例;另选27名健康人作为对照组.血清总三碘甲状腺原氨酸(TT3)、游离T3(FT3)、反T3(rT3)、总甲状腺素(TT4)、游离甲状腺素(FT4) 及促甲状腺激素(TSH) 均采用化学发光法检测,肝功能生化指标用RXL生化分析仪检测,凝血酶原时间(PT)用全自动血凝仪(血凝固法)检测.结果 从LC-A组到LC-C组随着肝硬化级别的增加,血清TT3和FT3水平逐渐降低,rT3渐次增高,TT4/rT3比值顺次下降,血清TT3分别与白蛋白、前白蛋白、载脂蛋白-A1和胆碱酯酶呈显著正相关(df=89,r值分别为0.568,0.260,0.317和0.599,P<0.05),与CTP分值及PT呈显著负相关(df=89,r值分别为-0.447和-0.297,P<0.01),TSH在各组间差异无统计学意义.共26例LC病人出现低T3综合征,LC-A组为0,LC-B组8例(22.9%),LC-C组18例(58.1%).经保肝、支持治疗1~2周后,随着肝功能好转低T3综合征也随之消失.心得安试验仅见FT4有所下降(16.84±3.16)vs (14.00±2.45) pmol·L-1,地塞米松试验未见甲状腺激素及TSH有明显变化.结论 肝硬化失代偿期随着肝功能的下降,发生低T3综合征的比例增多,与甲状腺激素转运蛋白合成功能减退、T4向T3转化减少有关,但随着病情好转低T3综合征便逐渐消失,无须补充甲状腺素.心得安或地塞米松试验对甲状腺功能未产生明显的影响,提示短期适量应用此类药物是安全的.     

The effects of ranitidine on pituitary-thyroid function.

Although several studies have examined the effects of cimetidine on pituitary-thyroid function, few have investigated ranitidine in this respect. We found no changes in thyroid-stimulating-hormone (TSH) or prolactin responses to TSH-releasing-hormone (TRH) in 10 patients with peptic ulcer disease given oral ranitidine. Serum total and free thyroxine (TT4 and FT4) concentrations declined slightly, whereas total and free triiodothyronine (TT3 and FT3) increased slightly following ranitidine. None of these changes achieved statistical significance. Both the ratio of TT4/TT3 and FT4/FT3, however, declined (P less than 0.05) following ranitidine. Thus ranitidine may have a minor influence on peripheral deiodination of thyroxine but has little effect on hormone production from the thyroid gland. The diagnostic value of biochemical tests of thyroid function is not seriously compromised in patients receiving ranitidine.     

Sensitivity of thyroid gland growth to thyroid stimulating hormone (TSH) in rats treated with antithyroid drugs.

Antithyroid drugs and phenobarbital (PB) have been shown to promote thyroid tumors in rats. It has been proposed that increased thyroid-stimulating hormone (TSH) mediates the thyroid tumor-promoting effect of antithyroid drugs and PB, and is increased because of decreased thyroxine (T4) concentration. However, PB is much less effective than antithyroid drugs at increasing TSH. It has been proposed that small increases in serum TSH produced by PB treatment is sufficient to promote thyroid tumors. However, the level to which TSH must be increased to stimulate the thyroid gland has not been reported. Therefore, we have examined the effect of increasing serum TSH concentration on thyroid growth by measuring thyroid gland weight and thyroid follicular cell proliferation. Serum TSH concentrations were increased by feeding rats various concentrations of propylthiouracil (PTU) or methimazole (MMI) for 21 days. Serum total T4, free T4, total T3 (triiodothyronine), free T3, and TSH concentrations were measured by radioimmunoassay. Thyroid follicular cell proliferation was measured by autoradiography and expressed as a labeling index (LI). PTU and MMI treatments reduced total and free T4 more than 95% by day 21, whereas total and free T3 were reduced 60%. TSH, thyroid follicular cell proliferation and thyroid weight were increased 560%, 1400%, and 200%, respectively, by day 21. TSH was significantly correlated with thyroid weight and LI. Moderate increases in serum TSH of between 10 and 20 ng/ml increased the number of proliferating thyroid follicular cells, but had no effect on thyroid weight. These results support that small increases in serum TSH can be sufficient to stimulate thyroid follicular cell proliferation. Furthermore, thyroid follicular cell proliferation may be more useful than thyroid weight alone for assessing alterations in thyroid growth in rats treated with chemicals that produce only small to moderate increases in serum TSH.     

皮质醇增多症治疗控制对促甲状腺素和甲状腺激素水平的影响

观察10例皮质醇增多症未治患者和8例治疗控制患者血中促甲状腺素（TSH）和甲状腺激素浓度的改变。结果显示未治组平均TSH、TT3、FT3血浓度明显低于正常低限，TT4稍低于正常，FT4略高于正常低限。治疗控制组平均TSH、TT3、FT3浓度明显上升，与未治组比较差别有显著性意义；TT4、FT4稍上升，与未治组比较差别无挺着性意义。在治疗技制组除TT3略低于正常外，TSH、FT3、TT4平均值均恢复正常。提示皮质醇增多症治疗控制后，合并存在的下丘脑－垂体－甲状腺轮功能紊乱可随之恢复。     

慢性心力衰竭患者甲状腺激素水平的变化

目的 探讨充血性心力衰竭（CHF）患者血清甲状腺激素水平的改变情况及其与病情的关系.方法 采用放射免疫法测定50例CHF患者（心功能Ⅱ级7例,Ⅲ级19例,Ⅳ级24例）和30例健康人血清三碘甲状腺原氨酸（T3）、四碘甲状腺原氨酸（T4）、游离三碘甲状腺原氨酸（FT3）、游离四碘甲状腺原氨酸（FT4）、促甲状腺激素（TSH）.结果 CHF组T3、FT3含量（1.95±0.55）nmol/L、（2.20±0.39）nmol/L,低于对照组的（2.4±0.50）nmol/L、（5.89±0.45）nmol/L（t=2.415,2.325,P〈0.05）;治疗后T3、FT3含量（2.19±0.53）nmol/L、（3.69±0.57）nmol/L,较治疗前显著升高（t=2.375,2.405,P〈0.05）;CHF心功能Ⅳ级患者T3、FT3含量（1.76±0.7）nmol/L、（1.99±0.45）nmol/L,明显低于对照组（t=2.245,2.375,P〈0.05）;血清TT3、TT4与心功能分级呈负相关（r=-0.933,-0.383,P均〈0.05）,血清FT3、FT4、TSH与心功能分级均无相关性.结论 血清甲状腺激素水平的改变可作为判断CHF严重程度的指标之一.     

Thyroid status and the levels of thyroid auto-antibodies in the sera of hyperthyroid and goitrous subjects

OBJECTIVES: To determine the prevalence of thyroid auto-antibodies in specimens sent to Parirenyatwa hospital laboratory for thyroid function testing and to compare the thyroid status of these patients with that of apparently healthy subjects. DESIGN: Cross sectional study. SETTING: Immunology and radio-immunoassay laboratories, Parirenyatwa hospital, Department of Chemical Pathology, and Blood Transfusion Services, Harare. SUBJECTS: 212 blood samples submitted for thyroid function testing and 230 blood samples from apparently healthy blood donors. MAIN OUTCOME MEASURES: Serum concentrations of free triiodothyronine (FT3), thyroxine (FT4), thyrotropin (TSH), and thyroid auto-antibodies; anti microsomal (M Ab) and antithyroglobulin (Ag Ab) antibodies. RESULTS: The hyperthyroid subjects had median serum TSH level of 0.027 mIU/L (Q1 = 0.006, Q3 = 0.052), median serum FT3 level of 15.895 pmol/L (Q1 = 10.563; Q3 = 30.111), and a median serum FT4 level of 45.513 pmol/L (Q1 = 30.256; Q3 = 63.910). The goitrous subjects had median serum TSH level of 0.390 mIU/L (Q1 = 0.157; Q3 = 0.745). The blood donor group had median TSH value of 0.724 mIU/L (Q1 = 0.471; Q3 = 1.170). (Normal ranges: TSH = 0.167 to 2.80) Amerlite TSH-30 diagnostic kit; FT3 = 3.4 to 7.2 pmol/L; FT4 = 11 to 24 pmol/L) Amelex-MAB diagnostic kits) Thirty nine percent of the hyperthyroid subjects had either positive M Ab or Tg Ab or both. None of the goitrous subjects and the blood donors tested positive for neither M Ab, nor Tg Ab. No significant difference was found between the blood donors and the goitrous subjects for serum FT4 (P = 0.51). However, significant differences were found between the goitrous, the blood donor and the hyperthyroid groups with regards to serum TSH, serum FT4, and serum FT3 levels (p = 0.001). CONCLUSION: Our findings indicate that the occurrence of thyroid auto-antibodies among the blood donors and the goitrous population was uncommon, but high in the hyperthyroid subjects. The increase of iodine intake through iodine prophylaxis could have had the side effects of iodine induced hyperthyroidism.     

Anticonvulsants and thyroid function

Serum total and free thyroid hormone concentrations were estimated in 42 patients with epilepsy taking anticonvulsants (phenytoin, phenobarbitone, and carbamazepine either singly or in combination). There was a significant reduction in total thyroxine (TT4), free thyroxine (FT4), and free triiodothyronine (FT3) in the treated group compared with controls. Free hormone concentrations were lower than total hormone concentrations, suggesting that increased clearance of thyroid hormones occurs in patients receiving anticonvulsants. Detailed analysis indicated that phenytoin had a significant depressant effect on TT4, FT4, FT3, and reverse T3 (rT3). Phenobarbitone and carbamazepine had no significant main effects, but there were significant interactions between phenytoin and carbamazepine for TT4 and FT4. phenobarbitone and carbamazepine for FT3, and phenytoin and phenobarbitone for rT3.     

Effects of recombinant growth hormone therapy on thyroid hormone concentrations

BACKGROUND AND OBJECTIVE: There are numerous, often contradictory reports on the effects of growth hormone (GH) therapy on thyroid function. The aim of this study was to assess the effect of such therapy on serum concentrations of thyroid hormones in GH-deficient children euthyroid prior to the treatment, and to determine the necessity of thyroid hormone administration in these patients. MATERIAL AND METHODS: The study included 32 GH-deficient patients in the first stage of sexual development, in whom disorders of thyroid function could be excluded. The inclusion criteria were based on clinical examination and levels of thyroxine (T4), triiodothyronine (T3), free thyroxine (fT4), free triiodothyronine (fT3), reverse triiodothyronine (rT3), thyrotropin (TSH) before and after stimulation with thyrotropin-releasing hormone (TRH). Recombinant growth hormone (rGH) (Genotropin 16U, Pharmacia) was administered at a dose of 0.7 U/kg/week. Fasting blood samples were drawn before treatment and after 3, 6, 9 and 12 months of therapy. Thyroid hormones were measured using RIA and IRMA methods. RESULTS: There were no physical signs of hypothyroidism in the patients examined during 12 months of rGH administration, and the satisfactory growth rate was achieved. T4 levels decreased in the first 3 months but remained within the normal range, and then returned to the values prior to the treatment. A similar trend was observed for fF4, with 28.5% of patients exhibiting fF4 levels below the normal in the 3rd month. An increase during the first 3 months of therapy was observed in the cases of T3 (statistically non-significant) and fT3, and these values then fell to levels within the normal range of patients' age. During treatment, TSH levels decreased but remained within the normal range. CONCLUSIONS: A transient decrease in T4 concentrations in the 3rd month with unchanged T3 and an increase in fT3 concentrations probably result from the effect of rGH on the peripheral metabolism of thyroid hormones. The results obtained do not support the use of thyroid hormone therapy with levothyroxine during the first year of rGH therapy in patients who are initially euthyroid.     

The effects of chronic ingestion of spironolactone on serum thyrotropin and thyroid hormones in the male rat

Male rats were fed spironolactone admixed with feed at doses of 6, 50, and 200 mg/kg/day for up to 13 weeks. After 13 weeks of treatment, there were dose-related increases in thyroid weight and follicular hypertrophy. Serum thyrotropin (TSH) concentrations were significantly increased throughout the treatment period. Serum thyroxine (T4) and triiodothyronine (T3) were significantly decreased at Weeks 2 and 4, but returned to control concentrations by Week 13. The TSH increase and transient T4 decrease suggested that the thyroid hypertrophy was a compensatory reaction to lowered thyroid hormone levels. To determine the effect of spironolactone ingestion on T4 synthesis and metabolism, male rats were fed spironolactone admixed with feed at 200 mg/kg for 2 weeks. The decrease in T4 was not due to decreased synthesis, since iodide uptake and organification were significantly increased by spironolactone treatment. Since uridine diphosphate glucuronosyl transferase activity was significantly increased by spironolactone treatment, it appears that, by increasing hepatic clearance of T4, spironolactone causes a decrease in the serum concentration of this hormone. The lower T4 level causes a release of feedback inhibition and an increase in TSH resulting in the increase in thyroid gland size and activity.