氟对鸡甲状腺组织结构的影响

目的 探讨氟对鸡甲状腺组织结构的影响。方法 选用250只1日龄蛋鸡,随机分成5组,每组50只,饲喂相同的全价日粮。第1组为对照组,第2,3,4,5组在日粮中添加不同水平的氟化钠,使日粮中氟含量分别为500,1000,1500,2000mg/kg,实验期150d。每30d采集1次样品,测定血清中氟含量,制作甲状腺组织切片,称量甲状腺重量,观察鸡的临床表现。结果 成功地复制出了不同程度的鸡慢性氟中毒模型。在早期,各氟中毒组鸡甲状腺的相对重量均不同程度地低于对照组,甲状腺滤泡面积减小,胶质减小。中后期,则均不同程度地高于对照组,滤泡直径和面积增大,胶质过度充盈,并出现由滤泡旁细胞组成的增生性结节。结论 氟化物对甲状腺的组织结构产生了严重的破坏作用,在早期引起鸡甲状腺萎缩,中后期则致甲状腺呈胶质性、结节性肿大。     

胰岛素样生长因子Ⅰ在碘缺乏和碘过量小鼠甲状腺形态变化中的作用

目的 观察碘缺乏和碘过量小鼠甲状腺胰岛素样生长因子Ⅰ(IGF-Ⅰ)的水平及在甲状腺形态变化中的作用.方法 选用Balb/c小鼠48只,体质量约16 g,雌雄各半.按体质量、性别将小鼠随机分为3组:碘缺乏组(LI,饲料中含碘量为50μg/kg,饮去离子水);适碘组(对照,NI,饲料中含碘量为300μg/kg,饮去离子水)、碘过量组(HI,饲料中含碘量为300μg/kg,饮水中含碘量14 700μg/kg);每组16只.喂养12周后处死,取小鼠甲状腺,测量甲状腺的绝对及相对质量,HE染色,光镜下观察小鼠甲状腺的形态学变化;RT-PCR法检测IGF-Ⅰ mRNA表达:免疫组化法检测甲状腺IGF-Ⅰ蛋白质表达.结果 小鼠甲状腺的绝对质量和相对质量,组间比较差异有统计学意义(F值分别为315.881、405.921,P均<0.01);其中LI组[(10.71±4.03)mg,(44.98±15.39)mg/100 g体质量]和HI组[(3.42±1.17)mg,(13.50±3.89)mg/100 g体质量]高于NI组[(2.11±0.53)mg,(8.35±1.98)mg/100 g体质量,P均<0.01].光镜下,LI组小鼠滤泡体积变小,数量增多,上皮细胞呈柱状或高柱状,增生呈复层,滤泡腔内胶质减少或缺如;而HI组小鼠发生了胶质蓄积,滤泡增大,未见滤泡增生.甲状腺IGF-Ⅰ mRNA表达,LI组(1.03±0.32)明显高于NI组(0.65±0.19),组间比较差异有统计学意义(F=7.518,P<0.01),HI组与NI组比较有下降趋势,但差异无统计学意义(P>0.05).甲状腺IGF-Ⅰ蛋白质表达,LI组小鼠甲状腺滤泡上皮细胞内棕黄色颗粒明显多于NI组和HI组,而HI组却少于NI组.结论 碘缺乏和碘过量小鼠发生甲状腺肿,甲状腺IGF-Ⅰ mRNA和蛋白表达的改变,可能参与碘缺乏和碘过量导致甲状腺形态改变的过程,甲状腺白分泌的IGF-Ⅰ在缺碘性和高碘性甲状腺肿形成过程中可能起重要调节作用.     

长期摄入过量碘大鼠甲状腺的形态学变化

目的观察大鼠长期摄入过量碘甲状腺的形态学变化。方法选用Wistar大鼠给予不同剂量的碘化钾,分别于实验3、6、12月时处死观察甲状腺质量、组织学变化、阳性增殖细胞数量等指标。结果低碘组大鼠甲状腺明显肿大,呈小滤泡性增生,阳性增殖细胞显著增多。各高碘组甲状腺虽未发生肿大,但发生了明显的组织学变化,主要表现为胶质蓄积,大滤泡增多,同时存在小滤泡增生;在5倍和10倍高碘(5HI,10HI)组两种变化均可见到,但在50倍和100倍高碘(50HI,100HI)组滤泡增生变得明显,阳性增殖细胞亦明显增多,但不及低碘组。结论长期摄入过量碘使大鼠甲状腺发生了明显组织学变化,但仍不足以形成甲状腺肿大;在50HI和100HI摄入时滤泡增生变得明显,提示甲状腺存在促甲状腺激素(TSH)刺激。     

摄入不同剂量碘对甲状腺肿复原的形态计量学研究

目的碘是人体维持正常生理功能不可缺少的元素,适量碘的摄入不仅可保证正常的生理功能,而且可以纠正碘缺乏.本实验是在成功复制缺碘性甲状腺肿大鼠模型的基础上,给予不同剂量的碘酸钾和碘油治疗后,观察大鼠甲状腺组织学改变,并进行了形态计量学研究,以进一步了解不同剂量碘的摄入和碘油对甲状腺的形态与结构的影响.方法将300只离乳1个月,体重80～100 g的Wistar大鼠,饲以低碘饲料(碘含量在40μg/kg左右)和去离子水3个月,出现明显的甲状腺肿大后,将其随机分为5组,各组均继续饲以低碘饲料,但在饮水中加入不同浓度的碘酸钾.其中低碘组(LI)继续饮用去离子水;适碘组(NI)、中碘组(M1)、高碘组(HI)的饮水中分别含有碘酸钾为400,1 200,3 000μg/L.碘油组(OI)1次口服10 μl(32%)碘油后饮用适碘组的饮水(即含400μg/L碘酸钾的水).在补碘实验开始后的1周时分别测量各组动物甲状腺湿重、甲状腺细胞滤泡面积、最大直径、最小直径、形状因子、滤泡和胶质占视场面积比.结果①各补碘组甲状腺的绝对重量和相对重量均较LI组有明显下降(P＜0.05),但各补碘组间差异无显著意义;②无论是滤泡的截面积,还是最大、最小直径,LI组与各治疗组之间均无明显差别;③细胞和胶质所占视场面积比显示,LI组甲状腺细胞大量增生,新生小滤泡较多,滤泡腔内胶质缺如;不同碘摄入的4个治疗组均使甲状腺滤泡有所恢复,大部分滤泡腔内充满胶质;④LI组与各治疗组间形状因子均未见改变,说明甲状腺滤泡始终较规则,且接近于圆形;⑤从小、中、大滤泡所占比例的分布可见,NI和MI组主要集中在中等滤泡的范围,说明NI和MI组大鼠甲状腺肿恢复较好;HI组出现小滤泡最多、大滤泡也较多的情况,是由于在低碘形成甲状腺肿后立刻给予大剂量碘的摄入,使机体处于高碘营养状态造成的;而OI组小滤泡最少,大滤泡最多,因为口服碘油后3 d,大量碘基本由尿液排出,在正常碘营养状态下其恢复好于HI组.结论适量补碘可以较好的纠正碘缺乏所造成的甲状腺肿,应避免补碘过量可能产生的副作用,提倡科学补碘.此外,形态计量学指标可以定量的分析和反映甲状腺组织在给予不同剂量碘和口服碘油后的结构变化,比单纯形态学观察更加客观、准确,其研究结果更加可靠.     

高碘对小白鼠甲状腺影响的观察研究

以高碘饲料喂养４组小白鼠，平均每只日摄碘量分别为：１组１μｇ，２组６μｇ，３组５０．８μｇ，４组１０１μｇ。１５０天后发现甲状腺肿和甲状腺炎。动物每日摄碘量和甲状腺的重量、甲状腺滤泡直径呈正相关，和动物的体重、甲状腺滤泡上皮细胞的高度呈负相关。甲状腺的组织学改变属巨滤泡性胶样甲状腺肿。超微结构显示细胞功能处于静止减弱的形态。８只动物（占１４％）甲状腺组织中有不同程度的灶性或弥漫性淋巴细胞浸润，和…     

轻、中度碘过量对碘缺乏大鼠甲状腺功能和形态的影响

目的探讨轻、中度碘过量对碘缺乏Wistar大鼠甲状腺功能和形态影响。方法碘缺乏大鼠以饮用1%过氯酸钾溶液制备,分成0μg/L、840μg/L和1680μg/L碘组。双蒸水(DDW)组饲以DDW和普通饲料。固相免疫放射法(IRMA)测定血清TSH,放射免疫法(RIA)测定血清TT3、TT4、rT3和甲状腺组织TT4。光镜、电镜下观察甲状腺形态学变化。图像分析系统测量大鼠滤泡上皮细胞高度和滤泡腔的面积。结果补碘90天时,碘过量组血清TSH明显低于低碘对照组(均P<0.05),但与DDW组相比差异无显著性。1680μg/L碘组血清TT3值明显低于低碘对照组和DDW(均P<0.05),碘过量组血清TT4值明显高于低碘对照组和DDW组(均P<0.001),血清rT3高于低碘对照组和DDW组,但是差异无显著性,碘过量组甲状腺组织TT4含量明显高于低碘对照组和DDW组(均P<0.001)。甲状腺的相对重量均明显高于DDW组和低碘对照组(P<0.001和P<0.05)。碘过量组随着时间延长,滤泡上皮变扁,滤泡周围毛细血管逐渐减少,巨滤泡形成,同时有部分滤泡增生。碘过量组非增生滤泡上皮细胞高度明显小于DDW组和低碘对照组(均P<0.001),1680μg/L碘组泡腔面积明显大于DDW组和低碘对照组(均P<0.001)。结论轻、中度过量碘(尿碘中位数,MUI为300和600μg/L)处理90天,使碘缺乏大鼠甲状腺功能亢进,低碘致甲状腺肿不能完全恢复,甲状腺滤泡异质性增加。     

碘缺乏与碘过多大鼠甲状腺定量形态学研究

目的　研究碘缺乏与碘过多对大鼠甲状腺形态结构的影响。方法　将 Wistar大鼠随机分为 3组 ,适碘组 (NI)、高碘组 (HI)、低碘组 (L I) ,观察喂养 12周、2 4周大鼠甲状腺形态结构的变化 ,应用 MIAS- 2 0 0 0型图像分析系统 ,对甲状腺滤泡及滤泡腔进行形态定量测定 ,获得 5项体视学参数 (平均体积 V、平均表面积 S、比表面积 S/ V、数密度 Nv及球形因子 SF)和 1项截面积的定量参数。结果　低碘组大鼠甲状腺滤泡及滤泡腔的 V、S及 SF均明显小于适碘组 ,而 S/ V和 Nv明显大于适碘组 ,上皮细胞体积明显增大 ;高碘组滤泡在实验过程中无明显改变 ,而滤泡腔 V、S在实验的 2 4周时均明显小于适碘组 ,上皮细胞体积增大。结论　碘缺乏导致大鼠甲状腺小滤泡增生性甲肿改变 ,而碘过多在实验中未形成甲肿 ,并随碘过多时间的延长 ,滤泡腔变小 ,上皮细胞增生。     

碘与酪氨酸交互作用对小鼠甲状腺形态变化的动态对比研究

目的动态研究高碘与高酪氨酸对小鼠甲状腺形态结构变化的影响。方法将150只昆明种小鼠随机分为对照组(NI)、高碘组(HI)、高酪氨酸组(Htyr)、高碘高酪氨酸组(HI+Htyr)和高碘模型组(HIM)5组。在实验10周、20周和30周时,测定小鼠甲状腺绝对质量与相对质量,观察小鼠甲状腺组织形态变化。结果 20周时,HI组小鼠甲状腺相对质量显著高于NI组;30周时,HI+Htyr组小鼠甲状腺相对质量显著高于NI组。光镜结果显示,HI组呈现典型的胶质性甲状腺肿;同时HI+Htyr组也呈现出胶质性甲状腺肿的改变,但滤泡腔胶质减少。结论补充适量的酪氨酸可以减轻高碘对甲状腺组织的损伤作用,延缓昆明种小鼠甲肿的发生,但不能阻止高碘甲状腺肿的形成,说明在水碘为300μg/L的情况下,碘对甲状腺肿的作用是主要的,酪氨酸的作用是次要的。     

老年人甲状腺功能

甲状腺形态学和功能在老年人的甲状腺已观察到许多形态改变,包括重量减轻、滤泡最大直径缩小,血管狭窄,结缔组织增生和细胞成分减少。尸检发现80岁以上者有发生微结节的高度倾向。除随年龄发生形态学改变外,其功能亦发生变化。近来Studer报告老年鼠甲状腺正常滤泡可转为对促甲状腺激素(TSH)不起反应的“冷”滤泡。老年鼠甲状腺放射自显影表明甚至在强烈的外源性或内源性TSH刺激下“冷”滤泡也不能碘化腔内的酪氨酸。小于5月龄鼠无“冷”滤泡,13月龄时     

氟对大鼠甲状腺形态和甲状腺过氧化物酶活性及蛋白表达的影响

目的 观察长期氟过量对大鼠甲状腺形态结构、甲状腺过氧化物酶(TPO)活性及TPO蛋白表达的影响,并探讨其可能的作用机制.方法 选用雄性SD大鼠40只,按体质量随机分为对照组、低氟组、中氟组、高氟组,每组10只.4组大鼠分别饮用含氟0.40(普通自来水)、15.00、30.00、60.00 mg/L的自来水,均食用普通粮食配制的饲料.喂养180 d后,将大鼠麻醉,取甲状腺组织.在400倍光镜下观察甲状腺组织形态学改变;改良愈创木酚法测定TPO活性；免疫印迹(Western blot)法检测TPO蛋白质表达水平.结果 光镜下,对照组甲状腺滤泡上皮细胞多为单层柱状或立方状,滤泡腔内充满粉红色胶质;低氟组甲状腺滤泡上皮细胞增生活跃;中氟组滤泡增大,滤泡腔内充满深染、黏稠的胶质滤泡；高氟组滤泡上皮细胞明显扁平,滤泡胶质过度浓集,少量滤泡腔甚至有融合,形成巨形滤泡或囊腔.对照组、低氟组、中氟组和高氟组甲状腺细胞TPO活性[(1.572±0.046)、(1.414±0.086)、(1.322±0.049)、(0.960±0.083)U/L]依次降低,组间两两比较差异有统计学意义(P均＜ 0.05)；TPO蛋白表达水平(0.335±0.011、0.156±0.027、0.084±0.020、0.045±0.002)依次下降,组间两两比较差异有统计学意义(P均＜ 0.05).结论 长期摄入过量氟可抑制甲状腺TPO活性和TPO蛋白的表达,进而影响甲状腺组织学改变.     

Evidence for co-ordinated changes between vascular endothelial growth factor and nitric oxide synthase III immunoreactivity, the functional status of the thyroid follicles, and the microvascular bed during chronic stimulation by low iodine and propylthiouracyl in old mice

Vasoactive and angiogenic factors are involved in the autocrine/paracrine thyroid regulation of microvascular bed during goiter development. In the thyroid of old mice, the presence of slowly functioning ('cold') follicles allowed us to study the microvascular regulation of each follicle in correlation with the immunohistochemical expression of vascular endothelial growth factor (VEGF) and nitric oxide synthase III (NOSIII). Mice aged 20 months did or did not receive a goitrogenic treatment (low iodine diet and propylthiouracyl), and their thyroids were processed for light and electron microscopy, and for autoradiography. The relative volumes (Vv) of the capillaries, the number of vessels per follicular area, the mean capillary area and the number of [(3)H]thymidine labeled nuclei were measured separately for 'hot' and 'cold' follicles. Already in control mice, the capillary bed surrounding 'hot' follicles was significantly larger than that seen around 'cold' follicles, because of larger diameters and twice the number of capillaries. This difference persisted whatever the length of the stimulatory treatment. During this treatment, the Vv of the capillaries increased to a larger extent around 'hot' follicles than around 'cold' ones. All vascular changes around 'cold' follicles were less extended and the increase in the capillary diameter was delayed. In control mice, the 'cold' follicles were negative for NOSIII and positive for VEGF while 'hot' follicles were positive for both. During stimulation, all follicles became progressively NOSIII positive. These data support the concept of 'angio-follicular units' in the thyroid and demonstrate their differential regulation in chronic stimulation during which local secretion of VEGF and NO is clearly involved.     

Autonomous growth and function of cultured thyroid follicles from cats with spontaneous hyperthyroidism.

Spontaneous feline hyperthyroidism is a unique experimental model of toxic nodular goiter. To determine whether feline toxic goiter is caused by extrathyroidal stimulating factors or by the intrinsic autonomy of follicular cells, primary cultures of enzymatically dissociated follicles from 15 hyperthyroid cat goiters and from 3 normal cat thyroid glands were embedded in collagen gels. Growth and function in chemically defined media were assessed by autoradiography after double labeling with 3H-thymidine and 131I-Na. Iodine organification in follicles from normal glands was TSH dependent, but intense radioiodine organification occurred in follicles from hyperfunctioning goiters even in the absence of TSH. Similarly, twice as many follicular cells of hyperfunctioning thyroid tissue, maintained without TSH in the medium, were labeled after exposure to 3H-thymidine than in follicles from normal glands. The results strongly suggest that intrinsic alterations of cell function lead to autonomy of follicular growth and function and subsequently to the development of hyperplastic nodules, causing thyrotoxicosis. The reason for the focal nature of the disease remains an unresolved challenge. Further investigation using this model may further understanding of the growth of autonomous endocrine tumors.     

Content and heterogeneity of distribution of iodine in human and bovine thyroid glands determined by neutron activation analyses

While performing activation analytical investigations on the actual concentration of the long-lived radioactive 129iodine in human and bovine thyroid glands the absolute natural nonradioactive 127 iodine content was determined. In all thyroid glands an uneven distribution of 127I was found (in human thyroids from 0 to 0.75 micrograms 127I /mg, in bovine thyroids from 0 to 3.5 micrograms 127I /mg). The mean value of iodine concentration in human thyroid glands ranged from 230 micrograms/g to 490 micrograms/g. This is important because TSH independent autonomy is found at a cellular and follicular level during the development from diffuse to nodular goiter. Both processes may, however, not be related to each other. The resolution of the method used in our study is between the microscopic and the scintigraphic level with an accuracy of +/- 1%, and it shows an intermediate heterogeneity of iodine in thyroid glands.     

Increased follicular heterogeneity in experimental colloid goiter produced by refeeding iodine excess after thyroid hyperplasia

Delayed morphological changes induced in mouse hyperplastic thyroid by refeeding iodine were analyzed by light and electron microscopy, stereology, and autoradiography. Thyroid hyperplasia was induced by a low iodine diet supplemented with 0.25% propylthiouracil for 10 days. Involution was obtained by discontinuing the propylthiouracil and returning either to a moderate iodine diet [(MID) 1 microgram I/day] or to an iodine-rich diet [(HID) 10 micrograms I/day] for 40 days. In other experiments, three cycles of hyperplasia (8 days) and subsequent involution (8 days) with MID or HID were brought about. Control animals were fed MID or HID. All animals were killed when 12-14 weeks old after injection of 10-50 microCi 125I. Double labeling, with repeated injections of [3H]thymidine from day 0 to day 7 of involution followed by 125I injection 4 h before killing, was also performed. When involutions were performed with MID, most morphological variables returned to control values. However, when involution was brought about with HID, the glandular weight, the number of follicles, and the relative volume of follicular lumina remained larger than in controls. Moreover, the 125I-labeling pattern of the follicles was altered. The proportions of unlabeled, and unevenly or partly labeled, follicles, which were fewer than 5% in control groups, represented 25-35% of all follicles after involution with HID, whereas they were unchanged with MID. In unlabeled follicles the epithelium was flattened, with a reduced number of microvilli. Partly labeled follicles were of two types. In some follicles a persistent ring reaction was observed, suggesting an abnormally slow mixing of thyroglobulin. In others, the 125I labeling was restricted to areas adjacent to the apex of a reduced number of cells, suggesting that some cells were iodinating thyroglobulin, whereas others were not. There was no relationship between the follicular 125I labeling and the frequency of [3H]thymidine-labeled cells. These results indicate that refeeding iodine excess after hyperplasia leads to the formation of a colloid goiter with new follicles, and to an increased heterogeneity of iodine metabolism among follicles and among cells.     

Recombinant human thyrotropin stimulates thyroid angiogenesis in vivo.

BACKGROUND: Endogenous TSH and rhTSH stimulate thyroid growth by a direct effect on thyrocytes. Our hypothesis was that rhTSH may also stimulate thyroid angiogenesis. STUDY DESIGN: A normal human thyroid tissue sample was grafted into the epigastric area of 14 nude mice. Mice were divided in two groups of 7. The first group (treated mice) received rhTSH stimulation (0.014 UI/mouse/day for 3 weeks), while the second group (control mice) had saline. Histological study with special focus on vascular characteristics was performed by image analysis at day 21 for each graft. VEGF immunostaining score, determined by immunohistochemistry, was defined as the percentage of labeled thyrocytes score, plus an intensity score. RESULTS: Thyroid follicles showed signs of increased colloid re-uptake activity in rhTSH group within a larger surface area than controls (p <0.01). Thyrocytes were taller in the rhTSH group (p <0.01). The diameter of capillary vessels was larger and the microvessels expansion more important in the rhTSH group (p <0.02). Relative capillary area, defined as the ratio between capillary area and follicular area, was also higher in the rhTSH group (p <0.02). VEGF immunostaining score was increased in the rhTSH group (p <0.01). CONCLUSION: rhTSH stimulates angiogenesis and local VEGF expression in normal human thyroid.     

Elevated levels of polyamines and histamine in adenocarcinomas of the thyroid.

The concentrations of polyamines (putrescine, spermidine, and spermine) and of histamine in normal and diseased thyroids were determined with an automated amino acid analyzer. A total of 39 specimens was investigated: 7 specimens of normal tissue, 6 adenocarcinomas, 2 specimens of tissues adjacent to adenocarcinoma, 13 specimens from treated Graves' disease, 7 follicular adenomas, 2 adenomatous goiters, and 2 specimens of Hashimoto's thyroiditis. Mean putrescine levels in tissues from normal thyroid, adenocarcinomas, Graves' disease, and follicular adenoma were 26, 143, 20, and 12 nmol/g wet tissue, respectively. The mean levels of both spermidine and spermine were slightly but significantly higher in adenocarcinomas than in other thyroid tissues. The molar ratio of spermidine to spermine was about 0.5 both in the normal and diseased thyroid tissues, except for specimens of thyroiditis. Histamine was detected in 3 of the 6 cases of thyroid carcinomas, and in case of adenomatous goiter. The data suggest that measurement of polyamines, especially putrescine, may be useful for diagnosis of thyroid adenocarcinomas.     

Mutant gene-induced disorders of structure, function and thyroglobulin synthesis in congenital goitre (cog/cog) in mice.

We have investigated thyroid structure and function in mice homozygous for the chromosome 15 mutation, congenital goitre (cog). Abnormal thyroidal hypertrophy and reduced iodine uptake in cog/cog mice were observed as early as day 18 of gestation, corresponding to the onset of thyroid function. Growth continued unabated in mutants throughout the 10-month period of observation. By 2 months of age, thyroid cell hypertrophy obliterated nearly all follicular lumina in cog/cog glands and by 10 months mean mutant thyroid mass exceeded that of age-matched littermates. Twenty-fold serum concentrations of thyrotrophin were significantly increased at all ages examined. While wild type (+/+) and heterozygote (+/cog) mice are indistinguishable from each other, thyroids of homozygote mutants (cog/cog) and the +/cog type are easily discernible from thyroids of the +/+ type by microscopic and thyroglobulin (Tg) analyses. Thyrofollicular cells of both cog/cog and +/cog genotypes contain large vesicles of accumulated, nonglycosylated proteinaceous material not observed in cells from +/+ mice. Autoradiography showed 125I was incorporated only into Tg within recognizable follicular lumina of thyroids from +/cog mice. Serum concentrations of tri-iodothyronine are depressed during development in cog/cog mice. Serum concentrations of thyroxine are depressed during postnatal development but increase progressively to normal concentrations by 10 months of age. Our analyses indicate that full size Tg is produced in thyroid cells from cog/cog mice, though in a greatly reduced quantity, and that Tgs which are several sizes smaller than normal are also produced in both homozygote and heterozygote thyroids.(ABSTRACT TRUNCATED AT 250 WORDS)     

Histopathogenesis of goiters

The basic mechanisms acting in the transformation of a normal thyroid gland into a toxic or nontoxic goiter are summarized: 1) Any goiter arises from multiplication of follicular epithelial cells forming new follicles. 2) In the follicular epithelium there are cell families with much higher than average growth potential. 3) Cells of an individual follicle are not identical but heterogeneous. 4) Each follicular cell has a certain level of autonomy of growth and of function.     

Goiter associated with acromegaly: sonographic and scintigraphic findings of the thyroid gland.

Elevation in serum human growth hormone (GH) level is known to be a factor that causes goiter development. The present study was designed to analyze sonographic and scintigraphic appearances of the thyroid in patients with acromegaly. The records of 48 consecutive patients with acromegaly were examined. Two patients had a history of operation for thyroid cancer. One had an atrophic thyroid gland after 131I treatment for Graves' disease. Goiter was palpable in 39 of the remaining 45 patients. Neither ultrasonography (US) nor scintigraphy was performed in 17 patients, including 6 with no palpable goiter and 11 with small diffuse goiter (group 1). Of the remaining 28 patients who underwent US, 14 had a moderately or markedly enlarged diffuse goiter (group 2), 13 were diagnosed as having adenomatous goiter (group 3), and 1 had a solitary cystic nodule. Among 11 patients in group 3 who underwent 123I or 99mTc thyroid scintigraphy, 6 showed uneven uptake, and 2 with undetectably reduced levels of thyrotropin (TSH) showed localized functioning areas. The mean serum TSH concentration in group 3 was significantly lower than that in group 1 or 2 (p<0.01). The duration of illness as acromegaly was significantly longer in group 2 and 3 as compared with group 1 (p<0.05). These results suggest that long-term stimulation by GH and insulin-like growth factor-I of thyroid follicular cells might be responsible for thyroid enlargement, presence of functioning lesions, slight overactivity of the thyroid, and the subsequent formation of multiple nodules in acromegalic patients. In conclusion, excluding two patients with thyroid cancer and one with Graves' disease, goiter was palpable in 39 of the 45 patients with acromegaly, among whom 14 (13 adenomatous goiters and 1 solitary cystic nodule) showed nodular enlargement.