EMG myokymia as a cause of ptosis in hypothyroidism

Ptosis is known to be associated with thyroid disorders. We describe two biochemically corrected hypothyroid patients presenting with isolated bilateral ptosis. EMG of the orbicularis oculi showed continuous grouped motor unit potentials. In the absence of obvious aetiology, it is hypothesised that focal demyelination of terminal branches to the orbicularis oculi may play a role in the generation of the discharges.     

An enzyme-linked immunosorbent assay for thyroxine in dried blood spotted on filter paper

We have developed a rapid and sensitive enzyme-linked immunosorbent assay (ELISA) for thyroxine (T4) in dried blood samples spotted on filter paper. The assay is carried out on microtiter plates without extraction or centrifugation steps. The detection limit of the assay is 5 pg/disc/well, equivalent to 1.25 micrograms/1 of whole blood or 2.5 micrograms/1 of serum. Intra- and inter-assay coefficients of variation for various T4 concentrations are 2.4-9.0% and 5.9-17.5% respectively. Correlation between the proposed ELISA method and the RIA is good (r = 0.900, n = 62, y(RIA) = 0.99x(ELISA) + 9.90). The ELISA method is useful for mass-screening of neonatal congenital hypothyroidism using dried blood samples on filter paper, is very simple and one person can assay more than 300 samples per day.     

多发性肌炎与甲状腺功能减退性肌病的鉴别诊断

目的为鉴别诊断多发性肌炎与甲状腺功能减退性肌病,对二者的异同点进行探讨。方法回顾分析12例多发性肌炎和10例甲状腺功能减退性肌病患者的临床表现、实验室检查资料。结果多发性肌炎与甲状腺功能减退性肌病在肌肉方面的临床表现相似,但急性炎症指标、自身抗体、肌肉病理检查结果多有不同,甲状腺功能检查结果明显不同。结论甲状腺功能检查有助于两病的鉴别,对于肌肉无力和肌酶升高的患者需常规检测甲状腺功能。     

碘缺乏甲状腺功能减退对仔鼠海马LTP的影响

目的研究碘缺乏、甲状腺功能减退对大鼠仔鼠海马长时程增强(LTP)的影响,为碘缺乏、甲状腺功能减退导致脑发育障碍的发病机制提供实验依据。方法分别选用低碘饲料及他巴唑诱导建立碘缺乏(低碘)及甲状腺功能减退(甲减)大鼠仔鼠动物模型,应用细胞外微电极记录单脉冲刺激海马CA3区在CA1区诱发的群体峰电位(PS),测量高频刺激(HFS)前后单脉冲刺激诱发的PS幅值与PS潜伏期及其变化。结果低碘组、甲减组仔鼠PS潜伏期在HFS前(22.6764±5.4314),(20.0139±3.3028)ms;后(21.4414±4.2231),(20.8598±3.2207)ms,均明显高于相应的对照组(17.4643±2.6242),(16.7467±2.6283)ms(P<0.05)。低碘组HFS(1.8885±0.6418)mV及甲减组HFS前、后PS幅值(2.0291±0.3553),(1.9836±0.5698)mV,均明显低于相应对照组(2.4064±0.4645)、(3.1610±1.0844)mV(P<0.05)。各组HFS后PS幅值与相应的HFS前PS幅值相比,低碘明显降低(P<0.05),9只仔鼠有2只产生LTP,4只产生长时程抑制(LTd);甲减组PS幅值明显降低,6只仔鼠2只产生LTP,4只产生LTD;而对照组PS幅值显著升高(P<0.01),6只仔鼠4只产生LTP,1只产生LTD。结论碘缺乏、甲状腺功能减退可损害仔鼠在体海马LTP的诱导。     

甲状腺功能低下与亢进大鼠模型的几项生化指标的检测

目的:探讨甲状腺功能低下(甲低)及甲状腺功能亢进(甲亢)模型大鼠的甲状腺功能改变对血钙和血磷的影响。方法:制备甲低及甲亢大鼠模型,测定其血清T3、T4、TSH、钙、磷的含量变化。结果:甲低大鼠血清T3、T4和TSH浓度分别为0.27±0.08nm o l/L、25.87±2.83nm o l/L和3.36±0.42mU/L,与对照组血清T3(0.97±0.11nm o l/L)和T4(68.74±7.57nm o l/L)相比较,均明显降低(P<0.0001),有极显著差异;而血清TSH较对照组TSH含量(1.72±0.43mU/L)显著升高(P<0.0001)。甲亢大鼠T3(9.24±1.56 nm o l/L)和T4(155.73±13.98nm o l/L)含量比对照组均显著升高(P<0.0001),而TSH含量仅为0.37±0.06mU/L,与对照组相比明显降低(P<0.0001)。对照组血钙(C a2+)和血磷(HPO42-)含量分别为2.37±0.30mm o l/L和2.56±0.10mm o l/L;甲低组血钙为2.27±0.15mm o l/L,血磷为2.33±0.10mm o l/L;甲亢组血钙含量为6.17±1.42mm o l/L,血磷含量为3.84±1.13mm o l/L。结论:甲亢大鼠血钙和血磷含量较正常大鼠明显升高。甲低大鼠血清钙、磷含量与对照组大鼠比较均有所下降,但无统计学意义。     

EFFECT OF ENVIRONMENTAL AND HYPOTHALAMIC FACTORS ON THYROTROPIN SECRETION IN THE HYPOTHYROID RAT

1. Fourteen days after hypothyroidism was induced either by propylthiouracil (PTU) treatment or by thyroidectomy, the serum thyrotropin (TSH) responses to morphine (5 or 20 mg/kg bw), ether stress (30 min) and cold exposure (60 min) were compared with those in normal rats. 2. The decrease in serum TSH levels after morphine and ether stress found in the normal rats were abolished or much reduced respectively. 3. The increase in serum TSH in response to cold exposure and the diurnal rhythm of serum TSH (lower level at night) were also absent in the hypothyroid rat. 4. The stimulating effects of low dose of thyrotropin releasing hormone (TRH) and the inhibitory effects of somatostatin and apomorphine were completely abolished, while the stimulating effects of a high dose of TRH were much reduced in the hypothyroid rat. 5. These results indicate that in the hypothyroid rat the effect of a lack of negative feedback action of thyroid hormone predominates, and that hypothalamic factors are probably unimportant in the regulation of TSH secretion.     

Altered thyroid status modulates portal pressure in normal rats

Abstract: Background & Aims: Disturbances in thyroid function in humans and experimental animal models have been associated with alterations in liver function and portal circulation. We have previously shown that hypothyroidism can significantly reduce portal pressure in portal vein ligated rats as well as inhibit the development of cirrhosis and fulminant hepatic failure following toxic liver injury. The aim of this study was to determine the effects of increased and decreased thyroid function on portal pressure in rats with normal liver histology and portal circulation. Methods: Three groups of 12 Wistar rats each were studied over a 30 day period: euthyroid (Group 1), hyperthyroid (Group 2) and hypothyroid (Group 3). Hyperthyroidism was induced by subcutaneous injection of triiodothyronine (400 μg/100g body weight) every ten days during the study period. Hypothyroidism was induced by methimazole (0.04% in drinking water) from 2 weeks prior to and throughout the 30 day study. Serum triiodothyronine (T3) and thyroid stimulating hormone (TSH) levels were determined to confirm the induction of hyper- and hypothyroidism. Portal pressure was assessed by direct catheterization of the portal vein prior to sacrifice. Indirect confirmation of changes in portal circulation was obtained by determining splenic weight at the time of sacrificing the animals. Animals were sacrificed at 10 day intervals throughout the 30 day study. Results: Triiodothyronine treated rats were hyperthyroid compared to controls, with an elevation in serum T3 levels (3.8±0.9 mmol/L vs 1.3±0.4 mmol/L, p < 0.05). In rats treated with methimazole, hypothyroidism was confirmed by a 7-fold increase in serum TSH compared to controls (1.8 ± 0.4 vs 0.24 ± 0.04 mmol/L, p < 0.01). Portal pressure was significantly higher in the triiodothyronine treated rats compared to controls (12.8 ± 1.7 and 9.6 ± 0.75 cm H₂O, p < 0.001). Splenic weights in hyperthyroid rats were significantly higher than in controls (579 ± 44 vs 478 ± 46 mg, p < 0.01). Portal pressure was significantly lower in the methimazole treated group compared to the control group (8.13 ± 0.68 vs 9.6 ± 0.75 cm H₂O, p < 0.01) as were splenic weights (400 ± 33 vs 478 ± 46 mg, p < 0.01). Conclusion: These studies demonstrate that disturbed thyroid function exerts significant hemodynamic effects on the portal circulation in normal rats and complements results from previous similar studies in cirrhotic animals.     

甲状腺功能减退性肌病误诊3例并文献复习

目的提高风湿免疫科临床医师对甲状腺功能减退性肌病的认识及诊断水平。方法分析3例误诊为结缔组织病的甲状腺功能减退性肌病病例,参考国内外文献探讨误诊的原因,并对甲状腺功能减退性肌病进行复习。结果山西医科大学第二医院风湿免疫科近半年收治了3例以"肌无力、肌酶谱升高"为主要表现的患者,初步诊断均为结缔组织病,其中2例给予糖皮质激素治疗,行甲状腺功能检查后均诊断为甲状腺功能减退症,结合患者病史、症状、体征及肌酶谱、肌电图等结果确诊为甲状腺功能减退性肌病,给予左旋甲状腺素钠片治疗,2例患者症状、体征及心肌酶谱、甲状腺功能均恢复正常。第3例患者在治疗中,临床表现及心肌酶谱也明显恢复。结论对临床出现肌无力、肌酶谱升高,但查体肌力、肌张力正常的患者,应考虑甲状腺功能减退性肌病的可能,对此类患者应该常规行甲状腺功能检查,以减少误诊误治。     

Analysis of the mechanisms underlying increased histogenetic cell death in developing cerebellum of the hypothyroid rat: determination of the time required for granule cell death

The connection between the date of formation of granule cells and their final position in the internal granular layer of the cerebellum has been described previously. In rats made hypothyroid since the end of gestation, the distribution of the pyknotic cells in the internal granular layer of the cerebullar cortex was also previously found to be age-related. In 14-day-old hypothyroid rats, it was compared with that of the granule cells which were labeled after a pulse of [³H]thymidine at various stages of development. It appeared that the localization of the dying cells corresponded roughly to that of granule cells labeled on day 9. Therefore the maximum time required for granule cell death was about 5 days. Since the migratory phase through the molecular layer lasted about two days, the granule cells died after a maximum time of 3 days following their deposition in the internal granular layer. Information concerning the time of survival of the dying granule cells was important for subsequent investigation of the mechanisms underlying increased granule cell death in the hypothyroid cerebellum and the corrective effects of thyroid hormone.