Red cell 2,3-diphosphoglycerate and oxygen affinity of hemoglobin in patients with thyroid disorders

We measured red blood cell 2,3-diphosphoglycerate (2,3-DPG), adenosine triphosphate (ATP), and the P50 value in vitro of the oxyhemoglobin dissociation curve, which is the oxygen tension at half saturation of hemoglobin, in order to quantitate red blood cell oxygen transport function in individuals who were diagnosed as hypothyroid, euthyroid, or hyperthyroid based on measurements of thyroxine (T4), triiodothyronine (T3), thyrotropin (TSH), and their clinical status. Hypothyroid (mean T4 2.8 microgram/dl, T3 49 ng/dl, TSH 37 microU/ml) and hyperthyroid (mean T4 14 microgram/dl, T3 271 ng/dl, TSH less than 0.7 microU/ml) patients had normal red cell 2,3-DPG and ATP levels and normal P50 values in vitro. The known changes in oxygen consumption produced by alterations in thyroid hormone levels in patients with hypothyroidism or hyperthyroidism did not affect red blood cell oxygen transport function.     

Fasting decreases thyrotropin responsiveness to thyrotropin-releasing hormone: a potential cause of misinterpretation of thyroid function tests in the critically ill

We have previously reported that caloric deprivation inhibits peripheral T4 metabolism and blunts the TSH response to TRH in euthyroid obese subjects. To determine whether these phenomena also occur in hypothyroid subjects, T4, T3, rT3, and the TSH response to TRH were measured initially and after a 60-h fast in seven hypothyroid patients. Short term fasting caused a 29% decrement in the maximum serum TSH increment and a 32% decrement in the integrated TSH response to TRH (P less than 0.01). In two subjects with mild hypothyroidism, basal TSH as well as the TSH response to TRH were reduced to levels within the normal range. Specifically, basal TSH values decreased from 7.6 to 3.5 microU/ml and from 11 to 4.1 microU/ml. In the seven subjects, mean serum T3 decreased significantly from 88 to 60 ng/dl, (P less than 0.05) and rT3, initially undetectable in six of seven subjects, rose to detectable or low normal values in four of seven subjects, serum T4 remained at 2.7 micrograms/dl during both study periods. We conclude that 1) fasting induces changes in both peripheral thyroid hormone metabolism and the hypothalamic-pituitary axis in hypothyroid individuals which are qualitatively similar to those that occur in euthyroid subjects; and 2) in certain hypothyroid subjects, fasting alone can decrease basal TSH values to within the normal range. If these data can be extrapolated to critically ill subjects whose caloric intake may be diminished, they suggest that basal TSH concentrations in moderately and severely hypothyroid critically ill subjects will accurately reflect the biochemically hypothyroid state. However, mild degrees of hypothyroidism in critically ill subjects might be overlooked due to the lowering effect of fasting or poor caloric intake alone on basal TSH concentrations.     

Recovery of thyroid function with a decreased titre of antimicrosomal antibody in a hypothyroid man with Hashimoto's thyroiditis

A 36 year old man with a diffuse goitre, signs of mild hypothyroidism, strikingly low levels of T4 (0.9 micrograms/dl) and T3 (24 ng/dl), elevated TSH (140 microU/ml) and elevated microsomal haemagglutination antibody (MCHA, 1:409 600), subsequently became non-goitrous and euthyroid with a decreased titre of antimicrosomal antibody without any medication. At the time of surgical biopsy, serum levels of T4 and T3 had risen to the normal range (4.6 micrograms/dl and 73 ng/dl, respectively), serum TSH had decreased to 30 microU/ml and the titre of MCHA to 1:25 600. Thyroid specimens showed Hashimoto's thyroiditis. The activity of thyroid peroxidase (TPO) was normal. The latest examination, 1 year and 3 months after initial evaluation, showed that the patient remained euthyroid with no goitre, that serum thyroid hormones were within the normal range (T4 7.7 micrograms/dl and T3 97 ng/dl), and that TSH was not detectable. The titre of MCHA decreased strikingly to 1:400.     

A sensitive thyroid stimulating hormone assay for screening of thyroid functional disorder in elderly Japanese

The use of a screening test for thyroid functional disorder by sensitive thyroid stimulating hormone assay in the elderly was investigated. The basal thyroid stimulating hormone levels predicted the response of thyroid stimulating hormone to thyrotropin releasing hormone; it was suppressed in 99 (99.0%) of 100 hyperthyroid patients. Therefore, not only primary hypothyroidism but also hyperthyroidism can be excluded when the serum thyroid stimulating hormone levels are normal. An epidemiological study was then performed on 2,421 (76.7%) of the Japanese general population aged 40 or over recruited from the residents in Hisayama town and also in 122 residents between 20 and 40 years of age. Additional free T4 measurement was necessary in about 10% of the residents with abnormal TSH levels to confirm the diagnosis of hyperthyroidism or distinguish latent from overt hypothyroidism. There was a significant correlation between age and serum thyroid stimulating hormone levels after logarithmic conversion (r = 0.1533, P less than .001). The prevalence of thyroid dysfunction found in 1,026 males and in 1,395 females aged 40 or over was, respectively: hyperthyroidism, less than 0.1% and 0.2%, latent (subclinical) hypothyroidism, 3.2% and 5.5%, and overt hypothyroidism, 0.4% and 0.7%. We conclude that the screening with this sensitive thyroid stimulating hormone assay and additional free T4 measurement is useful for detection of patients with thyroid functional disorder.     

Familial thyroid hormone resistance

Eight patients with thyroid hormone resistance were found in four generations of a kindred containing 19 members. Results of studies in this family are consistent with an autosomal dominant mode of inheritance for this disorder. The affected family members were clinically euthyroid but all had goiters and markedly increased serum thyroid hormone levels: thyroxine (T4) = 21.1 +/- 2.1 microgram/dl; triiodothyronine (T3) = 323 +/- 60 ng/dl; free T4 = 5.4 +/- 0.9 ng/dl; and free T3 = 1,134 +/- 356 pg/dl (mean +/- SD). Serum thyrotropin (TSH) levels were normal or slightly elevated in six patients and responded normally to the administration of thyrotropin-releasing hormone (TRH) and L-triiodothyronine. Two patients who had previously undergone subtotal thyroidectomy had elevated baseline serum TSH levels and exaggerated TSH responses to the administration of TRH suggesting subclinical hypothyroidism despite elevated total and free thyroid hormone levels. The absence of thyrotoxicosis and normal serum TSH levels despite elevated serum free T3 and T4 levels in the untreated members of this family are consistent with resistance of pituitary and peripheral tissues to the actions of thyroid hormones. In addition, the absence of hypothyroidism and normal responsiveness of serum TSH to TRH and L-triiodothyronine administration in untreated family members suggest that the thyroid has compensated for the hormone resistance by increased secretory activity under the control of pituitary TSH secretion.     

Amiodarone and thyroid function

Amiodarone blocks the action of thyroid hormone by the inhibition of 5′-deiodinase which reduces production of T₃ in peripheral tissues and possibly by blocking nuclear binding of T₃. Since the drug inhibits peripheral conversion of T₄ to T₃, many patients taking amiodarone have abnormal thyroid function studies (increased T₄ and rT₃; decreased T₃) despite being euthyroid. Treatment of patients with amiodarone generates an iodine excess, which contributes greatly to the significant incidence of altered thyroid status in this population. The diagnosis of hyperthyroidism and hypothyroidism can be difficult. However, using the overall clinical picture and the tolerance limits of hormone levels determined for patients remaining euthyroid on amiodarone therapy, the accurate diagnosis of clinically significant thyroid dysfunction can almost always be made. To screen for thyroid disease, thyroid function should be assessed before initiating therapy, semiannually during therapy or whenever clinical features of thyroid dysfunction occur. Subclinical hypothyroidism as denoted by modest increases in TSH levels do not require treatment or the discontinuation of amiodarone therapy. An appreciation of the mechanism of the interaction between amiodarone and thyroid hormone metabolism allows the clinician to recognize thyroid dysfunction at an early stage and initiate appropriate therapy, thereby minimizing the morbidity associated with forms of amiodarone toxicity.     

Effect of long-term amiodarone therapy on thyroid hormone levels and thyroid function

Both hyperthyroidism and hypothyroidism have been noted to occur in some patients treated with amiodarone for cardiac arrhythmias. To determine the frequency of the development of thyroidal abnormalities in patients receiving amiodarone, 45 euthyroid patients were prospectively evaluated. Serum samples were obtained for measurement of thyroxine, thyrotropin, triiodothyronine, and triiodothyronine resin uptake prior to initiation of amiodarone treatment and serially over a 12- to 27-month period during which amiodarone was administered. The patients were divided into four subgroups as follows: Group I (n = 22) had elevated thyroxine levels, Group IIA (n = 13) had normal thyroxine levels and normal thyrotropin levels, Group IIB (n = 7) had normal thyroxine levels and elevated thyrotropin levels, and Group III (n = 3) had subnormal thyroxine levels. Demographic factors (such as route of administration, cardiac diagnosis, sex of the patient, or indication for amiodarone therapy) and amiodarone levels had no significant effect on the thyroid hormone parameters. However, Group I patients were statistically older than the patients in the other groups. Linear regression analysis revealed a negative correlation for thyroxine levels and a positive correlation with thyrotropin levels with age for the whole group. The various groups were not statistically affected by duration of therapy, but a positive trend existed for increasing thyroxine levels. Although virtually all patients showed changes in their thyroid hormone levels, chemical hyperthyroidism (elevated thyroxine and triiodothyronine levels without symptoms) developed in only two patients (4 percent), and clinical hyperthyroidism (elevated thyroxine and triiodothyronine levels with symptoms) developed in no patients. Four patients (9 percent) became biochemically and clinically hypothyroid. Thus, amiodarone frequently influences thyroid hormonal parameters, but less commonly causes a change in actual thyroid function. However, hyperthyroidism and hypothyroidism do occur in a significant number of patients.     

Thyroid status in fifty patients with alcoholic cirrhosis.

Because the liver is of considerable importance in metabolism of thyroid hormones, plasma levels of thyroxine (T4), triiodotyronine (T3) with their unbound fractions (FT4 and FT3), reverse T3 (rT3)--an inactive isomer of T3-tyrotropin (TSH) and TSH response to thyrotropin releasing hormone (TRH; 250 micrograms i.V.) were determined by radioimmunoassays in 50 clinically euthyroid patients with alcoholic cirrhosis. T4 mean concentration (7.3 micrograms/dl) did not differ from normal values but T3 was decreased (101 vs 154 ng/dl; p less than 0.001) and was correlated with the degree of liver damage appreciated by a clinico-biological index. FT4 was elevated in patients (17.1 vs 13.1 pg/ml; p less than 0.02) although FT3 was slightly decreased (3.4 vs 4.5 pg/ml; p less than 0.10) with an increased FT4: FT3 ratio (7.0 vs 3.0; p less than 0.02). rT3 was elevated (592 vs 206 ng/100 ml; p less than 0.001) and correlated with FT4/FT3: rT3/T3 ratio (p less than 0.01) and with the severity of the cirrhosis. Basal TSH levels (3.3 microU/ml) and TSH responsiveness to TRH was normal though very scattered, and independant from T3 and T4 values. It may be concluded that: 1. euthyroidy in cirrhosis assessed by a normal responsiveness to TRH, results from a compensatory increase in FT4. 2. The low T3 and FT3 levels may proceed from an impairment of peripheral T4 in to T3 conversion with a deviation pathway towards rT3. 3. T3 and rT3 levels provide valuable index of the severity of the cirrhosis.     

Chronic administration of amiodarone and thyroid function: a follow-up study

In order to evaluate the effects of amiodarone on thyroid function in chronically treated patients, 43 consecutive patients, who had been taking a mean weekly dose of 1420 +/- 488 mg for more than 9 months (mean 16.5 months), were studied. In a first evaluation, three patients with hypothyroidism and two with hyperthyroidism were discovered. In the remaining 38 patients, mean T4 (131 +/- 38 nmol/L) and rT3 (0.85 +/- 0.3 nmol/L) levels were significantly higher than reference values (p less than 0.05 and p less than 0.001, respectively), and mean T3 levels (1.89 +/- 0.73 nmol/L) were significantly lower (p less than 0.001). Thirteen patients showed hyperresponsiveness to thyrotropin-releasing hormone (TRH) stimulation testing. In a second evaluation, performed 12 to 18 months later, two new cases of hypothyroidism were discovered. T3 levels showed significantly lower values (p less than 0.02) than in the first evaluation, whereas basal thyroid-stimulating hormone levels and levels 30 and 60 minutes after TRH stimulation were significantly higher than those in the first evaluation (p less than 0.001). Five new hyperresponders to TRH were found. In the present series, the progressive appearance of clinical thyroid dysfunction with an elevated total incidence (16%) is demonstrated. Moreover, a progressively high prevalence of hyperresponsiveness to TRH stimulation is shown. These findings indicate that chronic amiodarone administration may carry a high risk of thyroid dysfunction.     

The effect of iodide on serum thyroid hormone levels in normal persons, in hyperthyroid patients, and in hypothyroid patients on thyroxine replacement.

OBJECTIVE: To clarify the duration and the extent of the antithyroid effect of iodides in hyperthyroidism, and to investigate whether iodides have an additional peripheral effect on the metabolism of thyroid hormones, as has been reported for some organic iodine compounds. DESIGN: The effect on the peripheral thyroid hormone levels of 150 mg of potassium iodide daily (equivalent to 114 mg of iodide) for 3-7 weeks was compared in 21 hyperthyroid patients and 12 healthy controls. A possible effect of iodide on the peripheral metabolism of thyroid hormones was investigated by assessing the serum levels of thyroid hormone in 12 hypothyroid patients on thyroxine replacement for 2 weeks. PATIENTS: There were 21 thyrotoxic patients, 12 healthy hospital controls, and 12 patients with complete or near-complete hypothyroidism, on thyroxine replacement. MEASUREMENTS: The following were measured before and at weekly intervals after iodide administration: (1) pulse rate, (2) serum T4, (3) serum T3, (4) serum TSH, (5) serum thyroxine-binding capacity (TBC), (6) serum rT3, (7) serum thyroxine-binding globulin (TBG), (8) the free-T4 Index, calculated as T4/TBC. RESULTS: In the hyperthyroid patients serum T4, T3 and rT3 decreased, whereas serum thyroxine-binding globulin and thyroxine binding capacity increased. Serum T3, however, did not become completely normal in all cases. After 21 days, serum T4 and T3 started increasing again in some cases, but other patients remained euthyroid even after 6 weeks. In the normal controls there was a small but significant and consistent decrease in serum T4, T3 and rT3 and an increase in serum TSH. Finally, in the T4-treated hypothyroid patients there was no consistent change, except for an increase of serum T4 at 1 and 14 days and a decrease of serum TSH the first day. CONCLUSION: Iodides in hyperthyroidism have a variable and unpredictable intensity and duration of antithyroid effect. Their antithyroid effect is smaller in normal controls. They have no important effect on the peripheral metabolism of thyroid hormones.     

Thyroid hormone indices during illness in six hypothyroid subjects rendered euthyroid with levothyroxine therapy.

PURPOSE: We wanted to evaluate changes in the natural course of serum thyroxine (T4), tri-iodothyronine (T3), reverse tri-iodothyronine (rT3), and thyroid stimulating hormone (TSH) concentrations during hospitalization for an acute illness, in subjects rendered euthyroid with Levothyroxine (LT4) replacement therapy. METHODS: Six male subjects ranging in age 30 - 65 years with a history of primary hypothyroidism were included. They were euthyroid prior to hospitalization. LT4 continued to be administered orally in the same pre-admission daily dose. Serum, T4, T3, rT3, and TSH concentrations were determined on day of admission to the intensive care unit (ICU) for an acute illness. These were repeated during the first week on alternate days and again during a follow-up visit 1 week after discharge. Student's t-test, analysis of variance, and linear regression were used to analyze the data. RESULTS: Serum T4, T3 declined to a nadir and serum rT3 rose to its peak by day 3 of hospitalization before returning to pre admission euthyroid levels. Serum TSH declined initially but rose to supernormal levels on day 7 before normalization. Significant correlations were noted between TSH on one hand and T3/T4 (r = 0.76, p < 0.001) and rT3/T4 (r= - 0.64, p < 0.001) ratios. CONCLUSIONS: Alterations ensuing during a short stay in the hospital due to an acute illness in subjects with primary hypothyroidism rendered euthyroid with appropriate replacement therapy with Levothyroxine (LT4) are almost identical to those in normal subjects. These changes are probably secondary to altered thyroid hormone metabolism. The altered levels of thyroid hormones and TSH noted in these subjects are transient and therefore providers should refrain from initiating frequent changes in daily LT4 replacement dose during the acute illness in these subjects.     

Nuclear 3,5,3'-triiodothyronine receptors in circulating human lymphocytes in normal, hyper-and hypothyroid subjects

The relationship between nuclear receptors and thyroid function state has not been elucidated. We have determined the circulating lymphocyte nuclear T3R in normal subjects, in patients with hyper-and hypothyroidism and in hypothyroid patients on thyroid hormone substitution treatment, with 10 cases in each group. In hyperthyroid and hypothyroid patients, the nuclear affinity (Kd) for T3 was similar to that of normal subjects. In hyperthyroidism nuclear T3 MBC was unaltered, whereas in hypothyroidism the MBC was significantly increased to 8.06 +/- 0.80 fmol/micrograms DNA, being 2.1 times that of the control group. In hypothyroid patients treated with 90-120 mg desiccated thyroid extract daily the nuclear MBC was 4.34 +/- 0.72 fmol/micrograms DNA, being not different from that observed in euthyroid subjects. It was found that the nuclear T3 MBC was negatively correlated with serum levels of T3, T4, FT3, FT4 and rT3, but positively correlated with serum TSH concentration in hypothyroid patients. These results indicate hormonal modulation of the nuclear T3R which exhibits up regulation in hypothyroidism. The increase in nuclear T3R number might reflect a compensatory mechanism to the decreased serum concentrations of thyroid hormones.     

The spectrum of thyroid disorders in systemic lupus erythematosus

To study the spectrum of thyroid disorders in systemic lupus erythematosus (SLE). Hundred SLE patients as per American Rheumatology Association(ARA) classification criteria underwent clinical examination, including assessment of disease activity (SLEDAI) and laboratory evaluation for serum triiodothyronine (T3),free thyroxine (FT4), thyroid stimulating hormone (TSH), antithyroperoxidase (TPO) antibody and antithyroglobulin (TG) antibody. Hundred age- and sex-matched apparently healthy individuals served as control. Thirty-six (36%) lupus patients had thyroid dysfunction when compared to 8 (8%) of controls and all of them were women. Primary hypothyroidism was the commonest dysfunction in 14 (14%), while subclinical hypothyroidism and subclinical hyperthyroidism was seen in 12 (12%) and 2 (2%), respectively. Eight (8%) had isolated low T3 consistent with sick euthyroid syndrome. Eighteen (50%) of thyroid dysfunction were autoimmune in nature (autoantibody positive) and rest 18 (50%) were non-autoimmune. Euthyroid state with the elevation of antibodies alone was seen in 12 (12%) of the lupus patients. In contrast, only 5 (5%) of controls had primary hypothyroidism and 3 (3%) had subclinical hypothyroidism, while none had hyperthyroidism. SLEDAI score and disease duration were compared between lupus patients with thyroid dysfunction to those with normal thyroid function. A statistically significant association was found between SLEDAI and thyroid dysfunction of sick euthyroid type.SLE disease duration had no statistically significant association with thyroid dysfunction. Prevalence of thyroid autoantibodies in lupus patients was 30% when compared to 10% of controls. Ninety-six (96%) of the SLE patients were ANA positive, while 4 (4%) of them were ANA negative but were anti-Sm antibody positive. There were no suggestions of any other autoimmune endocrine diseases like diabetes or Addison’s disease (clinically and on baseline investigations) in our lupus cohort and hence no further work up was done for these diseases. Thyroid disorders are frequent in SLE and are multifactorial with a definite higher prevalence of hypothyroidism as well as thyroid autoantibodies.     

老年人血管性痴呆与甲状腺轴功能关系的研究

目的　探讨老年人血管性痴呆（VD）与甲状腺轴功能的关系。　方法　采用放射免疫分析法检测31例VD患者、22例不伴有痴呆的脑血管病（CVD）患者及22例同龄对照的血清三碘甲状腺原氨酸（T     

Studies on thyroid hormone autoantibody in two euthyroid cases with spuriously high value of serum free triiodothyronine]

Spuriously high value of serum free triiodothyronine (FT3: Amerlex free T3 kit, Amersham, UK.) was noted accidentally on routine laboratory examination of two clinically euthyroid patients (case 1: FT3; 18.5 pg/ml, FT4; 1.1 ng/dl, T3; 103 ng/dl, T4; 8.2 micrograms/dl, TSH; 1.74 microU/ml, case 2: FT3; 8.5 pg/ml, FT4; 1.1 ng/dl, T3; 137 ng/dl, T4; 8.9 micrograms/dl, TSH; 1.45 microU/ml), the former with poorly controlled diabetes (FBG 253 mg/dl, HbA1c 12.1%) and the latter with essential hypertension (184/108 mmHg). Although the hypertensive patient showed mild diffuse goiter, there was no evidence that the patients had autoimmune thyroid diseases because anti-thyroglobulin antibody tests measured by radioimmunoassay and MCHA, TGHA or TBII were all negative. Their serum levels of TBG were within the normal range. Further studies revealed that both patients' sera had unusual binding activity to labelled polyaminocarboxy T3 (125I-aT3) but not labelled T3 (125I-T3). Furthermore, this binding protein was precipitated by goat anti-human immunoglobulin G (IgG). The IgG purified from both patients' sera also showed strong binding activity to 125I-aT3, which was inhibited by unlabelled T3 in a dose dependent manner. In conclusion, we found anti-T3 antibody in two clinically euthyroid patients with no apparent evidence of complicating autoimmune thyroid diseases. The stronger binding activity to polyaminocarboxy T3 rather than T3 may lead to the spuriously high value of serum FT3. The mechanisms of the production of such autoantibodies in our cases should be further investigated.     

Relation of serum reverse T3 to amiodarone antiarrhythmic efficacy and toxicity

The relation of serum reverse T3 (rT3) to amiodarone efficacy and toxicity was studied in 31 patients with frequent and complex ventricular arrhythmias. Baseline studies included 48-hour Holter recordings and rT3 levels (normal 33 ng/dl or less). Amiodarone therapy was initiated with a 5 mg/kg infusion followed by 600 to 800 mg/day for 7 to 10 days, then 200 to 400 mg/day. Holters and rT3 levels were repeated every 1 to 3 months and amiodarone was titrated to achieve at least a 70% reduction in total ventricular premature complexes, at least a 90% reduction in couplets and abolition of ventricular tachycardia. The baseline rT3 level was 18 +/- 7 ng/dl (range 10 to 30) and patients were followed 12 +/- 9 months. Arrhythmia control was achieved in 25 patients (81%), including 21 patients with elevated rT3 levels (36 to 105 ng/dl) and 4 patients with normal rT3 (15 to 33 ng/dl). Six patients were uncontrolled with rT3 (27 to 90 ng/dl) and 14 patients had minor side effects with rT3 (27 to 123 ng/dl). Three of 4 patients in whom rT3 levels exceeded 130 ng/dl died suddenly (137 to 174 ng/dl before the event). Thus, amiodarone efficacy and minor toxicity occurs at rT3 levels less than 105 ng/dl and sudden death may be associated with levels greater than 130 ng/dl.     

Effect of thyroid hormones on the prolactin response to thyrotropin-releasing hormone in normal persons and euthyroid goitrous patients.

In nine euthyroid goitrous patients, increasing doses of T4 caused a significant decrease in the PRL response to TRH; the PRL response fell significantly at a dose of T4 of 100 micrograms/day for 1 month (P less than 0.02) and fell further with increasing doses so that at 300 micrograms T4/day, the PRL response was 40% of that in the untreated state. T4 treatment also blunted the PRL response to chlorpromazine (P less than 0.05) in a separate group of euthyroid goitrous patients. In contrast, there was only a small drop of the PRL response to TRH in normal subjects treated with T4 (n = 9) and none at all with T3 (n = 7). These data, together with previously published reports, suggest that thyroid hormone may affect PRL secretion in the presence of thyroid disease (hyperthyroidism, hypothyroidism, or euthyroid goiter), but that physiological amounts of thyroid hormone have little or no modulating effect on PRL secretion in normal persons.     

重组人生长激素治疗对生长激素缺乏症患者甲状腺功能的影响

为探讨生长激素治疗对甲状腺功能的影响及其机制，给１９例特发性生长激素缺乏症患者每日皮下注射重组人生长激素（ｒｈＧＨ）Ｇｅｎｏｔｒｏｐｉｎ０．１ＩＵ／ｋｇ体重，治疗１年，观察治疗前后甲状腺功能及血促甲状腺激素（ＴＳＨ）对静脉推注促甲状腺素释放激素（ＴＲＨ）的反应。经Ｇｅｎｏｔｒｏｐｉｎ治疗后，患者血清Ｔ４及ＦＴ４水平较治疗前明显下降（Ｐ＜０．０１）；治疗半年后，血清ＦＴ３水平亦较治疗前下降（Ｐ＜０．０５）；而血清Ｔ３、３，３′，５′－三碘甲状腺原氨酸及ＴＳＨ水平无明显变化（０．２＜Ｐ＜０．３）。治疗１年后，８例患者血清ＦＴ４水平降至正常范围以下，依此将患者分为治疗后甲状腺功能正常组及降低组，结果证实甲状腺功能降低组在治疗前或治疗后ＴＳＨ对ＴＲＨ兴奋的反应均较甲状腺功能正常组高（Ｐ＜０．０５）。血清ＴＳＨ对ＴＲＨ的反应增强提示患者治疗前就已有潜在的ＴＲＨ缺乏，后者可能是ｒｈＧＨ治疗过程中ＦＴ４及Ｔ４水平下降的潜在基础。因此在ｒｈＧＨ治疗过程中需监测特发性生长激素缺乏症患者的甲状腺功能，以及时给予替代治疗。     

Thyroxine and 3,5,3'-triiodothyronine content of thyroglobulin in thyroid needle aspirates in hyperthyroidism and hypothyroidism

Thyroglobulin (Tg) was obtained by fine needle aspiration from patients with untreated hyperthyroidism due to Graves' disease and untreated hypothyroidism to determine whether alterations in its T4 and T3 content could account for the disproportionately high serum T3 compared to serum T4 found in both diseases. For comparison aspiration was performed from normal thyroid tissue in euthyroid patients operated for solitary thyroid lesions. The average amounts of Tg aspirated were: normal 177 +/- 52 (SE) micrograms, n = 7, hyperthyroidism 82 +/- 32 micrograms (n = 8); hypothyroidism 4.6 +/- 1.9 micrograms, n = 9. The iodothyronine content of Tg was, normal, T4 3.7 +/- 0.5 mol/mol, T3 0.28 +/- 0.04 mol/mol, T4/T3 13.7 +/- 1.4; hyperthyroidism, T4 3.8 +/- 1.0, T3 0.59 +/- 0.15, T4/T3 6.8 +/- 1.1; hypothyroidism, T4 3.3 +/- 0.5, T3 0.54 +/- 0.09, T4/T3 6.8 +/- 0.7. The iodine content of Tg was 28 +/- 3.1 atoms/mol in the euthyroid subjects and 31 +/- 7.3 atoms/mol in hyperthyroid patients. Hence, both untreated hyperthyroidism and untreated hypothyroidism were characterized by Tg with a normal T4 but a relatively high T3 content. This is probably related to the prolonged hyperstimulation of functioning follicular cells present in both diseases. The relatively high T3 content of Tg could not alone explain the relatively high T3 production compared to T4 production in these two thyroid diseases.