Thyroidology最新文献

A patient with amiodarone-induced thyrotoxicosis and autonomous nodule was treated with percutaneous ethanol injection (PEI) in 8 sessions. Preinjection thyroid hormone levels showed a marked elevation, peaking before the third session. The thyroid hormone increments following each procedure never exceeded 20% of the preinjection levels. FT4 plasma levels thereafter declined to within the normal range by the sixth session (day 21), while FT3 levels, though markedly reduced, were still slightly elevated; also, the thyroid hormone increments following ethanol injection were not observed after the fifth session. These findings suggest that a significant, but not sustained, increase in thyroid hormone levels is induced by PEI and may account for the lack of acute deterioration of clinical status, which remained under control with medical treatment alone. Normal serum thyroid hormone levels were observed at the 3 and 12 month follow-up. The use of percutaneous ethanol injection therapy for amiodarone-induced hyperthyroidism should be restricted to patients with preexisting thyroid hyperfunctioning nodule, and it may be a practical alternative to surgery in addition to medical treatment. Special caution should be exercised with patients with severe underlying heart disorders, since their clinical status might seriously worsen in case of acute elevations of serum thyroid hormones following ethanol injection. To this purpose, a close monitoring of serum thyroid hormones is recommended in order to institute a prompt adjustment in their medical therapy and/or in their PEI protocol.

Thyroid hormones and the GH/IGF-1 system show considerable mutual interference which may have physiological, pathophysiological and clinical importance. GH therapy of children and adults may induce a fall in serum T4, which seems to be due to an effect on the deiodination of T4 to T3. Animal studies suggest that the alterations in thyroid hormones in tissue may be much more prominent than the changes observed in serum. It is possible that the GH deficiency seen in the majority of patients with pituitary/hypothalamic disorders may mask secondary hypothyroidism in some patients by giving a relatively high serum T4. GH therapy may then unmask the hypothyroidism. In accordance with such a mechanism GH deficient children evaluated thoroughly to exclude secondary thyroid failure before GH administration do not develop thyroid insufficiency during GH substitution therapy. It is suggested that thyroid insufficiency should be considered in GH deficient patients with low normal serum T4.

Radioiodine therapy has become a cornerstone of treatment of hyperthyroidism. However, the timing of its administration varies between 1) the time of initial diagnosis with concurrent therapy with beta adrenergic blocking drugs or 2) following induction of euthyroidism with thioamide, Propylthiouracil or Methimazole. This study assessed 24-HR 131I uptake values and the thyroid scan in 24 subjects with hyperthyroidism at the time of diagnosis and again after attaining the euthyroid state with Propylthiouracil or Methimazole. Propylthiouracil of Methimazole was withdrawn seven days prior to the second 24-HR 131I uptake and scan. In all subjects, as a group, 24-HR 131I uptake increased following antithyroid therapy as compared to the time of initial of diagnosis [76 + 5% Vs. 54 + 4%; p < 0.01]. The thyroid gland size decreased in nine of twenty-four subjects, but remained unchanged in the remaining subjects. Since 24-HR 131I uptake and the gland size are the major factors influencing the therapeutic radioiodine dosage, it is possible that initial therapy with thioamide drugs may reduce the therapeutic dose of 131I in subjects with hyperthyroidism belonging to both groups, i.e., Graves' disease and Multinodular toxic goiter by inducing a rise in 24-HR 131I uptake. Furthermore, the shrinkage of thyroid glands may further decrease the radioiodine dosage in patients with Graves' disease.

We measured serum concentrations of apolipoproteins (apo A-I, A-II, B, C-II, C-III and E) in patients with thyroid disease (hyperthyroidism; n = 44, hypothyroidism; n = 15) and in normal subjects (n = 89). We found that apoA-II, B and C-III concentrations revealed significant difference among three groups of the normal (apoA-II; 31.4 +/- 4.9 mg/dl, apoB; 85.8 +/- 16.3 mg/dl, apoCIII; 7.45 +/- 2.99 mg/dl), hyperthyroidism (apoA-II; 29.8 +/- 5.4, apoB; 63.4 +/- 18.9, apoC-III; 6.28 +/- 2.45) and hypothyroidism (apoA-II; 27.5 +/- 5.3, apoB; 108.0 +/- 30.9, apoC-III; 9.43 +/- 2.74). Thyroid hormones showed clear negative correlation to apoB (r = 0.70, p < 0.001). Furthermore, apoC-III was also found to be negatively correlated with thyroid hormone concentrations (r = 0.47, p < 0.001).

The goal of our present study has been to examine the effects of the atrial natriuretic factor (ANF) on the growth processes in rat thyroid lobes. In the initial in vitro experiment, thyroid lobes were preincubated with rat ANF (Sigma) for 30 min in RPMI 1640 medium with 3H-thymidine (2 microCi/ml), and later on 15% fetal calf serum (FCS), Hepes buffer and the remaining tested substances [TSH 20 mIU/ml, somatostatin (SS) 10(-7)M] were added. Preincubations with ANF were not conducted in the controls and in the group exposed to TSH alone. Incubations of all the examined groups (controls, TSH alone, ANF alone, ANF together with TSH or ANF together with SS) with 3H-thymidine were carried out for 4 hours. We obtained the following results: at none of the examined concentrations (10(-5)M, 10(-7)M, 10(-9)M), did ANF significantly affect the rate of 3H-thymidine incorporation in vitro. Neither did TSH alone nor ANF with TSH jointly significantly influence the process in question. However, we observed increased rates of the 3H-thymidine uptake, following the joint exposure of thyroid lobes to ANF (10(-7)M or 10(-9)M) and SS (10(-7)M), when compared to ANF alone. In the ex vivo in vitro experiment, direct intrathyroidal microinjections of ANF alone or jointly with TSH or SS, were carried out. Twenty four (24) hours after the microinjections, all the animals were sacrificed by decapitation, the thyroid lobes being collected and incubated for 4 hours with 3H-thymidine (2 microCi/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Ground glass nuclei are an important finding in the diagnosis of papillary carcinoma of the thyroid. However, they appear only in specimens in paraffin-embedded histological sections, and not in frozen sections or cytological specimens. This has led to the conclusion that they are an artifact of fixation and/or embedding. However, if this is the case, a question arises as to whether or not such an artifact can be of value as a definitive sign for establishing a diagnosis of papillary carcinoma. This study was undertaken to try to answer that question. 1) To confirm whether or not the author's microscopic observations were correct, we carried out automatic imaging analysis with the Interaktives Bild-Analysen System (IBAS). The author's microscopic observations were consistent with the data obtained by the IBAS. 2) Among 20 cases of papillary carcinoma, clear nuclei were observed in 11 cases (55%), and pseudoclear nuclei were noted in 20 cases (100%). When 1,000 papillary cancer cells were counted in 10 cases, the average incidences of clear nuclei and pseudoclear nuclei were found to be 0.51% and 18.3% respectively. Clear nuclei were seen in papillary carcinomas in all kinds of fixatives except one but were not seen in benign lesions. Even though ground glass nuclei are a type of artifact, we believe that their presence may be considered to be a characteristic feature of papillary carcinomas of the thyroid.

Papillary carcinoma of the thyroid occurring within a hyperfunctioning nodule is an extremely rare disorder. A case in a woman is reported. We believe that diagnostic and therapeutic procedures to be used in the case of a hot thyroid nodule must take this possible occurrence into account.

Thirty Tunisian patients with a voluminous multinodular goiter with cold nodules and inhabiting a region of mild iodine deficiency, have been studied. The 131 I fixation by the thyroid, three hours after ingestion was significatively higher than in normal population. Fourty six per cent of the patients have stable iodine urine contents less or equal to 0.39 mumol/L. Three serum concentrations were paradoxically abnormal: thyrotropin (TSH), thyroglobulin (TG) and gammaglobulin concentrations. Fourty seven per cent of the serum thyrotropin (TSH) levels were less than the normal values though the serum total triiodotyronine (TT3), tetraiodotyronine (TT4), free triiodotyronine (FT3), free tetraiodotyronine (FT4), antithyroglobulin antibodies, total protein, triglycerides and cholesterol concentrations were normal. Serum thyroglobulin (TG) rates were elevated, ranged from 2 to 10,180 ng/ml and twenty five per cent of our patients showed levels greater than 500 ng/ml. The gammaglobulin levels were greater than normal in sixty eight per cent of our patients though only 10% of our patients manifest antithyroglobulin antibodies.

Study objective: The aim of the study was to determine the incidence of thyroid dysfunction in an iodine sufficient area (Vigo city, Galicia, North-West of Spain).

Design: Case-finding study during a 3-year (1990-1992) period.

Subjects: Subjects from a random sample of the population with abnormal results on FT4, sensitive-TSH or antithyroid autoantibodies.

Measurements: Thyroid size by ultrasound study. FT4 by RIA; TSA Ab by radio receptor assays; TSH, Tg Ab and TMS Ab by IRMA.

Major results: Overall incidence of thyroid dysfunction was 97.96 per 100,000 per year (CI 95% 78.86-117.06); female 162.45, male 17.44. Incidence rate of hyperthyroidism was 52.37 per 100,000 per year (CI 95% 38.41-66.36); 24.24 for Graves' disease, 11.63 for nodular hyperthyroidism, 13.57 for iatrogenic hyperthyroidism and 2.90 for others causes. Incidence rate of hypothyroidism was 45.58 per 100,000 per year (CI 95% 32.55-58.620 27.15 for hypothyroid autoimmune thyroiditis, 8.72 for postoperative hypothyroidism, 4.89 for miscellaneous hypothyroidism, 1.93 for amiodarone induced hypothyroidism and 2.90 for secondary hypothyroidism.

Conclusions: This investigation provides extensive data on incidence of clinical and subclinical thyroid dysfunction and its different forms in an iodine sufficient area.