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Amiodarone is a widely-used anti-arythmic drug that induces an iodine overload and, in 1 to 23% of the patients, a thyrotoxicosis. In a few cases, the thyrotoxicosis may be refractory to conventional pharmacological therapy, thus leading to thyroidectomy. We report the thyroid gland pathology in 5 thyroidectomies that were performed for uncontrolled thyrotoxicosis, induced by amiodarone (4 cases) and by Colchimax, another iodine-rich drug (1 case). Two cases have been studied by electron microscopy. Pathologic findings were: [1] colloid transformation of the parenchyma, [2] areas of follicular disruption with numerous foamy macrophages in the colloid, [3] regenerative areas and [4] a moderate T lymphocytic infiltration. No lysosomal lamellar inclusion body was found by electron microscopy. These lesions may be rather specific of an iodine toxicity. The pathogeny is still misunderstood, and probably complex. It may essentially involve toxic mechanisms, as well as immunologic or allergic mechanisms.
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Although hypo- and hyperthyroid patients have different symptoms in the gastrointestinal tract, the mechanism of thyroid action on the gut remains poorly understood. Thus the aim of this study was to investigate the effect of hypo- and hyperthyroidism on gastric myoelectrical activity, gastric emptying, dyspeptic symptoms. Twenty-two hyperthyroid (median age 45, 15 females) and 11 hypothyroid (median age 42, 10 females) patients were included into the study. Dyspepsia score, hypo- and hyperthyroid symptom scale, abdominal ultrasonography and upper gastrointestinal endoscopy were performed. Gastric myoelectrical activity was measured by electrogastrograpy (EGG) before and after therapy both preprandially and postprandially and compared with age, gender, and body-matched controls (12 for hypothyroid, 15 for hyperthyroid patients). Radionuclide gastric emptying studies were performed with a solid meal. Hypothyroid patients revealed a significant increase in preprandial tachygastria as compared with controls (12.3% vs 4.8%). The percentage of preprandial normal slow waves (2.4-3.7 cpm) was below 70% (dysmotility) in 7 of 11 hypothyroid patients versus 2 of 12 controls (P < 0.05). Hyperthyroid patients revealed a significantly higher preprandial (3.1 vs 2.8) and postprandial (3.4 vs 3) DF when compared with the controls (P < 0.05). A higher percentage of postprandial taschygastria (7.9 vs 0) was present in hyperthyroid patients than in the controls (P < 0.05). The decrease on postprandial EGG power (power ratio < 1) was observed in 7 patients the in hyperthyroid group and 1 in controls (P < 0.05). The percentage of postprandial normal slow waves was below 70% in 10 of 20 hyperthyroid patients vs 1 of 15 controls (P < 0.05). After therapy these differences disappeared in the euthyroid state. The hypo- and hyperthyroid symptom scale correlated to dyspepsia score. Dyspepsia score in hyperthyroidism correlated to power ratios in hyperthyroid patients. We detected some correlations between serum levels of fT3 or fT4 and some EGG parameters in hypo- and hyperthyroidism. Dyspepsia score and hypo- and hyperthyroid symptom scale were improved significantly after therapy in the euthyroid state. In conclusions, we showed gastric dysrhythmia by EGG in both hypo- and hyperthyroid patients. Dyspeptic symptoms correlated to the activity of thyroid disease. After therapy, these findings and dyspeptic symptoms improved in the euthyroid state. Abnormalities of power ratios may be responsible of dyspeptic symptoms in hyperthyroid patients. EGG may be a useful and noninvasive tool for detecting gastric disturbances during hypo- and hyperthyroidism.
OBJECTIVE: Several abnormalities in the GH response to pharmacological stimuli have been described in hyperthyroidism. Both normal and high serum IGF-I levels have been reported, as well as a decrease in IGF-I bioactivity. We have evaluated the GH response to GH-releasing hormone (GHRH) in hyperthyroid patients and the effects of hyperthyroidism on serum IGF-I levels. The possible relations between nutritional status, thyroid hormones and IGF-I levels were also investigated. We also studied the influence of long-term beta-adrenoceptor blockade on the GH response to GHRH in these patients. DESIGN: In 18 hyperthyroid patients and in 12 control subjects, GHRH (100 micrograms) was administered as an i.v. bolus injection. Eight hyperthyroid patients and 8 control subjects received 50 micrograms GHRH i.v. Seven hyperthyroid patients were reevaluated after beta-adrenoceptor blockade. IGF-I and albumin levels were measured initially in all hyperthyroid patients and control subjects. Body composition was determined in 11 hyperthyroid patients and in a group of 33 matched normal controls. PATIENTS: Hyperthyroid patients were compared to control subjects. MEASUREMENTS: GH, TSH and free T4 were measured by immunofluorometric assay. IGF-I, total T3 and total T4 were measured by radioimmunoassay. Body composition was determined using a dual-energy X-ray absorptiometer. RESULTS: The GH response to 100 micrograms GHRH in hyperthyroid patients was blunted compared to control subjects. The mean peak GH levels and the area under the curve were significantly lower in hyperthyroid patients compared to control subjects (11 +/- 1 vs 27 +/- 5 micrograms/l and 820 +/- 113 vs 1879 +/- 355 micrograms/l 120 min, respectively; P < 0.01). IGF-I levels were significantly reduced in hyperthyroid patients compared to controls (131 +/- 10 vs 201 +/- 16 micrograms/l, respectively; P < 0.01). Ideal body weight, serum albumin levels and the lean body mass were also reduced in hyperthyroid patients. After beta-adrenoceptor blockade there were no changes in the blunted GH response to GHRH in hyperthyroid patients. CONCLUSION: Our data suggest that the blunted GH response to GHRH in hyperthyroidism is apparently not related to circulating IGF-I levels. It is possible that nutritional factors could play a role in the reduced circulating IGF-I levels found in these patients.
OBJECTIVE: Hyperthyroidism is associated with altered GH secretion. Whether this is due to changes of somatotroph responsiveness or reflects an alteration in negative feedback signals at the hypothalamic level is unknown. We therefore performed a series of studies to shed some light onto this issue. DESIGN: Study 1: GHRH (1 microgram/kg b.w.) was injected i.v. in 38 hyperthyroid patients and in 30 normal subjects; in 11 of the patients the GHRH test was repeated following methimazole-induced remission of hyperthyroidism. Study 2: hGH (2 U i.v.) or saline were administered 3 hours prior to GHRH; six hyperthyroid patients and six normal subjects were studied. Study 3: ten normal subjects and ten hyperthyroid patients were given 75 g oral glucose or water 30 minutes before GHRH. Study 4: 11 normal subjects and eight hyperthyroid patients were studied. TRH or vehicle were dissolved in 250 ml of saline solution and infused at a rate of 400 micrograms/h for 150 minutes. Thirty minutes after the beginning of the infusions, L-arginine (30 g infused over 45 min i.v.) was administered. PATIENTS: Hyperthyroid patients were compared to normal subjects. MEASUREMENTS: Growth hormone was measured by RIA at 15-minute intervals. RESULTS: GH responses to GHRH were subnormal in hyperthyroid patients. Following antithyroid drug treatment with methimazole, GH responses to GHRH increased in these patients in comparison to pretreatment values. Serum IGF-I levels, which were elevated before treatment, decreased after methimazole administration. Exogenous GH administration induced a clear decrease of GH responses to GHRH in both control and hyperthyroid subjects. On the other hand, oral glucose load decreased the GH responses to GHRH in normal but not in hyperthyroid subjects. TRH administration did not modify the GH responses to arginine in either normal subjects or hyperthyroid patients. CONCLUSIONS: Hyperthyroidism is associated with increased serum IGF-I levels and marked alterations in the neuroregulation of GH secretion. These changes involve decreased GH responsiveness to GHRH at the pituitary level and, at the hypothalamic level, a lack of suppressive effect of an oral glucose load. The normal inhibitory effect of exogenous GH administration but not of an oral glucose load in hyperthyroid patients suggests that these two feedback signals act through different mechanisms. The lack of effect of a TRH infusion on GH responses to L-arginine in normal and hyperthyroid patients makes an inhibitory role for TRH in GH secretion unlikely, at least in Caucasian subjects.
BACKGROUND: Hyperthyroidism is a common disease in the elderly. Although some studies on the prevalence of this thyroid disorder have been performed in the aged population, several aspects of hyperthyroidism, such as etiology and treatment effectiveness, have not been fully characterized in large series of aged patients. OBJECTIVE: The aims of the present study were to determine the frequency of the diverse etiologies of hyperthyroidism, and to assess the effectiveness of therapy in adult patients older than 55 years. METHODS: We performed a descriptive, observational, cross-sectional study in the setting of a hospital endocrinology clinic. We studied a group of 313 patients with hyperthyroidism. There were 246 women (78.6%, age 67.02 +/- 8.35 years) and 67 men (21.4% age 63.34 +/- 7.63 years). Overt hyperthyroidism was diagnosed in 167 patients (53.4%) and subclinical hyperthyroidism in the remaining 146 subjects (46.6%). In every patient we studied: the etiology; presence or absence of goiter; time of evolution from diagnosis; previously and presently used treatments; current thyroid functional status (free thyroxine and thyrotropin concentrations); adequacy of disease control, and thyroid autoimmune status. RESULTS: The different etiologies of hyperthyroidism were as follows: toxic multinodular goiter 43.1%; Graves' disease 21.4%; iatrogenic thyrotoxicosis 16.0%; toxic adenoma 11.8%; iodine-induced thyrotoxicosis 1.2%; subacute thyroiditis 1.0%; painless thyroiditis 0.3%; factitious thyrotoxicosis 0.3%; TSH-secreting pituitary adenoma 0.6%, and unknown etiology 3.8%. Etiology was related to age, sex, presence of goiter, degree of hyperthyroidism and autoimmune status. 77.6% of patients had been diagnosed in the last 5 years, and 91.3% in the last 10 years. Preferred therapies were thionamide drugs in patients with Graves' disease and radioiodine in patients with hyperthyroidism due to nodular disease. Surgery was performed in a limited number of patients. Periodic follow-up was used in patients with subclinical hyperthyroidism. Control of the disease was adequate in 65.3% and inadequate in 34.7% of patients who received any kind of previous therapy. In this group of patients, logistic regression analysis showed that the probability of attaining good control of hyperthyroidism was greater in patients with overt thyrotoxicosis compared to patients with subclinical thyrotoxicosis. CONCLUSION: In patients older than 55 years, toxic multinodular goiter is the most frequent etiology of spontaneous hyperthyroidism, followed by Graves' disease and toxic adenoma. Most patients with thyroid hyperfunction can be adequately controlled, provided that effective therapy is administered. Patients with overt hyperthyroidism seem to have a higher probability of attaining adequate control of their disease than patients with subclinical hyperthyroidism, regardless of age, sex or etiology.
There are many reports of glucose intolerance in adult patients with hyperthyroidism but few reports of glucose intolerance in hyperthyroid children. In this study, we measured plasma levels of glucose, insulin, glucagon and growth hormone in hyperthyroid children and control subjects by the use of three kinds of tolerance tests: an oral glucose tolerance test, an arginine tolerance test and an insulin tolerance test. In the oral glucose tolerance test, mean fasting glucose levels (79.6 +/- 1.4 mg/dl) rose to maximum levels (157.3 +/- 4.3 mg/dl) at 30 min in hyperthyroid children which were significantly higher than the levels in control subjects (p less than 0.01). The maximum levels of glucose fell slowly and returned to fasting levels at 180 min. In this test, plasma insulin levels increased from basal levels (12.7 +/- 1.9 microU/ml) to maximum levels (120.8 +/- 22.1 microU/ml) at 30 min in the prepubertal age group of hyperthyroidism. On the other hand, in the pubertal age group of hyperthyroidism, maximum levels of insulin were observed at 60 min, but not at 30 min. These maximum levels of insulin of both hyperthyroid age groups were significantly higher than those in the control subjects (p less than 0.05, p less than 0.01 respectively). There was no difference in insulin-glucose ratio at 30 min (delta IRI/delta BG) and insulinogenic index (I.I.) at 0 to 60 min between these two groups of hyperthyroid children and control subjects. However, I.I. at 0 to 120 min and 0 to 180 min decreased significantly in the pubertal age group of hyperthyroidism as compared with those in the control group (p less than 0.05, p less than 0.02 respectively). In the oral glucose tolerance test, plasma glucagon levels decreased from basal levels (74.1 +/- 4.3 pg/ml) to minimum levels (36.4 +/- 4.7 pg/ml) at 90 min in hyperthyroidism, which were significantly lower than those in the controls (p less than 0.05). However, there was no difference in -epsilon delta IRG/epsilon delta BG (cumulative glucagon response/cumulative glucose response) between the subjects with hyperthyroidism and the controls. On the other hand, lower responses of blood glucose, insulin, glucagon and growth hormone to arginine were observed in subjects with hyperthyroidism than in the controls. Moreover in the insulin tolerance test, there was no difference in glucagon and growth hormone response between the subjects with hyperthyroidism and the controls. Thus our conclusions are as follows: A marked increase in blood glucose after oral glucose load was observed in spite of normal insulin-glucose ratio in hyperthyroid children, suggesting the existence of peripheral insulin resistance.(ABSTRACT TRUNCATED AT 400 WORDS)