Radioiodine therapy in Graves disease.
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Antithyroid Agents↗
Biomedical subjects
J M Tibaldi
Publications and source records attributed to J M Tibaldi.
Postprandial hypoglycemia in islet beta cell hyperplasia with adenomatosis of the pancreas.
Organic hyperinsulinism causing hypoglycemia in adults is caused by insulinoma, islet hyperplasia, or a combination of adenomata and hyperplasia. We present a patient with long-standing symptoms of postprandial hypoglycemia occurring within 15 minutes of meals in the absence of fasting hypoglycemic symptoms. An intravenous glucagon stimulation test resulted in a rise of plasma insulin from 194 to 21,883 pmol/L at 7.5 minutes. Blood glucose simultaneously rose from 4.9 to 5.9 mmol/L. A glucose tolerance test revealed an exuberant insulin response. A euglycemic hyperinsulinemic clamp demonstrated incomplete suppression of plasma C-peptide. At surgery, three nodules were found and a 50-60% distal pancreatectomy was performed. The pancreas revealed a combination of multiple beta-cell islet adenomata and islet hyperplasia with no evidence of nesidioblastosis. The coexistence of islet adenomata with hyperplasia must be considered in the differential diagnosis of postprandial hypoglycemia.
Adenoma↗
Diabetic ketoacidosis and insulin resistance with subcutaneous terbutaline infusion: a case report.
Diabetic ketoacidosis may occur in women treated with intravenous beta-sympathomimetic agents for tocolysis. We describe diabetic ketoacidosis and transient severe insulin resistance in a woman with diabetes who was treated with subcutaneous terbutaline infusion. Subcutaneous terbutaline infusion may precipitate transient insulin resistance and diabetic ketoacidosis in women with diabetes.
Adult↗
Thyrotoxicosis in the very old.
The records of 25 patients older than 75 years of age with the diagnosis of hyperthyroidism were reviewed. The mean age of the group (22 women and three men) was 81.5 years, the eldest being 95 years old. Twenty-one patients had Graves' disease, three had multinodular goiter, and one had toxic adenoma. Major presenting symptoms included weight loss (44 percent), palpitations (36 percent), and weakness (32 percent). The average number of thyrotoxic symptoms was only two per patient. Two patients were asymptomatic. Clinical signs included fine skin (40 percent), tremor (36 percent), atrial fibrillation (32 percent), and tachycardia (28 percent). The thyroid was palpable in only three patients with Graves' disease. Mean blood thyroxine level was 15.6 micrograms/dl (range, 11.5 to 24); blood triiodothyronine level was elevated in only half of the patients. One patient had triiodothyronine toxicosis. Mean 24-hour radioiodine uptake was 52 percent. Five patients had normal uptake. No correlation could be established between age, clinical symptoms, signs, and hormone blood levels. Because signs and symptoms of hyperthyroidism in the very old may be too subtle for clinical diagnosis, all elderly subjects should have periodic screening of blood thyroxine levels.
Aged↗
Thyroiditis mimicked by metastatic carcinoma to the thyroid.
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Adult↗
Effects of nonthyroidal illness on thyroid function.
Despite the absence of thyroid disease, patients with nonthyroidal illness frequently have changes in serum thyroid hormone measurements that may suggest either hypothyroidism or hyperthyroidism. Serum T3 levels are frequently decreased mainly because of a decrease in the rate of T3 production from T4. The free T3 concentration may be either normal or reduced as well. The binding of T4 and T3 by the serum-binding proteins is almost always impaired, resulting in an increase in the dialyzable fraction (free) fraction. This is due to a decrease in the concentration of thyroxine-binding proteins and the presence of circulating inhibitors of binding. If serum T4 concentration remains within the normal range, the free T4 concentration can be increased. However, serum T4 is frequently decreased in patients with chronic and/or severe illness. The decrease in serum T4 in these patients, combined with an increase in the dialyzable fraction, results in normal free T4. In patients who are critically ill, none of the available methods for measurement of free T4 may give results that accurately reflect the euthyroid state. Since T3 is the major active thyroid hormone, it is surprising that patients with decreased serum T3 do not appear hypothyroid. The decrease in serum T3 is probably an adaptive change to nonthyroidal illness, which at least enables the sick patient to conserve protein. The clinical impression of euthyroidism is supported by the finding of a normal serum TSH level in most patients. Although TSH regulation may not be entirely normal in patients with nonthyroidal disease, it is likely that serum TSH will be increased in most sick patients who also have significant thyroid failure. The normal clinical findings in patients with decreased serum T3 may result from an augmentation of those biologic responses associated with the clinical manifestations of the euthyroid state. Several animal models of nonthyroidal disease or starvation show that cells have the ability to modulate some biologic responses to thyroid hormone. Further study should elucidate the mechanisms underlying these changes. This article has emphasized that no single laboratory measurement may reliably predict the thyroid state in patients with nonthyroidal disease. This fact emphasizes the need for careful clinical evaluation of these patients and judicious use of laboratory tests. Because the changes in thyroid hormone metabolism that occur in nonthyroidal disease probably represent adaptive changes to the illness, treatment with L-thyroxine to restore serum thyroid concentrations to the normal range is not indicated.
Blood Proteins↗
Animal models of nonthyroidal disease.
Rats bearing transplantable Walker 256 carcinoma provide an opportunity to assess thyroid function and activity during an interval of time when the tumor has not affected growth rate. Rats with tumor have decreased serum T4 and T3 concentration and decreased serum FT4 and FT3 as well. These changes are due to a decrease in binding of iodothyronines by the serum binding proteins, an increase in the fractional rate of T4 metabolism and a decrease in thyroidal secretion. The decrease in activity of the thyroid gland appears to be due to reduced sensitivity of the thyroid to circulating TSH. Despite decreased serum FT4 and FT3 concentrations, serum TSH remains normal, not increased as would be anticipated in a hypothyroidal animal. Nevertheless, a further experimental decrease in serum T4 and/ or T3 from the already reduced serum iodothyronine levels of the tumor bearing rat results in a normal increment in serum TSH. Thus, TSH secretion appears to be regulated normally despite decreased concentrations of pituitary nuclear T3. This finding suggests that tumor bearing rats have greater than normal sensitivity to T3 in their regulation of TSH secretion. Rats with Walker 256 carcinoma have decreased concentrations of hepatic nuclear T3 receptors and a decrease in T3 specifically bound to the receptors. The fractional occupancy of hepatic nuclear receptors appears relatively normal. The dose-response of alpha-GPD in relation to fractional nuclear T3 receptor occupancy appears shifted up and to the left in tumor bearing rats, whereas the curve for ME is shifted down to the right. The appearance rates of these enzymes are described by similar functions. These findings suggest that postreceptor factors in tumor bearing rats may result in augmentation of some and depression of other biologic responses to thyroid hormones. If the results of these studies are extended to sick patients, they may provide a possible mechanism whereby patients maintain the euthyroid clinical state despite a decrease in serum T3. Thus, postreceptor factors may enhance those thyroidal responses which characterize the euthyroid clinical state. Moreover, attenuation of other thyroidal responses related to conservation of protein may provide a distinct adaptive advantage to the patient with nonthyroidal illness with or without decreased food consumption.
Animals↗
Response of hepatic mitochondrial alpha-glycerophosphate dehydrogenase and malic enzyme to constant infusions of L-triiodothyronine in rats bearing the Walker 256 carcinoma. Evidence for divergent postreceptor regulation of the thyroid hormone response.
To characterize the hepatic response to L-triiodothyronine (T3) in an experimental nonthyroidal disease, we determined the activity of hepatic mitochondrial alpha-glycerophosphate dehydrogenase (alpha-GPD) and cytosol malic enzyme (ME) as a function of the saturation of the nuclear T3 receptor during constant T3 infusions in rats bearing the Walker 256 carcinoma. Groups of control and tumor-bearing rats were infused by minipumps (Alza Corp., Palo Alto, CA) with vehicle, 1.2 or 4.5 micrograms T3/100 body wt per day for 3 d. The range for serum T3 was 47.2 +/- 4.1 to 165 +/- 17.3 ng/dl for the control rats and 13.2 +/- 1.3 to 135 +/- 14.3 ng/dl for the tumor-bearing rats. Nuclear T3 receptor concentration was between 0.41 +/- 0.06 and 0.47 +/- 0.02 ng/mg DNA in control rats and was decreased in tumor-bearing rats to between 0.23 +/- 0.03 and 0.26 +/- 0.03 ng/mg DNA. Nuclear T3 receptor concentrations were not influenced by the T3 infusions. Specifically bound nuclear T3, determined by radioimmunoassay of extracts of isolated nuclei, was decreased nearly 50% in the tumor-bearing rats. However, the calculated percentage saturation of the T3 nuclear receptor remained similar in control and tumor-bearing rats at each level of T3 infusion. Dose-response curves for alpha-GPD and ME were curvilinear and showed an exponential increase in enzyme activity with progressive receptor saturation. In tumor-bearing rats, the activity curves or calculated appearance rate curves for alpha-GPD were shifted significantly upward and to the left, indicating greater sensitivity to T3, and those of ME were shifted downward and to the right, indicating decreased responsiveness to T3. Our findings suggest that cellular factors result in postreceptor amplification of the alpha-GPD response and diminution of the ME response to T3 in tumor-bearing rats. Augmentation of the alpha-GPD response may be a prototype for other hormonal responses that enable the tumor-bearing rat to maintain an apparent euthyroid state in association with decreased serum T3.
Animals↗