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PubMed1984

Hypermetabolic state and hypoxic liver damage.

The concept of a hypermetabolic state to explain metabolic tolerance to ethanol grew from the recognition that the rate of alcohol metabolism is, in general, limited by the rate at which mitochondria can reoxidize reducing equivalents and thus by the rate at which oxygen can be consumed by the liver. This relationship appears to be most important in conditions in which the alcohol dehydrogenase (ADH)/QO2 ratio is high and is not in conflict with observations suggesting that ADH can, under certain conditions, constitute a rate-determining step for ethanol metabolism in rodents. Liver preparations from animals fed alcohol chronically, in which an increase in ethanol metabolism is shown, consume oxygen at higher rates. This effect, concerning which there is discrepancy among investigators, depends on the type of preparation. Thyroid hormones play a permissive role in the development of the hypermetabolic state, while increased circulating levels of these hormones are not required. Antithyroid drugs inhibit both metabolic tolerance in vivo and the hypermetabolic state. While the hypermetabolic state requires an increased ATP utilization in the form of an adenosine triphosphatase, or an inhibition of ATP synthesis, the different mechanisms proposed for such an effect do not quantitatively account for the increases in oxygen consumption. In humans and animals chronically exposed to ethanol, but withdrawn, oxygen tensions in blood leaving the liver are significantly reduced. In some situations, low oxygen tensions in zone 3 of the hepatic acinus can reach critical hypoxic levels and may lead to cell necrosis. Studies in which the effectiveness of propylthiouracil is tested in human alcoholic hepatitis are discussed.

Adenosine Triphosphate↗

PubMed1984

Commentary on the hypermetabolic state and the role of oxygen in alcohol-induced liver injury.

Centrilobular hypoxia has been postulated as a mechanism for the development of hepatocellular necrosis and fibrosis in alcoholic liver disease. Chronic ethanol ingestion in rodents results in increased hepatic oxygen consumption and in a steeper fall in oxygen tension between the periportal and the pericentral area of the lobule, rendering the pericentral area susceptible to hypoxia. Hepatocellular necrosis occurs when ethanol-fed animals are exposed to low atmospheric oxygen. In man, the existence of a hypermetabolic state is more tenuous, but suggested by an increased rate of ethanol elimination after chronic ethanol consumption that has been linked to increased oxygen consumption in animals. Also, decreases in hepatic blood flow and hepatic vein oxygen tension were found in alcoholics with histological evidence of liver-cell necrosis as compared to those without necrosis. It is postulated that in man, reduction in the availability of oxygen to the liver may be caused by miscellaneous conditions such as anemia, respiratory depression or infection, cigarette-smoking, or reduction of hepatic blood flow, but the contribution of one or more of these factors remains to be proven. Trials of the effect of propylthiouracil (PTU) on alcoholic hepatitis are based on the effect of this drug in decreasing the ethanol-induced hypermetabolic state and in preventing hepatocellular necrosis in animals exposed to low atmospheric oxygen. A tentative conclusion of the two small trials that have been completed is that PTU may be beneficial in moderately ill patients with a low mortality, but not useful in severely ill patients with a high mortality.

Alcohol Dehydrogenase↗

PubMed1996

Thyroid hormone modulates inotropic responses, alpha-adrenoceptor density and catecholamine concentrations in the rat heart.

We investigated the influence of hyper- and hypothyroidism on basal parameters of isolated perfused hearts of rats. In addition the effects of different extracellular calcium concentrations ([Ca2+]o), the calcium entry promoter Bay K8644 and the alpha 1-adrenoceptor agonist methoxamine were investigated. Since alterations in alpha-adrenoceptor density could explain the increased sensitivity to methoxamine in hearts from hypothyroid rats, alpha 1-adrenoceptor density in the left ventricle was also established. Different time-schedules of exposure to hyper- and hypothyroidism were used to investigate whether the influence of chronic dysthyroid states on alpha 1-adrenoceptor density is transient and time-dependent. Simultaneously myocardial noradrenaline and adrenaline tissue concentrations were determined, since they might correlate with the observed changes. Hyperthyroidism was induced by feeding rats for 1, 4 and 8 weeks with 5 mg/kg L-thyroxine (T4)-containing rat chow. Hypothyroid rats were obtained by adding 0.05% propylthiouracil (PTU) to the drinking water during 1, 4 and 8 weeks. For the functional experiments animals were treated during 4 weeks, to mimic the clinical situation of a chronic endocrine disease. Langendorff hearts from hyperthyroid hearts showed an increased maximally developed relaxation velocity, whereas Langendorff hearts from hypothyroid rats showed an increased left ventricular pressure (LVP). We observed an increased maximal inotropic response to [Ca2+]o in hearts from both hyperthyroid and hypothyroid rats, indicating that both dysthyroid states interfere with the handling of calcium ions by the contractile apparatus. Unchanged responses to Bay K8644 in hearts from hyperthyroid and depressed responses in hearts from hypothyroid rats suggest that the involvement of L-type calcium channels is rather unlikely. Furthermore, the reflex increase in coronary flow in response to enhanced contractile force appeared to fail in hearts from hypothyroid rats. Sensitivity of the response to methoxamine was increased in hearts from hypothyroid rats, which was accompanied by a decrease in the number of myocardial alpha 1-adrenoceptors. Both T4 and PTU treatment resulted in a non-transient decrease of alpha 1-adrenoceptor density in left ventricular tissue. Furthermore, hypothyroidism increased the percentage of alpha 1A-binding sites, whereas in hyperthyroidism the distribution of the alpha 1-adrenoceptor subtypes was not affected. Myocardial tissue concentrations of noradrenaline and adrenaline were unchanged in hyperthyroid rats and decreased in hypothyroid rats. The present study indicates that thyroid hormones have a direct rather than a sympathetically mediated effect on alpha 1-adrenoceptor mediated myocardial functions.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

PubMed1986

Three-dimensional aspects of blood vessels in thyroids from normal, low iodine diet-treated, TSH-treated, and PTU-treated rats.

Three-dimensional images of blood vessels in thyroid glands from normal, low iodine diet-treated, thyroid-stimulating hormone (TSH)-treated and propylthiouracil (PTU)-treated rats were investigated by use of the corrosion-cast method. The vascular casts made by the injection of methacrylate resin were observed with the scanning electron microscope. In normal animals, each follicle is surrounded by a clearly defined basket-like capillary network, which is generally independent of adjacent networks, though a few anastomoses or common capillaries are sometimes seen. In low iodine diet-treated or TSH-treated animals, the capillaries in the basket-like network become markedly dilated and fuse with one another. Though the vascular casts of PTU-treated animals are similar to those of low iodine diet-treated or TSH-treated ones in some aspects, most basket-like networks become distorted and irregular in shape, and the capillaries are heterogeneously dilated and show many buds, branches and anastomoses. We consider that these peculiar changes in the thyroid of the PTU-treated animals are due not only to the elevation of serum TSH but also to other unknown factors. It is clear that the distribution and morphology of the thyroid capillaries are extremely affected and changed by functional states of the gland.

Animals↗

PubMed1984

In vivo shedding of apical plasma membrane in the thyroid follicle cells of the mouse.

Clusters of luminal dense bodies, limited by a triple-layered membrane, were found in all follicle lumina in thyroid glands of mice. After thyroxine treatment the number of luminal dense bodies increased, especially in the periphery of the lumen, where the intraluminal bodies often displayed a striking resemblance to microvilli. In hyperplastic goiters, obtained by feeding mice with propylthiouracil, luminal dense bodies were replaced by intraluminal vesicles. During goiter involution the vesicles were gradually replaced by luminal dense bodies; the presence of intermediate forms suggests that vesicles and dense bodies are basically the same formations. Luminal dense bodies were observed in colloid droplets indicating their removal by endocytosis. As demonstrated by electron-microscopic cytochemistry, luminal dense bodies contain a membrane-bound peroxidase, and electron-microscopic autoradiography after administration of 125I indicate that they possess an iodinating capacity. Our observations on mouse thyroid glands suggest that the luminal dense bodies, which appear as vesicles in hyperplastic glands, are formed by shedding of the apical plasma membrane of the follicle cell. The shedding process might be of importance for the turnover of plasma-membrane material.

Animals↗

PubMed1994

Enhancement of seminiferous tubular growth and spermatogenesis in testes of rats recovering from early hypothyroidism: a quantitative study.

Testicular weight and DNA content were markedly reduced (63 and 69%) in weanling Long-Evans rat pups rendered hypothyroid from birth by administration of propylthiouracil (PTU), a reversible goitrogen. These growth deficits worsened to > 80% by continuing hypothyroidism beyond weaning, to days 50 and 90. Recovery of thyroid function, brought about by discontinuing PTU at weaning, resulted in a paradoxical stimulation of testis growth, amounting to increased weight (40%), DNA content (60%) and size by 90 days, compared to age-matched controls. In the 25-day or older hypothyroid rats, testicular structure was immature and spermatogenesis markedly delayed, as evident by closed lumen and significantly reduced diameter of seminiferous tubules (38%), thickness of germinal layer (70%), and number of primary spermatocytes (86%), compared to control. Hypothyroidism did not alter the number of tubules per testis cross section. In the 90-day recovery rats, numbers of seminiferous tubules were unchanged but tubular diameter was significantly (20%) larger than in controls and spermatogenesis appeared very active as indicated by significantly increased germinal layer thickness (22%) and total number and density of primary spermatocytes (55% and 40%). The results show that although postnatal hypothyroidism is deleterious for testicular growth and spermatogenesis, recovery from this condition leads to enhanced seminiferous tubular growth and spermatogenesis.

Animals↗

PubMed1986

Thyroid-stimulating immunoglobulins and thyroid function tests in two siblings with neonatal thyrotoxicosis.

Thyroid function and serum TSI levels in two siblings with neonatal thyrotoxicosis are described. The first infant was treated with exchange transfusion and potassium iodide. The second infant was treated with intrauterine propylthiouracil followed by potassium iodide. In contrast to the first infant, the second infant had no clinical sign of neonatal thyrotoxicosis. He also had lower TSI levels with a biological half-life of 5 days. Only one of three assays showed some TSI activity in breast milk.

Adult↗

PubMed1988

Effect of infection with Spirometra erinacei plerocercoid on thyroid hormone in mice.

Young, male ICR mice were given tap water or distilled water containing 200 mg/l propylthiouracil (PTU) and were then infected with 10 plerocercoids of Spirometra erinacei to investigate the effect of plerocercoid infection on thyroid hormone in their hosts. Plerocercoid infection stimulated growth in PTU-induced hypothyroid mice as if they had never received PTU treatment: there were increases in weight in the liver, skeletal muscle, and spleen, as well as enhancement of the head and body length, in spite of a greater decrease in serum T4 levels than was observed in PTU-treated controls. Furthermore, the intact mice infected with plerocercoids showed a decrease in serum T4 levels as well as in the concentration of T4-binding globulin. These observations suggest that the growth stimulation and the decrease in concentrations of serum T4 and T4-binding globulin associated with plerocercoid infection in mice probably resulted from secretion of a growth hormone-like substance produced by plerocercoids of S. erinacei.

Animals↗

PubMed1984

Oxidations in kidney mitochondria of heat-exposed rats: regulation by cytochrome c.

Exposure of rats to higher environmental temperature (36-37 degrees C) decreased the capacity of their kidney mitochondria to oxidize succinate. The decrease was corrected on the addition of exogenous cytochrome c. Kidney mitochondria of heat-exposed animals showed decreased rates of H2O2 generation when alpha-glycerophosphate, but not succinate, was used as electron donor. These mitochondria also showed decreased activity of alpha-glycerophosphate dehydrogenase but not of succinate dehydrogenase. The content of cytochrome c in kidney mitochondria of heat-exposed animals was low even though the concentration of the pigment in the whole tissue did not decrease. Starvation as well as administration of an antithyroid agent like propylthiouracil simulated some of the effects of heat exposure on kidney mitochondria, but the cytochrome c-dependent reversal of inhibition of oxidation was obtained only in heat exposure.

Animals↗

PubMed1986

Influence of V1 and V3 isomyosins on the mechanical behaviour of rat papillary muscle as studied by pseudo-random binary noise modulated length perturbations.

Experiments were done on four-week-old rats, containing biochemically verified V1 only, and thyroidectomized adult rats, treated with propylthiouracil, verified to contain V3 only. Contracture tension was induced in isolated papillary muscles either by high potassium solution or 0.5 mmol l-1 Ba2+. Small amplitude length perturbations with peak-to-peak value not exceeding 0.15% L0 were applied to the activated muscle. Both the applied length perturbations and the corresponding resulting force changes were analysed by computer for dynamic stiffness and phase values. In order to reduce data acquisition time, pseudo-random binary noise length changes, rather than the conventional sinusoidal length changes, were used. The plot of the dynamic stiffness against frequency displays a minimum, akin to a resonance phenomenon. The frequency, fmin, at which this resonance occurs, reflects crossbridge kinetics. It was found that the fmin values for the two types of papillary muscles differed by a factor of two. Experiments were also done on chemically skinned muscles containing V1 or V3 isomyosin activated by different concentrations of either barium or calcium ions. It was found that fmin values of skinned fibres were higher than those obtained from intact fibres. However, for each type of muscle the fmin was independent of the activator used as well as the level of activation. The ratio of fmin for V3 to that for V1 remained the same as for intact preparations. We conclude that the difference in mechanical parameters did not arise a possible difference in excitation-contraction coupling mechanism, but rather is a difference in the dynamic properties of the two types of crossbridges.

Animals↗

PubMedDate not supplied

Energetic changes of myocardium as an adaptation to chronic hemodynamic overload and thyroid gland activity.

Pressure-overload cardiac hypertrophy and hypothyroidism were shown to be associated with a decreased maximum shortening velocity of the myocardium. To investigate the nature of these intrinsic myocardial changes, we studied the energetic consequences in left ventricular papillary muscles of the rat by using standard HILL planar vacuum-deposited antimony-bismuth thermopiles. To evaluate the economy of isometric force generation and maintenance, we analyzed the ratio of liberated heat and developed tension or developed tension-time integral in twitches and experimentally induced tetanic contractions. Hypothyroidism was induced by treatment with propylthiouracil (PTU), and hypertension by operative narrowing of the left renal artery of rats according to Goldblatt (GOP). In the myocardium of hypothyroid as well as hypertensive rats, initial heat per peak twitch tension and total activity-related heat per tension-time integral were significantly reduced compared to controls. In tetanic contractions, total activity-related heat per tension-time integral was also decreased in PTU and GOP myocardium when compared to controls. Thus, the economy of force generation and maintenance is improved in the myocardium of the experimental animals. The data is interpreted in terms of altered cross-bridge cycling rates which are shown to be associated with changes in the myosin isoenzyme pattern. The intrinsic changes of the myocardium due to pressure-overload hypertrophy and hypothyroidism are considered to be adaptive rather than pathologic reactions of the myocardium.

Adaptation, Physiological↗

PubMedDate not supplied

Alterations of mechanical parameters in chemically skinned preparations of rat myocardium as a function of isoenzyme pattern of myosin.

Myofibrillar ATPase activity, maximum unloaded shortening velocity, and isometric tension development were evaluated in left ventricular preparations of 5-week-old rats with a high endogeneous level of thyroid hormones and hypothyroid rats after 4-week treatment with propylthiouracil (PTU). The range of possible alterations of the above functional parameters was defined in relation to myosin isoenzyme distribution. The mechanical behaviour of the ventricular preparations was investigated in native myocardium as well as in the glycerinated state. The essential results of the present study is that alterations of myofibrillar ATPase activity and mechanical Vmax, evaluated in glycerinated preparations, are limited to a well-defined range of similar magnitude for both functional parameters: 32-40% of maximum values (obtained from rat myocardium with homogeneous myosin V1). Isometric tension was only insignificantly decreased in glycerinated preparations of the PTU-treated group. The alteration in the apparent maximum shortening velocity of native myocardium (V0) was of the same magnitude as changes in Vmax of chemically skinned preparations. Physical training revealed a shift in the direction of V1-type myosin with increased ATPase activity and shortening velocity; aging and pressure overload showed an opposite effect. The documented mechanical alterations do not contradict an adaptational interpretation of the myosin isoenzyme redistribution in pressure-induced hypertrophy.

Adenosine Triphosphatases↗

PubMed1992

Hormonal control of manganese transport in the mouse thyroid.

The present study deals with a possible mechanism controlling the transport of manganese (Mn), an essential trace element, from the circulation to the thyroid. Mice were pretreated with propylthiouracil (PTU) or triiodothyronine (T3), and a measurement of the thyroid:serum concentration ratio (T/S) of radioactive manganese (54Mn) was carried out. The T/S of 54Mn was greatly enhanced by PTU, but reduced by T3. Several methods were used to demonstrate that the T/S of 54Mn depends upon the level of thyroid-stimulating hormone (TSH) in the serum. First, bovine TSH was injected into mice; an increase in the T/S resulted. Secondly, serum thyroxine and T3 levels measured by radioimmunoassay (RIA) suggested that PTU produced an increase in serum TSH and T3 a decrease. However, direct measurement of mouse TSH by RIA for rat TSH failed to produce proof of any changes in TSH level, owing to poor cross-reactivity. Taking all the information into account, it is concluded that Mn-transport into the thyroid is controlled by the thyroid state.

Animals↗

PubMedDate not supplied

Changes in myosin and creatine kinase mRNA levels with cardiac hypertrophy and hypothyroidism.

Rats were treated with three methods which produce alterations in the expression of myosin isozymes: coarctation of the abdominal aorta, treatment with low doses of isoproterenol, and administration of propylthiouracil. The steady-state levels of the left ventricle mRNAs for alpha myosin heavy chain (alpha-MHC), beta myosin heavy chain (beta-MHC), M creatine kinase (MCK), and B creatine kinase (BCK) were then determined using Northern and slot blot hybridizations. Cardiac hypertrophy was induced by an acute systolic pressure overload, or beta adrenergic stimulation. At 7 days following systolic pressure overload, the induced cardiac hypertrophy was accompanied by alterations in the levels of MHC mRNAs, as has been previously reported. In RNA from left ventricles of treated animals alpha-MHC mRNA levels decreased by 15% by day 3 and 20% by day 7. In contrast, beta-MHC mRNA levels increased to 250% of control levels by day 3 and then declined to a value 150% of controls by day 7. Levels of MCK and BCK mRNAs showed little or no changes by day 3; at day 7 both MCK and BCK mRNAs showed decreases of 20% relative to controls. Cardiac hypertrophy induced by low doses of isoproterenol produced decreases of alpha-MHC mRNA levels to 70% of control values at day 3 and 50% at day 7. Over the same time periods there was an increase in the levels of the fetal mRNA isoform (beta-MHC) to 190%, then 130% of control values, respectively. At 3 days, both BCK and MCK mRNA levels had declined by approximately 20-25%. By 7 days, MCK mRNA levels had decreased by approximately 50% and BCK mRNA levels by 30%. Hypothyroidism induced by PTU treatment led to a 50% decrease in alpha-MHC mRNA levels by day 3, which then further decreased to 10% of control levels at day 7. beta-MHC mRNA levels increased to 350% of control levels at day 3 and then decreased to 275% of control levels at day 7. For creatine kinase mRNAs the level of the M isoform was increased by 30% at day 3, whereas there appeared to be no significant change in levels of B isoform mRNA at this time. At day 7 neither BCK nor MCK mRNA levels were significantly different from controls. These results show three treatments which produce an alteration in myosin mRNA isoforms produce little or no change in creatine kinase isoform mRNAs. Thus, the MHC and CK genes respond differently to either cardiac hypertrophy or a reduction in thyroid hormone levels.

Animals↗

PubMed2006

Treatment of post-partum thyrotoxicosis.

Thyrotoxicosis occurs more frequently during the post-partum period than at other times in women of childbearing age. Graves' disease and post-partum thyroiditis are two major causes of thyrotoxicosis in this period. The major task lies in differentiation of these two diseases in the post-partum period; since throtoxicosis caused by post-partum thyroiditis usually does not require treatment. The radioiodine uptake is elevated or normal in Graves' disease and low in post-partum thyroiditis, and TSH-receptor antibodies are positive in Graves' and negative in post-partum thyroiditis. Post-partum thyrotoxicosis due to Graves' disease may be treated with radioiodine but it requires radiation safety measurements for infant and is contraindicated if the mother is breast-feeding. Antithyroid drugs are the mainstay of the treatment of post-partum thyrotoxicosis. Recent investigations conclude that neither propylthiouracil nor methimazole cause any alterations in thyroid function and physical and mental development of infants breast-fed by lactating thyrotoxic mothers, and both can be safely administered in moderately high doses during lactation.

Antithyroid Agents↗

PubMed2003

Acute decrease in circulating T3 levels enhances, but does not normalise, the GH response to GHRP-6 plus GHRH in thyrotoxicosis.

In thyrotoxicosis there is an impaired GH response to GHRH, normal GH responsiveness to GHRP-6 and lack of synergistic GH response after simultaneous administration of both peptides. We have previously shown that the GHRH-induced GH release in these patients increases after an acute reduction of circulating T3 values with administration of iopanoic acid, a compound that inhibits peripheral conversion of T4 to T3. We have now studied the effect of a decrease in serum T3 levels on the GH response to GHRP-6 (1 microg/kg) plus GHRH (100 microg) in 9 hyperthyroid patients before and after 15 days of treatment with iopanoic acid (3 g every 3 days) and propylthiouracil (600 mg/day). Nine normal subjects were also studied. In all hyperthyroid patients iopanoic acid induced a rapid decrease and normalisation of serum T3 levels. In these subjects peak GH (microg/l; mean +/- SE) and AUC (microg/l x 120 min) values after GHRP-6 plus GHRH were significantly higher on day 15 compared to pretreatment values (peak, 18.3 +/- 3.0 vs 13.4 +/- 1.9; AUC, 1227.9 +/- 212.9 vs 968.5 +/- 160.4; p<0.05). Despite the significant enhancement of the GH responsiveness to GHRP-6 plus GHRH after treatment with iopanoic acid, this response remained significantly blunted when compared to controls both in terms of peak GH (18.3 +/- 3.0 vs 83.7 +/- 15.2; p<0.05) and AUC values (1227.9 +/- 212.9 vs 4956.5 +/- 889.3; p<0.05). In conclusion, our results show that an acute decrease of circulating T3 levels enhances, but does not normalise, the GH response to GHRP-6 plus GHRH in thyrotoxicosis. This could suggest that circulating T3 does not have a major role in the mechanisms involved in the synergistic effect of these peptides.

Adolescent↗

PubMed1997

Lactose intolerance following antithyroid drug medications.

We recently observed 2 lactase-deficient women with Graves' disease who consistently developed severe diarrhea after ingestion of thionamide (methimazole and propylthiouracil) tablets containing lactose as carrier. The strict temporal relationship between ingestion of lactose-containing tablets and appearance of intestinal symptoms, as well as the absence of side effects following ingestion of methimazole tablets without lactose as carrier, provided the clue for the diagnosis. To our knowledge, severe diarrhea resulting from carrier lactose has not been previously reported for antithyroid drugs, and should be considered in occasional cases of patients with gastrointestinal symptoms on thionamide therapy.

Adult↗

PubMed1986

Graves' disease and Hashimoto's thyroiditis: effects of high doses of antithyroid drugs on thyroid autoantibody levels.

We studied the effects of high doses of methimazole (MMI) or propylthiouracil (PTU) on thyroid-stimulating antibody (TSAb), antithyroid microsomal (MCHA) and antithyroglobulin (TGHA) levels in Graves' disease and Hashimoto's thyroiditis. Thirty Graves' hyperthyroid patients were treated for 14 +/- 8 months (mean +/- SD) with MMI, 60-80 mg daily or PTU, 900-1200 mg daily plus T3, 50-75 micrograms daily. Fifteen Hashimoto's thyroiditis patients (4 of whom hypothyroid) received 100-200 micrograms of T4 daily for 4-8 weeks prior to MMI, 60-90 mg daily or PTU, 900 mg daily for 12-16 weeks. In Graves' disease a decrease (p less than 0.001) in TSAb activity (20/25 patients) was observed: before therapy, 0.424 +/- 0.506 pmoles/mg wet wt and at the end of treatment, 0.189 +/- 0.23 pmoles/mg wet wt. The MCHA titers also fell (18/26 patients) from 1:10,403 +/- 20,197 to 1:3,476 +/- 5,252 (p less than 0.01) and was associated with a decrease in free T4 values (1.23 +/- 0.69 vs. 0.51 +/- 0.36 ng/dl; p less than 0.01). A fall of MCHA titers in T4-treated Hashimoto's thyroiditis patients (1:10,416 +/- 25,576) was found when compared with the value before T4 (1:25,920 +/- 39,973; p less than 0.001). However, the titers of MCHA (1:13,280 +/- 25,992) did not change on MMI or PTU plus T4 treatment. The TGHA titers fell in a single patient. No alterations were observed in serum immunoglobulins. Serum concentrations of the complement factor C'3 remained higher (p less than 0.01) than normal values in both Graves' disease and Hashimoto's thyroiditis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗