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PubMed1988

The different types of hyperthyroidism in Europe. Results of a prospective survey of 924 patients.

In a prospective multicentric study, 924 untreated hyperthyroid patients were investigated, coming consecutively within one year into 17 thyroid centers of 6 European countries. With the aid of clinical information, evaluation of thyroid scan and centrally assayed thyroid hormones, thyroid antibodies, TSH-binding inhibiting immunoglobulins (TBII), and urinary iodine, different types of hyperthyroidism could be shown. Two types of hyperthyroidism could be defined directly: autonomous adenoma in cases of hot nodules in thyroid scan and Graves' disease, defined as hyperthyroidism with eye symptoms, and/or measurable TBII levels. The remainder, called "non-classifiable", included TBII negative Graves' patients, comprising of Hashitoxicosis, toxic nodular goiter, and other multifocal autonomies. 9.2% of the patients had an autonomous adenoma, 59.6% Graves' disease, and 31.2% unclassified hyperthyroidism. The main and significant difference between these types were mean age, goiter size, nodularity, and severity of the disease, being especially expressed in Graves' disease. Graves' patients had significantly increased T3/T4 ratios. Using as additional criteria diffuse regular uptake and/or increased T3/T4 ratios for immunogenic types of hyperthyroidism at least half of the 31.2% unclassified hyperthyroidism are probably Graves' disease. Forming two groups of iodine-deficient areas (IDA) and iodine-sufficient areas (ISA) according to the urinary iodine, it was possible to elucidate some characteristics independently of local factors. Autonomous adenoma was more frequent in IDA (10.1%) than in ISA (3.2%). Differences in iodine supply are reflected in the three types of hyperthyroidism by a significant higher prevalence of goiter, thyroid nodularity, lower thyroid hormone concentrations, and a higher rate of T3 toxicosis in IDA.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2000

Constitutively activating TSH-receptor mutations as a molecular cause of non-autoimmune hyperthyroidism in childhood.

BACKGROUND: The glycoprotein hormone TSH (thyroid-stimulating hormone) and its receptor, the TSH-receptor (TSHR), play a crucial role in thyroid growth and function. Constitutively activating germline mutations within the TSHR gene were identified in patients with sporadic or familial non-autoimmune hyperthyroidism. Inheritance of these mutations is autosomal dominant. PATIENTS AND METHODS: We investigated two patients with neonatal onset of non-autoimmune hyperthyroidism and two families in whom the child and one parent are affected. RESULTS: Hyperthyroidism was difficult to treat in all of these patients and was complicated by premature craniosynostosis. Sequencing of all exons of the TSHR gene in one family with hyperthyroidism revealed a mutation in exon 10 (T6321), which was first identified in toxic adenomas and found to constitutively activate the TSHR. In the other family, we identified a new mutation in the first membrane spanning segment (G431S). In both patients with sporadic hyperthyroidism, a heterozygous mutation in exon 9 (S281N) was detected. The functional characterization of S281N and G431S demonstrated that both mutants were constitutively active. Therefore, these mutations are the molecular cause of non-autoimmune hyperthyroidism in the patients. CONCLUSIONS: For patients suffering from non-autoimmune hyperthyroidism, screening for mutations and their functional characterization is recommended. In case of an ineffective hyperthyroidism treatment, thyroidectomy should be performed to prevent lengthy anti-thyroid drug treatment and complications like premature craniosynostosis.

Child↗
PubMed1992

Hyperthyroidism due to inappropriate secretion of thyrotropin in 10 patients.

PURPOSE: The syndrome of inappropriate thyroid-stimulating hormone (TSH) secretion, characterized by elevated serum free thyroxine and triiodothyronine levels in association with measurable serum TSH concentrations, remains an uncommon cause of hyperthyroidism that is being recognized with increasing frequency. The hyperthyroidism may be due to either neoplastic pituitary TSH secretion or selective pituitary resistance to thyroid hormone. In an effort to better understand this rare cause of hyperthyroidism, we undertook a retrospective analysis of our institution's experience with this condition. PATIENTS: We reviewed our cumulative experience (10 patients) with hyperthyroidism due to the syndrome of inappropriate secretion of TSH. RESULTS: Six patients were diagnosed with TSH-secreting pituitary adenomas and four were found to have selective pituitary resistance to thyroid hormone. One patient with tumor had a TSH-secreting pituitary adenoma in the setting of multiple endocrine neoplasia syndrome. In all patients with tumor, hyperthyroidism was successfully treated with transsphenoidal adenomectomy with or without pituitary radiotherapy. All four patients with pituitary resistance had thyroid ablation or resection prior to their correct diagnosis. Therefore, therapy for this group of patients involved thyroid hormone replacement and efforts to suppress TSH hypersecretion. All 10 patients have done well clinically, with follow-up ranging from 2 weeks to 13 years. CONCLUSIONS: Adequate treatment exists for the two primary causes of TSH hypersecretion. TSH-secreting pituitary adenomas are treated with surgery and, if necessary, adjuvant pituitary radiotherapy. The results are generally good if the tumor is diagnosed and treated at an early stage. Primary therapy for hyperthyroidism due to selective pituitary resistance to thyroid hormone is aimed at suppression of pituitary TSH hypersecretion. The evaluation of any patient with hyperthyroidism must be thorough and, in some cases, should include measurement of TSH to determine the presence of inappropriate secretion. Eliminating this diagnosis will help avoid improper and potentially harmful treatment of hyperthyroid patients.

Adenoma↗
PubMed1993

Iodine-induced hyperthyroidism due to nonionic contrast radiography in the elderly.

PURPOSE: To identify the number of cases of hyperthyroidism that followed the performance of contrast radiography in elderly patients at a geriatric hospital in a non-iodine-deficient area and to determine the clinical course of the condition. PATIENTS AND METHODS: All patients over a 20-month period with biochemical hyperthyroidism (plasma free thyroxine level greater than 25.0 pmol/L and thyroid-stimulating hormone level less than 0.10 IU/L) were identified. Clinical features of hyperthyroidism and exposure to nonionic contrast media radiographs within the previous 12 months were sought. Follow-up extended from 6 to 22 months. RESULTS: A total of 28 patients with hyperthyroidism (aged 70 to 96 years) were identified. Seven patients (25%) had documented biochemical development of hyperthyroidism (five) or subsequent hyperthyroidism (two) 3 to 8 weeks after nonionic contrast media radiography. The four patients who underwent scanning had a multinodular thyroid, and thyroid antibodies were not detected in five of five patients. Although the condition appeared self-limited and six of six patients were euthyroid after 18 months, the condition was not benign; progress and recovery were adversely affected by hyperthyroidism. Four patients had a good response to treatment with an antithyroid drug (carbimazole). CONCLUSION: Iodine-induced thyrotoxicosis following contrast radiography was found in 7 of 28 cases of hyperthyroidism seen at a geriatric hospital. Although the condition appears ultimately self-limited, pharmacologic control of severe clinical features may be required. The frequency of this condition in a non-iodine-deficient area appears related to the more common occurrence of autonomous thyroid nodules in the elderly. Because performance of contrast radiography is more common in this age group, the recognition and treatment of iodine-induced thyrotoxicosis are of increasing clinical importance.

Age Factors↗
PubMed1980

Effect of experimental hyperthyroidism on protein turnover in skeletal and cardiac muscle.

Since experimental hyperthyroidism reduces skeletal muscle mass while simultaneously increasing cardiac muscle mass, the effect of hyperthyroidism on muscle protein degradation was compared in skeletal and cardiac muscle. Pulse-labeling studies using (3H) leucine and (14C) carboxyl labeled aspartate and glutamate were carried out. Hyperthyroidism caused a 25%-29% increase in protein breakdown in both sarcoplasmic and myofibrillar fractions of skeletal muscle. Increased muscle protein degradation may be a major factor in the development of skeletal muscle wasting and weakness in hyperthyroidism. In contrast, protein breakdown appeared to be reduced 22% in the sarcoplasmic fraction of hyperthyroid heart muscle and was unchanged in the myofibrillar fraction. Possible reasons for the contrasting effects of hyperthyroidism on skeletal and cardiac muscle include increased sensitivity of the hyperthyroid heart to catecholamines, increased cardiac work caused by the hemodynamic effects of hyperthyroidism, and a different direct effect of thyroid hormone at the nuclear level in cardiac as opposed to skeletal muscle.

Animals↗
PubMed1990

Oral and intravenous glucose-induced insulin secretion in hyperthyroid patients.

To elucidate glucose intolerance in hyperthyroidism, insulin response to oral (75 g) and intravenous (IV) (20 g) glucose administration was investigated in 18 hyperthyroid patients and six normal control subjects. In oral glucose tolerance tests (OGTT), plasma insulin and C-peptide levels in hyperthyroid patients were not significantly different from that in controls; however, an impaired blood sugar response was observed in hyperthyroid patients. In IVGTT, blood sugar, plasma insulin, and C-peptide levels were significantly higher in hyperthyroid patients than in controls. Insulin secretion in proportion to blood sugar stimulus (the sum of increment in insulin divided by the sum of increment in blood sugar after glucose load, sigma delta IRI/sigma delta BS) in IVGTT was similar in hyperthyroid patients and controls; however, that in OGTT was significantly lower in hyperthyroid patients. After thyroid function tests had returned to normal by treatment with thiamazole, glucose tolerance and sigma delta IRI/sigma delta BS in OGTT were almost normalized. These results indicate that decreased insulin secretion after oral glucose may have an important role in abnormal oral glucose metabolism in hyperthyroidism.

Administration, Oral↗
PubMed1994

Adaptive changes in transmembrane transport and metabolism of triiodothyronine in perfused livers of fed and fasted hypothyroid and hyperthyroid rats.

The transport and subsequent metabolism of triiodothyronine (T3) were studied in isolated perfused livers of euthyroid, hypothyroid, and hyperthyroid rats, both fed and 48-hour-fasted. T3 kinetics (transport and metabolism) during perfusion were evaluated by a two-pool model, whereas the metabolism of T3 was also investigated by determination of T3 breakdown products by chromatography of medium and bile. For comparison of groups, metabolism was corrected for differences in transport. Transport parameters in fed hypothyroid livers were not significantly changed as compared with euthyroid livers, whereas metabolism was decreased. In fed hyperthyroid livers, fractional transfer rate constants for influx (k21) and efflux (k12) were decreased and metabolism, corrected for differences in intracellular mass transfer, was increased. Furthermore, for transport in hyperthyroid liver it was shown that only total mass transfer (TMT) into the metabolizing liver compartment (not into the nonmetabolizing liver compartment) was decreased. Transport and metabolic parameters in fasted hypothyroid livers were decreased as compared with euthyroid fed livers. In fasted hyperthyroid livers, transport and metabolism were not significantly different as compared with that in euthyroid fed livers, so transport was increased versus hyperthyroid fed livers. It appeared therefore that fasting normalized the effects of hyperthyroidism on both the transport and metabolic processes of T3 in the liver. The present study demonstrates normal transport and decreased metabolism in livers of hypothyroid fed rats and decreased transport and increased metabolism in livers of hyperthyroid fed rats. In livers of hypothyroid fasted rats transport and metabolism were decreased, whereas in livers of hyperthyroid fasted rats transport and metabolism were not significantly different from that in euthyroid fed livers.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗
PubMed1995

Hyperuricemia in patients with hyperthyroidism due to Graves' disease.

The effects of hyperthyroidism on uric acid metabolism were investigated. First, the serum uric acid level was measured in 92 patients with hyperthyroidism due to Graves' disease, eight patients with subacute thyroiditis, six patients with hypothyroidism, and 70 sex- and age-matched controls. Second, the correlation between serum thyroxine (T4) and serum uric acid was obtained in hyperthyroid Graves' disease patients before and during antithyroid drug therapy. Finally, uric acid clearance (CUA) was determined in untreated patients with hyperthyroidism due to Graves' disease. Serum uric acid was significantly elevated in patients with hyperthyroidism, and the elevation correlated well with serum T4 before treatment as a group and during treatment in each patient. A significant elevation of serum uric acid was not present in patients with a transient mild thyrotoxicosis due to subacute thyroiditis. Serum uric acid was significantly decreased in patients with hypothyroidism. Renal excretion of uric acid clearly increased in hyperthyroid patients, and CUA also increased. The increase in CUA corresponded to the increase in renal plasma flow (RPF), which was measured by p-aminohippuric acid clearance. The fractional excretion of uric acid as determined by CUA/glomerular filtration rate (GFR) was similar and within the normal range in hyperthyroid patients and normal controls. A significant inverse correlation between CUA and serum uric acid concentration was present in hyperthyroid patients as in normal controls, indicating that the renal handling of uric acid in the tubule affected uric acid excretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

Calcium oxalate crystal formation in patients with hyperparathyroidism and hyperthyroidism and related metabolic disturbances.

The crystallization of calcium oxalate in the urine of patients with hyperparathyroidism and hyperthyroidism was studied using a mixed suspension mixed product removal (MSMPR) system. In addition, calcium metabolism in hyperthyroidism and its relationship to urolithiasis was investigated. The urines from all the three groups (normal subjects, hyperparathyroid and hyperthyroid patients) showed reduced nucleation rates and increased growth rates in comparison with the control synthetic urine. The nucleation rate was not significantly different between the three human urine groups, while the growth rate was significantly higher in the hyperparathyroid group compared to the normal and hyperthyroid groups. Crystal volume (suspension density) in the hyperparathyroid group was approximately twice that in the other two groups. Serum and ionized calcium levels in hyperparathyroid patients were higher than in normal subjects, while hyperthyroid patients had levels only slightly higher than those in normal subjects. The hyperparathyroid and hyperthyroid groups differed significantly from the normal group in urinary calcium excretion. These two groups also showed significantly higher levels of serum alkaline phosphatase and urinary hydroxyproline than did the normal group. Although hyperthyroid patients have a calcium metabolism similar to hyperparathyroid patients, the incidence of urolithiasis is no different between hyperthyroid and normal subjects. The results of both crystallization and calcium metabolism in hyperparathyroid patients were not significantly different between those with and without urolithiasis. The result of crystallization was also not significantly different between hyperparathyroid patients with and without hypercalciuria. This study suggests that hypercalciuria alone does not produce urinary stones and that urine from hyperparathyroid patients may contain promotors of calcium oxalate crystallization and calcium stone formation.

Calcium Oxalate↗
PubMed1988

Effects of piperonyl butoxide on halothane hepatotoxicity and metabolism in the hyperthyroid rat.

A series of experiments were conducted to examine the potential role of phase I metabolism in halothane-induced liver injury in the hyperthyroid rat. The metabolism of halothane was determined in both hyperthyroid (triiodothyronine, 3 mg/kg per day, for 6 days) and euthyroid rats and in animals pre-treated with the cytochrome P-450 inhibitor piperonyl butoxide (75-100 mg/kg, i.p.). It was found that the hyperthyroid state, which is associated with a substantial increase in sensitivity to the hepatotoxic effects of halothane, decreases both oxidative and reductive routes of halothane metabolism in the rat. The production of trifluoroacetic acid (TFA), an oxidative metabolite, as well as that of chlorodifluoroethylene (CDF) and chlorotrifluoroethane (CTF), 2 reductive metabolites, was significantly reduced in hyperthyroid animals. Consistent with these findings serum and urinary bromide levels resulting from the formation of TFA, CDF or CTF were significantly reduced. The only route of halothane metabolism significantly increased by the hyperthyroid condition was the defluorination of halothane. Piperonyl butoxide administration did not render euthyroid animals sensitive to the halothane-induced hepatotoxicity and had no effect on the defluorination of halothane in euthyroid animals. However, piperonyl butoxide markedly increased the hepatotoxicity of halothane in hyperthyroid rats and, except for a modest increase in debromination reactions, decreased all measured indices of halothane metabolism including the defluorination of halothane. Thus, none of the observed changes in halothane metabolism produced by triiodothyronine or piperonyl butoxide treatment could be consistently correlated to the increases in hepatotoxicity linked to these 2 treatments. Based on these studies we suggest that the halothane hepatotoxicity induced in the hyperthyroid rat results from effects produced by either the parent compound or an as yet unidentified metabolite. In addition, these studies further demonstrate that considerable mechanistic differences exist for halothane-induced hepatotoxicity when comparing euthyroid and hyperthyroid animal models.

Administration, Inhalation↗
PubMed1975

Gonadal steroids and gonadotropins in hyperthyroidism.

Gynecomastia occurs in about 20 to 40 per cent of men with hyperthyroidism. Serum concentrations of total estradiol-17beta, total testosterone, and luteinizing hormone are supranormal in these patients. Serum concentration of SHBG is also high in hyperthyroidism. This can explain the high serum testosterone, essentially completely but not the high serum estradiol-17beta; thus, whereas serum unbound testosterone is normal, serum unbound estradiol-17beta is above normal in hyperthyroid men. This balance in relative concentrations of unbound gonadal steroids is apparently quite favorable to the development of gynecomastia in hyperthyroidism. Increased peripheral tissue metabolism of androgens to estrogens seems to be the major factor responsible for high estradiol-17beta in hyperthyroidism; increased glandular secretion of estradiol-17beta may also be important. The mechanism of hypomenorrhea or amenorrhea in hyperthyroidism remains unclear. Changes in circulating estrogens, androgens, and luteinizing hormone in hyperthyroid women are similar to those in hyperthyroid men. The mid-cycle ovulatory peak of luteinizing hormone may be blunted in patients with scanty periods whereas it may be altogether absent in those with amenorrhea.

Androgens↗
PubMed2000

Variable bone mass recovery in hyperthyroid bone disease after radioiodine therapy in postmenopausal patients.

OBJECTIVES: Long-term follow-up of postmenopausal hyperthyroid females after radioiodine therapy, since hyperthyroidism is known to cause impressive bone loss which may increase the risk of bone fractures. METHODS: Bone mineral density (BMD) and biochemical parameters of bone metabolism in hyperthyroid postmenopausal patients were investigated before and 2 years after radioiodine therapy and compared with euthyroid age-matched controls. RESULTS: At baseline, the incidence of low BMD with t-scores more than 2.5 S.D. below normal was significantly higher in hyperthyroid patients (54%) than in controls (20%, P<0.001). Regardless of initial BMD values, osteocalcin (OC) was also higher in all hyperthyroid patients (P<0.0001). After 2 years, all treated patients were euthyroid and OC levels were in the upper normal range. In hyperthyroid patients with initially low BMD, bone density values had increased significantly by +6.5% (P<0.008) as compared with baseline values. In contrast, hyperthyroid patients with initially normal BMD showed a further decrease in lumbar BMD values of -4.3% despite radioiodine treatment. BMD in euthyroid controls decreased by -6.5% within 2 years. CONCLUSIONS: We conclude that hyperthyroid postmenopausal patients with generally increased bone turnover may show individual differences in bone loss and BMD recovery after radioiodine treatment. The mechanisms for this variable manifestation of osteoporosis have still to be elucidated, since this has implications for prophylactic and therapeutic strategies in these elderly patients.

Aged↗
PubMed1981

Effect of hyperthyroidism and hypothyroidism on lipid and carbohydrate metabolism of the perfused rat liver.

1. Liver from hyper- and hypo-thyroid male fed rats were perfused with whole blood and their metabolism was compared with euthyroid controls. 2. Hyperthyroid livers produced more bile than controls and hypothyroid livers produced less. 3. Glucose output by all livers was similar; glycogen declined only during perfusion of hyperthyroid livers. Lactate uptake increased in hyperthyroid but decreased in hypothyroid livers. These results may be explained by changes in oxidation of carbohydrate rather than in gluconeogenesis. 4. Secretion of triacylglycerol was decreased in hyperthyroid and not changed significantly in hypothyroid livers. 5. Fractional extraction of infused [1-14C]oleate was unaltered. Hyperthyroid livers oxidized more oleate to CO2 and ketone bodies, esterified less and incorporated less into lipoproteins of d less than 1.006. Hypothyroid livers oxidized and esterified oleate to the same extent as controls; their decreased O2 consumption was due to diminished oxidation of other (non-lipid) substrates; 14C-labelled ketone-body formation was increased, but at the expense of 14CO2 production. 6. Lipogenesis (measured with 3H2O) was unaltered in hyperthyroid but was decreased in hypothyroid livers. Incorporation of 3H and 14C into triacylglycerol relative to phospholipid decreased in hyperthyroid and increased in hypothyroid livers. Cholesterol synthesis was similar in all perfusions. 7. During oleate infusion, the cytosolic redox state, as indicated by the perfusate [lactate]/[pyruvate] ratio, was decreased in hyperthyroid and increased in hypothyroid livers. No change in [3-hydroxybutyrate]/[acetoacetate] was detected. 8. The importance of relating the concentration of plasma non-esterified fatty acids to the interpretation of metabolic data obtained under differing thyroid status is emphasized.

Animals↗
PubMed1996

A comparison of 20 or 40 mg per day of carbimazole in the initial treatment of hyperthyroidism.

OBJECTIVE: The optimal dosage regimen for carbimazole (CBZ) in the treatment of hyperthyroidism remains uncertain, despite clinical use of the drug for approximately fifty years. We have compared the early clinical and biochemical responses to 20 or 40 mg/day of CBZ given as initial treatment for hyperthyroidism. DESIGN: Prospective open multicentre trial. PATIENTS: Sixty-three patients presenting with hyperthyroidism. MEASUREMENTS: Serum total and free thyroid hormones, serum TSH and SHBG were measured at baseline and at 4 and 10 weeks after start of therapy. Weight, pulse and a symptom questionnaire were also monitored at 6 and 12 weeks. RESULTS: Patients randomized to a starting dose of 40 mg/day CBZ had lower total (98 +/- 10 vs 158 +/- 11 nmol/l, P < 0.001) and free T4 (19.4 +/- 2.6 vs 35.2 +/- 3.7 pmol/l, P < 0.001) and total (2.6 +/- 0.3 vs 4.3 +/- 0.4 nmol/l, P < 0.001) and free T3 (8.3 +/- 1.0 vs 13.7 +/- 1.2 pmol/l, P < 0.01) at 4 weeks than those receiving 20 mg/day. Clinical responses at 6 and 12 weeks (weight, pulse, symptom score) and SHBG concentrations were similar. Drug-related hypothyroidism was less likely to occur at 4 and 10 weeks in those patient who initially received 20 mg CBZ/day, but this dose was less effective at controlling hyperthyroidism in those with more severe hyperthyroidism with baseline TT4 > 260 nmol/l. CONCLUSIONS: In treating hyperthyroidism, 20 mg/day carbimazole is effective, convenient and has a lower risk than 40 mg/day of iatrogenic hypothyroidism in patients with mild or moderate hyperthyroidism. Higher doses are required for those with severe hyperthyroidism.

Adolescent↗
PubMed1997

Moderate hyperthyroidism reduces liver amino nitrogen conversion, muscle nitrogen contents and overall nitrogen balance in rats.

There are conflicting data on the effect of thyroid hormones on nitrogen metabolism. We determined the basal blood amino nitrogen (amino-N) concentrations, the urea nitrogen (urea-N) synthesis rate and the maximum hepatic capacity of urea nitrogen synthesis during saturating infusion of alanine, in moderately acutely (24 h) and chronically (7 days) hyperthyroid rats and compared this with changes in organ nitrogen contents in muscles and kidney, nitrogen excretion and nitrogen balance. Forty-three rats were made acutely hyperthyroid through administration of 5 microg 100 g(-1) triiodothyronine twice daily (T3: 2.2 +/- 0.7 vs. 0.87 +/- 0.04 nmol L(-1), P < 0.01). Fifty-one rats were made chronically hyperthyroid through administration of 12.5 microg 100 g(-1) thyroxine twice daily (T3: 2.63 +/- 0.18 vs. 0.87 +/- 0.04 nmol L(-1), P < 0.01). Weight gain was halved in this group. Both acute and chronic hyperthyroidism increased basal blood amino-N concentration in both groups by 16% (4.5 +/- 0.15 vs. 3.9 +/- 0.13 mmol L(-1) and 4.7 +/- 0.12 vs. 3.9 +/- 0.13 mmol L(-1), respectively, P < 0.01), and decreased basal urea-N synthesis rate in both groups by 30% [2.7 +/- 0.3 vs. 4.1 +/- 0.3 micromol (min x 100 g)(-1) and 3.1 +/- 0.3 vs. 4.1 +/- 0.3 micromol (min x 100g)(-1), respectively, P < 0.01]. The capacity of urea-N synthesis during saturation fell in both groups by 35% compared with controls [6.5 +/- 0.4 vs. 9.3 +/- 0.5 micromol (min x 100 g)(-1) and 5.7 +/- 0.5 vs. 9.3 +/- 0.6 micromol (min x 100g)(-1), respectively, P < 0.01]. Nitrogen contents in the muscles, soleus and extensor digitorum longus, of chronically hyperthyroid rats decreased by 22% and 11%, respectively, whereas kidney N-content increased by 12% (P < 0.05). N-balance and urinary urea-N excretion fell by 30%, whereas faeces-N excretion increased by 80% in hyperthyroid rats. Overall liver function assessed by galactose elimination capacity did not differ among groups. Both acute and chronic moderate hyperthyroidism increase blood amino-N and decrease basal and maximum rate of urea formation. Furthermore, chronic hyperthyroidism reduces N-contents of muscles, urinary urea-N excretion and N-balance. Thyroid hormones thus mobilize muscle-N, whereas amino-N in the liver is spared from irretrievable conversion into urea.

Amino Acids↗
PubMed2000

Serum insulin-like growth factor-I, insulin-like growth factor binding proteins, and bone mineral content in hyperthyroidism.

The mechanism by which thyroid hormones promote bone growth has not yet been elucidated. In vitro, thyroid hormones stimulate insulin-like growth factor-I (IGF-I) production by osteoblasts, which is important for the anabolic effects of the hormone on bone. To determine whether the IGF-I/IGF binding protein (IGFBP) profile is affected when thyroid hormone production is altered in vivo, we studied 36 women who had recently been diagnosed with hyperthyroidism (age: 29-67 years; 19 with Graves' disease, 17 with toxic nodular goiter) and 36 age-matched healthy women as controls. Serum IGF-I, and its binding proteins (IGFBP-3, IGFBP-4, and IGFBP-5), as well as bone mineral density (BMD) at the lumbar spine, femoral neck, and radius midshaft were measured before and 1 year after antithyroid (methimazole) treatment. Serum IGF-I levels were significantly increased in the hyperthyroid patients before treatment (214 +/- 18.2 ng/mL vs. 145 +/- 21.3 ng/mL; p < 0.05). There was no difference in IGF-I levels of patients with Graves' disease and toxic nodular goiter. Serum IGF-I concentrations returned to normal after treatment with methimazole. Serum IGFBP-3 and IGFBP-4 values were significantly elevated in the hyperthyroid group before treatment (3960 +/- 220 ng/mL and 749.7 +/- 53.1 ng/mL vs. 2701 +/- 180 ng/mL and 489.9 +/- 32.4 ng/mL; p < 0.05 and p < 0.01, respectively) and were reduced to those of controls after treatment. Serum IGFBP-5 of hyperthyroid subjects was not different from that of controls either before or after therapy. Serum free thyroxine showed a positive correlation with serum levels of IGF-I (r = 0.73, p < 0.05), IGFBP-3 (r = 0.59, p < 0.05), and IGFBP-4 (r = 0.67, p < 0.05) but not IGFBP-5. BMD at the radius midshaft was significantly lower in hyperthyroid patients at the start of the study and showed a positive correlation with serum IGF-I (r = 0.58; p < 0.001) and a negative correlation with IGFBP-4 (r = -0.61; p < 0.05). Radius BMD showed a 7.2% increase in the hyperthyroid group after 1 year of methimazole treatment, and the correlation between BMD and serum IGF-I disappeared. Our data indicate that thyroid hormones may influence the IGF-I/IGFBP system in vivo in hyperthyroidism. The anabolic effects of increased levels of IGF-I may be limited in hyperthyroidism due to the increases of inhibitory IGFBPs that can counteract the anabolic effects and contribute to the observed net bone loss.

Adult↗
PubMed1992

Hyperthyroidism and hepatic dysfunction. A case series analysis.

Liver dysfunction in hyperthyroid patients has not been well characterized. We analyzed the clinical records of 43 patients with hyperthyroidism to define the spectrum of clinical and liver test abnormalities. The patients were divided into three categories: (a) 18 patients with uncomplicated hyperthyroidism (HT) (b) 19 with hyperthyroidism and congestive heart failure (HT/CHF), and (c) 6 with hyperthyroidism and concomitant unrelated liver disease (HT/ULD). Hepatomegaly and/or spenomegaly were noted in 15 of 19 (79%) patients with HT/CHF as compared to 6 of 18 (33%) patients with HT and 3 of 6 (50%) patients with HT/ULD. Four patients with HT/CHF had ascites. Serum aminotransferase levels greater than 250 IU/L were noted in only 1 of 37 (3%) patients without unrelated liver disease. Patients with HT/ULD or HT/CHF had markedly low prothrombin time. Serum bilirubin levels as high as 323 microM were noted in patients with HT. No characteristic liver histology due to hyperthyroidism was noted. Severe liver test abnormalities, including deep jaundice and prolonged prothrombin time, can occur in patients with hyperthyroidism alone or with HT/CHF. This makes the diagnosis of concomitant, unrelated liver disease difficult until the hyperthyroidism has been controlled.

Adult↗
PubMed2001

Plasma isocitrate dehydrogenase as a marker of centrilobular hepatic necrosis in patients with hyperthyroidism.

Isocitrate dehydrogenase (ICDH) may be useful for differentiating centrilobular from periportal necrosis in rats with liver injury. In this study, we assessed the usefulness of ICDH as a marker of centrilobular necrosis in patients with hyperthyroidism. Isocitrate dehydrogenase and alanine aminotransferase (ALT) activities were measured in the plasma of 56 patients with hyperthyroidism, 16 patients with chronic viral hepatitis (CVH), and 17 controls. Isocitrate dehydrogenase levels were higher in patients with hyperthyroidism than in those with CVH or in the controls (p < 0.01 and p < 0.001, respectively), even though ALT levels were higher in patients with CVH than in patients with hyperthyroidism (p < 0.01). Isocitrate dehydrogenase/ALT ratios were also higher in patients with hyperthyroidism than in those with CVH (p < 0.0001). Isocitrate dehydrogenase correlated to ALT levels in patients with hyperthyroidism or CVH (p < 0.05). In a patient with hyperthyroidism, ICDH levels decreased progressively to normal, and the ALT level and thyroid function were normalized. Thus, the plasma ICDH or ICDH/ALT ratio might be useful for differentiating centrilobular from periportal necrosis and for monitoring the degree of hepatic necrosis in patients with hyperthyroidism.

Adult↗