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PubMed1993

Evaluation of thyrotropin secretion before and after TRH by third generation chemiluminescent assay. Assessment of subclinical hyperthyroidism.

The recent introduction of third generation assays for TSH has led to a considerable improvement of assay sensitivity. To assess the clinical significance of subnormal basal TSH (b-TSH) values (< 0.2 microU/ml), we investigated b-TSH and TRH-stimulated TSH (r-TSH) by means of a new, highly sensitive immunochemiluminometric assay in 105 euthyroid subjects, 45 patients with overt hyperthyroidism and 18 patients suspected of having subclinical hyperthyroidism. A weak, albeit statistically significant, correlation (r = 0.48) was found between b-TSH and r-TSH and also between b-TSH and delta-TSH (r = 0.31) in euthyroid subjects. Consideration of b-TSH alone correctly identified 90 % of euthyroid subjects in this group; 10 of 105 apparently euthyroid subjects presented delta-TSH suggesting subclinical hyperthyroidism. While b-TSH was detectable (> 0.04 microU/ml) in 8 of 45 (18%) of hyperthyroid patients, all (100%) were abnormal in both b-TSH and r-TSH. 14 of 18 (78%) of patients with subclinical hyperthyroidism exhibited a blunted TSH response to stimulation (delta-TSH < 2 microU/ml). These results suggest that although the new generation of TSH assays can be a valuable addition to the diagnostic arsenal of thyroid function tests, certain limitations must still be accepted. Specifically, b-TSH in the "grey zone" (0.1-0.2 microU/ml) appears to be a less than reliable predictor of thyroid function.

Adult↗
PubMed1989

Urinary N-acetyl-beta-D-glucosaminidase in the patients with hyperthyroidism.

Urinary N-acetyl-beta-D-glucosaminidase (NAG) was measured in patients with hyperthyroidism. The value of urinary NAG in these patients was higher than that in normal subjects and diabetic patients without diabetic nephropathy. This high level of urinary NAG in patients with hyperthyroidism decreased to the level of normal subjects after treatment of hyperthyroidism. Why urinary NAG increases in the patients with hyperthyroidism remains unknown. On the occasion of estimating the significance of the high level of urinary NAG, however, the possibility of the existence of hyperthyroidism has to be considered in addition to renal damage or hyperglycemia which have already been found to increase urinary NAG.

Acetylglucosaminidase↗
PubMed1983

[Immunogenic and non-immunogenic hyperthyroidism: attempts at a clinical differentiation].

In a retrospective study, 326 cases of thyroid hyperfunction but no scintigraphic demonstration of autonomous adenoma, were on the basis of certain primary and secondary criteria grouped as probably immunogenic or probably non-immunogenic hyperthyroid. Primary criteria were hormonal orbital signs and occurrence of thyroid antibodies. Secondary criteria concerned age, presence or absence of goitre and nodular goitre, scintigraphically silent areas and iodine contamination in relation to the onset of the disease. There was a significant difference between immunogenic and non-immunogenic hyperthyroidism by these criteria. In non-immunogenic hyperthyroidism, it is probable that suddenly raised iodine intake plays an important role in the initiation of hyperthyroid metabolic states. This was demonstrable in 82% of these patients, while in those with probably immunogenic hyperthyroidism iodine contamination (at 16%) seemed to be of less significance.

Age Factors↗
PubMed2001

Subclinical hyperthyroidism as a risk factor for atrial fibrillation.

OBJECTIVES: Atrial fibrillation is a well-known manifestation of hyperthyroidism. We studied whether subclinical hyperthyroidism with low serum thyrotropin concentrations and free thyroid hormone concentrations within the normal range in clinically euthyroid persons is a risk factor for subsequent atrial fibrillation. METHODS: We studied 23,638 persons. The subjects were classified according to their serum thyrotropin concentrations: group 1 comprised those with normal values of serum thyrotropin concentration (>0.4-5.0 mU/L) and free tri-iodothyronine and free thyroxine concentrations were within the normal range (22,300 subjects), group 2 comprised those with both low serum thyrotropin values (</=0.03 mU/L) and elevated free tri-iodothyronine and free thyroxine concentrations (725 subjects), and group 3 comprised those with low values of serum thyrotropin (<0.4 mU/L) and free triiodothyronine and free thyroxine concentrations were within the normal range (613 subjects). RESULTS: Atrial fibrillation was present in 513 persons (2.3%) in group 1 with normal values for serum thyrotropin, 100 (13.8%) in group 2 with overt hyperthyroidism, and 78 (12.7%) in group 3 with subclinical hyperthyroidism. The prevalence of atrial fibrillation in patients with low serum thyrotropin concentrations (<0.4 mU/L) was 13.3% compared with 2.3% in patients with normal values for serum thyrotropin (P <.01). The relative risk of atrial fibrillation in subjects with low serum thyrotropin and normal free tri-iodothyronine and free thyroxine concentrations, compared with those with normal concentrations of serum thyrotropin, was 5.2 (95% CI 2.1-8.7, P <.01). CONCLUSION: A low serum thyrotropin concentration is associated with a >5-fold higher likelihood for the presence of atrial fibrillation with no significant difference between subclinical and overt hyperthyroidism.

Atrial Fibrillation↗
PubMedDate not supplied

Investigation of red blood cell carbonic anhydrase, glucose 6-phosphate dehydrogenase, hexokinase enzyme activities, and zinc concentration in patients with hyperthyroid diseases.

We have recently reported on the activities of glucose-6-phosphate dehydrogenase (G6PD), hexokinase (HK) and carbonic anhydrase I (CA-I) and II (CA-II) isoenzymes obtained from erythrocytes of healthy subjects and untreated patients with hyperthyroid diseases. Also, erythrocyte zinc concentrations were measured. Red blood cell (RBC) zinc (Zn) concentration was measured by atomic absorption spectrophotometry. Activities of carbonic anhydrase II and I isoenzymes were determined with CO2-hydratase activity method by using selective inactivation with bromopyruvate. G6PD and HK enzyme activities were measured spectrophotometrically via absorbance change (at 340 nm) in NADPH formed as a result of the reactions catalysed by these enzymes. In statistical analysis of all these parameters, activity of CA-I was 4388 +/- 207 (EU/gHb) and 2881 +/- 869 (EU/gHb) in healthy and untreated hyperthyroid subjects, respectively. The activity values for CA-II were 5391 +/- 257 (EU/gHb) and 4688 +/- 12.6 (EU/gHb) in healthy and untreated hyperthyroid subjects. Glucose 6-phosphate dehydrogenase (G6PD) activity was 10.19 +/- 1.87 (EU/gHb) in healthy group and 4.92 +/- 2.49 (EU/gHb) in patient group. While hexokinase enzyme activity was 1.575 +/- 0.898 in healthy subjects, it was 0.651 +/- 0.418 (EU/gHb) in the patient group. While erythrocyte zinc concentration in the healthy subjects was 49.32 +/- 23.5 (mg/gHb), this concentration for patients with uncontrolled hyperthyroid diseases was significantly decreased to 29.62 +/- 4.26 (mg/gHb). As a conclusion, CA-I isoenzyme, G6PD, hexokinase activities and erythrocyte zinc concentration had decreased in untreated patients carrying hyperthyroid diseases as compared to those of the healthy subjects.

Adult↗
PubMed1996

Bone mass, bone turnover, body composition, and calcium homeostasis in former hyperthyroid patients treated by combined medical therapy.

It is still uncertain whether bone mass and bone turnover are completely normalized after treatment of hyperthyroidism. The aim of the present investigation was to determine bone mass, bone turnover, body composition, and calcium homeostasis in former hyperthyroid patients who had been euthyroid for at least 4 years following combined medical therapy. Thirty-nine former hyperthyroid patients and 67 normal sex- and age-matched controls participated. Height, body weight, and body composition were similar in the two groups. All patients were euthyroid. However, serum FT3I (free T3-index) was reduced by 9% (p < 0.01) in the patients compared to controls, serum FT4I was normal, while serum TSH was nonsignificantly reduced by 39%. No significant differences were observed between patients and controls with respect to total or regional bone mineral content (BMC) or density (BMD). The former hyperthyroid patients had slightly higher serum calcium (2.35 +/- 0.06 vs. 2.32 +/- 0.07 mmol/L, p < 0.05) and lower serum phosphate (1.15 +/- 0.15 vs. 1.24 +/- 0.15 mmol/L, p < 0.01) than their controls. Renal excretion of calcium and serum levels of magnesium, 1,25-vitamin D and intact PTH were unchanged. Renal excretion of pyridinoline was increased by 30% (p < 0.05) in the patients, whereas the remaining resorptive markers, renal excretion of hydroxyproline and deoxypyridinoline and serum cross-linked carboxy-terminal teleopeptide of type I collagen (ICTP) were unaltered. Among the formative bone markers the average serum carboxy-terminal propeptide of human type I procollagen (PICP) level was 12% lower (p < 0.05) than in the control group, whereas serum levels of osteocalcin and total and bone alkaline phosphatase were normal. In conclusion, former hyperthyroid patients treated by combined medical therapy have normal bone mineral content and density in spite of minor variations in thyroid hormones and skeletal homeostasis.

Biomarkers↗
PubMed1996

Recurrent hyperthyroidism in consecutive pregnancies characterized by hyperemesis.

A 34-year-old Caucasian woman was seen and evaluated for hyperemesis and abnormal thyroid function tests, consistent with hyperthyroidism, during her second pregnancy. Her hyperemesis and hyperthyroidism both resolved during the second trimester of this pregnancy. She recounted very similar symptoms of similar duration in her first pregnancy. She was again monitored in a third pregnancy during which hyperemesis and hyperthyroidism were once more documented, resolving during the second trimester. The recurrence of hyperemesis in three consecutive singleton pregnancies, with documentation of transient hyperthyroidism in two of these pregnancies, is suggestive of human chorionic gonadotropin (hCG)-mediated hyperthyroidism. Either the trophoblasts synthesized hCG of high thyrotropic grade or, alternatively, hCG could be modified in the maternal tissues, resulting in molecules with greater thyrotropic activity. These potential mechanisms are discussed.

Adult↗
PubMed1998

Normal serum concentrations of sex hormone binding-globulin in patients with hyperthyroidism due to subacute thyroiditis.

Serum concentrations of sex hormone binding-globulin (SHBG) were determined in patients with hyperthyroidism (n = 94; 12 men, 82 women) due to either Graves' disease (n = 59; 11 men, 48 women), autonomous thyroid adenomas (n = 23; 1 man, 22 women), or subacute thyroiditis (n = 12; all women). Elevated serum concentrations of SHBG were initially seen in 57 of 82 patients (69%) with hyperthyroidism due to either Graves's disease or due to autonomous adenoma. Elevated serum SHBG concentration was more frequent in patients with serum total thyroxine (TT4) concentrations greater than 15.0 microg/dL (32/39 [82%]; including 3 patients with autonomous adenoma) compared to those with serum TT4 concentration between 11.0 and 15.0 microg/dL (21/27 [77%]; including 7 patients with autonomous adenoma), or patients with an isolated elevation of serum total triiodothyronine (TT3) concentration (4/16 [25%]; including 2 patients with autonomous adenoma). Serum SHBG concentration normalized when patients became euthyroid. Only 1 of 12 patients in the hyperthyroid phase of subacute thyroiditis had an elevated serum concentration of SHBG. Serum concentrations of thyroid binding globulin (TBG) and transcortin (CBG) were normal in all but 1 patient. In patients with hyperthyroidism as a result of Graves' disease or autonomous adenoma serum SHBG concentrations were elevated with the greatest elevation found in patients with the highest serum T4 concentrations. The normal concentrations of SHBG in the hyperthyroid phase of subacute thyroiditis most likely reflects the shorter duration of exposure to increased thyroid hormone in this condition.

Adenoma↗
PubMed1999

Hyperthyroidism in pregnancy: diagnosis and treatment.

Hyperthyroidism due to autoimmune Graves' disease is the leading cause of thyrotoxicosis in pregnant women. The peak incidence of the disease is in the second through the fourth decade of life, which encompasses the reproductive years for women. Although menstrual irregularity is frequent in women with mild to moderate hyperthyroidism, convincing evidence that fertility is impaired is lacking. In general, 2 of every 1000 pregnancies have been reported to be complicated by hyperthyroidism. Hyperthyroidism associated with pregnancy may pose a challenging diagnostic and therapeutic dilemma. The current review focuses on the discussion of symptomatology and diagnosis of the disease, on therapeutic options available to women presenting with hyperthyroidism during gestation, and on the controversy surrounding maternal and fetal outcome in pregnancies complicated by thyrotoxicosis.

Adrenergic beta-Antagonists↗
PubMed2000

Increased lead excretion correlates with desoxypyridinoline crosslinks in hyperthyroid patients.

Lead is a widespread toxic metal that accumulates predominantly in human bone. Altered bone metabolism in hyperthyroidism is characterized mainly by bone resorption. Thus, we speculated that lead excretion could be increased in hyperthyroid patients. In 12 hyperthyroid patients (43.3 +/- 16.1 years) who were not previously occupationally exposed to lead, lead concentrations in blood (PbB), spot urine samples corrected by urine creatinine (PbUs), and in 24-hour urine samples (PbU24) were determined in the hyperthyroid state and after euthyroidism had been induced by therapy. Serum osteocalcin (OC) and desoxypyridinoline crosslinks (Pyr) served as specific markers for bone metabolism. After induction of euthyroidism (duration of antithyroid therapy: mean 17.3 +/- 6.9 weeks) PbB was reduced (3.7 +/- 2.6 vs. 5.7 +/- 4.7 microg/dL, p = 0.041) as was PbUs (0.39 +/-0.27 vs. 0.61 +/- 0.32 microg/mg Cr, p = 0.005). A fourfold decrease of PbU24 was associated with a 3.3-fold decrease of Pyr, and moreover there was a significant correlation between Pyr and PbUs (r = 0.58, p = 0.047). Concentration of total triiodothyronine correlated with Pyr (r = 0.66, p = 0.018), but not with PbB or PbUs. OC showed only a tendency to be increased before antithyroid medication, and did not correlate with either thyroid hormone or Pyr. Our results indicate that in hyperthyroid patients, even when not previously exposed to lead, lead excretion is increased due to bone resorption.

Adult↗
PubMed2005

Observations concerning the natural history of subclinical hyperthyroidism.

OBJECTIVE: To examine the natural history of a subnormal serum thyroid-stimulating hormone (TSH) concentration with normal concentrations of both serum free thyroxine (FT4) and free triiodothyronine (FT3) (subclinical hyperthyroidism). PATIENTS, DESIGN, AND MEASUREMENTS: A retrospective analysis was undertaken and yielded 16 ambulatory patients who had presented with subclinical hyperthyroidism and were longitudinally followed with measurements of serum TSH and both FT4 and FT3 for a cumulative follow-up of 11 to 36 months. Seven of the patients had subclinical Graves' hyperthyroidism as judged from the presence of thyroid-stimulating immunoglobulins (TSI) in serum, and 9 had multinodular goiter confirmed with ultrasound and no TSI. RESULTS: In the 7 patients with TSI, serum TSH reverted to normal in 5 patients, with disappearance or decrease of TSI in 4, within 3 to 19 months. In 1 patient, subnormal serum TSH accompanied by both normal FT4 and FT3 has persisted for 15 months, and in a second patient serum TSH reverted to normal within 9 months, but at follow-up 27 months later overt hyperthyroidism had emerged. In the 9 patients with multinodular goiter, subnormal serum TSH accompanied by both normal FT4 and FT3 persisted during cumulative follow-up that ranged from 11 to 36 months. CONCLUSIONS: This study suggests that the natural history of subclinical hyperthyroidism is variable, resolving or occasionally evolving in subclinical Graves' disease and persisting unchanged in multinodular goiter.

Adult↗
PubMed2006

The impact of overt and subclinical hyperthyroidism on skeletal muscle.

OBJECTIVE: Patients with overt hyperthyroidism (OH) commonly have proximal limb muscle weakness that improves after correction of hyperthyroidism. It is unclear, however, if patients with milder degrees of hyperthyroidism (referred to as subclinical hyperthyroidism or SCH) may also have a degree of muscle weakness. This may have clinical relevance as SCH patients are often elderly and may therefore have concurrent sarcopenia of aging and would represent a previously unrecognized complication of SCH. DESIGN: We measured both thigh strength and cross-sectional area in patients with OH (n = 30) or SCH (n = 24), both prior to treatment of hyperthyroidism and again at 6-9 months after the restoration of a euthyroid state. Euthyroid controls (n = 48) were studied at similar time intervals. MAIN OUTCOME: Prior to treatment, both knee flexor and extensor muscle strength was reduced in both patients with OH and SCH compared to controls (p < 0.05). After treatment all strength measurements improved in the OH group (p < 0.01) while in the SCH group the majority of muscle strength measurements improved (p < 0.05). Midthigh muscle cross-sectional area was reduced in both the OH and SCH group at baseline (p < 0.05) compared to controls and increased significantly following treatment (p < 0.05). There were no significant changes in any parameter in the euthyroid control (EC) group during the study period. CONCLUSIONS: The finding that muscle strength and cross-sectional area are reduced in SCH and improved after treatment lends support for the clinical decision to treat rather than observe this condition. This may have particular relevance to certain SCH patient groups including the elderly who are prone to falls and athletically active younger patients who require optimal skeletal muscle function.

Adolescent↗
PubMed1993

Radioiodine therapy for hyperthyroidism in young patients--perception of risk and use.

Although radioiodine is increasingly the treatment of choice in hyperthyroidism, there are regional differences in its use which reflect, in part, concerns regarding safety. We investigated attitudes amongst general practitioners and consultant physicians to the role of radioiodine therapy, and reviewed our own radioiodine prescribing in patients aged less than 40 to elucidate any influence of age and/or sex. We surveyed general practitioners in the former Central Birmingham Health District and consultant physicians in the West Midlands Region to investigate treatment preferences in hyperthyroidism and perceived risk from radioiodine of hypothyroidism, carcinogenesis and infertility. Of 230 general practitioner and 130 consultant physician respondents, less than 1% considered radioiodine the treatment of choice in a 25-year-old female presenting with hyperthyroidism. At relapse after antithyroid drug treatment in a 25-year-old female, only 16.5% of general practitioners and 23.9% of physicians advocated radioiodine, the greatest number preferring partial thyroidectomy. For a 65-year-old at presentation, 49.1% of general practitioners and 62.3% of physicians considered radioiodine the treatment of choice. More than 10% failed to note the risk of hypothyroidism following radioiodine, while 11-34% perceived increased risk of malignancy or infertility. Review of our own practice demonstrated that of 100 patients given radioiodine, 94% were cured of hyperthyroidism when reviewed at a mean of 2.4 years from latest treatment, 70% being hypothyroid. Females given radioiodine were treated less promptly following diagnosis of hyperthyroidism than males (2.2 +/- 0.26 years vs. 1.6 +/- 0.4) and were more likely to have received a preceding course of antithyroid drugs (78% vs. 57%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1997

The effect of hyperthyroidism on Müller's muscle contractility in rats.

The objective of this study was to determine if hyperthyroidism affects the responses of Müller's muscle to alpha-1 adrenoceptor agonists and consequently, if these responses might explain thyroid eyelid retraction. Sprague-Dawley adult rats (n = 37) were divided into control and treated groups and given either placebo or intraperitoneal triiodothyronine (250 micrograms/kg/d) for 1, 2, or 3 weeks. A suture was passed through their upper eyelid and connected to a force transducer that measured Müller's muscle contractions. Responses to phenylephrine (0.015-0.61 mmol) were compared with respect to peak amplitude and 50% duration of action. Mean maximum force values [+/-1 standard error of the mean (SEM)] in response to phenylephrine were 1.254 +/- 0.071 gr for controls and 0.963 +/- 0.062 gr for thyroid-treated subjects (p = 0.005). Mean 50% duration of response values (+/-1 SEM) were 9.143 +/- 1.108 min for controls and 5.763 +/- 0.973 min for thyroid-treated subjects (p = 0.014). Hyperthyroid rats had a significantly lower Müller's muscle response amplitude than control rats; however, duration of response was not significantly different between the groups. We believe that hyperthyroidism caused intrinsic changes in Müller's muscle that resulted in eyelid retraction. Based on hypotheses discussed in this article, we expect that further studies will localize these changes to the thyroid hormone receptor on Müller's muscle or calcium-triggered intracellular second messengers. Clinical significance would then be the ability to treat hyperthyroid eyelid retraction with drugs. This study provides the first evidence of functional impairment of Müller's muscle due to hyperthyroidism in an animal model.

Adrenergic alpha-Agonists↗
PubMed2000

Propranolol diminishes cardiac hypertrophy but does not abolish acceleration of the ischemic contracture in hyperthyroid hearts.

This study was undertaken to define the contributions of left ventricular hypertrophy (LVH) and increased adrenergic activity to the acceleration of ischemic contracture (IC) that occurs in chronic hyperthyroid rat heart. Acute and chronic hyperthyroidism (THYR) were induced by thyroxine administration for 2 and 14 days, respectively, and normal animals (NORM) served as controls. Isolated hearts were perfused in a Langendorff mode. NORM alpha acute, n = 6; THYR alpha acute, n = 8; and THYR alpha, n = 13; and NORM alpha, n = 13 were subjected to 20-min zero-flow global ischemia (I) and 45-min reperfusion (R). Additional THYR and NORM hearts treated with propranolol (prop) were subjected to 30-min I; THYR beta prop, n = 6 and NORM beta prop, n = 8, and THYR beta, n = 6, NORM beta, n = 8 served as controls. Acceleration of IC was measured by the time to peak contracture (Tmax). Left ventricular hypertrophy (LVH) was assessed by the ratio of left ventricular weight in milligrams (LVW) to animal body weight (BW) in grams. Cardiac hypertrophy developed in chronic but not acute hyperthyroidism. Propranolol reduced the extent of LVH. Contracture occurred earlier in chronic than in acute hyperthyroid and normal hearts. Propranolol did not alter contracture. In conclusion, IC is accelerated by thyroxine administration, and this is probably not due to LVH or increased beta-adrenergic activity. Propranolol diminishes LVH in hyperthyroidism.

Adrenergic beta-Antagonists↗
PubMed2001

Recovery of chronic hepatitis by treatment of concomitant hyperthyroidism.

A 15-year-old boy presented with biochemical and histological hepatic abnormalities consistent with chronic aggressive hepatitis and concomitant hyperthyroidism. After treatment with antithyroid therapy not only the hyperthyroidism subsided but also the hepatic function normalized. Two years later, the hyperthyroidism and liver function disorders relapsed in combination with a striking vitiligo and once again the liver function normalized after treating the hyperthyroidism. The liver biopsy sample taken in remission showed a normal picture without signs of hepatitis, fibrosis or cirrhosis. The diagnosis of a polyglandular syndrome was made, of which three types have been described. At this moment the patient fits best in type 3, which is a rather heterogenic group. Recovery of chronic hepatitis by treatment of concomitant hyperthyroidism has never been described before.

Adolescent↗
PubMed1977

The possible relation between postpartum exacerbation of hyperthyroidism and neonatal thyrotoxicosis.

Hyperthyroidism is generally considered to be ameliorated during pregnancy, and there appears to be a high incidence of postpartum exacerbation. These phenomena have to our knowledge not been related to neonatal thyrotoxicosis, a transient hyperthyroidism seen only in newborns of previous or current hyperthyroid mothers. The first of two siblings of a previously thyrotoxic mother had marked symptoms of neonatal thyrotoxicosis and high levels of thyroid hormones. The mother had not received antithyroid treatment during her first pregnancy. During her next pregnancy she was treated with propylthiouracil from the second trimester. This infant had only minimal thyrotoxic signs but almost as high levels of thyroid hormones during the neonatal period as the elder. The mother had no signs of postpartum exacerbation but her thyroid hormones were significantly elevated in the postpartum period analogous to the infants. Neither the mother nor the infants presented any increase in thyroid-stimulation hormone and long-acting thyroid stimulator during the hyperthyroid periods. The possibility is discussed, that postpartum exacerbation of hyperthyroidism and neonatal thyrotoxicosis may be related. They could be the result of a changed balance between a thyroid stimulator and an inhibitor after birth.

Female↗
PubMed1985

Treatment of hyperthyroidism with standard doses of radioiodine aiming at ablation.

Sixty patients with hyperthyroidism were treated with standard doses of 131I during 1969-83 in our department. The doses were 10-25 mCi (370-920 MBq), mostly 15 mCi (550 MBq). 38 of the patients have become hypothyroid, mostly within one year after treatment. There were 3 early relapses of hyperthyroidism; these patients became hypothyroid within one year after an additional dose of radioiodine. All hypothyroid patients had early substitution with l-thyroxine before overt clinical symptoms and signs had developed. There were no late relapses of hyperthyroidism. 15 patients had died during the follow-up; all were euthyroid or hypothyroid with adequate substitution. 28 of the 60 patients have been followed for 5-14 years, 14 for 2-5 years, 7 for 1-2 years and 10 for less than one year. Standard dose 131I treatment offers certain advantages compared with attempted individualized treatment. Late hypothyroidism after individualized dosage may be difficult to anticipate and detect, whereas early hypothyroidism after ablative standard dose treatment is easy to detect and control. Generally speaking, hypothyroidism is not to be regarded as a complication of radioiodine treatment for hyperthyroidism, but as its natural end result. The fixed dose schedule is especially well suited for regions where hyperthyroidism with no goitre or a small goitre is common.

Adult↗