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PubMed2000

Serum dehydroepiandrosterone, dehydroepiandrosterone sulfate, and pregnenolone sulfate concentrations in patients with hyperthyroidism and hypothyroidism.

BACKGROUND: Dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEA-S) have been suggested to have protective effects against cardiovascular disease, cancer, immune-modulated diseases, and aging. We examined serum concentrations of DHEA, DHEA-S, and pregnenolone sulfate (PREG-S) in patients with thyroid dysfunction. METHODS: Steroids extracted with methanol from serum sample were separated into an unconjugated fraction (DHEA) and a monosulfate fraction (DHEA-S and PREG-S), using a solid-phase extraction and an ion-exchange column. After separation of unconjugated steroids by HPLC, the DHEA concentration was measured by enzyme immunoassay. The monosulfate fraction was treated with arylsulfatase, and the freed steroids were separated by HPLC. The DHEA and PREG fractions were determined by gas chromatography-mass spectrometry, and the concentrations were converted into those of DHEA-S and PREG-S. RESULTS: Serum concentrations of DHEA, DHEA-S, and PREG-S were all significantly lower in patients with hypothyroidism (n = 24) than in age- and sex-matched healthy controls (n = 43). By contrast, in patients with hyperthyroidism (n = 22), serum DHEA-S and PREG-S concentrations were significantly higher, but the serum DHEA concentration was within the reference interval. Serum concentrations of these three steroids correlated with serum concentrations of thyroid hormones in these patients. Serum albumin and sex hormone-binding globulin concentrations were not related to these changes in the concentration of steroids. CONCLUSIONS: Serum concentrations of DHEA, DHEA-S, and PREG-S were decreased in hypothyroidism, whereas serum DHEA-S and PREG-S concentrations were increased but DHEA was normal in hyperthyroidism. Thyroid hormone may stimulate the synthesis of these steroids, and DHEA sulfotransferase might be increased in hyperthyroidism.

Adult↗
PubMed2005

Interactions among thyroid function, insulin sensitivity, and serum lipid concentrations: the Fremantle diabetes study.

CONTEXT: Recent observations in healthy subjects showed that insulin resistance modifies the relationship between serum cholesterol and thyroid function. OBJECTIVE: The aim of the study was to determine whether insulin sensitivity modifies the association between thyroid dysfunction and lipid parameters in diabetic patients. DESIGN: This is a cross-sectional study. SETTING: This is a community-based observational study. PATIENTS: One hundred seventeen females with type 2 diabetes who were not taking oral hypoglycemic therapy, insulin, or lipid-lowering therapy participated in the study. INTERVENTION: Serum TSH, insulin, total and high-density lipoprotein cholesterol, and triglycerides were measured. MAIN OUTCOME MEASURES: Age-adjusted multiple linear regression analysis of serum lipid concentrations and derived parameters, as functions of serum TSH and homeostasis model assessment-derived insulin sensitivity (HOMA-S), were measured. RESULTS: The relationship among serum lipid concentrations, serum TSH, and HOMA-S was significantly modified by an interaction term ln(TSH)*ln(HOMA-S). In three-dimensional graphs, there were strong positive associations between TSH and lipid parameters with adverse cardiac risks at low insulin sensitivity that were absent at higher insulin sensitivity. The effect was strongest for lipid risk factors associated with insulin resistance. CONCLUSIONS: The interaction between thyroid function and insulin sensitivity is an important contributor to diabetic dyslipidemia and may justify T4 replacement in some patients.

Aged↗
PubMed2005

Myocardial ultrastructure in cardiac hypertrophy induced by thyroid hormone--an acute study in rats.

The early responses of the myocardium ultrastructure under thyroid dysfunction conditions, hemodynamic parameters, cardiac hypertrophy and ultrastructural evaluations were performed in hypothyroid and hyperthyroid rats submitted to different doses [T4-25 and T4-100; 0.025 mg and 0.1 mg kg(-1) body weight (BW).per day, respectively)]. All groups were treated for 7 days. The animals were sacrificed, the hearts were excised and weighed and the left ventricle tissue samples were processed for transmission election microscopy. Systolic blood pressure (SBP) was not altered by administration of T4. An increased heart rate and ratio of heart weight to body weight (HW/BW) were found in the hyperthyroid rats. However, the SBP and HW/BW decreased significantly in hypothyroid rats. No significant ultrastructural alterations were detected when the hypothyroid and T4-25 groups were compared with the control group. Alterations of cardiomyocytes nuclei of these groups were also not detected. Notably, disorganization of intercellular junctions was observed in many cardiomyocytes of T4-100 group. The present results indicate that in the early stages of hyperthyroidism, the cardiac hypertrophy development was mainly due to direct effects of thyroid hormone. Despite cardiac hypertrophy development, there is no ultrastructural evidence of myocardial degeneration.

Animals↗
PubMed1994

Bone mineral density and metabolism in premenopausal women taking L-thyroxine replacement therapy.

BACKGROUND AND OBJECTIVE: Excess endogenous thyroxine causes bone loss, but the effects of exogenous thyroxine are disputed. We report on bone mass and metabolism in women taking L-thyroxine therapy. DESIGN: Cross-sectional and longitudinal studies. PATIENTS: Cross-sectional study: 40 healthy premenopausal women with autoimmune thyroiditis taking either physiological (serum TSH usually normal, 0.35-3.3 mU/l) or suppressive (serum TSH usually < 0.35 mU/l) doses of L-thyroxine; patients were also compared with previously acquired age and weight matched premenopausal volunteers with no history of thyroid dysfunction. Longitudinal study: 28 patients were followed-up > or = 1 year later. MEASUREMENTS: In all subjects bone mineral density (BMD) was measured at the anteroposterior lumbar spine and left hip (femoral neck, greater trochanter and Ward's area) using dual-energy X-ray absorptiometry, and physical activity assessed using the Framingham physical activity index. Serum osteocalcin (OC), PTH and vitamin D, and urinary pyridinoline and deoxypyridinoline excretion were measured in patients. RESULTS: Cross-sectional study: The patient groups were well matched for disease duration and physical activity although the suppressed group were slightly younger (mean 38.1 (SD 7.5) vs 43.3 (3.9) years, P < 0.05). BMD, serum OC, PTH and vitamin D, and urinary cross-link excretion did not differ significantly between the two groups. Multivariate analysis of the whole group suggested that BMD at the femoral neck and greater trochanter was related positively to weight and physical activity and negatively to thyroxine dose (microgram/kg/day) and patient age. At the lumbar spine BMD was reduced non-specifically in the presence of thyroid disease and treatment, but this effect appeared to decline with increasing duration of therapy. A similar analysis of the patient group suggested that urinary cross-link excretion correlated positively with thyroxine dose, and negatively with duration of treatment. Longitudinal study: Annualized changes in BMD were inversely related to thyroxine dose (microgram/kg/day) at all sites but achieved statistical significance only at the femoral neck and Ward's area. CONCLUSION: We did not find any effect of persistent historical TSH suppression on current bone mass, and this might relate to the relative insensitivity of older TSH assays. However, the cross-sectional and longitudinal data suggest that high daily doses of thyroxine in relation to patient body weight might adversely affect bone mass, particularly at the hip. These findings support the contention that excess exogenous thyroxine might predominantly deplete skeletal sites, such as the femoral neck, rich in cortical bone.

Absorptiometry, Photon↗
PubMed1990

Thoracic irradiation in Hodgkin's disease: disease control and long-term complications.

A total of 590 patients with Stage IA-IIIB Hodgkin's disease received mantle irradiation at the Joint Center for Radiation Therapy between April 1969 and December 1984 as part of their initial treatment. Recurrence patterns as well as pulmonary, cardiac and thyroid complications were analyzed. Pulmonary recurrence was more frequently seen in patients with large mediastinal adenopathy (LMA); 11% of patients with LMA recurred in the lung in contrast to 3.1% with small or no mediastinal disease, p = 0.003. Hilar involvement, when corrected for size of mediastinal involvement, was not predictive of lung relapse. Patients with LMA also had a high rate of nodal relapse above the diaphragm (40%) following radiation therapy (RT) alone as compared to similarly treated patients with small or no mediastinal adenopathy (6.5%), p less than 0.0001. This risk of nodal recurrence was greatly reduced (4.7%) for LMA patients receiving combined radiation therapy and chemotherapy (CMT), p less than 0.0001. Sixty-seven patients (11%) with hilar or large mediastinal involvement received prophylactic, low dose, whole lung irradiation. No decrease in the frequency of lung recurrence was seen with the use of whole lung irradiation. Radiation pneumonitis was seen in 3% of patients receiving radiation therapy alone. In contrast, the use of whole lung irradiation was associated with a 15% risk of pneumonitis, p = 0.006. The risk of pneumonitis was also significantly increased with the use of chemotherapy (11%), p = 0.0001. Cardiac complications were uncommon with pericarditis being the most common complication (2.2%). Thyroid dysfunction was seen in 25% of patients and appeared to be age-related. These data suggest that the long-term complications of mantle irradiation are uncommon with the use of modern radiotherapeutic techniques. The use of prophylactic whole lung irradiation is no longer recommended since its use did not reduce pulmonary relapse but did increase the risk of pneumonitis. Chemotherapy is also associated with an increased risk of pneumonitis, however, its use in patients with large mediastinal adenopathy appears justified.

Adolescent↗
PubMed1997

[Therapy of hypo- and hyperthyroidism in pregnancy].

Therapy of thyroid dysfunction needs a close cooperation between endocrinologist and gynecologist. In addition to a number of metabolic changes during pregnancy, the diaplacentar transfer of different substances (thionamides, antibodies) has to be considered. Pregnant women with overt and subclinical hypothyroidism should be treated using L-Thyroxine with the bTSH between 1 and 2 mU/l. Many of the women need an increase of the L-Thyroxine dose during pregnancy. Overt hyperthyroidism (mostly due to Graves' disease) has to be treated immediately after diagnosis using thionamides. Because thionamides cross the placenta, the dose should be as low as possible with the fT4 in upper level and bTSH in the lower level of normal range. Most studies show, that both methimazole (MI) and propylthiouracil (PTU) can be used in pregnancy. Although PTU is preferred especially in the USA, an advantage of PTU over MI is not proven. Surgery is necessary in only few cases of hyperthyroidism during pregnancy with the optimal time for surgery during the second trimester. In case of subclinical hyperthyroidism and HCG induced hyperthyroidism several controls of thyroid function should be performed to decide whether treatment is necessary.

Abnormalities, Drug-Induced↗
PubMedDate not supplied

Dual role of testosterone in fenvalerate-treated mice with respect to thyroid function and lipid peroxidation.

Effects of testosterone propionate (TP, 2.5 mg kg(-1) body weight) in fenvalerate-induced (120 mg kg(-1) body weight) thyroid dysfunction and lipid peroxidation were investigated in male mice. Testosterone propionate aggravated in the inhibition of hepatic type I iodothyronine 5'-monodeiodinase (5'D-I) activity, coupled with a decrease in serum triiodothyronine (T3) concentration in pesticide-treated mice. However, it could ameliorate the toxicity as indicated by decreased hepatic lipid peroxidation (LPO) with a marginal but significant increase in superoxide dismutase and catalase activities following fenvalerate treatment. While protective effects of testosterone on LPO indicated its antiperoxidative property, the decrease in 5'D-I activity could be because of the increased accumulation of fenvalerate in the tissues following TP administration.

Animals↗
PubMed1993

Treatment of amiodarone-induced hypothyroidism with potassium perchlorate.

The antiarrhythmic drug, amiodarone, induces thyroid dysfunction, which is potentially dangerous in cardiac patients. After discontinuation of the drug it takes several months before euthyroidism is restored. The potent antithyroid drug, potassium perchlorate (KClO4), is used successfully to treat amiodarone-induced thyrotoxicosis, but it is less well known as potential treatment in amiodarone-induced hypothyroidism. In this case report we describe the successful use of two courses of KClO4 treatment in a cardiac patient with severe amiodarone-induced hypothyroidism. The mechanisms responsible for the amiodarone-induced hypothyroidism and rationale for the use of KClO4 in this condition are discussed.

Amiodarone↗
PubMed1986

Natural history of dermatitis herpetiformis in southern Sweden.

A retrospective clinical survey of 96 patients with dermatitis herpetiformis (DH) was performed in two defined populations of 425,000 in southern Sweden. The incidence of DH was 1.05-1.13/100,000 inhabitants/year and the prevalence was approximately 20-25/100,000 inhabitants. In one-third of DH patients the age at onset was greater than 60 years. In women with DH a strong connection to thyroid dysfunction was observed, but also other conditions of probable autoimmune pathogenesis were found in both sexes. No connection to malignant disease was observed. DH seems to be less active the later in life it starts. Several patients with DH manage without dapsone or need dapsone just occasionally in connection with bouts. This is the case even without a gluten-free diet. Many mild cases of DH were observed without a gluten-free diet; therefore, this restricting regimen should be prescribed only in more active cases of DH.

Adolescent↗
PubMedDate not supplied

Nervous system role of iodocompounds in blood pressure regulation.

Approximately one-third of hypertensive patients with thyroid dysfunction become normotensive on restoration to the euthyroid state. Considerable evidence suggests that the nervous system is involved in these responses, but the mechanism has been obscure. New information demonstrates that iodothyronines are localized and processed in discrete neural systems in rat brain. Moreover, following a latent period, heart rate is significantly increased by intrathecal administration of triiodothyronine in a dose which sustains but does not increase heart rate when given intravenously. These observations add to existing biochemical and autoradiographic evidence that autonomic effects of iodocompounds may be mediated through direct neuroregulatory (neuromodulator and neurotransmitter) functions within the nervous system.

Animals↗
PubMed1993

Pregnancy after high therapeutic doses of iodine-131 in differentiated thyroid cancer: potential risks and recommendations.

Seventy female patients who had been treated with high doses of iodine-131 for differentiated thyroid cancer (DTC) and who had a subsequent pregnancy were evaluated. The total 131I dose ranged from 1.85 to 16.55 GBq (mean +/- SD = 4.39 +/- 25.20 GBq). Age at first therapy ranged from 15 to 36 years (mean +/- SD = 24.3 +/- 5.0 years) and the interval from 131I therapy to pregnancy varied from 2 to 10 years (mean +/- SD = 5.3 +/- 2.8 years). The estimated radiation dose to the gonads ranged from 10 to 63 cGy (mean +/- SD = 24.0 +/- 13.5 cGy). All patients were treated with L-thyroxine at doses capable of suppressing thyroid-stimulating hormone. Seventy-three children were followed-up and seven pregnancies are still in progress. One child was affected by Fallot's trilogy and three had a low birth weight through with subsequent normal growth; the others were healthy with subsequent normal growth. No newborn with clinical or biochemical thyroid dysfunctions was found. Two spontaneous abortions during the second month of pregnancy were recorded. One of two patients in question subsequently had two healthy children. On the basis of these data, previous administration of high 131I doses does not appear to be a valid reason for dissuading young female DTC patients from considering pregnancy. However, patients should be advised to avoid pregnancy after 131I administration for a period sufficient to ensure complete elimination of the radionuclide and to permit confirmation of complete disease remission, i.e. at least 1 year in our opinion.

Adenocarcinoma↗
PubMed1989

"Low T3 syndrome" in cirrhosis: effect of beta-blockade.

The so-called "low T3 syndrome" has frequently been reported in patients with cirrhosis. In this study, we aimed to determine whether administration of propranolol to such patients leads to further changes in plasma thyroid hormones, since it can affect their peripheral metabolism. Twenty cirrhotics (11 with ascites) whom we investigated showed no clinical evidence of thyroid dysfunction. The free fractions of plasma T3 and T4 (FT3, FT4) were determined by radioimmunoassay before and after the achievement of an effective beta-blockade by propranolol. The activity of the sympathetic nervous system also was evaluated by measuring plasma norepinephrine concentration. Under basal conditions, cirrhotics showed a reduced FT3 (2.45 +/- 0.11 SEM vs 3.55 +/- 0.16 pg/ml; p less than 0.001) and comparable FT4 (7.62 +/- 0.79 vs 9.2 +/- 0.42 pg/ml) and FT3/FT4 ratio (0.38 +/- 0.04 vs 0.42 +/- 0.013) with respect to healthy controls. When patients with ascites were considered apart, a reduction of FT4 was also found (6.78 +/- 0.74 pg/ml; p less than 0.01). In these patients, many of whom showed an increased plasma norepinephrine concentration, an inverse correlation between log FT3/FT4 and log plasma norepinephrine concentration was found (r = -0.79; p less than 0.01). The effective beta-blockade did not lead to significant changes in either FT3 or FT4 or FT3/FT4, whether the patients were considered as a whole (2.52 +/- 0.19 pg/ml, 9.3 +/- 1.41 pg/ml, and 0.36 +/- 0.04, respectively), or were split into groups according to the presence of ascites. When administered to cirrhotics, propranolol did not worsen thyroid hormone abnormalities, thus appearing to be safe in this respect. This may result from an impaired influence of the sympathoadrenergic system on thyroid hormone metabolism.

Adult↗
PubMed1985

Side effects and complications of amiodarone therapy.

To assess the incidence of adverse effects associated with long-term amiodarone therapy, we reviewed the records of 217 consecutive patients who were treated for refractory arrhythmia. After an average of 11.8 months of therapy, one or more side effects occurred in 113 patients (52%). These were considered clinically significant in 42 patients (19.3%), mandating discontinuation of amiodarone in 18 (8.3%). The untoward reactions requiring discontinuation of amiodarone included thyroid dysfunction, visual disturbances, pulmonary infiltrates, ataxia, cardiac conduction abnormalities, and drug interactions. The mild side effects included corneal microdeposits, skin rashes, and gastrointestinal symptoms. There was a weak correlation between blood levels of amiodarone, the daily dose, and the cumulative dose (r = 0.23, p = 0.015). Drug levels were higher in symptomatic patients (p less than 0.03), although they received lower doses of amiodarone. While amiodarone is associated with frequent side effects, they are generally mild and do not necessitate drug discontinuation. Careful monitoring of therapy is essential to detect the potentially serious adverse reactions which are encountered in nearly 20% of patients.

Amiodarone↗
PubMed2005

[Thyroid ophthalmopathy: clinical activity determination of thyroid ophthalmopathy as a prognostic factor of immunosuppressive treatment response].

OBJECTIVE: To determine the usefulness of the clinical, biochemical and thyroid imaging parameters in patients with thyroid-associated ophthalmopathy, in predicting their response to immunosuppressive treatment. METHODS: This retrospective study of 16 patients with thyroid ophthalmopathy considered a number of variables including sex, age, thyroid hormone levels, treatment of the thyroid dysfunction, clinical activity score (CAS), severity (NOSPECS) of the ophthalmopathy, signs in standardized A-mode ultrasonography, in CAT and/or NMR, and previously used treatments and their effectiveness. RESULTS: The average age of the patients was 50.81 (S.D: 11.89) years; there were 5 males (31.3%) and 11 females (68.8%). The ophthalmopathy was classified as active in 10/16 patients (62.5%) and inactive in 6/16 (37.5%); and as moderate in 9/16 (56.25%) and severe in 7/16 (43.75%) according to the severity defined in NOSPECS. Ultrasonography was diagnostic in 100% of the cases. The severity decreased significantly (p < or =0.05), however the clinical activity decrease did not reach significance (p=0.38) during immunosuppressive therapy. Better results were obtained during treatment of patients with a higher CAS (p=0.04) and in those with more severe ophthalmopathy (p=0.02). There was a tendency for the patients with higher levels of TSI to respond better to the treatment (p=0.06). CONCLUSIONS: The CAS is the best parameter to quantify the activity of the disease and predicting the response to treatment. The higher the CAS and the more severe the ophthalmopathy, the better the response to treatment. No association existed between thyroid function and the activity or severity of the ophthalmopathy; or the effectiveness of treatment.

Adult↗
PubMed2006

Thyroid hormone and gamma-aminobutyric acid (GABA) interactions in neuroendocrine systems.

Thyroid hormones (THs) have critical roles in brain development and normal brain function in vertebrates. Clinical evidence suggests that some human nervous disorders involving GABA(gamma-aminobutyric acid)-ergic systems are related to thyroid dysfunction (i.e. hyperthyroidism or hypothyroidism). There is experimental evidence from in vivo and in vitro studies on rats and mice indicating that THs have effects on multiple components of the GABA system. These include effects on enzyme activities responsible for synthesis and degradation of GABA, levels of glutamate and GABA, GABA release and reuptake, and GABA(A) receptor expression and function. In developing brain, hypothyroidism generally decreases enzyme activities and GABA levels whereas in adult brain, hypothyroidism generally increases enzyme activities and GABA levels. Hyperthyroidism does not always have the opposite effect. In vitro studies on adult brain have shown that THs enhance GABA release and inhibit GABA-reuptake by rapid, extranuclear actions, suggesting that presence of THs in the synapse could prolong the action of GABA after release. There are conflicting results on effects of long term changes in TH levels on GABA reuptake. Increasing and decreasing circulating TH levels experimentally in vivo alter density of GABA(A) receptor-binding sites for GABA and benzodiazepines in brain, but results vary from study to study, which may reflect important regional differences in the brain. There is substantial evidence that THs also have an extranuclear effect to inhibit GABA-stimulated Cl(-) currents by a non-competitive mechanism in vitro. The thyroid gland exhibits GABA transport mechanisms as well as enzyme activities for GABA synthesis and degradation, all of which are sensitive to thyroidal state. In rats and humans, GABA inhibits thyroid stimulating hormone (TSH) release from the pituitary, possibly by action directly on the pituitary or on hypothalamic thyrotropin-releasing hormone neurons. In mice, GABA inhibits TSH-stimulated TH release from the thyroid gland. Taken together, these studies provide strong support for the hypothesis that there is reciprocal regulation of the thyroid and GABA systems in vertebrates.

Animals↗
PubMed1997

Early effects of iodine deficiency on radial glial cells of the hippocampus of the rat fetus. A model of neurological cretinism.

The most severe brain damage associated with thyroid dysfunction during development is observed in neurological cretins from areas with marked iodine deficiency. The damage is irreversible by birth and related to maternal hypothyroxinemia before mid gestation. However, direct evidence of this etiopathogenic mechanism is lacking. Rats were fed diets with a very low iodine content (LID), or LID supplemented with KI. Other rats were fed the breeding diet with a normal iodine content plus a goitrogen, methimazole (MMI). The concentrations of -thyroxine (T4) and 3,5,3'triiodo--thyronine (T3) were determined in the brain of 21-d-old fetuses. The proportion of radial glial cell fibers expressing nestin and glial fibrillary acidic protein was determined in the CA1 region of the hippocampus. T4 and T3 were decreased in the brain of the LID and MMI fetuses, as compared to their respective controls. The number of immature glial cell fibers, expressing nestin, was not affected, but the proportion of mature glial cell fibers, expressing glial fibrillary acidic protein, was significantly decreased by both LID and MMI treatment of the dams. These results show impaired maturation of cells involved in neuronal migration in the hippocampus, a region known to be affected in cretinism, at a stage of development equivalent to mid gestation in humans. The impairment is related to fetal cerebral thyroid hormone deficiency during a period of development when maternal thyroxinemia is believed to play an important role.

Animals↗
PubMed1994

Angiotensin receptors in cardiovascular diseases.

1. Angiotensin II (AII) plays a major role in cardiovascular function via direct actions on the vasculature, kidney, adrenal, heart, brain and sympathetic nerves. The cellular effects of AII are extensive and encompass hypertrophy, hyperplasia and the deposition of extracellular matrix. 2. The actions of AII are mediated by the AT1 and AT2 membrane receptor subtypes, and additional forms of each subtype. Evidence is emerging that selective changes in AII receptor subtypes occur in cardiovascular diseases. 3. Thyroid dysfunction increased cardiac, liver and kidney AII receptor density but decreased adrenal gland receptor density. In the heart, there was a selective increase in AT2 receptor density. 4. Diabetes increased cardiac, liver and adrenal gland AII receptor densities but decreased kidney receptor density. 5. Hypertension increased AII receptor density in the heart and kidney. A corresponding increase in receptor mRNA was prevented by selective AT1 receptor antagonists. 6. The human heart contained AII receptors in all chambers; right atrial receptor density was increased in coronary artery bypass graft patients. 7. The presence of AII receptor changes in these models of cardiac hypertrophy and hypertension raises the possibility of using orally active, subtype-selective agonists and antagonists to treat particular forms of cardiovascular diseases.

Acromegaly↗
PubMed1990

Follow up of alterations in thyroid hormones and thyrotropin in patients of Hodgkin's disease given mantle radiation.

Thirty five patients with Hodgkin's disease who had received mantle radiotherapy to the neck were investigated for thyroid dysfunction serially over many years post radiation. No incidence of clinical hypothyroidism was noted; however, biochemical hypothyroidism (raised TSH, normal T3 and T4) was seen at some time during follow up in 22 patients. Thirteen had high TSH values at the first post radiation examination: in 6 they remained high during follow up and in seven they fell to normal or near normal without thyroxine substitution at any time. TSH abnormalities were seen by 2-3 years post radiotherapy and the return to normal, when it occurred, was seen by 4-6 years. It is advisable to follow up patients with abnormal TSH values following mantle radiation for a further 2-3 years and begin thyroxine substitution only if TSH abnormalities persist.

Adolescent↗