The value of thyroid parenchymal echogenicity as an indicator of pathology using the sternomastoid muscle for comparison

This study was undertaken to evaluate the diagnostic accuracy of comparison of the echogenicity of the thyroid gland with the sternomastoid muscle in diagnosis of thyroid disorders. Fifty healthy subjects underwent a thyroid ultrasound, and 80 patients with archived thyroid ultrasound examinations (50 thyrotoxicosis and 30 thyroiditis) were reviewed. Images were measured for the image density of the thyroid gland and the sternomastoid muscle, using a transmission densitometer. Healthy thyroid was relatively hyperechoic when compared with the sternomastoid muscle (100%). Of the thyrotoxic patients, 70% showed a relatively hyperechoic thyroid compared to 47% of the thyroiditis patients. Mean image density difference in healthy thyroid, thyrotoxicosis and thyroiditis ranged from 0.1 to 1, -0.42 to 0.83, and -0.55 to 0.58, respectively. In conclusion, the relative echogenicity of the thyroid gland when compared with the sternomastoid muscle may be useful to differentiate healthy thyroid from thyrotoxicosis and thyroiditis, but does not help to distinguish thyrotoxicosis from thyroiditis. An image density difference of less than 0.1 may be considered to be abnormal, whereas a value greater than 0.83 may be considered to be normal.     

Manifestation of primary hyperthyroidism after pituitary adenomectomy: a case report

We report a 47-year-old Japanese man who presented with visual disturbance due to a pituitary tumor with suprasellar extension. The patient had mild secondary hypothyroidism preoperatively, and was started on administration of levothyroxine sodium immediately before transsphenoidal surgery. After the operation, levothyroxine sodium was continued for several months. Pathological examination of the surgical specimen, together with endocrinological investigation revealed that the suprasellar tumor was a FSH-producing pituitary adenoma. Since 3 months after the operation, he has developed muscle weakness and finger tremor. He was found to be thyrotoxicosis, and levothyroxine sodium was discontinued. Seven weeks after levothyroxine sodium was discontinued, thyrotoxicosis continued, with a positive thyrotropin binding inhibitory immunoglobulin (TBII) and a high diffuse 123I-uptake by the thyroid. He was started on thiamazole 30 mg/day. Although his thyroid dysfunction improved within 2 months, hyperthyroidism worsened repeatedly on attempts to discontinue thiamazole, and he required continuous treatment at 2.5 mg/day. Patients with occult autoimmune thyroiditis rarely progress to thyrotoxicosis after operations on other endocrine organs such as the adrenal or parathyroid gland. In patients with pituitary adenoma, thyroid function and thyroid-associated autoantibodies should be investigated pre- and post-operatively.     

Histometry of lymphoid infiltrate in the thyroid of primary thyrotoxicosis patients. Relation of extent of thyroiditis to preoperative drug treatment and postoperative hypothyroidism

The thyroids of primary thyrotoxicosis patients prepared for partial thyroidectomy with propranolol contained much more lymphoid infiltrate than those prepared with carbimazole. No relation was found between the extent of lymphoid infiltrate in the thyroid and the development of postoperative hypothyroidism either between or within the two drug treatment groups. This study has shown that the extent of thyroid infiltrate should not be used as the major factor in predicting hypothyroidism after subtotal thyroidectomy for primary thyrotoxicosis.     

Thyrotoxicosis and lactate-producing angina pectoris with normal coronary arteries

Three patients with thyrotoxicosis are described, in whom the presenting symptom was severe cardiac pain at rest or on effort and who were admitted to hospital with suspected or proven myocardial infarction. All patients were studied by selective coronary arteriography and left ventriculography after thyroid function tests which confirmed thyrotoxicosis. There was no demonstrable disease of the major coronary arteries in any of the patients, yet myocardial infarction and left ventricular aneurysm were shown to be present in 1, and there was definite electrocardiographic evidence of ischaemia in all 3. In addition, under stress the myocardium of all 3 patients produced lactate. It is recommended that thyrotoxicosis be seriously considered in the differential diagnosis of cardiac pain, particularly in younger women. The cause of the pain seems related to the cellular effects of thyrotoxicosis on the myocardium and current views of these effects are summarised. Of the 3 patients, 1 died suddenly 6 months after becoming euthyroid, indicating that the disease may not be as benign as expected. A guarded prognosis and continued medical follow-up are recommended when thyrotoxicosis presents with angina pectoris even when normal coronary arteries have been demonstrated.     

Amiodarone-induced thyrotoxicosis: is there a place for surgery?

Amiodarone-induced hyperthyroidism has on most instances been reported as mild, and thyroid functions return to normal after discontinuation of the drug. Nevertheless, life-threatening amiodarone-induced thyrotoxicosis has also been described. Conventional treatments such as antithyroid drugs (thionamide) and corticosteroids are essentially ineffective or fail to alter the dramatic course of the thyroid crisis. This limited effectiveness of medical therapy, particularly in patients with previously neglected or unknown thyroid disease, prompted us to intervene surgically. We report a series of nine patients who underwent total or near-total thyroidectomy as a first-line therapy for five of them. Surgery resulted in rapid resolution of thyrotoxicosis with an uneventful postoperative course. This approach has the advantage of immediate effectivity, low risk of relapse, and appears to be the only treatment that permits continued therapy with amiodarone when the drug appears needed to control a life-threatening arrhythmia.     

Changes in thyroid volume in response to radioactive iodine for Graves' hyperthyroidism correlated with activity of thyroid-stimulating antibody and treatment outcome

This study investigated 1) the relationship between thyroid volume and thyroid function in radioactive iodine (RAI) treatment for Graves' disease, and 2) the activity of thyroid-related Ig in serum on the responsiveness of thyroid tissue to RAI. The changes in thyroid volume per megabecquerel (MBq) of 131I retained in thyroid tissue was calculated by ultrasonography as a quantitative indicator of the effect of RAI on thyroid volume. Of the 52 patients treated with 131I (3.7 MBq retained/g thyroid tissue), 26 patients showed thyrotoxicosis, 20 patients became euthyroid, and 6 patients developed hypothyroidism 6 months after therapy. The change in thyroid volume per MBq 131I was lower (P < 0.01) in the hyperthyroid patients than in the euthyroid or hypothyroid patients. The activity of thyroid-stimulating antibody in serum immediately before the therapy was greater (P < 0.01) in the hyperthyroid patients than in the euthyroid patients and was greater (P < 0.05) in the euthyroid patients than in the hypothyroid patients; it was inversely correlated with the changes in thyroid volume per MBq 131I (r = -0.667; P < 0.01). Accurate measurement of changes in thyroid volume during the course of RAI treatment provides evidence of the responsiveness of Graves' disease thyroid tissue to RAI, which is related to the outcome of thyroid function. Thyroid-stimulating antibody determination may be useful in deciding the appropriate dose of RAI to obtain euthyroidism instead of hyperthyroidism.     

Influence of clinical characteristics and parameters associated with thyroid hormone therapy on the bone mineral density of women treated with thyroid hormone

Reports of reduced bone mineral density (BMD) in patients receiving long-term replacement and suppression therapy with L-thyroxine have generated considerable interest and controversy. A substantial literature has evolved, with interpretation of conflicting results obscured by a variety of confounding factors. We examined the BMD measurements of 202 white women who were taking thyroid hormone to determine the contribution to BMD of a number of clinical characteristics and parameters associated with thyroid hormone therapy. Measurements of BMD (N = 335 over 2.6 +/- 1.6 years) of the spine (L2-L4) were performed in 195 subjects. The BMD of three sites of the hip was measured (N = 247 over 1.8 +/- 1.1 years) in 157 subjects. The BMD of the proximal radius was also measured (N = 172 over 1.8 +/- 1.2 years) in 124 subjects. Increasing age and a history of previous thyrotoxicosis had a deleterious effect on spine BMD. Body mass index (BMI) was positively correlated with spine BMD. Dose of thyroid hormone, duration of therapy, type of underlying thyroid disease, history of thyroidectomy, or serum-free thyroxine index did not influence either the initial BMD or the change in spine BMD over time. In the hip, age correlated with a decrease, and BMI with an increase in BMD. A history of previous thyrotoxicosis was associated with a decrease in hip BMD at all three sites (0.05 < p < 0.10). No other clinical parameters significantly influenced either the initial BMD or the change in hip BMD over time. Increasing age and dose of thyroid hormone, and a prior history of thyrotoxicosis had a deleterious effect on the BMD at the proximal radius. In summary, thyroid hormone therapy was not associated with a significant effect on BMD of the spine or hip, but a decreased BMD of the proximal radius was related to both previous thyrotoxicosis and to dose of thyroid hormone.     

Improved and effective assays of the glutamic oxaloacetic transaminase by the coenzyme-apoenzyme system (CAS) principle

257 patients have been reviewed 1-5 years (mean 3 years 2 months) after receiving one of five dose regimes of 125I for thyrotoxicosis. The cumulative incidence of hypothyroidism was 34% and of persistent thyrotoxicosis 17%. The group receiving doses between 351 and 500 muCi/g had the highest proportion of euthyroid patients (65%) with the lowest requirement for repeat therapy (46%). In the euthyroid patients, increasing dose of 125I was associated with progressive decline in mean thyroxine (T4) level and free thyroxine index (FTI) within the respective normal ranges, and increase in mean thyroid stimulating hormone (TSH) level to above the normal range. Euthyroid patients with elevated TSH levels had significantly lower T4 and FTI values compared with those with normal TSH, and showed a 3-4-fold increased rate of development of hypothyroidism over 1 year. Euthyroid patients with elevated T3 levels remained euthyroid during the subsequent year and mean T3 levels declined significantly, suggesting that abnormally elevated T3 levels after 125I do not generally indicate impending relapse of thyrotoxicosis. It is concluded that the potential admantages of 125I therapy for thyrotoxicosis in reducing the incidence of hypothyroidism have not been realized in practice.     

Changes in thyroid hormones by treatment with aspirin and prednisolone in subacute thyroiditis with hyperthyroidism

Thyroid functions were studied in 11 patients with subacute thyroiditis accompanied by signs and symptoms of hyperthyroidism, and were compared with 13 patients with untreated thyrotoxicosis in which serum T4 was elevated to the identical level. Serum T3 was also elevated in subacute thyroiditis but to a significantly lower extent than in thyrotoxicosis. Therefore the ratio of T4/T3 was significantly higher in subacute thyroiditis than in thyrotoxicosis. Although duration of thyroid swelling was shorter in the group treated by prednisolone than by aspirin, the accelerated ESR, thyroid tenderness and fever subsided almost similarly in the two groups. Serum T4 and T3 levels declined more rapidly in treatment with prednisolone compared with aspirin. In patients treated by aspirin initial increase in T3 level occurred transiently with simultaneous decrease in the T4/T3 ratio. These changes suggest the increase in peripheral conversion of T4 to T3. Even in severe cases of subacute thyroiditis associated with hyperthyroidism, aspirin treatment is an effective therapy and there is no recurrence following withdrawal of the medication.     

Elevated plasma adrenomedullin level in hyperthyroidism

Adrenomedullin is a recently discovered peptide that was first purified from phaeochromocytoma tissue and has marked vasodilatory activity, causing hypotension. In thyrotoxicosis, various haemodynamic changes are observed, including an increase in cardiac output and heart rate with a concomitant decrease in peripheral vascular resistance. To evaluate the mechanism underlying these haemodynamic changes in thyrotoxicosis, we measured the plasma adrenomedullin concentration in thyrotoxic patients with Graves' disease. The plasma concentration of adrenomedullin was elevated in hyperthyroid patients (14.7 +/- 5.7 pmol L-1) compared with euthyroid control subjects (5.6 +/- 1.3 pmol L-1) (P < 0.001). The correlation between the plasma adrenomedullin concentration and serum free thyroid hormone levels was marginally significant. The mean blood pressure was relatively low in the face of an elevated plasma adrenomedullin level. Adrenomedullin may therefore be responsible for the vasodilatation observed in thyrotoxicosis.     

Central hyperthyroidism

Central hyperthyroidism is a rare condition in which thyrotoxicosis results from primary overproduction of TSH by the pituitary gland with subsequent thyroid enlargement and hyperfunction. The two known causes of central hyperthyroidism are TSH-producing pituitary tumors (TSHomas) and the syndrome of PRTH. Both of these entities are characterized by clinical thyrotoxicosis, diffuse goiters, elevated circulating levels of free T4 and T3, and a nonsuppressed serum TSH. It is critical to distinguish central hyperthyroidism from the much more common types of primary hyperthyroidism, all of which have undetectable TSH values. TSHomas and PRTH can usually be differentiated from one another by measuring the serum alpha-subunit and the TSH response to intravenous TRH or exogenous thyroid hormone, and by pituitary imaging studies. TSHomas are usually benign adenomas arising from the monoclonal expansion of neoplastic thyrotropes. Causative oncogenes have not yet been convincingly identified. PRTH is a nonneoplastic disorder caused by inherited mutations in the gene for the thyroid hormone receptor beta; it is a poorly understood variant of GRTH. For unclear reasons, in PRTH, the pituitary gland is resistant to the feedback inhibitory effects of circulating thyroid hormones while peripheral tissues respond normally, causing patients to experience the toxic peripheral effects of thyroid hormone excess. TSHomas are best treated by transphenoidal surgical removal. Radiotherapy is indicated for inoperable or incompletely resected tumors. Octreotide administration is a useful adjunct for preoperatively reducing tumor size and for the medical management of surgical treatment failures. PRTH is ideally treated by chronically suppressing TSH secretion with medications such as D-thyroxine, TRIAC, octreotide, or bromocriptine. If such therapy is ineffective or unavailable, thyroid ablation with radioiodine or surgery may be employed with subsequent close monitoring of both thyroid hormone status and pituitary gland size.     

Opposite changes in serum soluble CD8 in patients at the active stages of Graves' and Hashimoto's diseases

Serum concentrations of soluble CD8 (sCD8) were examined by enzyme immunoassay in 154 patients with autoimmune thyroid diseases and 46 healthy controls. The numbers of peripheral CD8+ cells were also examined in the same subjects by flow cytometry. The serum concentrations of sCD8 were increased in patients with stimulative thyrotoxicosis caused by active Graves' disease, and decreased in patients with transient destructive thyrotoxicosis caused by the aggravation of Hashimoto's disease, and normal in euthyroid and hypothyroid patients with Graves' or Hashimoto's disease. The ratios of serum sCD8 levels to the numbers of CD8+ cells were increased in thyrotoxic patients with active Graves' disease, but not with active Hashimoto's disease, suggesting an increase in sCD8 production by CD8+ cells in active Graves' disease. The serum concentrations of sCD8 were correlated with the serum levels of thyrotropin receptor antibody (TRAb) and thyroid hormones in Graves' disease. These data indicate that serum sCD8 proteins change in opposite directions in the active stages of Graves' and Hashimoto's diseases, and may represent the disease activities.     

Plasma renin and aldosterone in thyroid diseases

The effect of thyroid hormones on the renin-angiotensin-aldosterone system has not been fully resolved. Highly specific immunoassays for measurement of renin, aldosterone, free T4 (fT4), free T3 (fT3) and ultrasensitive TSH enables a direct and more accurate measurement of these hormones. We investigated the relationship between plasma renin, aldosterone and thyroid hormones in the basal state and after intravenous frusemide. This is a cross-sectional study involving 37 patients with thyrotoxicosis, 42 rendered euthyroid with normal fT4, fT3 and TSH levels, 17 with euthyroid levels of fT4 and fT3 but suppressed TSH, and 11 with hypothyroidism. Basal plasma renin was significantly higher in thyrotoxicosis (63.4 +/- 9.8 microU/ml, mean +/- SEM) compared to euthyroid (32.7 +/- 4.4 microU/ml) and hypothyroid (26.7 +/- 9.8 microU/ml). Basal plasma renin for euthyroid with suppressed TSH (41.0 +/- 7.4 microU/ml) was significantly higher than hypothyroid (p = 0.02). Basal plasma aldosterones were not significantly different except for suppressed TSH (157.7 +/- 13 pg/ml), which was higher than normal (109.9 +/- 10.4 pg/ml; p = 0.04). Following frusemide, plasma renin and aldosterone were significantly increased in all groups. Plasma renin was highly correlated to fT3 (r = 0.405, p < 0.001), total T3 (r = 0.359, p < 0.001), fT4 (r = 0.331, p < 0.001) and TSH (r = 0.300, p < 0.001) in the basal state, but less to total T4 (r = 0.248, p < 0.01). Plasma renin correlated poorly to serum aldosterone (r = 0.212, p < 0.03). This study clearly showed that regulation of renin was mainly influenced by fT3, and that aldosterone response to frusemide was blunted in thyrotoxicosis despite normal electrolytes.     

The ulcer-associated cell lineage: the gastrointestinal repair kit?

We describe a 79 year old lady who presented with a cytologically confirmed anaplastic carcinoma of the thyroid gland eleven years after administration of radio-iodine for thyrotoxicosis. This is, we believe, the first such occurrence documented in the Irish literature.     

Recurrence of thyrotoxicosis after attack of allergic rhinitis in patients with Graves' disease

Graves' disease is frequently aggravated during antithyroid drug therapy; however, little is known of its aggravating factors. We studied 83 patients with Graves' disease who were euthyroid for at least 6 months under antithyroid maintenance therapy, and we examined the relationship between thyrotoxicosis relapse, attack of allergic rhinitis, and peripheral eosinophil increase. Forty-one patients showed thyrotoxicosis relapse; of these, 22 (54%) showed peripheral eosinophil increase, and 14 (34%) had attacks of allergic rhinitis. In the remaining 42 patients without thyrotoxicosis relapse, only 4 (10%, P < 0.001) showed an increase in peripheral eosinophils, and only 3 (7%, P < 0.01) had allergic rhinitis. Recurrence of thyrotoxicosis was observed with the increase in serum levels of TSH-receptor antibodies and increase in eosinophils 2 months after the attack of allergic rhinitis. Three patients with seasonal allergic rhinitis showed thyrotoxicosis relapse at the same time of year within 2 consecutive years. Our findings indicate that allergic rhinitis can be an aggravating factor of Graves' disease and suggest that the preceding increase in peripheral eosinophils can be a predictive indicator of recurrence of thyrotoxicosis during antithyroid drug therapy.     

Isolation of a pentraxin-like protein from rainbow trout serum

To investigate the outcome of Graves' thyrotoxicosis after antithyroid drug management, data from 81 patients, treated in Chang Gung Memorial Hospital at Taipei and Linkou from October 1981 to March 1990, were analyzed. The gender ratio of female to male was 59:22. The mean age of onset was 33.1 +/- 10.5(15-60) year-old. All the patients were treated with antithyroid drug (Thionamide group) for a duration of 11 to 63 months (mean +/- SD = 28.1 +/- 9.8 months). Forty of 81 patients (49.4%) were remained remission after up to 2 years of follow-up. Those patients relapse usually occurred within 2 years after discontinuation of treatment (34/41), and only one exceptional case relapsed after 3 years. Three conditions affected the relapse rate. Patients with larger goiter (grade II-III) and shorter duration of treatment (< 23 months) had a higher relapse rate than those-with smaller goiter (grade O-I) [29/46 vs. 12/35; chi 2 = 6.576, p = 0.010; p = 0.015 in stepwise logistic regression (LR)] and longer duration of treatment (> or = 23 months) (15/20 vs. 26/61; chi 2 = 6.316, p = 0.012; p = 0.020 in LR). Patients with higher pre-treated serum triiodothyronine (T3) level (T3 > or = 300 ng/dl) had a higher relapse rate than those with lower T3 level (T3 < 300 ng/dl) in univariate analysis (30/50 vs. 11/31, chi 2 = 4.601, p = 0.032), but no significant difference by LR (P = 0.094). Other clinical parameters including age, sex, past history, family history, thyroxine (T4) level, T3/T4 ratio, thyroid autoantibodies, staging of ophthalmopathy, responsiveness to thyrotropin-releasing hormone stimulation test at the end of treatment, and whether combined treatment with thyroxine had no significant difference between the relapse and remission groups. These data suggest: (a) patients with larger goiter (grade II-III had higher relapse rate; (b) most of the recurrent thyrotoxicosis patients relapsed within two years after drug withdrawal; (c) continuing treatment for more than twenty-three months produces better outcome; (d) patients with Graves' thyrotoxicosis should be followed up for at least three years after withdrawal of antithyroid drug.     

The interaction of cationic liposomes with the skin-associated bacterium Staphylococcus epidermidis: effects of ionic strength and temperature

OBJECTIVE: Treatment with recombinant interferon-alpha (rIFN-alpha) may induce autoimmunity. We have evaluated the effect of rIFN-alpha on pre-existing thyroid disease with special reference to changes in TSH receptor antibody. DESIGN AND PATIENTS: Five patients, who had a history of autoimmune thyroid disease diagnosed between 2 and 16 years earlier (three patients had Graves' disease while two had Hashimoto's thyroiditis), were treated with rIFN-alpha for chronic hepatitis C. Before, during and after rIFN-alpha therapy, we determined thyroid function, antithyroid antibody, thyroid echogenicity and the surface phenotype of the peripheral and intrathyroidal lymphocytes. RESULTS: Four of the patients developed overt hypothyroidism after 4-7 months of rIFN-alpha therapy, and two of them had a preceding history of low-uptake thyrotoxicosis. Recovery of thyroid function was observed in all four patients. Strongly positive blocking type TSH receptor antibody was detected and an increase in the percentage of CD19 positive cells in the intrathyroidal lymphocytes was also observed in three of the patients even though the goitre size increased in two of them. One of the patients became thyrotoxic later when stimulating type TSH receptor antibody became positive. Another patient suffered from reversible hypothyroidism although stimulating type TSH receptor antibody remained strongly positive throughout the clinical course. CONCLUSIONS: Our data thus indicated a high incidence of an unusual type of reversible hypothyroidism with TSH receptor antibodies in patients with chronic hepatitis C and pre-existing autoimmune thyroid disease after recombinant interferon-alpha therapy through a mechanism involving both the humoral and cellular immune systems.     

Prospective study on thyroid autoimmunity and dysfunction related to chronic hepatitis C and interferon therapy

This study was designed to assess patients with chronic hepatitis C (CHC) for the presence of thyroid autoimmunity and dysfunction, to evaluate the risk of thyroid disorders associated with interferon (IFN) therapy, and to survey the outcome of possible treatment-related thyroid injury. Out of 104 consecutive untreated patients (30 women and 74 men; mean age, 52.7 years), 8 (7.7%) were found seropositive for thyroid autoantibodies (ThyAb), whereas seropositivity in healthy controls was 1/98 (1.3%). The relative increase in risk of developing thyroid autoimmunity associated with CHC was 760% (95% CI, 220-1300%). No patients had abnormalities of thyroid function tests, but on IFN treatment, 3/3 patients showed a rapid over-range rise in circulating thyrotropin, which returned to normal after therapy discontinuation. In the other 5 seropositive patients who refused treatment, thyroid function remained normal. Out of the 58 initially seronegative patients who consented to IFN treatment, 9 (15.5%) developed thyroid autoimmunity. Seven of them (77.7%) had thyroid dysfunction: hypothyroidism in 4 cases, transient thyrotoxicosis in 2 cases. The last patient developed TSH-receptor antibodies and Graves' disease, requiring methimazole therapy. Thyroid function recovered in the former 6 cases following IFN discontinuation. In the 28 initially seronegative patients who refused IFN and participated in a preliminary tauroursodeoxycholic acid trial, antithyroglobulin antibodies alone appeared in one case, but no thyroid dysfunction was observed. The relative risk of thyroid autoimmune disorder associated with IFN therapy was 342% (28-636%). The patients with CHC were unlikely to develop thyroid dysfunction in the absence of IFN therapy, in spite of being ThyAb seropositive. Moreover, a considerable proportion of seronegative patients, when IFN-treated, developed thyroid autoimmunity and then thyroid dysfunction. Both in seropositive and seronegative patients immediate IFN discontinuation normalized thyroid function and hormone replacement therapy was not necessary.     

131 iodine: medical use. Carcinogenic and genetic effects

131 radioiodine is used for treating patients with thyrotoxicosis and differentiated thyroid carcinoma. Its therapeutic effect is related to the radiation dose delivered to the thyroid tissue. The radiation dose is related to its radioactive concentration (ratio between the radioactive uptake and the mass of functional tissue) and its effective half-life. Follow-up studies of patients exposed to 131I did not demonstrate any tumorigenic effect of 131I on the thyroid gland in adults, but do exclude such an effect in children. The dose delivered to other tissues is relatively low, and significant risk of cancer and leukemia has been found only in patients exposed to high cumulative activities of 131I (> 15 GBq). No genetic effect has been found in the studies of the outcome of pregnancies in women exposed to 131I for thyroid carcinoma. These data indicate that there is no scientific reason to avoid the use of 131I even in young patients when therapeutic benefits can be obtained.     

Inhibition in the senso-motor cortex of cats

The clinical course from birth and serial measurements of serum T3, T4 and TSH in an infant with untreated neonatal thyrotoxicosis are reported. The thyroid hormone levels fell exponentially with time at rates very much slower than those previously reported for the maternally-transmitted thyroid stimulating antibody generally thought to cause the disorder. Steady physiological levels of thyroid hormones were achieved after 110 days (serum T3 = 3.4 NMOL/L, T4 = 118 nmol/l). TSH first rose to a measurable level after about 90 days.