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Syncope due to hypersensitivity of carotid sinus developed in a patient with laryngeal carcinoma. After implantation of a ventricular demand pacemaker a marked vasodepressor component became evident leading to further episodes of fainting. Only after implantation of an AV-sequential pacemaker and additional oral medication with ephedrine syncopes could be prevented.

Basing on the results of the European and Austrian survey on the management of hyperthyroidism due to Graves' disease the theoretical backgrounds of the combination of thyrostatic treatment with thyroid hormones and with beta blocking agents are discussed. A suspected lack of compliance of a hyperthyroid patient is probably the only strong argument for the use of combination therapy with thyroid hormones. Some countries in Europe prefer this way of treatment, whereas other countries decline it. In Austria the opinion of the necessity of thyroid hormones in thyrostatic treatment is also not unanimous, the majority, however, preferring it. In contrast, the supporting use of beta blocking agents especially in highly symptomatic patients stands beyond debate. However, monotherapy with beta blockers for preparation of subtotal thyroidectomy in hyperthyroid patients is generally declined, probably because of the danger of a postoperative thyrotoxic crisis. Most colleagues agree (as well in Europe as in Austria) that the combination of thyrostatic drugs with beta-blockers is the best choice for the preparation of subtotal thyroidectomy, saving time and thereby costs and reducing the danger of a postoperative thyrotoxic crisis.

The present concept for the etiology of thyroid disease permits the definition of three separate entities occuring with hyperthyroidism: Graves' Disease, Toxic Nodular Goitre, Autonomous Adenoma. Physiopathological properties of these entities lead to a rational therapeutic strategy for each one of them.

Plasma calcitonin and 6-oxo-Prostaglandin-F1 alpha (6-oxo-PGF1 alpha), one of the stable metabolite of prostacyclin, were determined in patients with malignant and non-malignant diseases of the lung. 11 out of 14 patients with small cell carcinoma and only 3 out of 17 patients with other histological types of lung cancer had abnormally elevated plasma calcitonin levels. 6-oxo-PGF1 alpha levels were significantly higher in patients with different types of lung cancer, compared to a control group with non-malignant lung disease. Combining the results of calcitonin and 6-oxo-PGF1 alpha measurements led to improved specificity and efficiency for the correct differentiation between small cell and non-small cell carcinoma of the lung; the predictive value for the diagnosis of small cell carcinoma approached 90%.

These studies were performed to test the hypothesis that ether link cleavage (ELC) is an important pathway for the metabolism of thyroxine (T(4)) in the phagocytosing human leukocyte. When tyrosyl ring-labeled [(125)I]T(4)([Tyr(125)I]T(4)) was incubated with phagocytosing leukocytes, 50% of the degraded label was converted into [(125)I]3,5-diiodotyrosine ([(125)I]DIT). Of the remaining [Tyr(125)I]T(4) that was degraded, two-thirds was recovered as [(125)I]-nonextractable iodine ([(125)I]NEI), and one-third as [(125)I]iodide. The production of [(125)I]DIT was not observed when phenolic ring-labeled [(125)I]T(4) ([Phen(125)I]T(4)) was used, although [(125)I]NEI and [(125)I]iodide were produced. None of these iodinated compounds were formed in leukocytes that were not carrying out phagocytosis. The fraction of T(4) degraded by ELC was decreased by the addition of unlabeled T(4) and by preheating the leukocytes, findings which suggested that the process was enzymic in nature. ELC was enhanced by the catalase inhibitor aminotriazole, and was inhibited by the peroxidase inhibitor propylthiouracil, suggesting that the enzyme is a peroxidase and that hydrogen peroxide (H(2)O(2)) is a necessary cofactor in the reaction. To test this hypothesis, studies were performed in several inherited leukocytic disorders. ELC was not observed in the leukocytes of patients with chronic granulomatous disease, in which the respiratory burst that accompanies phagocytosis is absent. ELC was normal in the leukocytes of two subjects homozygous for Swiss-type acatalasemia, and aminotriazole enhanced ELC in these cells to an extent not significantly different from that observed in normal cells. ELC was normal in the leukocytes of a patient with myeloperoxidase deficiency, but could be induced by the incubation of [Tyr(125)I]T(4) with H(2)O(2) and horseradish peroxidase in the absence of leukocytes. The in vivo occurrence of ELC in the rat was confirmed by demonstrating the appearance of [(125)I]DIT in serum from parenterally injected [(125)I]3,5-diiodothyronine, but no [(125)I]DIT was produced when [(125)I]3',5'-diiodothyronine was administered. FROM THESE FINDINGS WE CONCLUDE THE FOLLOWING: (a) ELC is the major pathway for the degradation of T(4) during leukocyte phagocytosis, and accounts for 50% of the disposal of this iodothyronine; (b) the NEI and iodide formed by phagocytosing cells are derived from the degradation of the phenolic and tyrosyl rings of T(4), although ELC per se accounts for only a small fraction of these iodinated products; (c) the process by which ELC occurs is enzymic in nature, and its occurrence requires the presence of the respiratory burst that accompanies phagocytosis; (d) the enzyme responsible for ELC is likely to be a peroxidase, although a clear role for myeloperoxidase as the candidate enzyme remains to be established; (e) iodothyronines are also degraded by ELC in vivo, and the quantitative importance of this pathway in various pathophysiological states requires further investigation.

Pathologically low serum total triiodothyronine (T3) concentrations are a characteristic finding in patients with severe non-thyroidal illnesses. No adequate explanation has yet been offered for this phenomenon. We have, therefore, investigated the serum concentrations of total thyroxine (T4), total T3 and total 3,3',5'-triiodothyronine (reverse T3)--the metabolically-inactive metabolite of thyroxine--and of TSH in 13 patients with acute myocardial infarction, in 12 patients with compensated liver cirrhosis, in 9 patients with decompensated liver cirrhosis and in 15 patients with chronic renal failure on chronic intermittent haemodialysis by radioimmunoassay. The values obtained were compared to corresponding values of a normal control group (n - 23). According to our results the decrease in serum T3 combined with normal T4 concentrations in severe non-thyroidal illnesses seems to be a consequence of an alteration in thyroxine degradation. Two different possibilities of alteration can be considered: 1. inhibition of the overall deiodinationof T4, leading to low total T3 serum concentrations with concomitant normal to low reverse T3 serum concentrations (chronic uraemia), 2. a shift in the monodeiodination of T4 towards enhanced reverse T3 production, leading also to low total T3 concentrations, but with a concomitant increase in reverse T3 serum concentrations (myocardial infarction, liver cirrhosis). The results obtained in our patients with liver cirrhosis show, moreover, that this alteration of T4 metabolism depends on the severity of the illness.

The Fibrinogen Thrombin Adhesive System (FTAS) enables local haemostasis to occur in parenchymatous organs without tissue damage. The aim of this study was to investigate the degradation of FTAS and the process of wound healing after partial kidney resection in rats using FTAS for induction of local haemostasis. In 28 rats partial kidney resection was performed bilaterally. Haemostasis was achieved with Fibrinogen Thrombin Adhesive System. Four experimental groups were formed. Group A (n = 3): Haemostasis with unlabelled FTAS, subcutaneous injection of 0.1 ml = 60 mu Ci Na 125I. Group B (n = 3): Haemostasis with unlabelled FTAS, subcutaneous injection of 0.1 ml = 60 mu Ci 125I FTAS. Group C (n = 6): Haemostasis with 125I labelled FTAS. Group D (n = 16): treated like Group C. In Groups A - C 125I-elimination in 24 h urine samples was determined with a gamma-scintillation counter. Pairs of animals in Group D were killed after 2, 6, 12 and 24 h and 3, 7, 14 and 21 days. Kidneys were examined under the light and electron microscope and by autoradiography. In animals of Groups B and C two peaks of 125I excretion were observed: one peak within the first 48 h postoperatively which corresponded to the amount of free iodine injected with FTAS (FTAS contains 15% free iodine); a second peak after 120 h which was most probably due to the degradation of FTAS. Fibrinolysis was not observed. FTAS was resorbed mainly by macrophages. The time course of wound healing paralleled that of physiological fibrinogen concentration. Renal parenchymal damage was not observed.

A 41-year-old male patient developed amiodarone-induced thyrotoxicosis after 29 months of treatment with amiodarone. Thyrotoxicosis was readily reversible after cessation of the drug and did not need specific thyrostatic treatment. In contrast to what was expected, thyroglobulin serum concentrations, that were normal during the first 2 yr of follow up, decreased drastically to undetectable levels during and after the thyrotoxic phase. Although no explanation can be offered for this phenomenon, it seems important to point out the fact that measurement of thyroglobulin is of only limited value in the diagnosis of thyroid dysfunction in patients treated with amiodarone. Low levels do not exclude thyrotoxicosis.

The binding of 125I-insulin to insulin receptors on circulating mononuclear leukocytes was studied in ten patients with hyperthyroidism and 20 euthyroid normal volunteers. The hyperthyroid patients demonstrated significantly elevated glucose levels following an oral glucose load, despite normal insulin secretion. The infusion of insulin resulted in a delayed hypoglycaemic effect in the hyperthyroid patients; however, the inhibition of the endogenous insulin secretion as indicated by suppression of C-peptide levels was not different from euthyroid control subjects. Insulin binding to monocytes was significantly decreased in the hyperthyroid patients. Scatchard analysis of binding data indicates that a decrease of receptor number rather than receptor affinity seems to be the cause of the lowered insulin binding in hyperthyroid patients with diffuse toxic goitre. The findings of decreased insulin receptor number, mild degree of glucose intolerance despite normal insulin secretion and the delayed hypoglycaemic effect following insulin infusion suggest that peripheral insulin resistance could be involved in the highly complex pathophysiology of glucose intolerance in hyperthyroidism.

Fluid and electrolyte homeostasis is impaired in patients suffering from hypothyroidism and myxedema because myxedema induces retention of salt and water. We have measured plasma levels of human atrial natriuretic peptide (hANP) in 8 female patients who had been totally thyroidectomized because of thyroid carcinoma. Estimations of the hormone were done 4 weeks after diagnostic withdrawal (searching for iodine retaining metastases) and after 2 weeks and 4 weeks of reinitiation of thyroid suppressive therapy by L-thyroxine. hANP levels, although within the normal range (10-80 ng/l) throughout the study, were positively linked to the amount of pericardial effusion (determined by echocardiography), which was highest initially and decreased or vanished with duration of L-thyroxine therapy. Additionally, a positive correlation between thyroid hormone levels and hANP was obtained when the counteracting effect of pericardial effusion was allowed for by partial correlation analysis. Our findings might facilitate explanation of mild polyuria in hyperthyroidism and impaired water excretion in hypothyroidism.

Carcinomas of the thyroid gland display large pathological and clinical variation. Favourable prognostic factors accompary well-differentiated tumours, whereas poorly differentiated or anaplastic carcinomas tend to invade early and are usually rapidly fatal. Experience has demonstrated the difference in rate of growth, subsequent recurrence and late spread even in identically well-differentiated thyroid carcinomas. Biological difference must be the underlying reason for the clinical difference in behaviour of histologically similar cancers. This report demonstrates the correlation between in vivo radioactive iodine uptake, tumour staging and recurrence-free interval in 30 thyroid carcinomas. The uptake by well-differentiated carcinomas staged T2N0M0 is significantly higher than that by tumours staged T3N1M0, whereas the latter show a higher uptake than those tumours staged T3N1M0. A high tumour uptake rate is correlated with long recurrence-free interval (up to 24 months) within all groups of staging and vice versa.

During starvation the response of TSH to TRH decreases in many subjects. This could be due to an increased sensitivity to TSH secretion to circulating thyroid hormones. To study this hypothesis, 13 subjects were starved twice for 2-day periods. After both starvation periods, a standard TRH test (200 micrograms TRH, iv) was performed; during 1 starvation period 15 micrograms T3 were injected iv 24 h before the TRH test. The TRH tests were also performed while on normal nourishment, once without pretreatment and once 24 h after the iv injection of 15 micrograms T3. The spontaneous decrease of the TSH response to TRH was seen in 10 of 13 subjects. In these 10 subjects it decreased from 18.0 +/- 1.9 to 9.7 +/- 1.2 microU/ml (mean +/- SEM; P < 0.001). The additional inhibition of the TRH test with T3 was small compared with the one observed under normal conditions. In starvation, T3 decreased the maximal TSH response from 9.7 +/- 1.2 to 8.4 +/- 1 microU/ml (P = NS), while during the control period the maximal TSH response fell from 18.0 +/- 1.9 to 11.4 +/- 1.3 microU/ml (P < 0.001). These data indicate a diminished effectiveness of T3 in inhibiting TSH secretion and are consistent with the hypothesis of a more generalized resistance of target organs to T3 during starvation in man.

This review deals with the question whether hypertriglyceridemia represents an independent risk factor for the development of cardiovascular disease. The accepted definition of hyper- and "borderline"-hypertriglyceridemia is presented as well as its most frequent causes. After discussion of the hypotheses of the possible ways of mechanisms by which elevated serum triglycerides may be atherogenic the available epidemiologic data are analysed: summarizing these results it can be stated that in contrast to previous statements hypertriglyceridemia seems to be an independent risk factor for the development of cardiovascular disease, even after correction for other risk factors like total cholesterol, smoking, familial history, age or similar well known factors. Even the Framingham study that in earlier studies denied an independent role of the serum triglycerides showed recently that serum triglycerides correlated significantly with coronary heart disease after correction of other risk factors, especially in women. In conclusion, the recommendations of the European and American Consensus Conferences for patients with hypertriglyceridemia are presented: these conferences agree that even borderline hypertriglyceridemia should be investigated for its cause and treated by diet and if this fails by drugs.

Neuroadenolysis of the pituitary (NALP) is an efficient measure for treatment of severe pain in patients with bony metastases. It is especially recommended for primary carcinomas of the breast or prostate. The procedure, transsphenoidal puncture of the pituitary under radiographic control and instillation of up to 2 ml 95% alcohol, is simple. The pathomechanism of the analgesic effect is still unknown. Extensive determinations of the anterior pituitary hormones LH, FSH, HPRL, ACTH, and HGH were done before and up to 14 days after NALP in six consecutive patients receiving this treatment. The pituitary was stimulated with releasing hormones LHRH (100 mug) and TRH (200 mug) before and 3 days after NALP. Determinations of hormone parameters were done 25 and 60 min after injection. The results showed that hormone production by the adenohypophysis becomes unevenly suppressed. The following results are significant (P<0.05): (1) LH: poststimulation values are extremely suppressed; (2) FSH: basal values decrease; (3) ACTH: basal values decrease after the 6th day. The antalgic effect of NALP is independent of its hormonal consequences. NALP produces hormonal suppressions of various degrees, and is not a "chemical hypophysectomy".

Elevation of Thyroxine-binding globulin (TBG) in serum may lead to abnormally high total-thyroxine (T4) concentration. Causally hyper-TBG-aemia can either be acquired (estrogentherapy; hepatitis etc.) or familial. In a family-study with 3 generations 6 persons were found with this rare anomaly. Analysis of the pedigree is in accordance with an X-chromosomal transmission. Five of the affected family members were clinically euthyroid and had normal T4/TBG and effective thyroxine ratios (ETR). In one patient hypothyroidism was detected by these indirect parameters despite a normal T4-concentration. Changes in serum levels of thyroxine binding proteins make it difficult to diagnose a disturbance in thyroid function. However indirect parameters for free T4 (ETR, T4/TBG) as well as the TRH-Test allow a clear diagnosis in such patients.

Investigations of a patient with the benign adult form of osteopetrosis (Albers-Schönberg) revealed that the clinical symptoms correlated with a high bone metabolism, high calcium incorporation in bone, increased osteoclast activity and probably reactive increase of calcitonin in the blood.

Thyroid function was investigated in 41 patients on chronic treatment with amiodarone. 27% of the patients had elevated total thyroxine levels together with elevated free thyroxine levels. Thyrotropin (TSH) secretion was completely suppressed in 15% of the patients. Elevated free or total thyroxine levels were frequently observed together with normal TSH secretion, although 5 of the 6 patients with suppressed TSH had markedly elevated levels. Triiodothyronine (T3) levels were low normal or below the normal range in all patients but one. This was the only patient who apparently developed amiodarone-induced hyperthyroidism. The clinical symptoms of this patient were equivocal. Thyroid function parameters including T3 levels returned to normal only 3 months after withdrawal of the drug. The patient did not need any thyrostatic treatment. The duration of treatment with amiodarone did not influence thyroid hormone concentrations, although there was an insignificant trend of increasing total thyroxine levels after a year of treatment. There was, moreover, no significant influence of the dose (200-500 mg orally/day) of amiodarone on thyroid hormone levels. Our results show that the usual screening parameters of thyroid function, namely total and free thyroxine serum concentrations, are not reliable in patients on chronic amiodarone treatment. The incidence of amiodarone-induced hypothyroidism was 2.4%. We did not observe an amiodarone-induced hypothyroidism, although there was one patient with increased TSH levels but normal T3 and thyroxine levels.

Platelet retention was investigated using a standardized technique with a glass pearl column in 18 patients with malignant thyroid disease treated by thyroidectomy before and after high-dose radioiodine treatment (80 or 150 mCi). As compared with the normal controls platelet retention was significantly lower in 13 hypothyroid patients in whom thyroidectomy had been undertaken at least 6 months previously and hormone substitution therapy had been interrupted 3 weeks before the period of investigation. The remaining 5 patients, studied about 18 days following thyroidectomy, were euthyroid and displayed platelet retention values within the lower limits of the normal range except for one patient with markedly reduced values. Thyroid substitution therapy with synthetic preparations induced recovery of platelet retention in both groups examined over a 4 week period, the increase being highly significant in the group of hypothyroid patients. A transient increase in platelet retention was observed 24 hours after a therapeutic dose of radioiodine, and initial values being regained after a further 24-hour period. This phenomenon was found in both, the euthyroid and hypothyroid group, however, it was more pronounced in the latter patients. Our results indicate a dependence of platelet retention on thyroid hormone concentration. The observed transient increase after radioiodine may be due to a radiation effect.

Basal and thyroid-releasing hormone-stimulated (200 micrograms/m2) prolactin and thyroid-stimulating hormone (TSH) levels were measured in 31 patients with hypopituitarism (13 isolated growth-hormone deficiencies and 18 multiple pituitary hormone deficiencies). The results were compared with the prolactin response in 76 healthy prepubertal children. Normal prolactin concentrations were found in 13 patients whereas 11 had increased levels. TSH levels were either normal or increased in patients who were considered to have hypothalamic disorders. Decreased prolactin response was present in 7 children, 6 of whom had multiple pituitary deficiencies. Their TSH response was decreased as well, indicating pituitary failure. There was good overall correlation of peak prolactin with peak, TSH concentrations. Some patients with 'isolated' growth hormone deficiency had an abnormal prolactin response indicating an additional hormonal deficiency. All patients with low levels of serum thyroxine had abnormal prolactin or TSH levels, high in some, low in others. Two euthyroid patients with increased prolactin stimulation became hypothyroid during treatment with growth hormones, thus questioning whether prolactin is a more sensitive indicator of early thyroid insufficiency than thyroxine or TSH levels.

12 patients with impaired left ventricular function were submitted to left ventricular ejection fraction measurements before and after increasing doses of PGE1 administered by i.v. or i.a. infusion. 6 responders out of the 12 patients showed a significant (p less than 0.01) improvement in LVEF, whereas the LVEF remained unchanged in the remaining 6 patients. 4 of the responders had received intravenous and 2 had received intraarterial PGE 1. Afterload reduction, venous tonisation, increased myocardial contractility and metabolic effects may be causative factors. These results suggest that PGE 1 therapy may be of therapeutic benefit in some patients with impaired LVEF.

In isolated K+ (16.2 mM)-arrested cat hearts perfused at constant pressure adenosine infusions (0.8 mumoles - min-1 - 100 g-1 for 10 min) caused an increase in myocardial 14C-glucose uptake and release of 14CO2 + H14CO3- AND 14C-lactate simultaneously with a rise in coronary flow. The ratio of the release of 14CO2 + H14CO3- to that of 14C-lactate and the specific activity of lactate in the effuate were not altered. In K+ -arrested hearts perfused with constant volume neither glucose uptake nor glucose breakdown were influenced by 0.8 or 100 mumoles - min-1 - 100 g-1 adenosine with 0.1 - 5 mM glucose in the perfusion medium. It is concluded that adenosine does not affect directly the myocardial glucose carrier system, aerobic or anaerobic glucose breakdown or glycogenolysis, but enhances glucose uptake secondarily by increasing coronary flow. This interpretation is substantiated by the finding that mechanically produced increases in perfusion volume caused similar increases in myocardial glucose uptake as were observed with comparable adenosine-induced coronary flow increments.

Salivary electrolytes (potassium and calcium), as well as serum digoxin levels were measured in 114 patients receiving digoxin or one of its derivatives. The mean value of the product of salivary potassium (mVal/I) and calcium (mVal/i in digoxin-treated patients without signs of digitalis intoxication (group 1) was 235 +/- 137 (SD) and with digitalis intoxication (group 2) 404 +/- 161 (SD). The difference in these values was not of statistical significance. The mean serum digoxin levels were 1.38 +/- 0.6 ng/ml (SD) in group 1 and 2.97 +/- 0.7 ng/ml (SD) in group 2; this difference is highly significant (p less than 0.001). Both salivary electrolytes and serum digoxin levels were falsely elevated in 11% of group 1 patients. 50% of the cases in group 2 showed salivary electrolyte values within the range of group 1, but there was only 1 patient with a serum digoxin level of below 2 ng/ml. It can, thus, be concluded that measurement of the salivary electrolytes is a test of only limited value in the assessment of digitalis intoxication, whereas determination of the serum digoxin level is a valuable diagnostic tool.

The, in non-thyroidal illnesses, frequently occurring changes in the serum concentrations of peripheral thyroid hormones, are shown in patients with acute myocardial infarction, compensated and decompensated cirrhosis of the liver, renal insufficiency and in rheumatoid arthritis. The observed changes, (pathological) low total triiodothyronine, low or normal total thyroxine, and normal thyrotrophine), can make the diagnosis of hyperthyroidism impossible. Only in control measurements, after cessation of the simultaneous non-thyroidal illness, the peripheral thyroid hormone concentrations are found to be in the hyperthyroid range. The only way to establish the diagnosis, (or confirm the clinical suspicion), is to prove non-responsiveness of the pituitary to a TRH-stimulus. TRH-tests have, however, no diagnostic value in illnesses that affect pituitary function directly, such as terminal renal insufficiency. The diagnosis of hypothyroidism can be established by measurement of the basal thyrotrophine serum concentration (elevated) or by measurement of the serum concentrations of 3,3'5'-triiodothyronine (reverse T3), which is, according to a recent report, observed to be significantly decreased.

Thyroid hormone serum concentrations were measured in clinically apparently euthyroid patients suffering from diseases that have symptoms in common with thyroid dysfunction. The diseases investigated were: anorexia nervosa (n = 13), myocardial infarction (n = 13) cirrhosis of the liver (n = 19), terminal renal insufficiency (n = 30) and rheumatoid arthritis (n = 14). In each group, the patients were divided into groups according to the degree of their disease. A relative decrease in 3,5,3'-triiodothyronine (TT3) serum levels is the most pronounced effect of all the non-thyroidal ailments investigated. Individual observations show that total and free thyroxine levels can also be lowered by some acute illnesses. Moreover, the extent of the decrease in TT3 serum levels depends significantly on the severity of the non-thyroidal illness. This phenomenon was observed in all ailments investigated. Based on our findings it is concluded that the diagnosis of thyroid dysfunction may be extremely difficult in many non-thyroidal illnesses. This study should help the clinician to evaluate laboratory hormone data correctly in respect to the diagnosis of thyroid dysfunction in patients with non-thyroidal illnesses.

The effect of withdrawal of suppressive therapy with thyroid hormones (200 micrograms L-thyroxine/day) on serum biochemical profiles and blood cell counts were studied in ten athyreotic thyroid carcinoma patients. After 14 days off therapy, all patients but one were still clinically and biochemically euthyroid. Twenty-eight days without thyroid hormones resulted in severe clinical and biochemical (TT4, TSH) hypothyroidism. At that time, the following parameters changed significantly: CPK activities increased (in five of ten patients above normal) as well as activities of SGOT, SGPT, and LDH (means and s.d.s within the respective normal ranges). Total cholesterol and triglycerides increased within the normal range. There were minimal but significant increases of serum creatinine and of mean corpuscular volume of erythrocytes as well as decreases of serum sodium and calcium. Our study underlines the importance of further investigation if pathologic biochemical or hematologic parameters are obtained in athyreotic patients after 4 wk withdrawal of thyroid hormone therapy.

A screening method for detection of congenital hypothyroidism is presented in detail in cooperation with the "Austrian Program for Inborn Errors of Metabolism". Screening is performed by measuring the total T4-content of 1/8 inch filter paper dots filled with dried blood of newborns. The strategy for recall of newborns with borderline or pathological T4-values used, results in a definite diagnosis on day 55 of life. The advantages of additional TSH determination in the filter paper dots are discussed. So far (Sept. 1976) 8645 newborns have been investigated, covering the regions of Vienna and Carinthia (Austria). Preliminary studies reveal a slight dependency of the measured T4-values on the day of sampling. Two congenitally hypothyroid children have been diagnosed so far, corresponding fairly well with the reported frequency in the literature (1 : 6000).

In 16 healthy volunteers tolbutamide tests or i.v. glucose tolerance tests were performed with and without previous oral administration of 1000 mg diftalone. Blood sugar and serum insulin were assayed in regular intervals. Both with and without previous administration of diftalone blood glucose after tolbutamide did not show any difference. IRI response to tolbutamide, measured by planimetrical integration showed a statistically significant augmentation (0.05 greater than p greater than 0.01) after diftalone. Glucose assimilation (K-value) after diftalone was decreased (0.05 greater than p greater than 0.01) yet within normal range. For the accompanying insulin levels however no statistically significant difference was observed. In addition a normalisation of pathological tolbutamide test after diftalone could be noted in five patients with subclinical diabetes. Our results indicate that diftalone seems to have the following three actions: 1. Enhancement of the tolbutamide action. 2. direct augmentation of IRI secretion, 3. a peripheral action on glucose metabolism.

In pseudohypoparathyroidism type I pharmacologic dosis of vitamin-D can correct hypocalcemia. Several authors who had investigated vitamin-D-metabolism in these patients, found impaired renal conversion of 25-hydroxyvitamin-D to 1,25-dihydroxy-vitamin-D. Treatment of 2 patients with pseudohypoparathyroidism type I with vitamin-D-3 and 1 alpha-Hydroxycholecalciferol consecutively resulted in a nonuniform response with regard to the normalisation of serum-calcium. This led us to the conclusion that the disturbances of vitamin-D-metabolism in pseudohypoparathyroidism type I is heterogenous.

10 worker suffering from occupational vitiligo due to p-tert. butyl phenol have been observed in an Austrian resin factory. The dust concentration and its content of p-tert. butyl phenol in the working area were measured. On the basis of these results preventive measures were taken to reduce the exposure of the workers to p-test butyl phenol. In the presented cases an involvement of internal organs--as described by Rodermund et al. (1975)--could not be observed.

A total of 45 patients have received surgical treatment for distant metastases in 41 follicular and four papillary carcinomas. Fifty-four metastatic lesions were removed. In the majority of cases (n = 25, 46%), surgical intervention was indicated on the basis of oncologic data (reduced administration of radioiodine). Sixteen patients (30%) underwent surgery to relieve pain, and 13 other patients (24%) had surgical treatment of pathologic fracture. At the time of surgery, 29 patients (64%) had only one resectable metastasis, while 16 patients (36%) had further nonresectable metastases (six in the bone, 10 in the bones and lungs). In the course of 53 operations, metastases were resected from bone in 46 cases, from the lungs and greater omentum in two cases, and from the skin, suprarenal gland, pleura, and intra-abdominal lymph node in one case each. A total of 25 metastases (17 bone, eight soft tissue) could be removed by resection. In 16 patients, the resulting bone defect was filled with bone cement after resection of the metastases. Osteosynthesis was necessary in another six cases, while seven required the implantation of an endoprosthesis. Thirty-eight patients died between 1 and 136 months after surgical treatment. Twenty-six (58%) died of their primary disease after an average 49.3 months, seven (15%) died with their carcinomas of other causes after an average of 12 months, and five (11%) died intercurrently after an average of 16 months. Seven patients (15%) are still alive after 12 to 264 months (average, 99.3 months); four of them are without recurrence and three have metastases. Five of these patients exhibit normal activity, while the activity of the other two is limited by the progress of the carcinoma or as a result of surgical treatment. The estimated cumulative survival rate (Kaplan-Meier) was 44.8 +/- 11.2% for 5 years and 32.7 +/- 11.0% for 10 years after removal of a solitary metastasis. Analysis of these patients shows that the surgical removal of resectable metastases can be a valuable complement to nuclear medical therapy. The complicated surgical treatment of metastases is justified by the favorable effect it has on prognosis and on the patient's quality of life.