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Biomedical subjects

T Friis

Publications and source records attributed to T Friis.

At least 55 records · Page 3Linked to original sources
PubMed1982

Evidence of a correlation between thyrotrophin receptor binding inhibition and thyroid adenylate cyclase activation by immunoglobulins in Graves' disease before and during long-term antithyroid treatment.

In the present study we have measured in parallel thyrotrophin binding inhibiting immunoglobulins (TBII) and thyroid adenylate cylase stimulating immunoglobulins (TACSI) in patients with Graves' disease (GD) both before and during long-term antithyroid treatment. A statistical model based on the calculation of the differences (TACSI-TBII) is presented, comparing the changes in this parameter to the analytical variation. The correlation between TBII and TACSI in 52 patients with GD before treatment was: r = 0.58, P less than 0.0001. During long-term antithyroid treatment of GD the 2 activities changed in parallel in 39 of 45 patients followed. In a few patients discrepancies were observed, and 1 patient, initially TACSI positive, developed adenylate cyclase inhibiting IgG during treatment but without detectable TBII. In conclusion, 1) TBII and TACSI are significantly correlated in patients with GD both before and during long-term antithyroid treatment, 2) in some patients discrepancies between TBII and TACSI suggest, that these IgGs are heterogeneous with varying capacity for stimulation of the adenylate cyclase and receptor binding, and 3) adenylate cyclase inhibitory IgG without TBII activity was demonstrated in GD.

Adenylyl Cyclases↗
PubMed1982

The oral TRH stimulation test. A new diagnostic tool in "non-toxic" multinodular goitre.

We have developed a 28-hour TRH stimulation test based on the FT3I response to repeated oral TRH stimulation. The normal FT3I response in 15 controls was greater than or equal to 40 arb.U. Twenty-five euthyroid patients with multinodular goitre were studied. Fourteen had normal FT3I responses and normal basal levels of serum T4, FT4I, serum T3 and FT3I. Eleven patients had FT3I responses below 20 arb.U. Although the patients' individual basal values of serum T4, FT4I, serum T3 and FT3I were within the normal range, the median values of FT4I, serum T3 and FT3I were significantly elevated compared to the controls, suggesting that these patients were in a "pretoxic" condition. This assumption seems to be supported by the fact that 3 of these patients subsequently became frankly hyperthyroid, whereas all patients with normal FT3I response remained euthyroid. A comparison between the TSH response to i.v. TRH and the FT3I response to oral TRH showed concordance in 21 of the 25 patients studied.

Administration, Oral↗
PubMed1981

Urinary excretion of free and conjugated 3',5'-diiodothyronine and 3,3'-diiodothyronine.

RIAs for the estimation of 3',5'-diiodothyronine (3',5'-T2) and 3,3'-diiodothyronine (3,3'-T2) in human urine have been established. The urinary excretion of both glucuronide and sulfate conjugates of T2 and of T4, T3, and rT3 were estimated by means of enzymatic deconjugation. In healthy controls, the mean excretion (picomoles per 24 h) of free T4 was 1820, that of free T3 was 813, that of free rT3 was 77, that of free 3',5'-T2 was 13, and that of free 3,3'-T2 was 674. The total excretion of free and conjugated T4 was 2941, that of T3 was 1283, that of rT3 was 791, that of 3',5'-T2 was 709, and that of 3,3'-T2 was 2688. Significant amounts of sulfated T4 and T3 could not be demonstrated, amounts of sulfated T4 and T3 could not be demonstrated, whereas the excretion of sulfated rT3 was higher than that of glucuronidated rT3 (P less than 0.001). In contrast, glucuronidated and sulfated 3',5'-T2 as well as glucuronidated and sulfated 3,3'-T2 were found in the urine in equal amounts. In hyperthyroidism, the excretions of free and glucuronidated iodothyronines were increased, whereas the increase of the excretions of sulfated iodothyronines were less pronounced, only reaching statistical significance for 3,3'-T2 (P less than 0.02). In hypothyroidism, the excretions of both free, glucuronidated and sulfated iodothyronines were reduced. Significant amounts of sulfated T4 and T3 could not be demonstrated in urine from hyperthyroid or hypothyroid patients. Our data demonstrate that the amounts of free iodothyronines excreted in the urine vary considerably, suggesting active renal handling. The amounts of urinary glucuronidated and sulfated conjugates of the different iodothyronines studied vary considerably and are affected by thyroid function.

Cross Reactions↗
PubMed1981

Kinetic studies of thyroxine, 3,5,3'-triiodothyronine, 3,3,5'-triiodothyronine, 3',5'-diiodothyronine, 3,3'-diiodothyronine, and 3'-monoiodothyronine in patients with liver cirrhosis.

Turnover studies of T4, T3, rT3, 3',5'-diiodothyronine (3',5'-T2), 3,3'-diiodothyronine (3,3'-T2), and 3'-monoiodothyronine (3'-T1) were performed in 10 patients with alcoholic cirrhosis of the liver and 9 euthyroid, healthy controls using the single injection, noncompartmental approach. The kinetics of all 6 iodothyronines were studied in the same individuals. A newly developed, simple and reproducible gel separation technique, followed by antibody extraction, was used for the quantitation of tracer in serum. Serum T4, T3, and 3,3'-T2 levels were reduced in patients with liver cirrhosis, whereas serum rT3 and 3',5'-T2 levels were increased, Serum 3'-T1 levels were unaltered. A general tendency toward reduced MCRs was observed. The following median MCRs (liters per day per 70 kg BW) were found (cirrhotics vs. controls): T4, 1.13 vs. 1.19 (P = NS); T3, 16 vs. 20 (P less than 0.05); rT3, 81 vs. 147 (P less than 0.01); 3',5'-T2, 131 vs. 279 (P less than 0.01); 3,3'-T2, 533 vs. 1116 (P less than 0.01); and 3'-T1, 375 vs. 539 (P less than 0.05). The production rates (nanomoles per day per 70 kg BW) of T4, rT3, and 3,'5'-T2 were not significantly altered in patients with cirrhosis (cirrhotics vs. controls): 100 vs. 117, 47.5 vs. 52.0, and 14.5 vs. 13.9, respectively. In contrast, the following pronounced reductions in production rates of T3, 3,3'-T2, and 3'-T1 were found: 19.1 vs. 38.8 (P less than 0.01), 13.2 vs. 36.8 (P less than 0.01), and 15.7 vs. 28.6 (P less than 0.05), respectively. Assuming that thyroidal secretion contributes little rT3 and 3',5'-T2, the conversion rates from T4 to rT3 and further to 3',5'-T2 were calculated and found to be unaffected in patients with liver cirrhosis (48% vs. 34% in controls and 34% vs. 26% in controls, respectively). No tendency toward major changes in the activity of the nondeiodinative metabolic pathways was observed. In conclusion, our data show that liver cirrhosis profoundly changes the kinetics of all iodothyronines studied. Further, the 5-deiodination of T4 and rT3 is unaffected in patients with liver cirrhosis. In contrast, a general inhibition of the 5'-deiodinations seems to exist in patients with liver cirrhosis. Thus, our data are compatible with the existence of a common 5-deiodinase and a common 5'-deiodinase for the sequential deiodination of the iodothyronines in man.

Adult↗
PubMed1981

A radioimmunoassay of serum 3,5-diiodothyronine.

A radioimmunoassay (RIA) for serum 3,5-diiodothyronine (3,5-T2) was developed using small Sephadex G 25 (fine) columns. Prior to the RIA an alcohol extraction of 3,5-T2 from serum and an evaporation of the extract was performed. The recovery of 3,5-T2 added to serum was in mean (plus or minus SEM) 101 plus or minus 11%. The lower detection limit was 0.012 pmol/column corresponding to 14 pmol/l using 3 ml serum. Due to a 5% cross-reaction of 3,5-T2 antibody with 3,5,3'-triiodothyronine (T3) individual correction for T3 present in serum was necessary. Serum 3,5-T2 levels in 52 éuthyroid controls were (mean plus or minus SD) 105 plus or minus 51 pmol/l. Serum levels were higher in men (125 plus or minus 56 pmol/l. Serum levels were higher in men (125 plus or minus 56 pmol/l) than in women (84 plus or minus 34 pmol/l, P less than 0.005). In 17 hyperthyroid subjects serum 3,5-T2 levels were elevated (232 plus or minus 187 pmol/l, P less than 0.005). In hypothyroid patients and patients with non-toxic goitre serum 3,5-T2 levels did not differ significantly from control values, whereas 8 patients with liver cirrhosis had severely reduced serum 3,5-T2 concentrations (20 plus or minus 23 pmol/l, P less than 0.001).

Adolescent↗
PubMed1981

Serum 3'-monoiodothyronine levels in normal subjects and in patients with thyroid and non-thyroid disease.

Serum 3'monoiodothyronine (3'-T1) levels were estimated by means of a specific radioimmunoassay (RIA) preceded by an ethanol extraction. The recovery of 3'T1 was in mean (+/-SEM) 110 +/- 9%, and the lower detection limit was 23 pmol/l. Serum levels of 3'T1 in 34 euthyroid healthy subjects were (median (range)) 55 pmol/l (less than 23 - 168 pmol/l), in 13 hyperthyroid patients 133 pmol/l (70 - 265 pmol/l) (P less than 0.01) and in 13 hypothyroid patients less than 23 pmol/l (less than 23 - 68 pmol/l) (P less than 0.01). In 11 patients with chronic renal failure serum 3'-T1 levels were highly increased 285 pmol/l (115 - 1538 pmol/l) (P less than 0.01) and correlated inversely to creatinine clearance (R = -0.68, P less than 0.05). In patients with liver cirrhosis serum 3'-T1 levels were unaffected, whereas in 19 patients with endogenous depression studied before and after recovery from the depression serum levels decreased from 70 pmol/l (less than 23 - 248 pmol/l) to 30 pmol/l (less than 23 - 95 pmol/l) (P less than 0.01). Administration of propranolol 40 mg b.i.d. for 2 weeks did not affect serum 3'-T1 levels. The study shows that 3'-T1 is present in serum from euthyroid man and varies with thyroid function. Further, it is suggested that 3'-T1 in contrast to other iodothyronines primarily is eliminated by the kidneys.

Adult↗
PubMed1981

Prognostic value of thyrotrophin binding inhibiting immunoglobulins (TBII) in longterm antithyroid treatment, 131I therapy given in combination with carbimazole and in euthyroid ophthalmopathy.

Thyrotrophin binding inhibiting immunoglobulins (TBII) were measured in 27 patients with Graves' disease during and after longterm antithyroid treatment. The median observation period after treatment was 24 months. During the first 6 months of treatment the TBII index increased significantly in both the relapse and the remission group, but during the rest of the treatment and the observation no further change was observed. Patients with a TBII index below 0.35 at drug withdrawal (n = 8) all relapsed and patients with values above 1.00 (n = 5) all stayed in remission. There was a significant correlation between the TBII index at drug withdrawal and the time elapsed before a relapse. Graves' disease was treated with 131I in combination with carbimazole in 22 patients. The TBII index of these patients decreased after 131I and increased towards normal values during longterm observation of median 33 months. Of 4 patients with euthyroid ophthalmopathy one was TBII positive. This patient became overt hyperthyroid after an observation period of two years of prednisone treatment. It is concluded, that the TBII index is of some prognostic value after longterm antithyroid treatment, but is of no clinical importance following 131I treatment.

Adult↗
PubMed1979

Serum T4, T3 and reverse T3 during treatment with propranolol in hyperthyroidism, L-T4 treated myxedema and in normal man.

Serum concentrations of T4, T3 and reverse T3 were studied in two hyperthyroid groups (n = 13 and 11), in a group of normals (n = 9) and in a group of L-T4 substituted patients (n = 7) with severe pretreatment hypothyroidism. Serum T4 did not change except in one of the hyperthyroid groups change to in which a slight decrease was found. In all groups a significant fall in serum T3 and a significant rise in serum reverse T3 were found. An expected increase in serum TSH in the normal and in the L-T4 substituted groups could not be demonstrated.

Adult↗
PubMed1979

The influence of propranolol on the extrathyroidal metabolism of 3,3',5'-triiodothyronine (reverse T3).

The effect of propranolol 80 mg daily on the metabolism of 3,3',5'-triiodothyronine (reverse T3, rT3), 3,3',5'-triiodothyronine (T3) and thyroxine (T4) was studied by means of a non compartmental kinetic method in seven females with severe pretreatment hypothyroidism. The patients were maintained euthyroid on a constant L-T4 replacement therapy. Serum rT3 levels increased significantly during propranolol (p less than 0.02). This increase was explained by a decrease in metabolic clearance rate (MCR) (p less than 0.02), since the conversion rate from T4 and the distribution volume of rT3 were unchanged. By contrast the decreased serum levels of T3 were due to a significant decreased conversion from T4 (p less than 0.02) in spite of a decreased MCR. The results are compatible with the assumption of two different monodeiodinating enzymes, a 5-deiodinase responsible for the diodination of T4 to rT3 and a 5'-deiodinase responsible for the deiodination of T4 to T3.

Female↗
PubMed1979

Osteoporosis in hyperthyroidism estimated by photon absorptiometry.

The degree of osteoporosis in hyperthyroidism before and during treatment with carbimazole was studied by photon absorption technique of the right forearm and calcaneus. In addition serum total calcium, serum ionized calcium, serum phosphorus and serum alkaline phosphatase were determined. A group of 96 patients suffering from untreated hyperthyroidism (85 women and 11 men) was studied (79 of these patients were also followed during treatment) and compared to a control group of 157 persons (107 women and 50 men). The women were divided into two groups: less than or equal to 45 years old and more than 45 years old. In all groups untreated hyperthyroid patients showed lower bone densities compared to the control group, but this was only significant in women. During treatment all groups showed a significant increase in density. After 3-6 months of treatment bone density in the calcaneus increased 12% and in the forearm 1.5%; after 6 months - 3 years 33% and 31%, respectively. At that time bone density was normalized. There was no correlation between bone density in hyperthyroid patients and duration and severity of the disease. The biochemical changes were characterised by increases in serum alkaline phosphatase (26%), serum total calcium (16%) and serum ionized calcium concentration (17%) in cases of untreated hyperthyroidism. Serum phosphorus concentration did not change. A correlation was found between elevation of the alkaline phosphatase and decreased bone density.

Adult↗
PubMed1979

Subclinical hypothyroidism in Addison's disease.

Fourteen patients with Idiopathic Addison's disease (IAD) were studied in order to detect a possible subclinical hypothyroid state. All were clinically euthyroid with normal serum thyroxine (T4) and serum 3,5',5'-triiodothyronine (T3). Eleven had circulating thyroid microsomal antibodies in blood. The mean basal serum TSH was significantly higher than that of the control group but only three patients had values above the upper normal range. The mean value of serum T4 was decreased as compared to that of the normal persons, while serum 3,3',5'-triiodothyronine was elevated. 7.5 mU bovine thyrotrophin per kilogram body weight injected intravenously caused a rise in serum T3 not different from the response in normals. However, as well increasing serum TSH as increasing microsomal antibody titer correlated significantly to decreasing thyroidal release of T3. Our results suggest that clinically euthyroid patients suffering from IAD might have a beginning thyroidal insufficiency because of a progressive immunological damage of the thyroid.

Addison Disease↗