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Biomedical subjects

K Liewendahl

Publications and source records attributed to K Liewendahl.

At least 91 records · Page 5Linked to original sources
PubMed1983

Assessment of thyroid function with hormone assays.

Measurement of serum thyroid hormone and TSH levels provide diagnostic information in the majority of patients with thyroid dysfunction. The test strategy in hyperthyroidism differs from that in hypothyroidism. Serum T4 is a good test for hyperthyroidism in patients with normal thyroid hormone-binding protein levels. When binding proteins are abnormal serum free T4 is a much more accurate test for hyperthyroidism than serum T4. Serum T3 and the TSH response to TRH are useful tests for the early diagnosis of hyperthyroidism. Serum TSH is a very sensitive indicator of primary hypothyroidism rising already at the subclinical stage of the disease. Serum T4 and free T4, but not serum T3, are useful for the verification of clinical hypothyroidism. Determination of the TRH-stimulated TSH level is important for the differential diagnosis of pituitary and hypothalamic hypothyroidism. It is imperative to recognize that thyroid tests are often abnormal in various non-thyroidal diseases and that administration of drugs can affect these tests. Serum rT3 is of some value for the assessment of thyroid function in patients with non-thyroidal disease.

Humans↗
PubMed1982

Effect of parenteral nutrition on the blood levels of insulin, glucagon, growth hormone, thyroid hormones and cortisol in catabolic patients.

The changes in plasma insulin (IRI) glucagon (IRG), IRI:IRG ration, growth hormone (HGH), cortisol and thyroid hormones during two different but isocaloric parenteral nutrition regimens were investigated in 11 malnourished patients and 21 postoperative patients. The nutrition program which used glucose as a non-nitrogen energy source favoured anabolism by a higher rise in plasma IRI and by a higher rise in the initially low plasma IRI:IRG ratio in both malnourished and postoperative patients more than the alimentation regimen with glucose and lipid. The glucose program augmented the IRI:IRG ratio to an average of 5.5 +/- 1.2 (SEM) in malnourished patients and to 8.4+/-2.7 in postoperative patients. The corresponding values for the glucose-lipid program were 3.9+/- 1.0 and 1.9 +/- 0.4. In malnourished patients the difference between the anabolic effect of these nutrition regimens was further increased by a fall in the plasma HGH level to 0.7 +/- 0.3 microgram/l during fat infusion. Over a period of four days both alimentation programs similarly increased in the initially low serum T3 and free T3 index to the normal reference interval and decreased serum rT3 to a subnormal level (0.18+/-0.7 nmol/l) in malnourished patients. In postoperative patients the only change in thyroid hormones which was dependent on the four-day parenteral nutrition was the decrease in the initially elevated serum rT3 to the normal reference interval by both alimentation programs (by 54% in the glucose and by 30% in the glucose-lipid program).

Adult↗
PubMed1982

Susceptibility to proteolysis of thyroglobulin from rats and guinea-pigs treated with excess iodide.

The effect of excess iodide on proteolysis of in vivo 125I-labelled thyroglobulin (Tg) from rats and guinea-pigs was investigated in vitro using preparations of thyroid lysosomes and exogenous proteases (Pronase). Lysosomes were obtained by centrifugation of pig thyroid homogenates. This lysosomal preparation induced maximal proteolysis of Tg at pH 3.6 to 4.6 and was stimulated by KCl. Treatment of rats with excess iodide for up to 28 days had no effect on the proteolysis of Tg by lysosomes or Pronase. Decreased resistance of Tg to proteolysis by lysosomes and pronase was observed in guinea-pigs treated with excess iodide for 3 days, whereas Tg from guinea-pigs treated for longer time periods had increased resistance to proteolysis. This difference in the susceptibility to proteolysis of Tg provides an explanation why long-term administration of excess iodide is goitrogenic in guinea-pigs but not in rats.

Animals↗
PubMed1981

Bone lesions in chronic myelogenous leukaemia.

The incidence and site of bone lesions in 33 patients with chronic myelogenous leukaemia were studied by performing bone scintigraphy and radiography. The scintigrams were abnormal in 67% and the radiographs in 29%. Increased juxta-articular uptake of radiographs was observed particularly in acute phase patients, whereas areas of focal uptake were detected in many chronic phase patients. Nearly all patients suffered from bone pains before the development of demonstrable osseous lesions. Hypercalcaemia was found in one patient with blastic transformation and bone lysis. Two patients with extensive bone destruction were treated with vincristine, prednisone and local irradiation in spite of haematological remission. No haematological relapse has occurred in these two patients during follow-up for 12 and 41 months, respectively.

Adolescent↗
PubMed1980

Peripheral insensitivity to thyroid hormones in a euthyroid girl with goitre.

A 9-year-old girl was euthyroid with a small goitre, exophthalmos, scaphocephalic skull, minor sketelal abnormalities, and raised serum thyroid hormone concentrations. Other members of the family did not have goitres and their thyroid hormone levels were normal. From age 3 years the patient was treated for Graves's disease, but after 4 years treatment was stopped because of enlargement of the goitre. Despite increased serum thyroxine (T4), free T4 (FT4), and triiodothyronine (T3), basal serum TSH, and the TSH response to thyrotropin-releasing hormone (TRH) were normal. Pituitary refractoriness was present because full suppression of the TSH response to TRH was achieved only after daily administration of 500 micrograms thyroxine. Urinary excretion of hydroxyproline, and the activity of red cell glucose-6-phosphate dehydrogenase remained normal when excess T4 was administered, demonstrating the tissue resistance to thyroid hormones. Peripheral lymphocytes were found to have nuclear receptors for T3 with normal affinity, but the relatively low binding capacity indicated that the biochemical defect might be a deficiency of nuclear receptor protein. The findings in this patient differ somewhat from previously reported cases of peripheral resistance to thyroid hormones.

Child, Preschool↗
PubMed1980

Effect of anticonvulsant and antidepressant drugs on iodothyronines in serum.

Serum iodothyronine concentrations were measured in patients on long-term therapy with one or two anticonvulsant drugs. Diphenylhydantoin (DPH) and carbamazepine (CBZ) reduced the serum levels of thyroxine (T4) free T4 index, reverse triiodothyronine (rT3) and 3,3'-diiodothyronine (3,3'-T2), whereas the depressant effect on the serum levels of triiodothyronine (T3) and free T3 index was small but statistically significant. In patients administered DPH and phenobarbital (PB) or CBZ and primidone (PD) the serum iodothyronine levels were also depressed, except for normal T3 and free T3 index. Patients receiving only PB or PD had normal serum levels of total and free thyroid hormones, but decreased concentrations of rT3 and 3,3'-T2. Only supratherapeutic concentrations of DPH and CBZ added in vitro to control sera significantly reduced the number of T4 and T3-binding sites, as reflected in increased T4 and T3 uptake test results. This indicates that the DPH and CBZ-induced decrease in thyroid hormone concentrations in vivo is not due to a displacement of thyroid hormones from their binding sites on serum proteins. The antidepressant drugs amitriptyline and mianserin had no effect on the thyroid hormone levels in serum.

Adult↗
PubMed1980

Thyroid hormone resistance.

General resistance to the action of thyroid hormones is characterized by increased levels of thyroid hormones and normal thyroid hormone binding proteins but clinical euthyroidism. There is a wide clinical spectrum ranging from patients with congenital goitre and signs of subclinical hypothyroidism to subjects with no physical abnormality. In the most affected patients special physical features have been described. Serum thyrotrophin (TSH) and the response to thyrotrophin releasing hormone (TRH) is mostly normal but may fluctuate being at times elevated and even markedly increased values may be encountered. Studies on lymphocytes and fibroblasts indicate that a decreased affinity of thyroid hormones for nuclear receptors, a decreased binding capacity of the receptors or some post-receptor mechanism may be responsible for these changes. Hitherto, six families, comprising 24 patients and seven single cases, have been described. The pedigrees are compatible with dominant inheritance. Selective refractoriness of the pituitary thyrotrophs to thyroid hormones has been described in five patients with hyperthyroidism. Excessive secretion of TSH is the cause of hyperthyroidism. In four of the cases reported TRH caused an exaggerated TSH response and TSH was partially suppressible by additional exogenous thyroid hormone. The response of TSH and the behaviour of the alpha- and beta-subunits of TSH distinguish this syndrome from TSH-induced hyperthyroidism due to pituitary tumours. The underlying mechanisms are unknown.

Female↗
PubMed1979

Suppression of the TSH response to TRH by thyroxine therapy in differentiated thyroid carcinoma patients.

Absent response of serum thyrotrophin (TSH) after stimulation with 200 micrograms synthetic thyrotrophin-releasing hormone (TRH) was used as a criterion of adequate suppression of TSH in the treatment of thyroid carcinoma patients with thyroxine. The mean causing total suppression of the response was 223 micrograms of thyroxine per day. At this dose level about 40% of the patients had serum thyroxine concentrations above the upper reference interval and only 10% had elevated triiodothyronine concentrations. In some patients the TSH response to TRH varied between absent and low normal when tested at long intervals. The ideal dose of thyroxine is obviously slightly higher than the smallest one causing total suppression of the TSH response to TRH, i.e. about 250 micrograms a day. The individual dose must be found using the TRH stimulation test because serum thyroid hormone levels cannot be used as a guideline for adequate dosage. In some patients the thyroid remnant of apparently normal thyroid tissue was not totally suppressed although the thyroxine dose was definitely above the level causing suppression of the response to TRH.

Adenocarcinoma↗
PubMed1979

Abnormal thyroid function tests in devere non-thyroidal illness: diagnostic and pathophysiologic aspects.

In vitro thyroid function tests were studied in twenty-three patients with serious non-thyroidal illness. All had reduced protein binding of serum thyroxine (T4) and serum triiodothyronine (T3) as reflected in increased T4 and T3 uptake tests. The mean T4-binding prealbumin (TBPA) capacity and concentration were about one third the normal levels, whereas the decrease in R4-binding globulin (TBG) was much smaller. Increased serum free fatty acids and reverse T3 were frequently observed, but in vitro displacement of thyroid hormones from their binding sites was achieved only with much high concentrations of these compounds. Other still unrecognized substances significantly inhibiting binding of thyroid hormones might, however, occur in sera of severely ill patients. Evidence in favour of this possibility was the disproportionately high serum T4 by TBG-binding assay relative to T4 by radioimmunoassay. In most of the patients the dual-stage free T4 was elevated, whereas the single-stage free T4 index (CT4I) was within the reference interval. However, neither of these indices reflected the moderately increased dialysable free T4 concentration very accurately. The free T3 index was depressed in most of the patients, whereas the dialysable free T3 concentration was not affected. For practical purposes the combination of normal serum T4 and CT4I in a severely ill patient indicates absence of an associated thyrometabolic disorders.

Adult↗
PubMed1978

Nuclear binding of triiodothyronine and thyroxine in lymphocytes from subjects with hyperthyroidism, hypothyroidism and resistance to thyroid hormones.

Binding of triiodothyronine (T3) and thyroxine (T4) to nuclei of intact human lymphocytes was studied. The binding characteristics were analysed by Scatchard's method. In lymphocytes from euthyroid healthy subjects there was a single set of saturable nuclear T3 and T4 binding sites with an apparent mean equilibrium association constant of 3.3 X 10(10) l/mol and 1.7 X 10(10) l/mol, respectively. The estimated mean maximal specific binding capacity for T3 was 50 fmol/mg DNA and for T4 was 55 fmol/mg DNA, indicating that these two hormones may have a common receptor. In hyperthyroid and hypothyroid patients nuclear affinity for T3 and T4 was very similar to that for euthyroid reference subjects. In hyperthyroidism, T3 and T4 binding capacity was unaltered, whereas in hypothyroidism it was nearly twice as high as in euthyroidism. Lymphocytes from three members of a family with hereditary peripheral resistance to thyroid hormone action were studied. One set of saturable T3 and T4 nuclear binding sites with affinity constants similar to those in the euthyroid group was found. However, in these subjects the estimated binding capacity for T3 and T4 was rather low, indicating that the biochemical defect in this family might be a mild deficiency of nuclear receptor protein. Incubation with diphenylhydantoin and salicylate added in vitro did not alter the binding of T3 and T4 to lymphocyte nuclei. Nuclear binding was also not affected in patients receiving therapeutic amounts of diphenylhydantoin.

Adult↗
PubMed1978

Thyroid function tests in patients on long-term treatment with various anticonvulsant drugs.

Thyroid function tests were studied in patients undergoing long-term treatment with various anticonvulsant drugs. Previous reports that diphenylhydantoin induces a decrease in the serum concentrations of total and free thyroxine (T4) and triiodothyronine (T3) without a change in the TSH concentration were confirmed. Diphenylhydantoin had no effect on reverse T3. Carbamazepine was also found to decrease serum T4, the free T4 index and T3 but, with the exception of T3, the decrease was smaller than that induced by diphenylhydantoin. Dipropylacetic acid did not influence the serum thyroid hormone concentrations, and neither did primidone. This demonstrates that the interaction between anticonvulsant drugs of different chemical structure and thyroid hormone metabolism is diverse. None of the drugs tested altered serum TSH or the T3 uptake test for the estimation of unsaturated thyroid hormone binding-capacity in serum. These two tests are considered diagnostically more dependable than the measurement of thyroid hormones in serum when diphenylhydantoin and carbamazepine are administered.

Adolescent↗
PubMed1978

Acute effects of alcohol on anterior pituitary secretion of the tropic hormones.

The plasma or serum concentrations of GH, TSH, LH, PRL, testosterone, cortisol, T4, and T3, and the values of the T3 uptake test were monitored in 12 healthy male volunteers for a period of 20 h after administration of one large dose of ethanol (1.5 g/kg BW). The effects of TRH and LRH on the secretion of TSH, PRL, and LH were studied in these subjects once during the period of acute alcohol intoxication (4 h after the start of drinking) and once during the hangover period (14 h after the start of drinking). Each subject served as his own control by drinking water only during another experimental session. Alcohol had no significant effect on basal concentrations of GH, TSH, LH, T4, T3, or testosterone. The concentration of cortisol in plasma was elevated during the whole 20-h period after ingestion of alcohol, as compared with the control values. Alcohol also did not significantly alter the effects of TRH and LRH on plasma TSH and LH levels at 4 and 14 h. During the hangover period, the PRL response to TRH was totally blocked, but during alcohol intoxication, there was a slight increase in the PRL response to TRH. The lack of response of PRL to TRH during the hangover suggests that withdrawal symptoms are associated with increased dopaminergic activity in the hypothalamus.

Adolescent↗