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Biomedical subjects

M Weissel

Publications and source records attributed to M Weissel.

At least 91 records · Page 5Linked to original sources
PubMed1984

[Thyroid functional parameters during anti-arrhythmia therapy with amiodarone].

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.

Adolescent↗
PubMed1983

[The effect of nonthyroidal diseases on the serum hormone level of the thyroid gland function regulation cycle].

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.

Adolescent↗
PubMed1983

[Disorders of hormone metabolism in chronic uremia].

Uremia is accompanied by a variety of "true" and "laboratory" endocrine disorders, due in part to impaired degradation of hormones because of failing kidney function and in part to the interference of the uremic environment with extrarenal degradation or synthesis and secretion of certain hormones. "True" endocrine disorders, like hyperparathyroidism or hypogonadism, that are associated with renal insufficiency are in contrast with "laboratory" endocrine disorders in uremia, where pathological serum hormone levels lack clearcut clinical evidence for dysfunction of the respective endocrine organ (e.g. thyroid gland). This lack of a direct cause and effect relationship in uremia may be due to the fact that immunoassayable hormone levels may include cross reacting components without biological activity in uremia and to the fact that the uremic environment may alter hormonal effects on target organs. This review tries to give a survey of the big amount of available clinical and laboratory data for uremia induced changes in the following hormones: growth hormone and somatomedins, prolactin, cortisol and adrenocorticotrope hormone, the gonadal and thyroid function as well as parathyroid hormone action. The knowledge of these uremia-induced changes should facilitate the clinician the diagnosis of an additional primary endocrine ailment in a uremic patient and should, on the other hand, spare these patients unnecessary treatment for a suspected endocrine disorder.

Adrenocorticotropic Hormone↗
PubMed1983

[Familial increase in thyroxine binding globulins in the blood].

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.

Child↗
PubMed1983

Ether link cleavage is the major pathway of iodothyronine metabolism in the phagocytosing human leukocyte and also occurs in vivo in the rat.

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.

Amitrole↗
PubMed1982

Prolactin and thyrotrophin response to thyrotrophin-releasing hormone in growth hormone deficiency.

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.

Adolescent↗
PubMed1981

Partial rat kidney resection using autologous fibrinogen thrombin adhesive system.

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.

Animals↗
PubMed1980

[Osteopetrosis (Albers-Schönberg) (author's transl)].

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.

Adult↗