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E M Erfurth

Publications and source records attributed to E M Erfurth.

46 records · Page 3Linked to original sources
PubMed1990

Plasma neuropeptides in hyperthyroidism.

Plasma levels of the neuropeptides, vasoactive intestinal polypeptide (VIP, neuropeptide Y (NPY), calcitonin gene-related peptide (CGRP), substance P, and galanin were determined in 15 hyperthyroid patients before and at 3 occassions during 38 weeks of treatment. Treatment was performed with either 131I alone or with carbimazole, with combination of carbimazole and thyroxine, or with subtotal thyroidectomy. Before and after 11 (+/- 4), 24 (+/- 6) and 38 (+/- 5) weeks of treatment, plasma neuropeptide levels were analysed. A group of 9 premenopausal women served as controls. During hyperthyroidism, mean plasma level of CGRP was higher than in controls (P less than 0.001). In contrast, the mean plasma levels of the other measured neuropeptides did not differ from those in the controls. Mean serum level of tree T4 was lowered from 81.9 +/- 30.1 to 23.9 +/- 8.6 pmol/l and mean serum level of free T3 was lowered from 27.3 +/- 7.9 to 6.7 +/- 2.3 pmol/l during the course of the treatment. After 11 weeks of treatment, mean plasma NPY level was significantly increased (P = 0.004) compared to pretreatment levels. However, after 38 weeks of treatment, mean plasma NPY level had returned to control values. The mean plasma CGRP level was significantly reduced at 11 and 38 weeks of treatment compared to pre-treatment value (P = 0.002 and P = 0.004, respectively). Mean plasma level of neurotensin slowly declined during the treatment (P = 0.003). In contrast, mean plasma level of VIP, of substance P, and of galanin did not differ from control value before or after treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Suppressed plasma prolactin response to thyrotropin-releasing hormone in hyperthyroidism reproduced by thyroxine but not by triiodothyronine administration to normal subjects.

In 10 hyperthyroid women studied in the follicular phase of the menstrual cycle, basal plasma PRL was normal, but PRL release after TRH was significantly suppressed compared with that in 11 control women. The suppressed PRL response to TRH was not explained by changes in serum estradiol or sex hormone-binding globulin. It recovered after treatment of hyperthyroidism. When normal women were treated with T4 (0.5 mg daily for 6 to 10 days), their mean serum free T4 level increased to about 70% of that in the hyperthyroid patients, whereas their serum free T3 levels increased to a lesser degree. During T4 administration, these women had PRL changes similar to those of the hyperthyroid patients. When the normal women took T3 (60-120 micrograms for 6 to 8 days), their serum free T3 increased to almost the level of the hyperthyroid patients, but the TRH stimulated PRL release remained close to the control level. The PRL increase after dopaminergic blockade with metoclopramide was significantly suppressed in hyperthyroid patients, and they had no PRL response to TRH after pretreatment with metoclopramide. In conclusion, the PRL changes in hyperthyroidism were reproduced by administration of T4, but not by administration of T3 to healthy women. The site of action is suggested to be pituitary, but additional hypothalamic effects cannot be excluded.

Adult↗
PubMed1987

Increased plasma gonadotropin levels in spontaneous hyperthyroidism reproduced by thyroxine but not by triiodothyronine administration to normal subjects.

In nine hyperthyroid women studied in the follicular phase of the menstrual cycle basal plasma LH concentrations and LH and FSH responses to GnRH were increased compared to those in nine normal women. The increased gonadotropin levels could not be related to changes in body weight or plasma estradiol or serum sex hormone-binding globulin levels, and they approached normal levels during or after treatment of hyperthyroidism. When normal women were treated with T4 (0.5 mg daily for 6-10 days), their mean serum free T4 level increased to about 60% of that in the hyperthyroid patients, while their serum T3 levels increased to a lesser degree. During T4 administration these women had gonadotropin changes similar to those of the hyperthyroid patients. When the normal women took T3 (60-120 micrograms for 6-8 days), their serum T3 level rose almost to the level in the hyperthyroid patients, but basal and GnRH-stimulated LH and FSH remained close to control levels. Dopaminergic blockade with metoclopramide did not alter the gonadotropin response to GnRH in any subject group. We conclude that serum T4 is of greater importance than serum T3 for at least short term gonadotropin regulation.

Adult↗
PubMed1986

Thyroid hormone metabolism in thyroid disease as reflected by the ratio of serum triiodothyronine to thyroxine.

In 77 euthyroid subjects the mean ratio between serum triiodothyronine (S-T3) in nmol/l X 10(3) and serum thyroxine (S-T4) in nmol/l was 22.4 with a standard deviation of 4.3. The distribution of the ratio was close to Gaussian. It was not changed in subjects under estrogen effect. The ratio was increased in hypothyroid subjects suggesting a mechanism preserving S-T3 better than S-T4 in thyroid failure. This mechanism seemed independent of TSH as the increasing S-T3/S-T4 ratio in primary hypothyroidism was not correlated to serum TSH (S-TSH), and patients with hypothyroidism of pituitary origin, without any increase in S-TSH, had a significantly elevated S-T3/S-T4 ratio. In subjects taking thyroxine, S-T4 but not S-T3 increased with the dose of thyroxine, leading to decreasing S-T3/S-T4 ratios. This indicates a mechanism that keeps S-T3 within normal limits also when the S-T4 supply is high. This applied also to athyreotic subjects on thyroxine and to subjects on thyroxine plus carbimazole, suggesting that the mechanism is independent of thyroid tissue, uninfluenced by carbimazole, and probably operates via the peripheral metabolism of T4. Changes in the S-T3/S-T4 ratio can be achieved by several mechanisms, and the specificity of ratio changes is low. However, by investigating the ratio S-T3/S-T4 in selected clinical states we can depict the ability of the organism to protect its normal S-T3 level in situations with divergent S-T4 concentrations, even if details about the mechanisms cannot be explained.

Adolescent↗
PubMed1984

Normal reference interval for thyrotropin response to thyroliberin: dependence on age, sex, free thyroxin index, and basal concentrations of thyrotropin.

We measured the thyrotropin response (delta TSH) to 200 micrograms of thyroliberin in 131 subjects without thyroid dysfunction or other disease and with basal values for thyroid function that were within the normal reference intervals for our laboratory. By univariate and multivariate statistical methods we found delta TSH to be significantly influenced by the basal concentration of thyrotropin (TSH0) and the free thyroxin index (FT4I). When the effects of variations in TSH0 and FT4I were eliminated, delta TSH in men under 40 years of age did not differ from that in women. A decrease in delta TSH with increasing age was found in men but not in women. Thus a reference interval for delta TSH should consider TSH0, FT4I, and, in men, age. On the basis of multiple linear regression analysis, we constructed a formula for delta TSH reference intervals that takes into account individual values for TSH0 and FT4I. The formula should be applicable for women, regardless of age, up to 77 years and for men under 40 years. For older men a correction for the age-related decrease in delta TSH must be applied.

Adult↗
PubMedDate not supplied

Plasma levels of persistent organohalogens and hormone levels in adult male humans.

In this study the authors assessed the possible relationship between high dietary exposure to persistent organohalogens (OHS) through fatty fish from the Baltic Sea and hormone levels in adult men. Blood samples were drawn from 110 men who consumed varying amounts of fish (i.e., 0-32 meals per month) for analysis of plasma levels of 18 polychlorinated biphenyl (PCB) congeners, 5 hydroxy-PCBs, 1,1,1-trichloro-2,2-bis(4-chlorophenyl)-ethane (p,p'-DDT), 1,1-dichloro-2,2-bis(4-chlorophenyl)-ethene (p,p'-DDE), hexachlorobenzene, and 2,2',4,4'-tetrabromodiphenyl ether. In addition, plasma levels of follicle-stimulating hormone, luteinizing hormone, prolactin, plasma thyrotropin, free and total T3, free and total T4, and free testosterone were analyzed. The authors adjusted for age, and the only significant associations that remained were negative correlations between 2,2',4,4'-tetrabromodiphenyl ether and plasma thyrotropin (p < .001), and between pentachlorophenol and follicle-stimulating hormone (p = .04). The authors expected that there would be some significant correlations that resulted from pure chance. High consumption of organohalogen-polluted fish did not appear to affect plasma concentrations of pituitary, thyroid, or testosterone hormone levels in male adults.

Adult↗
PubMedDate not supplied

Effects of lead on the endocrine system in lead smelter workers.

In this study of the effects of lead on the endocrine system, 77 secondary lead-smelter workers (i.e., 62 active and 15 retired) were compared with 26 referents. Lead concentrations were determined in plasma with inductively coupled plasma mass spectrometry (i.e., index of recent exposure), in blood with atomic absorption spectrophotometry, and in fingerbone with K x-ray fluorescence technique (i.e., index of long-term exposure). In addition, pituitary hormones were determined in serum by fluoroimmunoassay, and thyroid hormones and testosterone in serum were determined with radioimmunoassay. Nine lead workers and 11 referents were challenged with gonadotrophin-releasing hormone and thyrotrophin-releasing hormone, followed by measurements of stimulated pituitary hormone levels in serum. Median levels of lead in plasma were 0.14 microg/dl (range = 0.04-3.7 microg/dl) in active lead workers, 0.08 microg/dl (range = 0.05-0.4 microg/dl) in retired lead workers, and 0.03 microg/dl (range = 0.02-0.04 microg/dl) in referents (1 microg/dl = 48.3 nmol/l). Corresponding blood lead concentrations were 33.2 microg/dl (range = 8.3-93.2 microg/dl), 18.6 microg/dl (range = 10.4-49.7 microg/dl), and 4.1 microg/dl (range 0.8-6.2 microg/dl), respectively. Respective bone lead levels were 21 microg/gm (range = -13 to 99 microg/gm), 55 microg/gm (range = 3-88 microg/gm), and 2 microg/gm (range = -21 to 14 microg/gm). Concentrations of basal serum hormone (i.e., free thyroid hormones, thyrotrophin, sex hormone binding globulin, and testosterone) were similar in the 3 groups. There were no significant associations between the hormones mentioned herein and blood plasma, blood lead, and bone lead levels. In the challenge test, stimulated follicle-stimulating hormone levels were significantly lower in lead workers (p = .014) than in referents, indicating an effect of lead at the pituitary level. Also, there was a tendency toward lower basal stimulated follicle-stimulating hormone concentrations in lead workers (p = .08). This effect, however, was not associated with blood plasma level, blood lead level, or bone lead level. In conclusion, a moderate exposure to lead was associated with only minor changes in the male endocrine function, particularly affecting the hypothalamic-pituitary axis. Given that sperm parameters were not studied, the authors could not draw conclusions about fertility consequences.

Adult↗