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Biomedical subjects

W H Hackeng

Publications and source records attributed to W H Hackeng.

At least 73 records · Page 4Linked to original sources
PubMed1984

Changes in nephrogenous cyclic AMP excretion and plasma cyclic AMP following treatment of hyperthyroidism.

Plasma cyclic AMP (PcAMP) concentration and the excretion of cyclic AMP/dl GF were estimated in 11 thyrotoxic patients before and after medical treatment. PcAMP concentrations were significantly higher during hyperthyroidism (2.30 +/- 0.69 vs 1.88 +/- 0.71 nmol/dl; P less than 0.05), and total urinary cyclic AMP (TcAMP) excretion showed no significant changes (3.24 +/- 0.64 vs 3.44 +/- 1.77 nmol/dl GF). Nephrogenous (NcAMP) excretion rose significantly (1.00 +/- 0.82 vs 1.68 +/- 1.31 mmol/dl GF; P less than 0.025). The increase in NcAMP excretion correlated significantly with the decrease in serum T3 levels (r = -0.46; P less than 0.05). Serum iPTH levels showed no significant change. Both the serum Ca, corrected for serum total protein and TmPO4/GFR declined after treatment (respectively 2.44 +/- 0.13 vs 2.33 +/- 0.08 mmol/l; P less than 0.05 and 1.18 +/- 0.29 vs 1.05 +/- 0.22 mmol/l; P less than 0.05). It is concluded that the rise in NcAMP excretion corroborates the concept of increasing parathyroid activity following the treatment of hyperthyroidism.

Adolescent↗
PubMed1983

Diminution of prolactin and increase of thyrotrophin response to thyrotrophin releasing hormone occurring independently of changes in basal level of these hormones during treatment of hypothyroidism.

In order to study the effect of rising thyroid hormone levels in hypothyroidism upon prolactin responses to TRH, in relation to changes in basal prolactin concentration and to changes in TSH responses, we followed 18 patients by performing TRH tests before and after 14, 28, 42 and 56 d on gradually increasing levothyroxine dosages, plus a final test when euthyroidism was achieved. Basal prolactin rose initially, at day 14, followed by a return on days 28, 42 and 56 to a level similar to the pretherapeutic value, while at euthyroidism prolactin had fallen below the original value. The area under the prolactin response curve on TRH stimulation was unchanged at 14 d, notwithstanding the rise of basal prolactin concentration. At 28, 42 and 56 d the responses declined progressively along with basal prolactin concentrations that remained equivalent to the pretreatment level. The TSH response to TRH rose at 14, 28, and 42 d along with a continuous downward course of basal TSH. Thus, substitution with L-thyroxine inhibited the responsivity of prolactin but enhanced that of TSH to TRH. The fact that these changes occurred in opposite directions, appears to rule out a negative feed-back effect of T4 on hypothalamic TRH secretion. The effects on responses were shown to occur independently of those on basal secretion of prolactin and TSH.

Feedback↗
PubMed1983

Thyroxine and triiodothyronine levels in Snell mice.

Since no data are available concerning thyroid hormone levels in Snell dwarf mice from birth on, a cross-sectional study was performed of L-thyroxine (T4) and L-triiodothyronine (T3) levels in blood or serum as a function of age of several litters, starting at birth. In normal Snell mice T4 levels in blood and serum are changing with age. T4 increases during the first 2 weeks of age and declines thereafter, until adult levels of about 50 nmol/l are reached at 21 days of age. Serum T3 values are in the range of 2-3 nmol/l. They do not show such an age-related pattern. From birth on in each litter there was a clear separation between animals with low T4 levels in blood and the others. This separation was possible at all subsequent days until 9 days of age, when dwarfs can be recognized by eye. Above that age the low T4 values were associated with dwarfism. This suggests that dwarfs are hypothyroid already at birth. Serum T3 in dwarfs falls below the normal range only after 4 weeks of age, resulting in a lower T4/T3 ratio than normal. The half life time of exogenous T4 in serum of dwarfs is in the range of 13-18 h and not different from normal. For T3 t1/2 is 9.5-11.1 h. Dwarf mice become euthyroid by treatment with 0.1 microgram T4 per day. 1 microgram T4 was needed to reach a physiological level of T3. These data suggest that the peripheral conversion of T4 to T3 is slower in dwarfs than in normals. Treatment with hGH, prolactin, glucagon, insulin, testosterone and oestradiol had no influence on serum T4. As expected TSH was stimulatory. Similar results were obtained for serum T3, with the exception of prolactin which caused slightly increased levels of serum T3.

Animals↗
PubMed1983

Cyproheptadine and desmethylcyproheptadine directly inhibit the release of adrenocorticotrophin and beta-lipotrophin/beta-endorphin activity from the neurointermediate lobe of the rat pituitary gland.

Cyproheptadine and its metabolite desmethylcyproheptadine were shown to suppress directly the release of adrenocorticotrophin (ACTH) and beta-lipotrophin/beta-endorphin activity from the neurointermediate lobe of the pituitary gland incubated in vitro. Neither compound affected the release of ACTH from the anterior pituitary gland. Serotonin stimulated the release of ACTH and beta-lipotrophin/beta-endorphin activity from the neurointermediate lobe, but did not influence the (desmethyl)cyproheptadine-mediated inhibition of hormone release. These results indicate that serotonin and cyproheptadine affect hormone release by the neurointermediate lobe by a direct action. The effect of cyproheptadine, however, might not be exerted by a serotonin receptor.

Adrenocorticotropic Hormone↗
PubMed1982

Concomitant secretion of calcitonin, beta-endorphin and ACTH from medullary thyroid carcinoma in vivo and in vitro.

The present study was performed to investigate the possible synthesis of a common precursor molecule for calcitonin (CT), adrenocporticotropin (ACTH) and beta-lipotropin (beta-LPH)/ beta-endorphin (beta-EP) by the human medullary thyroid carcinoma (MTC). In a patient with MTC but without Cushing's syndrome, the response of plasma CT, ACTH and cortisol levels to a calcium infusion, lysine vasopressin (LVP) and dexamethasone were measured. A parallel increase of these hormones in response to calcium and LVP was seen, while there was a paradoxical increase of CT during dexamethasone infusion. Incubation of MTC fragments obtained at surgery showed a significant correlation of the secretion of CT, ACTH and beta-LPH/ beta-EP in response to calcium, LVP and dexamethasone. The concomitant release of these hormones in vivo and in vitro could be compatible with the synthesis of a common precursor molecule for CT, ACTH and beta-LPH/ beta-EP in MTC, although this was not substantiated by gel-chromatography of the tumor extract. Corticotropin releasing factor, a regulator of the normal processing of pro-opiococorticoid precursor molecule in the anterior pituitary gland, is also able to activate ACTH, beta-LPH/ beta-EP and calcitonin secretion from the malignant C-cell of the thyroid.

Adrenocorticotropic Hormone↗
PubMed1982

Enhanced calcitonin release in chronic renal failure depending on the absence of severe secondary hyperparathyroidism.

In 27 patients with end-stage chronic renal failure an elevated calcitonin (CT) and parathyroid hormone was found. On stimulation with Ca i.v. there were 9 cases in whom delta CT proved to be higher than the maximal response of 50 pg ml-1 in controls. Supranormal CT responses were found predominantly in patients with normal alkaline phosphatase, who as a group increased their CT from 94.5 +/- 61 to 142.0 +/- 94 pg ml-1 (p less than 0.02). In contrast to this, patients with elevated alkaline phosphatase who also had a higher level of parathyroid hormone maintained unchanged CT on Ca stimulation. It is concluded that in chronic renal failure with severe secondary hyperparathyroidism, delta CT on stimulation is normal, while an enhanced delta CT often exists when hyperparathyroidism is of insufficient degree to cause a raised alkaline phosphatase.

Adult↗
PubMed1981

[Hyperparathyroidism in hemodialysis patients: studies on parathyroid regulation and classification problems (author's transl)].

In a series of 22 patients undergoing chronic intermittent hemodialysis the response in secretion of parathyroid hormone (PTH) to an acute increase in serum calcium (Ca) concentration was studied. All patients had raised levels of predialysis PTH. Ca concentrations were measured by means of atomic absorption spectrophotometry and PTH concentrations were determined by radioimmunoassay. A close, significant, linear, negative correlation was demonstrated by regression analysis when Ca concentrations were correlated to changes in PTH, expressed as a percentage of the initial predialysis PTH value (100%). This finding supports the assumption that the function of the parathyroid gland at cellular level is similar in all patients, irrespective of very different predialysis PTH concentrations in peripheral blood. The results together with findings in literature were used to describe secondary hyperparathyroidism as a disease which shows typical phases during progression. Some still obscure phenomena of secondary hyperparathyroidism can be explained by discriminating between parathyroid function at a cellular and an organ level. The classification of hyperparathyroidism in regulative and autonomous forms only seems to be applicable when referred to the cellular level.

Calcium↗
PubMed1981

Bilateral occurrence of pheochromocytoma in patients with the multiple endocrine neoplasia syndrome type 2A (Sipple's syndrome).

Two kindreds with the multiple endocrine neoplasia type 2A syndrome were studied. Of one of these we examined 150 members, 20 of whom were treated with thyroidectomy for medullary carcinoma and nine with bilateral adrenalectomy for pheochromocytoma. Of the second kindred 50 members were examined, seven of whom were thyroidectomized and seven treated with bilateral adrenalectomy. Pheochromocytomas were invariably found on both sides, even in four cases in which the adrenals on one side appeared to be completely normal, not only at preoperative roentgenologic examination but also on inspection during the operation. The microscopic finding of micronodules and a cluster of abnormal medullary cells identical with those found in pheochromocytomas in one of the apparently normal adrenals represents a first stage in the development of diffuse medullary hyperplasia as well as nodular hyperplasia. This is in accordance with the fact that in the MEN type 2A syndrome pheochromocytomas are always multicentric and multiple in origin. On the basis of these findings we conclude that all patients with the MEN 2A syndrome who show symptoms and signs of active pheochromocytoma should be subjected to bilateral adrenalectomy, even when one or both of the adrenals appear to be normal at roentgenologic investigation.

Adrenal Gland Neoplasms↗
PubMed1981

Value of serum calcitonin estimation in clinical oncology.

In 132 consecutive patients with carcinoma of various organs, a higher serum immunoreactive calcitonin (ICT) concentration (median level 50 pg/ml) was found than in 68 normal subjects (median level 20 pg/ml). The incidence of hypercalcitoninaemia was 40%. All 9 patients with primary liver-cell carcinoma were hypercalcitoninaemic. On the other hand, none of the 7 patients with a carcinoma of the breast had raised ICT levels. In bronchogenic cancer a relationship between ICT and cell type was found, with a predominance of high ICT in patients with oatcell and other undifferentiated types, whereas in squamous-cell carcinomas and adenocarcinomas of the lung hypercalcitoninaemia was relatively rare. When we divided all our patients according to differentiation of the tumour cell, it was found that the lower the degree of differentiation, the higher the ICT concentration, whereas opposite results were observed for CEA. When ICT and CEA were estimated concurrently, we found at least one marker increased in 70% of our patients. Our results demonstrate that patients with metastases in the liver have more frequently and increased ICT. In addition, we conclude that lifespan can be expected to be lower in patients with high ICT levels. In a longitudinal study of 46 patients, there was a positive correlation between change in serum ICT and tumour mass.

Aged↗
PubMed1981

Dissociation between changes in immunoreactive parathormone and its biological indices induced by cimetidine in primary hyperparathyroidism.

In three out of four patients with primary hyperparathyroidism, 2 000 mg of cimetidine daily caused a reduction of immunoreactive parathormone (iPTH) when measured at 8.30 and 11.30 on days 16 and 17 on treatment. Serum Ca, PO4 and maximal tubular reabsorption of PO4 remained unchanged. Excretion of cAMP/100 ml GFR remained elevated to at least the same extent as before treatment. Two patients, in whom cimetidine treatment was continued for an additional 4 weeks, did not show further hormonal or biochemical changes compared with the evaluation on days 16 and 17. We conclude that reduction of iPTH is not accompanied by any change in biological activity of this hormone. The reason for this discrepancy remains unclear.

Cimetidine↗
PubMed1981

Characteristic changes in the concentrations of some peptide hormones, in particular those regulating serum calcium, in acute pancreatitis and myocardial infarction.

In order to further investigate hormonal changes and possible metabolic consequences in acute pancreatitis, 10 cases with a mild form of the disease was studied. The influence of tissue injury per se on the hormones in question was assessed from comparison with the hormone levels in the course of myocardial infarction (MI) in 9 cases. Insulin and glucose showed no consistent changes. Glucagon was suppressed on admission, 22 +/- 10 pg . ml-1, compared with the ultimate concentration, 40 +/- 20 pg . ml-1 (p less than 0.05), and with the initial value in MI, 74 +/- 32 pg . ml-1 (p less than 0.01). Serum calcitonin (CT) was strongly elevated initially, 348 +/- 313 pg . ml-1, compared with the ultimate level, 24 +/- 7 pg . ml-1 (p less than 0.001), and with the normal initial level in MI, 43 +/- 44 pg . ml-1 (p less than 0.01). Serum CT elevations were time-related to a slight reduction in corrected serum Ca, which might reflect a biological expression of this substance. In pancreatitis, parathyroid hormone (PTH) remained normal and unchanged throughout the study, whereas patients with MI had an increased level of this hormone on admission, 0.19 +/- 0.08 microgramEq . 1(-1), compared with the ultimate concentration, 0.09 +/- 0.03 microgram/q . 1(-1) (p less than 0.02) and with the initial concentration in pancreatitis, 0.11 +/- 0.06 microgramEq . 1(-1) (p less than 0.05). Supranormal PTH levels were found in more than half of the infarction patients on days 0 and 1.

Acute Disease↗
PubMed1980

Serum concentrations of immunoreactive calcitonin in patients with hypergastrinaemia.

In order to test tthe hypothesis that chronically elevated serum gastrin levels induce hypercalcitoninaemia, we have measured serum calcitonin levels in patients with chronic hypergastrinaemia. Basal serum calcitonin concentrations were found to be elevated in 2 of 23 patients with Zollinger-Ellison syndrome, but not in 16 patients with hypergastrinaemia due to achlorhydria or a single patient with primary hypergastrinaemia of antral origin. Both Zollinger-Ellison patients with hypercalcitoninaemia (0.31 and 0.79 ng/ml) had multiple endocrine adenomatosis type 1, but no medullary carcinoma of the thyroid. The hypercalcitoninaemia in these patients does not seem to be related to multiple endocrine adenomatosis type 1, since serum calcitonin was normal in 12 normogastrinaemic patients with hyperparathyroidism from families with multiple endocrine adenomatosis type 1. We conclude that chronically elevated serum gastrin levels do not result in hypercalcitoninaemia.

Calcitonin↗