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Biomedical subjects

R Pelkonen

Publications and source records attributed to R Pelkonen.

At least 127 records · Page 7Linked to original sources
PubMed1980

Bomocriptine treatment of patients with acromegaly resistant to conventional therapy.

Eleven patients with active acromegaly resistant to conventional therapy were treated with bromocriptine for 15 (12--22) months by increasing the daily dose stepwise from 5 to 10--60 mg. A satisfactory response was achieved in all but one of the eight patients, in whom the mean diurnal level of serum GH was less than 50 ng/ml, whereas patients with grossly elevated serum GH levels responded poorly. In the longterm, no overall effects on glucose tolerance or plasma insulin (IRI) levels were observed but the chemical diabetes of three patients ameliorated in two. On the other hand, a dose-dependent acute suppressive effect of bromocriptine on plasma IRI response to oral glucose was observed, suggesting a direct effect of bromocriptine on the release of insulin from beta cells. Bromocriptine seems to be a good alternative in the treatment of patients with acromegaly who have not responded to conventional therapy.

Acromegaly↗
PubMed1980

Glucocorticoid receptors in adrenocorticoid disorders.

Circulating human lymphocytes contain glucocorticoid receptors (GR). To see if adrenocortical imbalance is associated with changes in the level of GR, several patients with hypo- and hypercortisolism were studied. Peripheral lymphocytes were prepared by Ficoll-Hypaque gradients and were then subjected to a whole cell-binding assay measuring the total cellular receptor pool, with [3H]dexamethasone as the ligand. There were no significant differences in the cellular content of GR among healthy controls, 10 patients with Cushing's syndrome, and 3 patients suffering from Addison's disease; the absolute levels of GR were 4850 +/- 1340, 4900 +/- 2160, and 5640 +/- 1110 (mean +/- SD) receptors/cell, respectively. The mean equilibrium dissociation constants of the interaction of [3H]dexamethasone with the receptor were also about the same in the 3 groups (1-2 X 10(-8) M). Thus, aberrations in glucocorticoid balance strong enough to produce clear-cut clinical symptoms do not result in major alterations in the level of the peripheral GR. We also studied an additional patient who had hypercortisolism due to an adrenal adenoma but only slight clinical signs of hypercortisolism; interestingly, her cellular GR level was only 30% of normal. The lymphocytic GR content was also below normal in 2 patients with anorexia nervosa.

Addison Disease↗
PubMed1980

Post-encephalitic hypothalamic-pituitary insufficiency.

Pituitary function was investigated in 3 patients who developed hypothalamic-pituitary insufficiency after viral meningoencephalitis. In 2 patients the causative agents were probably Influenza-A-and Herpes simplex virus whereas in the third patient it was not identified. The pattern of hormonal deficiencies indicated that all the central regulatory areas - hypothalamus, pituitary stalk and pituitary gland - may be injured after viral meningoencephalitis. Usually, the hormonal deficiency is permanent but it can also be transient.

Adult↗
PubMed1978

Pituitary function after pituitary apoplexy.

Pituitary function was studied in nine patients who had recovered from pituitary apoplexy. All the patients recovered spontaneously; none required immediate surgery. Four of the patients had acromegaly, two had pituitary-dependent Cushing's syndrome, and a "functionless" pituitary adenoma was found in three. Low serum growth hormone concentrations were observed in three patients with acromegaly whereas the concentration remained increased in the fourth one. Of the two patients with Cushing's syndrome, a selective ACTH-deficiency developed in one and Nelson's syndrome appeared with excessive secretion of ACTH in the other. Transient or persistent hypofunction of the anterior pituitary occurred in al patients. Three patients underwent hypophysectomy after respective intervals of three, eight and 12 months after pituitary apoplex. The operation revealed a hemorrhage in one functionless adenoma and a large cyst in another one. In the third patient who had acromegaly, no signs of the pituitary apoplexy were observed at operation.

Acromegaly↗
PubMed1978

Somatostatin inhibits the pentagastrin-induced release of serum calcitonin in medullary carcinoma of the thyroid.

The effect of somatostatin on the secretion of calcitonin was studied in four patients with medullary carcinoma of the thyroid (MCT). The basal serum calcitonin level was markedly elevated in all cases. A bolus injection (100 microgram) of somatostatin followed by an intravenous infusion (5 microgram/min) for 60 min suppressed the basal calcitonin level in three of the four patients by 24-42%, while it had no inhibitory effect in one case. In another experiment, the pentagastrin-stimulated (6 microgram/kg s.c.) calcitonin release was partially blocked by a simultaneous i.v. injection of somatostatin (200 microgram) in all four patients studied. These experiments add human calcitonin to the list of hormones whose release in inhibited by somatostatin.

Adult↗
PubMed1978

Ultrastructural and steroidogenic characteristics of an androgen-producing adrenocortical tumour.

A 16-year-old female patient with an adrenal tumour was studied. Clinically she had progressive hirsutism, showed high urinary 17-oxosteroid excretion with normal plasma cortisol. Plasma C19-steroids, both unconjugated (including testosterone) and sulphate-conjugated, were greatly elevated. On surgical exploration an adrenal tumour was histologically an adenoma. On ultrastructural analysis the cells in all zones of the adjoining adrenal were considered normal. Although the tumour cells had the general appearance of a steroid-secreting cell their structure diverged from the cells of every subzone of the cortex. This was the case particularly with mitochondria and lipid inclusions. The only endogenous unconjugated steroids detected in the adjoining cortex were corticosterone and cortisol while in tumour tissue these were present in lesser amounts. The tumour tissue contained large amounts of C19-steroids, 11beta-hydroxy-androstenedione being quantitatively most significant. On the basis of the steroid profile an impaired defect of 21-hydroxylation in tumour cells leading steroid synthesis from corticosteroidogenesis to the C19 pathway is proposed.

Adenoma↗
PubMed1977

Association of serum lipids and obesity with cardiovascular mortality.

Serum lipid concentrations, relative body weight, and smoking habits were assessed in a cohort of 1648 middle-aged Finnish men who were subsequently followed for seven years. Multivariate analysis showed that serum triglyceride and cholesterol concentrations and smoking were all independently associated with cardiovascular mortality. High serum triglyceride concentrations increased the risk of cardiovascular death only when they exceeded 1.7 mmol/l (150 mg/100 ml), but this occurred at all cholesterol and relative body weight levels. Obesity influenced death rates only in men with raised serum lipid levels, while smoking was associated with increased mortality when any combination of the other factors was present. Men who had raised triglyceride concentrations combined with smoking or obesity had the highest risk of cardiovascular death.

Cardiovascular Diseases↗
PubMed1977

Response of plasma insulin to small doses of tolbutamide in obesity and acromegaly.

The early response of plasma insulin (IRI) to successive intravenous doses of 50, 100 and 200 mg of tolbutamide was studied in nondiabetic obese subjects, in acromegalic patients, and in healthy controls. The smallest dose raised the plasma IRI level within two minutes in all subjects. The insulin response was correlated with the basal IRI in controls and in obese subjects but not in acromegalic patients. At each tolbutamide dose level the mean IRI response of obese subjects was about three times greater than in controls. In acromegalic subjects an increased response was observed only after the 200 mg dose of tolbutamide. The results suggest that in obesity the stimulus-secretion coupling of insulin output is normal but the number of secretory units is increased. In acromegaly the insulin release pattern is compatible with an increased number of secretory units which, however, are relatively insensitive to tolbutamide, probably due to an elevated serum growth hormone level.

Acromegaly↗