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Biomedical subjects

H E Carlson

Publications and source records attributed to H E Carlson.

At least 91 records · Page 5Linked to original sources
PubMed1978

Chromosome banding studies in two patients with XXXXY syndrome.

In 2 adult male patients with 49 chromosomes, an XXXXY sex chromosome constitution was confirmed by trypsin-Giemsa banding sites. Clinical findings as well as fingerprint ridge counts were typical of the syndrome. Primary hypogonadism was documented by finding low serum testosterone and raised serum LH and FSH levels. Several radiological abnormalities, not previously described in this syndrome, were seen in 1 patient.

Adult↗
PubMed1978

Comparison of inhibitory effects of 3,5,3'-triiodothyronine (T3), thyroxine (T4), 3,3,',5'-triiodothyronine (rT3), and 3,3'-diiodothyronine (T2) on thyrotropin-releasing hormone-induced release of thyrotropin in the rat in vitro.

In order to compare, in vitro, the TSH suppressive effects of iodothyronines, rat pituitary quarters were first preincubated with T4, T3, rT3, or 3,3'-diiodothyronine (T2) in Gey and Gey buffer containing 1% bovine serum albumin for 2 h at 37 C and then incubated at 37 C for 1 h with the iodothyronine under study and TRH. TSH released into the medium during incubation was compared to that released by control pituitary fragments, which were not exposed to iodothyronines. All four iodothyronines (T3, T4, rT3, and T2) were able to significantly inhibit the TRH-induced release of TSH from pituitary fragments in a dose range of 0.015-2.2 microgram/ml. However, much larger doses of sodium iodide (1.25 mg/ml) and diiodotyrosine (10 and 30 microgram/ml) had no significant effect on the release of TSH. Among T3, rT3, and T4, T3 was the most potent and rT3 was the least potent. The relative potency of T3:T4:rT3 appeared to be approximately 100:12:1 when estimated from the lowest doses that caused significant inhibition of TRH-induced release of TSH, and approximately 100:6:0.5 when estimated from the doses that caused 50% inhibition of TSH release; the TSH inhibiting potency of T2 was similar to that of rT3. The activity of T4 could not be explained entirely on the basis of contamination of T4 with T3 or by in vitro conversion of T4 to T3. Similarly, the available data suggested that rT3 and T2 possess some, albeit modest, intrinsic TSH-Suppressive activity. TSH-inhibiting activities of T3, T4, and rT3 were also studied using pituitary fragments from starved and iodine-deficient rats. There was no evidence of a change in the sensitivity of the thyrotroph to either T3 or T4 in starvation. Similarly, comparison of the responses to several doses of rT3 did not indicate any significant abnormality in the sensitivity of the thyrotroph to rT3 in starvation or iodine deficiency. However, comparison of the TSH-suppressive effects of T4 in the iodine-deficient and normal rat indicated a significant increase in the sensitivity of the thyrotroph to T4 in iodine deficiency. A similar trend was also evident in the effect of T3 in iodine deficiency, but it fell short of statistical significance.

Animals↗
PubMed1978

Effect of thyroid hormones on the prolactin response to thyrotropin-releasing hormone in normal persons and euthyroid goitrous patients.

In nine euthyroid goitrous patients, increasing doses of T4 caused a significant decrease in the PRL response to TRH; the PRL response fell significantly at a dose of T4 of 100 micrograms/day for 1 month (P less than 0.02) and fell further with increasing doses so that at 300 micrograms T4/day, the PRL response was 40% of that in the untreated state. T4 treatment also blunted the PRL response to chlorpromazine (P less than 0.05) in a separate group of euthyroid goitrous patients. In contrast, there was only a small drop of the PRL response to TRH in normal subjects treated with T4 (n = 9) and none at all with T3 (n = 7). These data, together with previously published reports, suggest that thyroid hormone may affect PRL secretion in the presence of thyroid disease (hyperthyroidism, hypothyroidism, or euthyroid goiter), but that physiological amounts of thyroid hormone have little or no modulating effect on PRL secretion in normal persons.

Adolescent↗
PubMed1978

Effect of human chorionic gonadotropin on thyroid function in euthyroid men.

The effect of large doses of commercial hCG on thyroid function was studied in eight men who received 100,000 or 150,000 IU hCG iv. These large doses of hCG produced definite thyroidal iodine release (TIR) responses in all eight men. The TIR after hCG administration was more delayed and of lesser magnitude than the TIR responses to TSH and TRH. There were no significant changes in serum T4, T3, or TSH for 48 h after hCG administration. No clinical side effects were noted in the subjects after iv administration of these large doses of hCG. The results of this study indicate that hCG is a weak thyroid stimulator in man.

Adult↗
PubMed1978

Hyperprolactinemia in multiple endocrine adenomatosis, type 1.

Three cases are described in which hyperprolactinemia occurred as a feature of multiple endocrine adenomatosis, type 1 (MEA-1); enlargement of the sella turcica varied from gross to absent, and serum prolactin (PRL) levels ranged from 21 to 1,000 ng/ml in these cases. Since PRL-secreting pituitary tumors may occur with variable presentation in MEA-1, periodic measurements of serum PRL levels should be carried out to detect this abnormality.

Adult↗
PubMed1977

Prolactin deficiency in pseudohypoparathyroidism.

Because thyrotropin deficiency may occur in pseudohypoparathyroidism, we studied pituitary function in two families with this condition. Six of eight patients had impaired pituitary prolactin secretion after administration of thyrotropin-releasing hormone and chlorpromazine, with preservation of other anterior pituitary functions. Peak serum prolactin levels after thyrotropin-releasing hormone and chlorpromazine in the prolactin-deficient patients were significantly lower than normal. Administration of diethylstilbestrol for five days, which normally enhances prolactin responses to thyrotropin-releasing hormone, had no effect on prolactin secretion in these patients. Although antilactotroph antibodies were not demonstrable, hypothyroidism or decreased thyroid reserve in four and antithyroid and antiparietal-cell antibodies in several family members suggest that an associated autoimmune process may be responsible for the prolactin deficiency.

Adolescent↗
PubMed1977

Osmotic control of the release of prolactin and thyrotropin in euthyroid subjects and patients with pituitary tumors.

The effects of acute changes in serum osmolality on basal serum PRL and TSH levels and on responses of prolactin (PRL) and thyrotropin (TSH) to the thyrotropin-releasing hormone (TRH) analogue, N3im-methyl-TRH, were studied in ten euthyroid subjects and in three patients with PRL-secreting pituitary tumors. An oral water load of 20 ml/kg had no effect on basal serum PRL or TSH levels but did result in an increased PRL response to methyl-TRH in the ten euthyroid patients. Intravenous infusion of 5% sodium chloride in the ten euthyroid subjects significantly depressed basal serum PRL levels but had no effect on the PRL response to methyl-TRH. Infusion of hypertonic saline significantly decreased the TSH response to methyl-TRH. In the three patients with pituitary tumors, oral water loading and hypertonic saline infusion had no significant effect on the basal serum PRL and TSH or the PRL and TSH responses to methyl-TRH. The patients with pituitary tumors had a higher basal serum osmolality and a proportionately higher serum concentration of arginine vasopressin than the euthyroid patients. These data suggest that changes in osmolality in euthyroid patients may have a direct effect on the anterior pituitary's PRL and TSH response to a releasing factor.

Adult↗
PubMed1977

Lack of effect of thyroid hormones on the growth hormone response to thyrotropin-releasing hormone in acromegaly.

Serum growth hormone (GH) responses to thyrotropin-releasing hormone (TRH) were evaluated in 14 patients with acromegaly following treatment with thyroid hormones. After an initial TRH test, seven patients received L-triiodothyronine, 100 mug daily for seven days; the GH response to TRH was not significantly altered by this treatment. Similar findings were noted in two acromegalic subjects who were tested with TRH before and after longer periods of administration of L-thyroxine. Four of five additional subjects with acromegaly who had received replacement doses of thyroid hormones for an average of 6.6 yr demonstrated GH responses to TRH which were similar to those seen in subjects not receiving thyroid hormones. Acute or long-term administration of replacement doses of thyroid hormones seems to have minimal effect on the GH response to TRH in acromegaly.

Acromegaly↗
PubMed1977

The role of vasopressin and prolactin in abnormal salt and water metabolism of obese patients before and after fasting and during refeeding.

Arginine vasopressin (AVP) and prolactin (PRL) concentrations were measured in the plasma of grossly obese subjects to determine if abnormalities in salt and water homeostasis could be related to these hormones. Acute oral water loads and hypertonic saline infusions were administered during baseline obesity, after prolonged fasting, and after hypocaloric refeeding. Only 64.7%, 46.1%, and 70.1% of a water load was excreted during the respective three stages. Pre-water load plasma AVP levels were normal, but after the water load the obese failed to suppress AVP secretion in a normal fashion; this defect was corrected after fasting and with refeeding. Salt loading resulted in appropriate osmolality and AVP responses. Serum prolactin levels, normal at baseline during all phases, rose slightly after water loading during fasting. Hypertonic.saline produced no changes in prolactin levels in the obese or in the normal controls. In the disordered salt and water metabolism of the obese, persistently high AVP values during water loading appeared to be a factor in the delay of water excretion. In the observed water retentionduring dietary restriction and refeeding, secretion of AVP and PRL did not appear to have a major regulatory function.

Adult↗
PubMed1977

Effect of dexamethasone on prolactin and TSH responses to TRH and metoclopramide in man.

We studied the effects of administration of dexamethasone, 2 mg orally every 6 h, for 5 days on the thyrotropin-releasing hormone (TRH)-induced release of prolactin (PRL), thyrotropin (TSH), triiodothyronine (T3) and thyroxine (T4) in 9 normal men and on the metoclopramide-induced release of PRL in 7 normal men. Dexamethasone suppressed the baseline serum levels of PRL, TSH and T3. The administration of dexamethasone blunted the PRL and TSH response to TRH; the blunted TSH response resulted in a decreased T3 and T4 response to TRH after dexamethasone. Following dexamethasone administration, the PRL response to metoclopramide, a dopamine antagonist which acts at the hypothalamicpituitary level to stimulate PRL secretion, was blunted in 7 normal men. The data suggest that short-term administration of pharmacological doses of glucocorticoids suppress the secretion of PRL and TSH by a direct effect on the anterior pituitary gland.

Adult↗
PubMed1977

Cimetidine, an H2-antihistamine, stimulates prolactin secretion in man.

Intravenous administration of cimetidine, a histamine (H2) receptor antagonist, provoked an immediate 2 to 3-fold rise in serum prolactin concentrations in 8 normal men; serum thyrotropin, growth hormone, thyroxine, and triiodothyronine were not significantly affected. Diphenhydramine, an H1-antagonist, was without effect on any of the hormones measured. The results suggest that histamine may have an important function in the regulation of prolactin secretion in man.

Adult↗
PubMed1977

Alterations in basal and TRH-stimulated serum levels of thyrotropin, prolactin, and thyroid hormones in starved obese men.

To investigate further the alterations in pituitary-thyroid function seen during starvation, we have measured basal and TRH-stimulated serum levels of thyrotropin (TSH), prolactin (PRL), growth hormone, thyroxine (T4), triiodothyronine (T3), free T4, free T3, and reverse T3 during prolonged fasting in seven obese men. Fasting was associated with a significant decrease in serum (4, (3, and free T3, while there was an increase in serum reverse T3; these values tended to return toward pre-fast levels as the fast continued beyond 3 weeks. No significant changes were seen in basal serum TSH, PRL, growth hormone, or free T4. Although the TSH response to TRH was diminished during fasting, PRL, T4, and T3 responses were unchanged. In addition to transient alterations in the peripheral metabolism of T4, these findings suggest that alterations in the thyroid hormone binding capacity of serum carrier proteins may occur during fasting. The blunted TSH response to TRH despite reduction of serum T3 concentration suggests that subtle alterations in hypothalamic-pituitary function may also occur.

Adult↗
PubMed1977

Altered responsiveness to hypophysiotrophic hormones of perifused rat pituitary tumours.

Since growth hormone (GH) and prolactin (Prl) secretion by human pituitary tumours is often influenced by the hypophysiotrophic hormones thyrotrophin-releasing hormone (TRH) and somatostatin (SRIF), we have examined the responses of several transplantable rat pituitary tumours to these substances in a perifusion apparatus. The MStT/W15 tumour did not alter its secretion of GH and Prl in response to TRH, SRIF, or a partially purified porcine hypothalamic extract containing GH-releasing activity; normal rat pituitaries show clear responses to each of these substances. Theophylline and dibutyryl cyclic AMP each provoked increased GH and Prl release from the tumour. A second specimen of the MStT/W15 tumour and a specimen of the MStT/W5 tumour behaved in a manner identical to the original MStT/W15, showing no response to TRH or SRIF, but releasing both GH and Prl when theophylline or dibutyryl cyclic AMP was given. The MtT/F4 tumour increased its secretion of GH in response to TRH, 10 mug/ml, and theophylline, but no effect was seen with lower concentrations of TRH or with SRIF; Prl secretion by the F4 tumour was increased by theophylline, but TRH and SRIF had no effect. The autonomy demonstrated in these experimental tumours may be due to a loss of specific hypophysiotrophic hormone receptors or of secretory activating mechanisms.

Animals↗
PubMed1977

The effect of stressful diagnostic studies and surgery on anterior pituitary hormone release in man.

The hormonal response of the anterior pituitary was studied in 10 normal males undergoing treadmill exercise testing, in 5 male patients undergoing diagnostic gastroscopy, and in 8 male patients undergoing elective surgery under general anaesthesia. Serum TSH was depressed below the baseline value at 2 and 3 h post-treadmill exercise, at 1, 2 and 3 h post-gastroscopy and from 10 min through 2 h post-surgery. Serum triiodothyronine was depressed below the baseline value at 10 min through 2 h post-surgery. Serum prolactin, growth hormone and cortisol were elevated by all three stressful procedures. Both gastroscopy and surgery resulted in an elevation of serum luteinizing hormone levels. There was no significant change in serum FSH levels in any of the three procedures. The post-stress depression in TSH levels could result from the suppressive effect at the hypothalamic-pituitary level of high serum levels of cortisol generated by the stress of the procedures.

Adult↗