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Biomedical subjects

H E Carlson

Publications and source records attributed to H E Carlson.

At least 19 recordsLinked to original sources
PubMed1992

Postmenopausal uterine bleeding due to estrogen production by gonadotropin-secreting lung tumors.

Two postmenopausal women are described who had uterine bleeding due to hormone production by lung tumors--a large cell carcinoma in one case and a choriocarcinoma in the other. Both tumors stained positively for one or more placental peptides (human chorionic gonadotropin [hCG], placental lactogen, or pregnancy-specific beta-1 glycoprotein) and both patients had extremely elevated serum levels of hCG, suggesting the tumors had some placental-like endocrine function. Clinical and hormonal data supported the concept that the uterine bleeding resulted from estrogen excess due to steroid bio-transformation by the tumors.

Biopsy↗
PubMed1992

Prolactin responses to phenylalanine and tyrosine in phenylketonuria.

In normal subjects, ingestion of tyrosine or phenylalanine stimulates prolactin (PRL) secretion. In patients with phenylketonuria (PKU), we found normal PRL responses to phenylalanine, demonstrating that conversion of phenylalanine to tyrosine is not necessary for PRL stimulation. PKU patients also showed greater PRL responses to tyrosine during dietary phenylalanine restriction than when consuming an unrestricted diet; this finding is consistent with inhibition by phenylalanine of tyrosine transport across the blood-brain barrier. Such competitive inhibition of a normal brain function may serve as a model for some of the neurotoxic effects of phenylalanine in PKU.

Adolescent↗
PubMed1992

Multiple hamartoma syndrome (Cowden's disease) associated with renal cell carcinoma and primary neuroendocrine carcinoma of the skin (Merkel cell carcinoma).

A case of multiple hamartoma syndrome (Cowden's disease) associated with renal cell adenocarcinoma and primary neuroendocrine carcinoma of the skin is described. Neither of these neoplasms has been documented previously in association with this genodermatosis. A search for epidermal growth factor receptor (c-erb-B protooncogene) gene abnormalities in the kidney, liver, and thyroid, as well as in tissue of the primary neuroendocrine carcinoma, was negative. Serum obtained from the patient before his death contained elevated levels of both chromogranin A (2641 ng/mL; normal level, less than 20 ng/mL) and calcitonin (517 pg/mL; normal level, less than 200 pg/mL), suggesting that the patient's principal tumor was neuroendocrine in origin.

Aged↗
PubMed1992

Differential tissue regulation of the insulin-like growth factors in rats bearing the MStT/W15 pituitary tumor.

The content of insulin-like growth factors, IGF-I and IGF-II, was measured in tissues of rats bearing a transplantable mammosomatotrophic tumor, MStT/W15. Serum IGF-I was elevated in tumor-implanted rats [2,557 +/- (SE) 419 vs. 891 +/- 100 ng/ml], and tumor tissue concentrations of IGF-I were increased (321 +/- 16 ng/g) in comparison to control liver tissue (160 +/- 5 ng/g) or control pituitary (80 +/- 3 ng/g). The IGF-I levels were significantly increased in most peripheral tissues in the tumor-bearing rats with the exception of the liver. In support of this finding, messenger RNA for prepro IGF-I was likewise not increased in the livers of tumor-bearing rats, nor was there an increase in the growth hormone-dependent IGF-binding protein, BP-3, in the liver or serum of these animals. All tumors had detectable levels of prepro IGF-I mRNA which was, however, less than 50% of that noted in normal control liver. The tumors also expressed an IGF-BP which was identified as IGF-BP-2 by immunoblotting. Serum concentrations of IGF-II were similar in control and tumor-bearing animals (approximately 70 ng/ml). IGF-II levels in the tumor (90 +/- 5 ng/g) were significantly higher than levels in control liver (34 +/- 2 ng/g), but similar to those found in normal pituitary (165 +/- 24 ng/g). In peripheral tissues, IGF-II concentrations were selectively increased in skeletal muscle and heart of tumor-bearing rats. These data demonstrate tissue-specific regulation of IGF-I and IGF-II. Paradoxically, the liver does not appear to be stimulated over control levels by high serum growth hormone levels, since neither IGF-I peptide, IGF-I mRNA, nor IGF-BP-3 levels are increased in livers of tumor-bearing rats. This suggests that the increase in serum IGF-I in these animals is due to increased production of IGF-I by the tumors themselves and by nonhepatic peripheral tissues and further that hepatic responsiveness to growth hormone is diminished in these tumor-bearing animals.

Animals↗
PubMed1992

On the nature of serum prolactin in two patients with macroprolactinemia.

OBJECTIVE: To further characterize the high molecular weight (MW) forms of prolactin (PRL) present in patients with macroprolactinemia. DESIGN: Case reports with laboratory investigations. SETTING: Academic medical centers. PATIENTS: Two patients with macroprolactinemia. INTERVENTIONS: Measurements of PRL concentrations before and after chromatographic separations. RESULTS: The majority of serum PRL had an estimated MW of at least 669 kd in the first patient and approximately 171 kd in the second. During a pregnancy, a new form of PRL (MW 291 kd) appeared in the first patient's serum and persisted for at least 3 years. Immunoprecipitation and polyacrylamide gel electrophoresis under reducing and denaturing conditions revealed that the largest form of PRL (MW 669 kd) was composed mostly of 25 kd glycosylated PRL; intermediate forms (171 kd and 291 kd) were composed of roughly equal portions of 25 kd glycosylated PRL and 23 kd nonglycosylated PRL, whereas "little" PRL in these patients was composed primarily of 23 kd nonglycosylated PRL. Injection of the first patient's serum into rats demonstrated that the human PRL (hPRL) immunoreactivity was cleared from the serum more slowly than the PRL from sera containing predominantly little hPRL; after stimulation with thyrotropin-releasing hormone in the second patient, serum PRL concentrations decayed more slowly than observed in normal subjects. CONCLUSIONS: Large forms of serum PRL are at least partially glycosylated. These large forms are heterogeneous, both within and among patients. Delayed clearance may account for increased serum PRL concentrations in patients with macroprolactinemia.

Adult↗
PubMed1991

CSF and endocrine studies of premenstrual syndrome.

Eight women with prospectively documented premenstrual syndrome (PMS) underwent multiple samplings for estradiol, progesterone, prolactin, cortisol, and plasma 3-methoxy-4-hydroxyphenylglycol (MHPG) during an asymptomatic midcycle (late follicular) and a symptomatic premenstrual (late luteal) phase of the menstrual cycle. Cerebrospinal fluid (CSF) was collected for analysis of MHPG, norepinephrine (NE), 5-hydroxyindoleacetic acid (5-HIAA), dihydroxyphenylacetic acid (DOPAC), gamma-aminobutyric acid (GABA), homovanillic acid (HVA), tyrosine, tryptophan, beta-endorphin, prostaglandins, adrenocorticotropic hormone (ACTH), and arginine vasopressin (AVP). In subsequent months, a dexamethasone suppression test (DST) and a thyrotropin-releasing hormone (TRH) stimulation test were performed during midcycle and premenstrual phases. Significant results included increased CSF concentrations of MHPG in the premenstrual, as compared with the midcycle, phase of the cycle, and increased plasma cortisol concentrations during the midcycle phase. The DST showed a 62% overall rate of nonsuppression, irrespective of menstrual cycle phase. Though there were no abnormalities of thyrotropin-stimulating hormone (TSH) after TRH stimulation, the mean delta maximum prolactin values after TRH stimulation were higher than reported normal values both at midcycle and premenstrually. These pilot data suggest hormonal axes that might be worthy of further systematic investigation in future studies of PMS.

Adult↗
PubMed1990

Evidence for an intracerebral action of phenylalanine in stimulation of prolactin secretion: interaction of large neutral amino acids.

Phenylalanine stimulates PRL secretion when given orally or iv to normal individuals. To differentiate between hypothalamic and pituitary sites of action, we examined the effects of concurrent infusion of valine on the PRL response to iv phenylalanine in eight normal men. Since large neutral amino acids share the same high affinity blood-brain barrier transport system, entry of phenylalanine into the brain will be diminished by the simultaneous presence of high serum concentrations of valine; the pituitary, lying outside the blood-brain barrier, is not subject to these competitive effects. Valine significantly blunted the PRL response to phenylalanine, supporting an effect of phenylalanine within the blood-brain barrier to stimulate PRL release.

Adult↗
PubMed1989

Stimulation of pituitary hormone secretion by neurotransmitter amino acids in humans.

The effects of several neurotransmitter amino acids on pituitary hormone secretion were examined in normal humans. Oral administration of 10 g of glutamic acid stimulated the secretion of prolactin (PRL) and cortisol to approximately twice baseline values, with no effect on GH, TSH or LH. Aspartic acid (10 g), taurine (5 g), and cysteine (5 or 10 g) had no consistent effect on any hormone measured, although the lack of effect of aspartic acid may relate to the modest increments in serum concentration achieved. Glutamic acid may be an important modulator of PRL and ACTH secretion in humans.

Adrenocorticotropic Hormone↗
PubMed1989

Desipramine increases circulating growth hormone in elderly depressed patients: a pilot study.

Serial blood samples were collected from 15 elderly depressed inpatients, ages 62 to 95 years, following random assignment to a 50 mg oral test dose of desmethylimipramine (DMI) or amitriptyline (AMI). Nine female and six male subjects began the 210-min study at 0800h. Serum growth hormone (hGH), cortisol, and prolactin (hPRL) were determined by radioimmunoassay. Baseline hormone concentrations were related to self and observer ratings of anxiety and depression. There was a trend for the hGH, cortisol, and hPRL concentrations to decline during the period of study. This trend for all three hormones reversed in those subjects receiving DMI, beginning approximately 90 min after drug ingestion. The DMI-induced increase of hGH reached statistical significance at the very end of the sampling period. There was an apparent latency in the DMI-induced effect for all three hormones. There was no stimulatory effect of AMI on hGH, cortisol, or hPRL. The female subjects had higher baseline hGH levels than the men. In addition, a significant negative correlation was found between baseline hPRL levels and self ratings of anxiety.

Aged↗
PubMed1989

Aspartame and its constituent amino acids: effects on prolactin, cortisol, growth hormone, insulin, and glucose in normal humans.

Because large doses of phenylalanine stimulate prolactin secretion in man, we studied the acute effects of oral doses of aspartame (0.534 g, equivalent to the amount of aspartame in approximately 1 L beverage), aspartic acid (0.242 g), and phenylalanine (0.3 and 1.0 g) on serum prolactin and other hormones in normal humans. Prolactin was not stimulated by any of the aspartame meals, aspartic acid, or 0.3 g phenylalanine; a small rise in serum prolactin, similar to that produced by a high-protein mixed meal, followed ingestion of 1.0 g phenylalanine. Serum growth hormone showed no statistically significant changes in response to any of the experimental meals whereas cortisol and insulin fell slightly and glucose rose slightly during each of the meals. We conclude that these doses of aspartame do not alter secretion of prolactin, cortisol, growth hormone, or insulin in normal individuals.

Administration, Oral↗
PubMed1989

Serum prolactin and aging: basal values and changes with estrogen use and hypothyroidism.

We studied basal serum prolactin in older (greater than age 50) men (N = 501) and women (N = 384) using younger adults for comparison and excluding those taking medications. Serum prolactin rose slightly with increasing age in men; it fell slightly in women until age 80, when it rose slightly. Men and women were not different except for the higher value in women at age 20 to 29. Serum prolactin did not fall after the menopause, while estrogen treatment had no effect on older women and caused only a slight rise in older men. Thyroid deficiency had only a minimal effect and did not raise the serum prolactin above 25 ng/ml. The prevalence of clearly elevated values (greater than 20 ng/ml) was only 1.3% in women and 0.6% in men above age 50; there is little evidence for a significant prevalence of prolactin-secreting adenomata in older persons. In older persons, prolactin-secreting tumors are uncommon, and neither thyroid failure nor estrogen therapy are good explanations for a clearly elevated serum prolactin.

Adult↗
PubMed1989

Prolactin stimulation by protein is mediated by amino acids in humans.

In normal humans, ingestion of protein stimulates PRL secretion. I investigated the mechanism of this effect by feeding free amino acids, both singly and in combination, to normal subjects. The serum PRL response to a high protein liquid mixed meal was duplicated by ingestion of an equivalent free amino acid mixture, indicating that intact protein or peptides are not required. The time course of the response and the presence of normal responses in two vagotomized subjects suggest that neither traditional gut hormones nor vagus nerve activity is involved in this response. Of the single amino acids tested, phenylalanine and tyrosine were the most potent stimulators of PRL secretion and can account for most, if not all, of the PRL-releasing activity of the mixed meal. D-Phenylalanine, the biologically inactive optical isomer, was nearly ineffective in releasing PRL. Administration of naloxone, phentolamine, or propranolol did not alter the PRL response to the various test meals, indicating that neither opioid, alpha-adrenergic, nor beta-adrenergic stimulation is involved in meal-induced PRL secretion.

Adult↗
PubMed1987

Lack of effect of warfarin on L-thyroxine metabolism.

The effect of a single 50 mg dose of warfarin sodium on thyroxine monodeiodination was examined in eight healthy human subjects. There was no evidence that warfarin inhibits 5'-monodeiodination, although such inhibition exists in rats.

Adult↗
PubMed1986

Carbidopa plus L-dopa pretreatment inhibits the prolactin (PRL) response to thyrotropin-releasing hormone and thus cannot distinguish central from pituitary sites of prolactin stimulation.

Contrary to a previous report, pretreatment of normal men with carbidopa plus L-dopa (Sinemet 25/250) markedly inhibited the PRL response to TRH, a stimulus that acts directly on the pituitary. Thus, the results of carbidopa/L-dopa testing cannot be used to determine whether agents that stimulate PRL secretion act on the pituitary or at a higher central nervous system level.

Adult↗
PubMed1986

Responses to glucagon infusion in pseudohypoparathyroidism.

Single or graded doses of glucagon (Eli Lilly) were given to patients with pseudohypoparathyroidism (PsHP) type I to examine the possible presence of hormone resistance. The doses of glucagon ranged from 0.25-15 micrograms/kg. The following individuals were studied: 13 normal subjects, 5 patients with low erythrocyte N-protein activity (PsHP type Ia), and 7 patients with normal erythrocyte N-protein activity (PsHP type Ib). Two additional patients with treated primary hypothyroidism who were relatives of a patient with PsHP type Ib were also studied. The patients with PsHP type Ia had blunted plasma cAMP responses to all glucagon doses. In contrast, the patients with PsHP type Ib had normal cAMP responses to glucagon infusion. However, the 2 relatives of the patient with PsHP type Ib had clearly decreased cAMP responses to glucagon infusion; both had normal renal responses to PTH and were clinically and biochemically euthyroid at the time of study. Glucose responses to glucagon were normal in both PsHP groups; the glucose response per unit cAMP response was slightly, but not significantly, enhanced in PsHP type Ia patients. Glucagon resistance appears to be a common finding in patients with PsHP type Ia, but not in those with PsHP type Ib. However, the observation of reduced glucagon responsivity in association with familial hypothyroidism in a kindred with PsHP type Ib suggests the possibility that this disorder may also cause disturbances in several hormone systems.

Adolescent↗
PubMed1986

Impotence in scleroderma.

Hormonal, neurologic, and vascular factors affecting potency were evaluated in 10 men with scleroderma and in 10 age-matched men with rheumatoid arthritis. Impotence was reported by 6 of the patients with scleroderma and none with rheumatoid arthritis. Studies of serum testosterone, free testosterone index, follicle-stimulating hormone, luteinizing hormone, prolactin, estradiol, thyroxine, and thyrotropin did not show a hormonal basis for impotence in any patient. Neurologic causes were not found on physical examination. Penile blood pressures were markedly abnormal in 4 impotent patients, intermediate in 2 impotent and 3 potent patients, and normal in 11 potent patients. A history of claudication and diminished ankle blood pressures indicated large vessel disease in 2 impotent patients; the remaining 4 impotent men had normal ankle pressures, suggesting that their poor penile blood pressures and impotence were due to small vessel disease, perhaps the small artery lesions of scleroderma.

Adult↗
PubMed1986

Cowden disease: gene marker studies and measurements of epidermal growth factor.

Cowden disease (CD) is a familial syndrome characterized by tumors of the skin, oral mucosa, breast, thyroid, and intestinal epithelium. Since the syndrome is inherited as an autosomal dominant, we examined a battery of gene markers in a family with CD to detect linkage between the CD gene and known marker genes. There was no positive evidence for linkage of a CD locus with any of the markers; other investigators can add to our data to confirm and extend these findings. Additionally, we measured epidermal growth factor (EGF) in body fluids from CD patients and controls to determine if elevated EGF levels might be responsible for the widespread epithelial proliferation in CD. EGF levels in saliva, serum, plasma, and urine were similar in CD patients and control subjects. Although alterations in growth factors or their receptors may play a role in CD, excess circulating EGF is not responsible for the manifestations of the syndrome.

Adult↗