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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↗
PubMed1979

Thyrotropin-releasing hormone and thyroid hormones in amniotic fluid.

Immunoassayable TRH (iTRH) was measured in 50 amniotic fluid specimens with a mean concentration of 207 +/- 26 (SE) pg/ml. This iTRH demonstrates parallelism with the standard curve for synthetic TRH. With increasing gestational age there is an increase in iTRH levels in amniotic fluid with a decrease in 3,3',5'-triiodothyronine levels (rT3), while thyroxine levels (T4) remain unaltered. Preliminary data suggest that iTRH levels in amniotic fluid that are less than 150 pg/ml after 32 weeks of gestation may correlate well with low Apgar scores at birth. There was no correlation of rT3 or T4 amniotic fluid levels with the Apgar scores.

Amniotic Fluid↗
PubMed1979

Pituitary and peripheral resistance to thyroid hormone.

A 32-year-old Caucasian male, clinically euthyroid, with paranoid schizophrenia and granulocytopenia, had elevated total and free serum T4 and T3; serum TSH was normal (2.7 +/- 0.7 micronU/ml). There was no goitre present, no evidence of Graves' disease, and no evidence of pituitary tumour. He had a normal response to methyl-TRH, with a TSH increment of 14.6 micronU/ml, T3 increment of 212 ng/dl, and T4 increment of 4.7 microgram/dl; baseline value and decreased the TSH increment in response to methyl-TRH. T3 therapy (100 microgram/day) decreased the thyroidal radioactive iodine uptake to less than half the baseline prolactin was normal with a normal response to methyl-TRH to 4.1 micronU/ml. Iodine therapy caused an increase in his baseline TSH with an increase in the TSH response to TSH. The metabolic clearance rates (MCR) and production rates (PR) of T3 and T4 were increased. Baseline serum levels of glycoprotein hormone alpha-subunit were normal and showed a slight increase in response to methyl-TRH, similar to normal subjects. This patient has evidence of partial pituitary and peripheral resistance to thyroid hormone; his only evidence for hyperthyroidism is the elevated MCR and PR of T3 and T4.

Adult↗
PubMed1979

Effect of chronic metoclopramide therapy on serum pituitary hormone concentrations.

The effect of chronic (3--9 months) therapy with metoclopramide on serum levels of pituitary and thyroid hormones was studied in 4 males and 1 female. The mean serum prolactin concentration during metoclopramide therapy was significantly higher than after discontinuation of metoclopramide. Serum prolactin concentrations increased acutely after each dose of metoclopramide. Serum prolactin concentrations increased acutely after each dose of metoclopramide, and gradually returned to normal by 6--12 h. There was no sifgnificant differences in the serum TSH, T3, T4, GH, and gonadotrophin levels during and after metoclopramide administration. In the male subjects the mean serum testosterone was normal, but significantly lower during metoclopramide therapy.

Adult↗
PubMed1979

Effect of endogenous hyperprolactinemia on human lower esophagel sphincter pressure.

The cause of gastroesophageal reflux occurring during pregnancy is not completely understood but may be related to changes in the hormonal environment specifically related to pregnancy. To evaluate the possible role of prolactin, one of the hormones elevated during pregnancy, we studied the effect of endogenously elevated serum prolactin concentrations, induced by I.V. thyrotropin-releasing hormone (TRH), on lower esophageal sphincter pressure (LESP) in normal subjects. Elevated prolactin concentrations (P less than 0.0001), did not change LESP over a 60-minute period. Serum gastrin concentration did not change significantly at any time during the study. We conclude: 1. acute elevations of serum prolactin comparable to the concentrations that occur during pregnancy did not change LESP; 2. there is no evidence that the hypothalamic regulating factor TRH affects serum gastrin concentration in man.

Adult↗
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↗