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Biomedical subjects

A G Frantz

Publications and source records attributed to A G Frantz.

At least 55 records · Page 3Linked to original sources
PubMed1979

Plasma beta-endorphin and beta-lipotropin in the human fetus at delivery: correlation with arterial pH and pO2.

Beta-endorphin-like immunoactivity was measured in the umbilical cord plasma of 45 term human fetuses. Mean concentration was 91 +/- 16 (SEM) pg/ml,an the normal adult level of 30.7 +/- 2.7 pg/ml. This immunoactivity was further characterized in 10 cases by Sephadex G-50 chromatography to separate beta-endorphin from beta-lipotropin (beta-LPH). Mean beta-endorphin and beta-LPH concentrations were 57 +/- 12.8 and 455 +/- 101 pg/ml, respectively. Both were higher (P less than 0.01) than the mean beta-endorphin and beta-LPH concentrations reported in the adult. The mean molar beta-endorphin to beta-LPH ratio was 0.35 in the fetus and 0.36 in the adult. In 17 fetuses whose umbilical arterial and venous concentrations were measured separately, mean beta-endorphin-like immunoactivity was higher in the artery than in the vein. A highly significant negative correlation (r = -0.831; P less than 0.001) was present between umbilical arteiral pH and beta-endorphin-like immunoactivity. A negative correlation (r = -0.611; P less than 0.005) with arterial pO2 was also noted. We conclude that high levels of beta-endorphin-like immunoactivity, composed of both beta-endorphin and beta-LPH, circulate in the human fetus at term, and that hypoxia and secondary acidosis may be major stimuli to the release of these peptides.

Adult↗
PubMed1979

The specificity of serum prolactin as a diagnostic indicator of pituitary adenoma.

Serum prolactin levels were determined in 205 patients with a variety of intracranial diseases, including 70 cases with pituitary tumors. It is concluded that although the absence of elevated prolactin levels does not help to rule out pituitary pathology, the presence of hyperprolactinemia is highly specific for diseases of the pituitary and hypothalamus, and prolactin determination should be part of the regular work-up of pituitary tumor suspects. Excluding known causes of hyperprolactinemia, such as tranquilizing drug ingestion, the presence of neurological disease outside the hypothalamic-pituitary area was not associated with increased serum prolactin concentrations.

Acromegaly↗
PubMed1978

Prolactin.

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Amenorrhea↗
PubMed1978

The pathophysiology of hyperprolactinemic states and the role of newer ergot compounds in their treatment.

Studies of prolactin secretion in humans have confirmed the concept, derived originally from animal investigations, that prolactin is predominantly controlled by tonic inhibition from the hypothalamus. The locus of action of dopamine and dopaminergic agents such as the ergot alkaloids inhibiting prolactin secretion appears to be primarily at the pituitary level, though a hypothalamic action to increase secretion of prolactin inhibitory factor may also contribute. Prolactin hypersecretion, through any of several possible mechanisms, is frequently but not always found in patients with galactorrhea. Recent studies have shown that hyperprolactinemia is considerably more common than was previously appreciated among patients without galactorrhea. It is present in at least two-thirds of all patients with pituitary tumors and in a significant minority of patients with secondary amenorrhea. Its clinical measurement in these conditions is therefore of considerable diagnostic importance. Whatever the pathophysiology of its production, hyperprolactinemia of all forms is responsive to treatment with the newer ergot alkaloids. The potential use of these agents for therapeutic purposes, particularly in the treatment of infertility, appears to be wider than was originally anticipated.

Acetonitriles↗
PubMed1977

Galactorrhea: a study of 235 cases, including 48 with pituitary tumors.

An analysis of 235 patients with galactorrhea (5.5 per cent males) showed that 20 per cent of all patients, and 34 per cent of women with associated amenorrhea, had radiologically evident pituitary tumors; these patients had the highest serum prolactin concentrations. The largest single group (32 per cent) consisted of women with idiopathic galactorrhea without amenorrhea; prolactin was normal in 86 per cent of these cases. Five patients had the empty-sella syndrome. Prolactin response was tested in selected patients by thyrotropin-releasing hormone, chlorpromazine, L-dopa, 24-hour sampling and other means. Tests with thyrotropin-releasing hormone were most useful in identifying patients with pituitary tumors. Surgery and radiotherapy lowered prolactin to a similar degree in patients with tumor, but galactorrhea, and amenorrhea often persisted after treatment. The ergot derivatives, bromergocryptine and lergotrile mesylate, lowered prolactin in all 18 patients with idiopathic hyperprolactinemia or pituitary tumor, stopped galactorrhea in over 50 per cent, restored menses in over 70 per cent, and allowed pregnancy in three.

Acromegaly↗
PubMed1977

Studies on the nature of thyroidal suppression during acute falciparum malaria: integrity of pituitary response to TRH and alterations in serum T3 and reverse T3.

The nature of the suppression of the pituitary-thyroid axis during infection was studied by testing the integrity of thyrotropin (TSH) and prolactin (PRL) responses to thyrotropin-releasing hormone (TRH) during acute falciparum malaria in human volunteers. During infection, TSH responses to TRH were found to be intact while PRL secretion was slightly increased. That serum T3 levels abruptly declined during infection while serum T4 was stable or increasing suggested an alteration in peripheral degradative pathways and prompted the measuremnt of reverse T3. Changes in serum T3 concentration were found to be accompanied by reciprocal changes in reverse T3. These observations allow some clarification of previously unknown aspects of thyroidal economy during infection.

Humans↗
PubMed1977

High vasopressin concentrations in human umbilical cord blood--lack of correlation with stress.

Marked elevations in the vasopressin concentrations in human umbilical cord blood have been reported previously (4, 8). This could either be a part of generalized increase in the activity of fetal endocrine system at the time of birth, a phenomenon that has led to the concept of fetal participation in the onset of labor, or simply due to the stress of delivery. The present study is an attempt to examine the later possibility. Plasma vasopressin was determined by radioimmunoassay [9] in separately collected arterial and venous blood from the umbilical cords of 24 babies spontaneously delivered and 14 babies born after Caesarian Section in the absence of labor. Arterial acid-base determinations were done in each case. The Apgar Score was evaluated by one individual. In order to obtain a general idea of circulating concentration of this hormone in the neonatal period, vasopressin concentrations were determined in the systemic venous blood of 12 normal and 10 stressed babies. Vasopressin concentrations in the umbilical arterial blood of babies born after spontaneous delivery were remarkably high, as compared to all the other groups. Despite a wide range, between 5-2200 pg/ml, there was no correlation between the magnitude of vasopressin elevation and the severity of fetal asphyxia (Fig. 1). The present finding in part, confirms and expands previously observed increased vasopressin levels in the cord blood after spontaneous vaginal delivery. In addition, a lack of correlation between fetal asphyxia and the vasopressin levels suggests that these high levels may not be related to this form of stress.

Acid-Base Equilibrium↗
PubMed1976

Diagnosis and evaluation of patients with an enlarged sella turcica.

A prospective analysis of the roentgenographic and laboratory parameters in 100 patients with an enlarged sella turcica was made. Seventy-five patients had no visual symptoms: 27 had primary intrasellar tumor; 25 had the empty sella syndrome: 13 had an extrasellar process; and in 10, no final diagnosis was made because air study was omitted. However, these patients remained asymptomatic for up to three years. Eighteen of the patients with a primary intrasellar tumor had symptomatic pituitary dysfunction; nine were asymptomatic. Five of 14 patients studied had elevated plasmaproa prolactin levels. of the 25 patients with the empty sella syndrome and the 10 patients in whom no final diagnosis was made, none had any clinical endocrine or visual abnormalities, although in 10 of these 35 patients, results of laboratory studies were compatible with pituitary dysfunction. In these cases, air study was necessary to differentiate a clinically silent pituitary tumor from the empty sella syndrome. This emphasizes the high incidence of the empty sella syndrome in patients with enlarged sella, and also confirms the high incidence of hyperprolactinemia in patients with pituitary tumors.

Adenoma↗
PubMed1976

The effect of ambient temperature on the growth hormone and prolactin response to exercise.

The effect of a standardised exercise procedure on plasma growth hormone (HGH) and prolactin has been assessed in 10 normal human subjects. Each subject was tested in an ambient temperature of 40 degrees and on a subsequent day at a temperature of 10 degrees. At 40 degrees exercise produced an increase in HGH in all 10 subjects, while in the cold only 1 showed a rise in the hormone during exercise. An increase in prolactin with exercise at 40 degrees occurred in some of the subjects, but these changes were small in comparison with those of HGH. Prolactin levels did not increase during exercise in the cold.

Adolescent↗
PubMed1976

Absence of nocturnal elevation of plasma prolactin concentrations in Cushing's disease.

The mean prolactin concentration during sleep and the per cent change (increase) and increment in the nocturnal elevation of plasma prolactin concentrations were significantly reduced (P less than .01, less than .01, and less than .001, respectively) in 6 untreated patients with clinically active Cushing's disease, compared with concentrations seen in normal subjects. There was no significant difference between mean-awake and mean-sleep plasma prolactin concentration in these patients, in contrast to that seen in normal subjects. In contrast, patients with hypercorticism secondary to adrenal adenoma (n = 2) or receiving long-term, high-dose corticosteroid therapy (n = 6) did not differ significantly from normal subjects in the percentage change seen in the nocturnal elevation of their plasma prolactin concentrations. Although mean prolactin concentration during sleep was reduced in these two categories of hypercorticism, a significant difference was still present between mean-awake and mean-sleep plasma prolactin concentration. (The nocturnal increment in plasma prolactin concentrations in these patients with hypercorticism compared with that of normal subjects was reduced, P less than .02). The difference between the percentage change and nocturnal increment observed in patients with Cushing's disease versus that seen in these two categories of hypercorticism was significant at P less than .02 and P less than .01, respectively. Four untreated patients with localized hypothalamic tumors also showed a significant reduction in the percentage change and increment in the nocturnal elevation of plasma prolactin concentrations (P less than .05 and P less than .02). In contrast to these findings, the prolactin responses to thyrotropin-releasing hormone (indicative of pituitary responsiveness) in patients with Cushing's disease, patients with adrenal adenoma, or those receiving chronic corticosteroid therapy, were all within the normal range seen in sex-matched control subjects. These findings provide additional evidence for the suggestion that there is altered hypothalamic function in patients with Cushing's disease.

Adrenal Cortex Hormones↗
PubMed1976

Effect of acute increases in serum triiodothyronine on TSH and prolactin responses to TRH, and estimates of pituitary stores of TSH and prolactin in normal subjects and in patients with primary hypothyroidism.

Previous investigators have shown that daily administration of TRH to normal individuals leads to diminishing TSH responses which were believed due to rising serum T3 with subsequent feedback inhibition of the pituitary. Patients with primary hypothyroidism were examined in the present study to test this hypothesis, since their T3 cannot increase after TRH. Bi-daily TRH (100 mug) was given to 4 patients for 3 consecutive days, and repeated on a 4th day following oral T3 (50 mug). TSH and PRL responses were unchanged during these 3days of serial TRH and were unaltered by T3 administration on the fouth day. In 5 other hypothyroid subjects studied before and during 3 consecutive days of T3 administration, TSH but not PRL responses to TRH appeared to decrease slowly but progressively. These observations led us to re-examine TRH responses in normal subjects given T3, since other workers had reported that 50 mug T3 completely abolished TSH response. Responses to TRH in 11 normals on a control day were compared to those observed 1 hour after oral T3. In spite of marked increases in serum T3, there was no significant difference between the mean TSH responses of the two studies.

Clinical Trials as Topic↗