Insulinoma misdiagnosed as intractable epilepsy.
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Adult↗
Biomedical subjects
E Rasio
Publications and source records attributed to E Rasio.
The rete mirabile of the eel: a useful model for the study of transcapillary passage of MR contrast agents.
Our purpose was to study the capillary leakage of MR contrast media using a pure capillary model, the rete mirabile of the eel. The rete is a countercurrent-exchange organ composed of an arterial and a venous capillary system that can be catheterized and perfused. Substances are introduced at the arterial input by a constant infusion, and their steady-state concentrations are measured at the arterial and venous outputs. The capillary leakage of four MR contrast agents--Gd-DOTA(MW = 561 D), carboxymethyldextran-Gd-DTPA (MW = 38,900 D), albumin-Gd-DTPA (MW = 92,000 D), AMI-227 (400,000 D<MW<900,000 D)--was characterized by reference to radioactive tracers (3HHO, 22Na, 14C-sucrose, 125I-albumin) by two parameters. These parameters were the concentration ratio of the venous output over the arterial input [C(VOUT)(%)] and the permeability coefficient (P). The transcapillary pathway mechanisms for carboxymethyldextran-Gd-DTPA and albumin-Gd-DTPA were studied by electron microscopy. P values for Gd-DOTA (9.4+/-3.6 x 10(-7) cm/s) and albumin-Gd-DTPA (11.8+/-5.5 x 10(-7) cm/s) were close to P values for 14C-sucrose, while P values for carboxymethyldextran-Gd-DTPA (6.4+/-4.9 x 10(-7) cm/sec) were similar to P values for 125I-albumin. The lowest permeability was observed with AMI-227 (2.7+/-2 x 10(-7) cm/sec). Vesicular transport was demonstrated for carboxymethyldextran-Gd-DTPA and albumin-Gd-DTPA. The transcapillary passage of several MR contrast agents can be characterized with the rete mirabile model. Molecular weight is the major factor influencing transport.
Air Sacs↗
Hypothalamic-pituitary-adrenal axis in abdominal obesity: effects of dexfenfluramine.
OBJECTIVE: Hyperactivity of the HPA axis is a possible mechanism underlying abdominal obesity. We aimed to evaluate in premenopausal women with abdominal obesity, (i) the hypothalamic-pituitary-adrenal (HPA) axis responses to direct pituitary stimulation with corticotrophin releasing hormone (CRH) and to opioid blockade with naloxone, and (ii) the interaction between short-term serotoninergic activation with dexfenfluramine (dF), a serotonin-release agonist, and these responses. DESIGN AND SUBJECTS: Eight obese women (mean BMI, 35 kg/m2) with waist to hip ratio (WHR) > 0.85 were tested with CRH (1 microgram/kg i.v.) and naloxone (125 micrograms/kg i.v.) before and at the end of two treatment periods with dF (15 mg twice daily for 7 days) and placebo (washout 7 days) in a cross-over design. Eight normal weight control women were tested with CRH and naloxone. RESULTS: Prior to treatment, ACTH and cortisol responses to naloxone (areas under the curve) were significantly higher in obese women then in control women (P = 0.027 and P = 0.035 respectively) dF treatment resulted in significant (P < 0.05) reduction of ACTH and cortisol increments. In contrast, ACTH and cortisol responses to CRH were not significantly different in obese and control subjects and were unaffected by dF treatment. CONCLUSION: We conclude that women with abdominal obesity have hyperreactivity of the HPA axis to opiod blockage and that dexfenfluramine treatment reduces this hyperactivity.
Adrenocorticotropic Hormone↗
Carl Arthur Goresky (August 25, 1932-March 21, 1996)
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Journal Article↗
[Effect of ranitidine on blood alcohol and glucose levels after ingestion of alcohol].
Are alcohol and glucose blood levels modified in fasting subjects taking ranitidine? This experience tries to simulate normal life conditions. Nine men, volunteer, aged from 24 to 29 years old, without any digestive symptoms, ate a standard lunch after five hours of fasting, took 0.35 g of alcohol per kg. Ethanol blood levels, glycemia and blood levels of insulin and glucagon were taken at regular intervals every 10 to 15 minutes during all the experiment (120 minutes). After the initial experiment, all subjects took 150 mg of ranitidine p.o. b.i.d. during seven days. Afterward they were submitted to the same protocol. Between both experiments no differences were found on blood levels of ethanol. Peak concentration, decreasing rate, and biodisponibility (estimated by area under the curve) did not change. There was a tendency to have a faster decrease in glucose blood level (p < 0.05). This study does not show any significant modification of ethanol metabolism after taking ranitidine p.o.; those results are differing from data already found with studies using cimetidine.
Adult↗
Effects of dexfenfluramine treatment on body weight and postprandial thermogenesis in obese subjects. A double-blind placebo-controlled study.
The purpose of this study was to determine the effects of dexfenfluramine on body weight and post-prandial thermogenesis in obese subjects. Thirty obese subjects, men and women, with an excess weight between 20 and 80% of the ideal weight and aged from 20 to 60 years, participated in this double-blind, placebo-controlled study. During the treatment period, the subjects were not submitted to caloric restriction. Basal metabolic rate and postprandial thermogenesis (following a 400 kcal test meal) measurements were made by indirect calorimetry. Metabolic parameters such as glucose, insulin, thyroid hormones, free fatty acids, beta-hydroxybutyrate, total cholesterol and triglycerides were also measured before the test meal. These measurements were done at baseline, after one week and after three months of treatment. Following the three month treatment period, the mean weight loss of the dexfenfluramine group was 4.6 +/- 1.6 kg (s.e.) (P < 0.01) whereas the placebo group maintained the initial weight. The mean weight loss in the dexfenfluramine group represented 15% of the initial overweight. There was no significant change in either group in basal metabolic rate and postprandial thermogenesis following one week and three months of treatment (P > 0.05). The caloric intake after the treatment period was significantly reduced in the dexfenfluramine group (from 1631 +/- 103 kcal (s.e.) to 1353 +/- 109 kcal (s.e.); P < 0.05); in the placebo group, the changes were not significant (P > 0.05). The plasma concentrations of tri-iodothyronine, total cholesterol and triglycerides were significantly reduced in the dexfenfluramine group (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Growth hormone-releasing factor increases serum prolactin concentrations in normal subjects and in patients with pituitary adenomas.
We have examined the serum growth hormone (GH) and prolactin (PRL) response to growth hormone releasing factor (hGRF-(1-44)NH2 (GRF) 1 microgram/kg i.v. bolus) in 16 acromegalic patients (eight of whom were hyperprolactinaemic), 13 patients with microprolactinoma, and 14 healthy subjects. The GH responses to TRH and to the somatostatin analogue SMS 201-995 were also studied in acromegalic patients. In these, and in patients with microprolactinoma, GH responses after GRF (P less than 0.001 vs saline) were variable. The absolute GH increase (calculated as area under the curve) in acromegalic patients (2489 +/- 920 micrograms/l min), or in patients with microprolactinoma (1322 +/- 279 micrograms/l min) was not different from that in controls (2238 +/- 633 micrograms/l min). In addition, a significant increase in PRL release was observed after GRF in comparison to saline in acromegalic patients (P less than 0.01), in patients with microprolactinoma and in normal subjects (P less than 0.001). The PRL increase was significantly correlated with basal PRL levels in acromegalic patients (r = 0.99, P less than 0.001) and in patients with microprolactinomas (r = 0.61, P less than 0.05). Furthermore, a significant correlation was found between GH rise after GRF and basal GH, and between GH rise after GRF and GH decrement after SMS in patients with acromegaly. These results suggest that GRF can stimulate PRL release by actions on the normal pituitary and on pituitary adenomas, including microprolactinomas. Moreover, the data suggest that in acromegaly there is a relative functional deficiency of hypothalamic somatostatin.
Acromegaly↗
Temporal changes in prolactin and corticosterone response during chronic treatment with d-fenfluramine.
In order to elucidate the mechanism of development of tolerance to the anorectic effect during chronic treatment with d-fenfluramine (d-F), we examined the temporal changes induced by d-F in food intake and prolactin (PRL) and corticosterone secretion. Male Sprague-Dawley rats were treated for 14 days with d-F (2.5 mg/kg i.p.) or saline twice daily and were given free access to food and water. Groups of 8 rats were sacrificed 30 min after d-F or saline injection at days 1, 4 and 14 for measurements of serum PRL and corticosterone. Food intake and weight gain were reduced significantly by d-F during the first 2-3 days of treatment but not thereafter. Compared with saline, d-F initially increased PRL (57 +/- 9 vs. 7 +/- 0.7 ng/ml) and corticosterone (42 +/- 2 vs. 14 +/- 3 micrograms/dl) serum concentrations. At 4 days, PRL was still significantly increased (43 +/- 5 vs. 10 +/- 4 ng/ml) but corticosterone returned to basal levels. At 14 days, PRL and corticosterone concentrations in the d-F group were not different from corresponding values in the saline group. To verify whether the loss of corticosterone and PRL responses to d-F was not due to a depletion of hormone stores, direct stimulation of corticosterone with corticotrophin and of PRL with metoclopramide were made at days 4 and 14, respectively. Corticotrophin (0.25 mg/kg i.p.) increased corticosterone concentrations similarly in d-F-treated (45 +/- 8 micrograms/dl) and in saline-treated rats (51 +/- 7 micrograms/dl).(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Clinical pancreas transplantation: a learning curve of its management.
In this evolving experience, acceptable patient and graft survival after PTX appear best secured by the use of whole duodenopancreatic grafts, enteric drainage, triple immunosuppression induced by OKT3, and the monitoring of postprandial blood glucose and serum amylase for detection of rejection.
Adult↗
The effect of d-fenfluramine on anterior pituitary hormone release in the rat: in vivo and in vitro studies.
Administration of d-fenfluramine, a serotonin-releasing drug, to male rats induced a dose-dependent increase in both serum prolactin and corticosterone concentrations. Serum growth hormone levels increased, but not significantly, at a dose of 1.25 mg/kg i.p. and decreased significantly at higher doses. When rats were pretreated with the serotonin uptake inhibitor fluoxetine (10 mg/kg i.p.) 30 min prior to injection of d-fenfluramine (5 mg/kg i.p.), the serum prolactin response to d-fenfluramine was partially inhibited, whereas the growth hormone response was not significantly modified. Fluoxetine pretreatment increased the serum corticosterone to the same level as did d-fenfluramine. d-Fenfluramine's effect on prolactin and growth hormone release was further tested in a hypothalamic-pituitary in vitro system. The addition of d-fenfluramine (5-500 ng/mL) for 30 min to rat hypothalami resulted in an enhancement of prolactin and growth hormone-releasing activities. These were expressed as the ability of the media in which the hypothalami had been incubated to stimulate prolactin and growth hormone release by cultured pituitary cells. The data suggest that the effect of d-fenfluramine on prolactin secretion is exerted through the hypothalamus and is probably mediated, at least partially, by a serotoninergic mechanism. The mechanism of d-fenfluramine's effect on corticosterone and growth hormone release needs further evaluation.
Animals↗
Decreased sensitivity to insulin in women with microprolactinomas.
To determine whether there exists an altered sensitivity to insulin in hyperprolactinemia, we studied, in 15 women with microprolactinomas, the insulin effects on glucose, PRL, GH, and cortisol before and after successful adenoma removal. Our results show that in women with microprolactinomas, the sensitivity to insulin is lower in hyperprolactinemia than in normoprolactinemia achieved by selective adenomectomy.
Adenoma↗
Acromegaly: biochemical assessment of cure after long term follow-up of transsphenoidal selective adenomectomy.
This study reports the clinical and biological follow-up 5-11 yr after transsphenoidal selective adenomectomy in 25 patients with acromegaly. Eight patients had microadenomas, and 17 had macroadenomas. Initial normalization of plasma GH levels (basal values, less than 5 ng/ml; glucose-suppressed concentrations, less than 2.5 ng/ml) was achieved in all 8 patients with microadenomas and in 13 patients with macroadenomas. Of these, 3 patients with normal GH levels and dynamics had relapse of GH hypersecretion after intervals between 1-6 yr after microadenoma removal. Recurrence of pituitary adenoma was documented by surgery in 1 patient and by computed tomographic scanning in 2 others. Normal basal and glucose-suppressed plasma GH concentrations were maintained 7.4 +/- 0.5 (+/- SEM) yr after adenomectomy in 7 patients with microadenomas and in all 10 patients with macroadenomas. Thus, 88% of the patients with microadenomas and 59% of the patients with macroadenomas were cured, and the overall cure rate was 68%. We conclude that recurrence of acromegaly after successful surgery may occur late after adenoma removal and that it cannot be predicted by normal postoperative GH levels and dynamics. However, in view of the overall cure rate, transsphenoidal adenomectomy remains a most valuable treatment for acromegaly.
Acromegaly↗
Recurrence of hyperprolactinemia after selective transsphenoidal adenomectomy in women with prolactinoma.
To assess the long-term prognosis for women with prolactinoma after selective transsphenoidal adenomectomy, we followed 44 patients for 6.2 +/- 1.5 years. Group 1 (28 patients) had microprolactinomas, and Group 2 (16 patients) had macroprolactinomas. After surgery, normal plasma prolactin levels, resumption of menses, and cessation of galactorrhea were observed in 24 Group 1 patients (85 per cent) and 5 Group 2 patients (31 per cent). Hyperprolactinemia recurred in 12 of the 24 Group 1 patients and in 4 of the 5 Group 2 patients after 4 +/- 1.3 and 2.5 +/- 1.6 years of remission, respectively. There was no radiologic evidence of tumor recurrence in any patient, and no relation was found between the occurrence of pregnancy after surgery and the recurrence of hyperprolactinemia. Clinical and biologic features before surgery could not predict the long-term outcome. However, the immediate postoperative level of plasma prolactin was significantly lower in patients in whom normal prolactinemia (6.4 +/- 1.1 ng per milliliter) was maintained than in those who relapsed (11.7 +/- 1.5 ng per milliliter) (P less than 0.02). We conclude that recurrence of hyperprolactinemia after successful surgery is frequent but delayed. The immediate postoperative level of plasma prolactin may be a predictive risk factor.
Adenoma↗
Glucose utilization and nitrogen balance in the obese on a protein-lipid hypocaloric diet.
Glucose utilization and insulin and growth hormone responses were evaluated in eight obese women by three rapid intravenous glucose tolerance tests (IVGTT): during a control period, and after 1 and 3 weeks of a 750 kcal/day protein-lipid diet (1 kcal = 4.1855 kJ). Weight loss averaged 454 g/day during the 1st week and 238 g/day for the 2nd and 3rd weeks of the diet. Nitrogen balance was maintained in equilibrium. Plasma insulin concentrations fell by 50% within 1 week of dieting; growth hormone levels were not modified. The net rate of glucose disappearance dropped from 0.98 to 0.65 and 0.68% min, the glucose pool from 16.2 to 13.3 and 13.4 g, and glucose utilization from 158 to 88 and 87 mg/min during the control period, and at 1 and 3 weeks of dieting, respectively. The insulinogenic index decreased from 0.41 to 0.24 to 0.16 with successive IVGTT's. The glucose volume of distribution was not modified with dieting. It is concluded that a hypocaloric protein-lipid diet induces (i) a carbohydrate intolerance not related to a negative nitrogen balance and (ii) a rapid initial weight loss which cannot be ascribed to a depletion of the glucose volume.
Adolescent↗
Effects of naloxone on insulin-induced release of pituitary hormones.
To evaluate the role of endogenous opiates on the regulation of the pituitary hormonal stress response, we have studied in six normal subjects the insulin-induced secretion of PRL, GH, and ACTH with and without naloxone, a specific opiate antagonist. During hypoglycemia, naloxone infusion reduced plasma PRL levels at 90 min, lowered the overall GH response, and enhanced that of ACTH. These observations suggest that endogenous opiates have a modulatory role in the stress-induced secretion of pituitary hormones.
Adrenocorticotropic Hormone↗
[Prolactinoma in the female. Clinical and biological study; preoperative evaluation in 200 women].
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Adenoma↗
[Prolactinoma in the male. Preoperative evaluation of 40 patients].
Forty male patients with a prolactinoma were studied. The majority of tumors were large. Eight (20%) were microadenomas. Loss of libido and sexual impotence, the most frequent symptoms, were found in 82,5% of cases. Gynecomastia with galactorrhea was noted in six cases. Seven patients had hypopituitarism and nine visual field defects. Prolactin levels ranged from 30 to 7,000 ng/ml. The mean baseline prolactin value was higher in the group of invasive adenomas or enclosed adenomas with a suprasellar expansion. The LH-RH test, performed on twenty-eight patients, showed an abnormal response in 80% of the cases.
Adenoma↗
[Prolactinoma in the female. Therapeutic results in 200 women].
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Adenoma↗