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F Cordido

Publications and source records attributed to F Cordido.

At least 19 recordsLinked to original sources
PubMed1998

Acute changes in free-fatty acids (FFA) do not alter serum leptin levels.

Leptin, the product of the ob gene, is a recently discovered hormone secreted by adipocytes. Serum leptin concentrations increase in correlation with the percentage of body fat, but besides that little is known about the physiological actions of leptin in humans. The aim of this study was to assess the influence of changes in circulating free-fatty acids on serum leptin levels. Increases in plasma FFA levels (p < 0.02) were obtained in a group of normal subjects following the administration of intralipid plus heparin (250 ml 10% Intralipid plus 5000 U heparin). FFA reduction was achieved through the administration of acipimox (250 mg, orally, at 0 min and at 210 min), a lipid-lowering drug devoid of side effects, to a group of normal (p < 0.02) and obese subjects (p < 0.05). An increase in circulating FFA levels in normal subjects (n = 6), following administration of a lipid-heparin infusion, failed to modify plasma leptin levels as assessed by the area under the curve (AUC; mean +/- SE 892 +/- 168 for placebo vs 896 +/- 260 following intralipid plus heparin). Similarly, whereas acipimox pretreatment induced a reduction in FFA levels compared to placebo in normal (n = 6) and obese subjects (n = 8), it also failed to modify plasma leptin levels at any time-point studied. The results indicate that short-term reduction or increase in circulating FFA are not associated to changes in plasma leptin levels.

Adult↗
PubMed1998

Effect of acute pharmacological reduction of plasma free fatty acids on growth hormone (GH) releasing hormone-induced GH secretion in obese adults with and without hypopituitarism.

In obesity, there is a markedly decreased GH secretion. The diagnosis of GH deficiency (GHD) in adults is based on peak GH responses to stimulation tests. In the severely obese, peak GH levels after pharmacological stimulation are often in the range that is observed in hypopituitary patients. To distinguish obese subjects from GHD patients, it will be necessary to demonstrate that reduced GH responsiveness to a given test is reversible in the former, but not in the latter, group. Recent studies have shown that reduction of plasma free fatty acids (FFA) with acipimox in obese patients restores their somatotrope responsiveness. There are no data evaluating GH responsiveness to acipimox plus GHRH in obese adults with hypopituitarism. The aim of the present study was to evaluate the effect of acute pharmacological reduction of plasma FFA on GHRH-mediated GH secretion in obese normal subjects and obese adults with hypopituitarism. Eight obese patients with a body mass index of 34.2+/-1.2; eight obese adults with hypopituitarism, with a body mass index of 35.5+/-1.9; and six control subjects were studied. All the patients showed an impaired response to an insulin-tolerance test (0.15 U/kg, i.v.), with a peak GH secretion of less than 3 microg/L. Two tests were carried out. On one day, they were given GHRH (100 microg, i.v., 0 min), preceded by placebo; and blood samples were taken every 15 min for 60 min. On the second day, they were given GHRH (100 microg, i.v., 0 min), preceded by acipimox (250 mg, orally, at -270 min and -60 min); and blood samples were taken every 15 min for 60 min. The administration of acipimox induced a FFA reduction during the entire test. Normal control subjects had a mean peak (microg/L) of 23.8+/-4.8 after GHRH-induced GH secretion; previous acipimox administration increased GHRH-induced GH secretion, with a mean peak of 54.7+/-14.5. In obese patients, GHRH-induced GH secretion was markedly reduced, with a mean peak (microg/L) of 3.9+/-1; previous administration of acipimox markedly increased GHRH-mediated GH secretion, with a mean peak of 16.0+/-3.2 (P < 0.05). In obese adults with hypopituitarism, GHRH-induced GH secretion was markedly reduced, with a mean peak (microg/L) of 2+/-0.7; previous acipimox administration did not significantly modify GHRH-mediated GH secretion, with a mean peak of 3.3+/-1.1 (P < 0.05). The GH response of obese patients and obese adults with hypopituitarism was similar after GHRH alone. In contrast, the GH response after GHRH plus acipimox, was markedly decreased in obese adults with hypopituitarism (mean peak, 3.3+/-1.1), compared with obese patients (mean peak, 16.0+/-3.2) (P < 0.05) and control subjects (mean peak, 54.7+/-14.5) (P < 0.01). In conclusion, GH secretion, after GHRH-plus-acipimox administration, is reduced in obese adults with hypopituitarism patients, when compared with obese normal patients. Testing with GHRH plus acipimox is safe and is free from side effects and could be used for the diagnosis of GHD in adults.

Adult↗
PubMed1997

Hypopituitarism due to lymphocytic hypophysitis in a patient with retroperitoneal fibrosis.

We present a 78-year-old woman with clinical acute hypopituitarism in whom pathologic findings showed lymphocytic hypophysitis and retroperitoneal fibrosis. Lymphocytic hypophysitis should be included in the differential diagnosis of hypopituitarism at any age. The association with idiopathic retroperitoneal fibrosis suggest an autoimmune origin for this entity.

Aged↗
PubMed1996

Acipimox-mediated plasma free fatty acid depression per se stimulates growth hormone (GH) secretion in normal subjects and potentiates the response to other GH-releasing stimuli.

Increases in plasma free fatty acids (FFA) inhibit the GH response to a variety of stimuli; however, the role of FFA depression in GH control is far from understood. In the present work, FFA reduction was obtained by the administration to normal subjects of acipimox, a lipid-lowering drug devoid of side-effects. Each subject tested underwent two paired tests. In one, acipimox was administered orally at a dose of 250 mg at -270 min and at a dose of 250 mg at -60 min; in the matched test, placebo was given at similar intervals. To induce GH release, four stimuli acting through different mechanisms were used: pyridostigmine (120 mg, orally) at -60 min, GHRH (1 microgram/kg, iv) at 0 min, GH-releasing peptide (GHRP-6; His-D-Trp-Ala-Trp-D-Phe-Lys-NH2; 1 microgram/kg, iv) at 0 min, and finally, GHRH plus GHRP-6 at the same doses at 0 min. GH secretion was analyzed as the area under the secretory curve (AUC; mean +/- SE, micrograms per L/120 min). Acipimox pretreatment alone (n = 6) induced a reduction in FFA levels compared with placebo treatment. The FFA reduction led to a sustained GH secretion that increased from 2.4 +/- 1.8 micrograms/L at -120 min to 14.2 +/- 4.0 at 120 min. The GH AUC for placebo was 266 +/- 100, and that for acipimox was 1781 +/- 408 (P < 0.05). In the pyridostigmine-treated group (n = 6), the acipimox-pyridostigmine AUC (2046 +/- 323) was higher (P < 0.05) than the placebo-pyridostigmine AUC (764 +/- 101), but was not different from the AUC of acipimox alone. Previous FFA reduction nearly doubled the GHRH-mediated GH secretion (n = 6; placebo-GHRH AUC, 1817 +/- 365; acipimox-GHRH test, 3228 +/- 876; P < 0.05). A similar enhancement was observed when the stimulus employed was GHRP-6 (n = 6; placebo-GHRP-6 AUC, 2034 +/- 295; acipimox-GHRP-6, 4827 +/- 703; P < 0.05). Furthermore, even the most potent GH stimulus known to date, i.e. GHRH plus GHRP-6, was enhanced by the FFA suppression (placebo-GHRH-GHRP-6 AUC, 2034 +/- 277; acipimox-GHRH-GHRP-6, 5809 +/- 758; P < 0.05). The enhancing effect of lowering FFA levels was additive regardless of the stimulus employed. These results indicate that 1) FFA reduction per se stimulates GH secretion with a delayed time of action; 2) FFA reduction enhanced in an additive manner the GH secretion elicited by such different stimuli as pyridostigmine, GHRH, and GHRP-6; and 3) the observation that FFA reduction enhanced the response to the most potent GH stimulus, GHRH plus GHRP-6, suggests that FFA suppression acts by a separate mechanism. FFA reduction may have value in the clinical setting for assessing GH reserve.

Adolescent↗
PubMed1996

Impaired growth hormone secretion in obese subjects is partially reversed by acipimox-mediated plasma free fatty acid depression.

GH secretion in response to provocative stimuli is blunted in obese patients. On the other hand, increases in plasma free fatty acids (FFA) inhibit the GH response to a variety of stimuli, and FFA levels in plasma are increased with obesity. To ascertain whether FFA might be responsible for the GH secretory alterations of obesity, we studied spontaneous and stimulated GH secretion in 31 obese patients after FFA reduction by acipimox, a lipid-lowering drug devoid of serious side-effects. Each subject underwent two paired tests. In one, acipimox was administered orally at a dose of 250 mg at -270 min and at a dose of 250 mg at -60 min; in the matched test, placebo was given at similar intervals. To induce GH release, three stimuli acting through different mechanisms were used: pyridostigmine (60 mg, orally, at -60 min), GHRH (100 micrograms, iv, at 0 min), and GHRH plus GH-releasing peptide (GHRP-6; His-D-Trp-Ala-Trp-D-Phe-Lys-NH2; both at a dose of 100 micrograms, iv, at 0 min). GH secretion was analyzed as the area under the secretory curve (AUC; mean +/- SE; micrograms per L/60 min). Acipimox pretreatment alone (n = 13) induced a large reduction in FFA levels compared with placebo treatment. The FFA reduction led to a slight GH rise (AUC, 123 +/- 47), not different from that in the placebo group (61 +/- 15). In the pyridostigmine-treated group (n = 6), the acipimox-pyridostigmine AUC (408 +/- 107) was significantly higher (P < 0.05) than that in the placebo-pyridostigmine group (191 +/- 25). Furthermore, the GHRH-mediated (n = 6) AUC of GH secretion in the placebo test (221 +/- 55) was tripled by FFA reduction due to acipimox, with an AUC of (691 +/- 134; P < 0.05). Even the most potent GH stimulus known to date, i.e. GHRH plus GHRP-6, was enhanced by FFA suppression. In fact, the placebo-GHRH-GHRP-6 AUC was 1591 +/- 349, lower (P < 0.05) than that in the acipimox-GHRH-GHRP-6 test (2373 +/- 242). The enhancing effects of FFA lowering on GHRH-mediated and GHRH- plus GHRP-6-mediated GH release were synergistic. These results indicate that in obese subjects, unlike normal weight subjects. FFA reduction per se does not stimulate GH secretion. A reduction in FFA with acipimox, however, increased pyridostigmine-. GHRH-, and even GHRH- plus GHRP-6-mediated GH release, suggesting that FFA reduction operates through a different mechanism from that of these three stimuli. The abnormally high FFA levels may be a contributing factor for the disrupted GH secretory mechanisms in obesity.

Adolescent↗
PubMed1996

[Utility of magnetic resonance in the etiologic diagnosis of hypopituitarism].

The diagnosis of hypothalamic-pituitary disorders relies on a combination of clinical and biochemical data and imaging techniques. During the last decade, computed tomography (CT) has been the best technique for the evaluation of the hypothalamuspituitary region, but in recent years magnetic resonance (MR) has improved the diagnostic efficiency of CT. We retrospectively review the clinical records of 40 hypopituitary patients from the endocrinology unit of our hospital. The aim of the present study was to establish the role of MR in the etiologic diagnosis and anatomic definition of hypopituitarism, when compared with CT. Secondarily, we studied the different pituitary hormones in this condition. The diagnoses were: 12 postsurgical hypopituitarism, 10 empty sella turcica, 7 Sheehan's syndrome, 5 idiopathic hypopituitarism, 3 pituitary disgenesis, 2 craniopharyngioma and 1 macroprolactinoma. GH was the most commonly affected hormone, followed by gonadotrophins, corticotrophin and thyrotrophin (100%, 94%, 76% and 68% respectively). In 24 patients both MR and CT studies were performed. MR was diagnostic in 22 patients, and CT in 15 patients (p < 0.05). MR offered improved diagnostic or anatomical data in 16 patients of the 24 in whom both techniques were performed (p < 0.05). We conclude that MR allows a better definition of the hypothalamus-pituitary region than CT, contributing to the etiologic diagnosis and improving the anatomical findings. Empty sella turcica should be considered a common cause of hypopituitarism.

Adolescent↗
PubMed1995

Effect of combined administration of growth hormone (GH)-releasing hormone, GH-releasing peptide-6, and pyridostigmine in normal and obese subjects.

Growth hormone (GH) secretion in response to all provocative stimuli is decreased in patients with obesity. Recently, we found that the combined administration of GH-releasing hormone (GHRH) and the hexapeptide GH-releasing peptide-6 (GHRP-6) induced a large increase in plasma GH levels. To gain further insight into the disrupted mechanism of GH regulation in obesity, we investigated whether the inhibition of somatostatinergic tone with pyridostigmine could further increase the GH response to combined administration of GHRH and GHRP-6. In normal subjects, administration of GHRH plus GHRP-6 induced a marked increase in plasma GH with a peak at 30 minutes (mean +/- SEM, 76.7 +/- 9.7 micrograms/L), which was similar to that obtained after pretreatment with pyridostigmine (74.7 +/- 9.4 micrograms/L). In obese patients, combined administration of GHRH plus GHRP-6 induced a clear increase in GH secretion with a peak at 15 minutes of 42.2 +/- 10.0 micrograms/L, which was also unaffected after pretreatment with pyridostigmine (38.4 +/- 5.8 micrograms/L). The GH response was lower in obese patients than in controls as assessed by the area under the curve after administration of both GHRH plus GHRP-6 (1,846 +/- 396 v 4,773 +/- 653, P < .01) and pyridostigmine plus GHRH plus GHRP-6 (1,989 +/- 372 v 5,098 +/- 679, P < .005). In conclusion, these data suggest that GHRP-6 can behave as a functional somatostatin antagonist, and that somatotrope responsiveness to the combined administration of GHRH plus GHRP-6 is largely independent of somatostatinergic tone.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Amyloid goitre: CT and MR findings.

Two cases of amyloid goitre presented as an enlarged thyroid mass with cystic components. Solid parts of the goitre showed high attenuation on computed tomography (CT) and moderate hypointensity on T1 and T2-weighted images. Fine needle aspiration was negative for amyloid, but pathological studies of surgical specimens demonstrated amyloid infiltration of the thyroid interstitium and regressive colloid cysts. In a patient at risk for systemic amyloidosis, thyroid enlargement with a cystic component suggests amyloid goitre. In this case, needle biopsies should be directed to solid areas of the mass because amyloid material may not be present in the cysts.

Adult↗
PubMed1994

Persistent GHRH-induced PRL secretion in Cushing's syndrome, obesity and exogenous hypercortisolism.

Endogenous Cushing's syndrome, obesity and chronic glucocorticod treatment are characterized by blunted GH secretion. The administration of GHRH is capable of stimulating a small but significant PRL increase in normal subjects. The current study was designed to determine plasma PRL levels in response to GHRH, studied in three different situations characterized by a blunted GH secretion. Obese patients (n = 6) with a weight over 30% of ideal body weight, patients with active Cushing's syndrome, and normal volunteers treated with dexamethasone 22 mg per os over two days before the pituitary challenge were studied. As a control group 18 normal subjects of similar age and sex were studied. GH and PRL was determined at intervals after GHRH (1 microgram/kg). GHRH-induced GH secretion was markedly reduced in patients with obesity, patients with endogenous Cushing's syndrome and volunteers treated with dexamethasone. In contrast, GHRH-induced PRL secretion was not affected in these three clinical situations. In summary, in three situations characterized for an impairment of the somatotroph cell, due to a primary intrinsic defect or to a functional hypothalamic alteration, there is a persistent GHRH-induced PRL secretion, suggesting that prolactin could be released by mammosomatotrophs that function normally in spite of hyposomatotropism.

Adult↗
PubMed1993

Massive growth hormone (GH) discharge in obese subjects after the combined administration of GH-releasing hormone and GHRP-6: evidence for a marked somatotroph secretory capability in obesity.

GH secretion in response to all provocative stimuli is decreased in patients with obesity. However, the precise mechanism causing this impairment in GH release is unknown. His-DTrp-Ala-Trp-DPhe-Lys-NH2 (GHRP-6) is a synthetic compound that releases GH in a dose-related and specific manner in several species, including man. To gain further insight into disrupted GH secretion in obesity, GHRP-6 and GH-releasing hormone (GHRH) at a dose of 100 micrograms, i.v., were administered either alone or in combination in a group of 19 obese subjects. In a group of obese patients, GHRP-6 induced GH secretion, with a GH peak (mean +/- SEM) of 15.7 +/- 4.4 micrograms/L and an area under the curve (AUC) of 674 +/- 187, which were larger than those after GHRH stimulation (6.8 +/- 1.1 and 412 +/- 71, respectively). Enhancement of the endogenous cholinergic tone was obtained in another group of obese subjects by means of pyridostigmine (120 mg, orally). Pyridostigmine administered 60 min before GHRP-6, increased both the mean GH peak (32.2 +/- 6.9) and the AUC (1413 +/- 537) after GHRP-6 administration. In a separate group of subjects, the combined administration of GHRP-6 and GHRH induced a massive discharge of GH, with individual responses ranging from 14-86 micrograms/L. GHRP-6 plus GHRH induced a mean GH peak of 42.2 +/- 10.9 and an AUC of 1894 +/- 784 (P < 0.05), clearly indicating a potentiating (synergic) action when the two compounds were administered together. These data show that GH responses to GHRP-6 were almost twice those to GHRH in obese patients. The stimulatory effect exerted by pyridostigmine on GHRP-6-induced GH secretion supported the view of increased somatostatinergic tone in obesity. Finally, the massive GH discharge that followed the administration of GHRH plus GHRP-6 was not observed after any stimulus in obesity, clearly indicating that the impaired GH secretion is a functional and potentially reversible state.

Adolescent↗
PubMed1992

[Different etiology of thyrotoxicosis as a function of previous prevalence of goiter].

BACKGROUND: The high incidence of goiter is believed to modify the characteristics and etiology of thyrotoxicosis. The aim of the present was to study the etiologic types and clinical characteristics of thyrotoxicosis of patients from two areas of different endemic goiter. METHODS: Two hundred twelve patients (184 women and 28 males) were studied with clinical and analytical data of thyrotoxicosis. The patients were consecutively seen in the endocrinology units of two different hospitals over the last 4 years. One hundred eight patients pertained to the area of the Xeral Hospital in Lugo (inland zone) and 104 pertained to the area of the Juan Canalejo Hospital from La Coruña (coastal zone). The clinical data of thyrotoxicosis, thyroxin concentration and thyroid gammagraphies were evaluated. RESULTS: The different etiological types were: Graves disease (GD): Lugo: 20 (19%), La Coruña 57 (55%; p less than 0.001). Toxic multinodular goiter (TMG): Lugo 53 (49%), La Coruña 29 (28%; p less than 0.001). Toxic adenoma (TA): Lugo 23 (21%), La Coruña 13 (13%). Hyperthyroidism by iodine: Lugo: 8 (7%), La Coruña 3 (3%). Other diagnosis: Lugo: 4 (3%), La Coruña 2 (2%). Although the frequency of thyrotoxicosis was much greater in women the percentage distribution of the etiologic types was similar in the two sexes. Symptoms were more frequent in patients with GD with respect to TMG. The presence of auricular fibrillation was more frequent in patients with TMG (38%) than in those presenting GD (4%; p less than 0.01). CONCLUSIONS: Toxic multinodular goiter is the most common cause of thyrotoxicosis in the zones of high endemic goiter. On lowering endemic goiter the percentage of TMG is lowered and that of Graves disease is raised. The symptomatology of thyrotoxicosis is more evident in GD with relation to other etiologic types, but auricular fibrillation is more frequent in TMG. The high prevalence of toxic nodular goiter and hyperthyroidism by iodine suggests the important pathogenic role of the increase of the ingestion of iodine in the form of iodized salt or drugs with iodine.

Aged↗
PubMed1992

Platelet function in diabetic retinopathy: levels of beta-thromboglobulin and platelet factor 4.

Altered platelet function has been reported in diabetic patients. This article reports plasma levels of beta-thromboglobulin and platelet factor 4 as measures of in vivo platelet activity in diabetic and control groups. Both beta-thromboglobulin and platelet factor 4 were significantly higher in diabetics than in controls (p < 0.01). The levels observed were not significantly affected by age, sex, diabetes type or whether the diabetic had nonproliferative or proliferative retinopathy, but beta-thromboglobulin levels were significantly higher in diabetics of less than 10 years standing than in those who had suffered diabetes for over 20 years (p < 0.05).

Adolescent↗
PubMed1991

Corticosteroid-induced growth hormone secretion in normal and obese subjects.

OBJECTIVE: In normal subjects, corticosteroids stimulate growth hormone (GH) secretion at 3 hours. Obesity is associated with blunted GH secretion. In order to clarify both the deranged mechanism of GH secretion in obesity and the corticosteroid mechanism of action we have assessed in normal and obese subjects the effects of dexamethasone, pyridostigmine (a drug capable of suppressing somatostatin release) and GHRH. We also compared in normal subjects the stimulatory effect of three different corticosteroids on plasma GH levels. DESIGN: In both normal and obese subjects the following tests were carried out: placebo; dexamethasone alone (4 mg i.v. at 0 minutes); and dexamethasone plus pyridostigmine (120 mg p.o. at 60 minutes). In normal subjects we also studied the effects of hydrocortisone (100 mg i.v. at 0 minutes) and deflazacort (a corticosteroid that does not cross the blood-brain barrier) (60 mg i.v. at 0 minutes). In obese subjects we also assessed the effect of dexamethasone plus GHRH (100 micrograms i.v. at 150 minutes) on plasma GH levels. PATIENTS: Ten normal subjects and 22 obese subjects were studied. Normal controls were within 10% of their ideal body weight. Obese subjects had a body mass index of 37.1 +/- 1.1 (mean +/- SEM). MEASUREMENTS: Plasma GH levels were measured by radioimmunoassay. RESULTS: Dexamethasone-induced GH secretion in normal subjects (28.6 +/- 7.8 millimicron/l, P less than 0.05). Corticosteroids did not alter GH levels in obese subjects. Pretreatment with pyridostigmine increased dexamethasone-induced GH release in normal subjects (40.8 +/- 6.8 millimicron/l) but this did not achieve statistical significance. Dexamethasone plus pyridostigmine did not alter GH levels in obese subjects (8.0 +/- 1.6 mU/l). In some subjects, dexamethasone pretreatment potentiated GHRH-stimulated GH secretion, while in half the subjects the basal GH levels were not altered. In control subjects, hydrocortisone and deflazacort caused GH release similar to dexamethasone. CONCLUSIONS: Corticosteroids are a new and selective stimulus of GH secretion. They do not cause GH release in obese subjects. Their relative independence from cholinergic control suggest that they act by reducing somatostatin secretion.

Adrenal Cortex Hormones↗