New diagnostic criteria for diabetes and mortality in older adults.
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Adult↗
Biomedical subjects
F Cordido
Publications and source records attributed to F Cordido.
Hyperleptinemia in uremic patients undergoing conservative management, peritoneal dialysis, and hemodialysis: A comparative analysis.
We performed a cross-sectional study in a wide sample of patients with chronic renal failure undergoing conservative therapy (CTh) (n = 79), peritoneal dialysis (PD) (n = 75), and hemodialysis (HD) (n = 51), with the aim of analyzing the impact of the different modes of therapy on serum leptin levels. We used a multivariate approach, taking into consideration the potential effects of other epidemiological, dialysis-related, nutritional, and hormonal factors on serum leptin. Leptin levels were higher in patients treated with PD (median, 36 ng/mL) than in those undergoing CTh (10.8 ng/mL) or HD (5.4 ng/mL) (P < 0.0005). This difference persisted after controlling for gender, body mass index, and fasting insulin levels, suggesting that imbalances in these factors may only partially explain the differences found between the three modes of therapy. Leptin levels showed a significant negative correlation with peritoneal protein losses in PD patients but were poorly associated with factors such as proteinuria, daily peritoneal glucose absorption (PD), renal function, or adequacy of dialysis. Leptin and insulin-like growth factor-I (IGF-I) were significantly correlated in PD patients, but the study design did not allow for establishing a meaning for this correlation. In conclusion, serum leptin levels are increased in PD patients when compared with CTh or HD patients. Differences in gender distribution, fat mass, and insulin levels may partially explain these findings, but other undefined factors also may have a role in producing these results.
Adolescent↗
The use of growth hormone (GH) secretagogues in the diagnosis of GH deficiency in humans.
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Adult↗
Serum leptin levels in women throughout pregnancy and the postpartum period and in women suffering spontaneous abortion.
OBJECTIVE: In pregnancy, important changes occur in the body weight of the mother, caused by sodium and water retention and by an increase in body fat tissue, but the mechanisms that regulate maternal and foetal changes in fat mass are poorly understood. Leptin is a hormone produced by adipocytes in order to regulate food intake and energy expenditure at the hypothalamic level in man. In order to verify whether leptin participates in the changes in body composition during pregnancy and postpartum, 630 healthy women were studied at specific time periods and leptin and auxological parameters were determined. DESIGN: A cross-sectional study in which leptin levels were measured in women at specific time periods related to pregnancy. Each woman was assessed only once. PATIENTS: 630 women participated in the study, and were divided into categories as follows: Group A, 29 internal controls, with no previous or current pregnancy; Group B, 73 women in the first trimester of pregnancy; Group C, 60 women in the 24 h before delivery; Group D, 212 women in the 24 h postpartum; Group E, 93 women in the eightH postpartum week (2 months group); Group F, 71 women in the sixteenth postpartum week (4 months group); Group G, 20 women in the sixth month postpartum; Group H, 23 women one year postpartum; Group I, 20 women two years postpartum; finally Group J, of 29 women who had suffered spontaneous abortion in the first trimester of pregnancy and were studied in the 24 h after the stillborn delivery. MEASUREMENTS: Serum leptin levels were measured in duplicate by radioimmunoassay using commercial kits. Height and weight was measured and BMI (kg/m2) calculated. RESULTS: Compared with serum leptin in the control group (11.7 +/- 1.0 micrograms/l), a non significant (NS) increase was observed in the first trimester of pregnancy (14.3 +/- 1.4 micrograms/l), with no parallel changes in body weight. A reduction in leptin occurred in the 24 h after delivery (9.4 +/- 1.4 micrograms/l, P = 0.02). After delivery a progressive increase in leptin concentrations was observed, 13.3 +/- 1.5 micrograms/l at two months (NS) and 17.4 +/- 2.6 micrograms/l at four months (P = 0.035 vs controls). Afterwards leptin values decreased towards normal values at 6, 12 and 24 months after delivery 14.4 +/- 1.8 micrograms/l; 12.9 +/- 1.6 micrograms/l; and 10.1 +/- 1.1 micrograms/l respectively (all NS). With the exception of the postpartum group, a significant correlation was observed between leptin concentrations and body weight or BMI in each group of women studied. In the women who suffered spontaneous abortion in the first trimester of pregnancy a reduction in leptin levels occurred (8.8 +/- 1.0 micrograms/l, P = 0.001 vs first trimester group). CONCLUSION: Serum leptin concentrations rose slightly during pregnancy, fell following delivery and subsequently increased during the first six months postpartum. These variations were unrelated to changes in body composition, and may be responsible for the postpartum weight gain observed in some women. Abnormally low serum leptin levels were observed in women suffering spontaneous abortion in the first trimester of pregnancy.
Abortion, Spontaneous↗
Prevalence of pregnancy and postpartum thyroid dysfunction in a homogeneous population of Spain.
To determine the prevalence of pregnancy and postpartum thyroid dysfunction in the Spanish population, 691 women divided into six cohorts were studied. Biochemical hypothyroidism was observed in 9.4%, 4.4%, 1.9%, 4.6% and 4.8% at the first trimester of pregnancy, at delivery and at the second, fourth and sixth to twelfth postpartum months, respectively. Biochemical hyperthyroidism was observed in 6.7%, 0.8%, 1.9%, 4.6% and 2.4% in the same cohorts of subjects. Thyroiditis was observed in 4%, 0%, 0.6%, 6.2% and 7.3% in the cohorts studied. No depression or psychological alterations were detected either in pregnancy or in the postpartum period. Our data suggest that if screening for thyroid dysfunction is to be recommended in the postpartum period, this must be based on biochemical parameters.
Autoantibodies↗
Regulation of growth hormone secretion by signals produced by the adipose tissue.
The neuroregulation of growth hormone (GH) secretion and the state of the adipose tissue reserves are closely related. GH exerts lipolytic actions on the adipose tissue and low body weight enhances secretion of GH while obesity is associated with reduced levels of GH and blocked release of GH when challenged by all stimuli. The mediators of the regulation exerted by the adipose tissue on the GH/insulin-like growth factor-I axis are not fully understood, but in the last few years two relevant factors have emerged--free fatty acids (FFA) and the adipocyte-produced hormone leptin. FFA and GH integrate a classical feedback loop and a rise in FFA blocks GH secretion. This action is rapid, dose-related and exerted at the pituitary level with no evident hypothalamic participation. A pharmacological reduction in FFA enhances secretion of GH and eliminates the GH blockade of obesity and Cushing's syndrome. The discovery of leptin has expanded our knowledge of the way in which the adipose tissue participates in some neuroendocrine actions. Obesity is associated with elevated levels of serum leptin while undernutrition and fasting lead to low leptin. In fasted rats, the pattern of GH pulsatility is eliminated with a near absence of spontaneous peaks, but the administration of leptin by the intracerebroventricular (i.c.v.) route restores the altered pattern. When fed rats receive antileptin antibodies i.c.v the normal pattern is reversed to an absence of pulses, reminiscent of the fasting state. These results are the first demonstration that, at least in experimental animals, leptin is a relevant factor in GH regulation. Leptin has no direct pituitary action and its action at the hypothalamic level appears to be mediated by neuropeptide Y, being the final step in a reduction in the somatostatin tone. On the other hand, the action of GH on leptin levels seems to be tenuous in humans, but in the near future it will be possible to investigate the action of leptin on human GH. As the hypothalamic neuroregulation of GH secretion in humans is unlike that in the rat, a crucial point for elucidation will be the actions, if any, and the mechanisms by which leptin participates in GH regulation in humans, as well as its alterations in disease states.
Adipose Tissue↗
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↗
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↗
[Early detection and control of risk factors in diabetic nephropathy].
Diabetic nephropathy is an important complication of diabetes. Established nephropathy is preceded by a long silent phase of incipient nephropathy characterized by a subclinical increase in albumin excretion know as microalbuminuria (30-300 mg/d). There is evidence that the progression of nephropathy and its associated mortality can be ameliorated by a number of interventions if started at a nearly stage: glycaemic control, that should be optimized as far as possible, and hypertension control. Angiotensin-converting enzyme (ACE) inhibitors are promoted as first-line agent for treating hypertension in diabetic patients; as well as their systemic hypotensive action, these drugs may have an additional beneficial effect in reducing intraglomerular pressure.
Albuminuria↗
[Central diabetes insipidus secondary to infundibuloneurohypophysitis].
In up to a third of cases, central diabetes insipidus (DIC) is idiopathic although the percentage varies in different series. Since antibodies against magnicellular neurons were detected in some patients, a possible autoimmune basis for certain cases of apparently idiopathic DIC was speculated. Lymphocytic infundibuloneurohypophysitis, an inflammatory process that affects the infundibulum, pituitary stalk and neurohypophysis with distinctive radiologic, histologic and evolutive characteristics, has recently been described as a cause of central diabetes insipidus. We describe a patient in whom the clinical and radiologic characteristics suggest the diagnosis of DIC secondary to infundibuloneurohyphysitis.
Adult↗
Amiodarone and thyroid function.
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Amiodarone↗
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↗
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↗
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↗
[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↗
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↗
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↗
[Adrenal insufficiency in amyloidosis secondary to rheumatoid arthritis].
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Adrenal Gland Diseases↗