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R Astorga

Publications and source records attributed to R Astorga.

At least 37 records · Page 2Linked to original sources
PubMed1999

Outbreak of septicaemic colibacillosis in Japanese quail (Coturnix coturnix japonica).

We have carried out an aetiological and pathological study of an outbreak of septicaemia caused by the O165 serogroup of Escherichia coli in Japanese quail (Coturnix coturnix japonica) which resulted in high mortality (90%). After treatment with amoxicilin in drinking water (200 mg/l), morbility and mortality rates dropped markedly. Microbiological studies showed that the organism responsible was an atypical E. coli strain, on the basis of the non-fermentation of lactose (ONPG-), which belonged to the O165 serogroup and was highly virulent for 1-day-old chickens.

Animals↗
PubMed1999

The presence of muramidase released protein and extracellular factor protein in various serotypes of Streptococcus suis isolated from diseased and healthy pigs in Spain.

A total of 142 strains from different serotypes of Streptococcus suis isolated in Spain from diseased pigs (88 strains) and healthy carrier pigs (54 strains) were studied for the presence of a muramidase released protein (MRP) and an extracellular factor (EF). The following five phenotypes: MRP+EF+, MRP+EF-, MRP-EF+, MRP+EF* and MRP*EF- were detected. A high percentage of S. suis serotype 2 strains isolated from diseased pigs (84 per cent) belonged to phenotype MRP+EF+, but this phenotype has also been noticed in other serotypes (serotypes 1, 1/2 and 14). Both proteins were detected in S. suis serotype 2 strains (26%) isolated from healthy carrier pigs and one of both proteins in serotypes 1 and 14 (phenotype MRP+EF*). The isolation of S. suis strains from healthy pigs which have shown both proteins may support the epidemiological significance of these carriers in the maintenance, transmission and distribution of virulent strains within and between swine farms.

Animals↗
PubMed1999

The growth hormone (GH)-releasing hormone-GH-insulin-like growth factor-1 axis in patients with fibromyalgia syndrome.

Fibromyalgia (FM) is a painful syndrome of nonarticular origin, characterized by fatigue and widespread musculoskeletal pain, tiredness, and sleep disturbances, without any other objective findings on examination. Interestingly, some of the clinical features of FM resemble the ones described in the adult GH-deficiency syndrome. Furthermore, insulin-like growth factor (IGF)-1 levels are frequently reduced in patients with FM. To gain further insight into the mechanisms leading to dysregulation of the GH-IGF-1 axis in these patients, we assessed 24-h spontaneous GH secretion, GH responses to GHRH, and IGF-1 and IGF binding protein (BP)-3 levels before and after 4 days treatment with human (h)GH. We found that, in comparison with controls, patients with FM exhibited a marked decrease in spontaneous GH secretion as assessed by mean GH secretion (2.5 +/- 0.4 microg/L in controls vs. 1.2 +/- 0.1 microg/L in FM, P < 0.05), pulse height (4.7 +/- 0.8 microg/L in controls vs. 2.5 +/- 0.3 microg/L in FM, P < 0.05), and pulse area (4.7 +/- 1 min/mg x L in controls vs. 2.3 +/- 0.3 min/mg x L in FM, P < 0.05). In contrast, GH responses to GHRH (100 microg, i.v.) were similar in controls (mean peak, 13.5 +/- 2.5 microg/L) and in patients with FM (12.2 +/- 3 microg/L). Finally, treatment with hGH (2 IU, s.c. daily), over 4 days, led to a clear-cut increase in plasma IGF-1 and IGFBP-3 levels in patients with FM. In conclusion, our data show that patients with FM exhibited a marked decrease in spontaneous GH secretion, but normal pituitary responsiveness to exogenously administered GHRH, thus suggesting the existence of an alteration at the hypothalamic level in the neuroendocrine control of GH in these patients. Furthermore, our finding of increased IGF-1 and IGFBP-3 levels after GH treatment, over 4 days, opens up the possibility of testing the therapeutic potential of hGH in patients with FM.

Adult↗
PubMed1999

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↗
PubMed1998

Adding metformin versus insulin dose increase in insulin-treated but poorly controlled Type 2 diabetes mellitus: an open-label randomized trial.

To compare the effect of adding metformin to insulin therapy with a moderate increase in insulin dose alone in insulin-treated, poorly controlled Type 2 diabetic patients, 47 consecutive such patients (baseline daily dose >0.5 IU kg(-1) and HbA1c >8%) were openly randomized either to a combination of their previous insulin schedule plus metformin (2.55 g daily in three divided doses, n = 24) or to a moderate insulin dose increase (20% of baseline, n = 23). The patient status/biochemical profile was assessed at entry and at 4 months. Among those assigned to insulin + metformin, 18 took the drug. Upon an intention-to-treat basis, patients assigned to insulin dose increase had a statistically significant weight gain (1.16+/-1.9 vs 0.3+/-4.5 kg, p < 0.05). Patients assigned to the insulin + metformin regimen experienced a significantly greater fall in HbA1c (-1.87+/-2.16 vs 0.03+/-1.68%, p < 0.01), total cholesterol (-0.56+/-0.89 vs 0.14+/-0.72 mmol l(-1), p < 0.05) and LDL-cholesterol (-0.51+/-0.73 vs 0.19+/-0.6 mmol l(-1), p < 0.01). These data suggest that adding metformin to insulin in poorly controlled Type 2 DM patients offers an advantage in terms of glycaemic control and lipid plasma profile.

Aged↗
PubMed1998

Enhanced growth hormone (GH) responsiveness to GH-releasing hormone after dietary restriction in patients with Cushing's syndrome.

OBJECTIVE: In patients with Cushing's syndrome, decreased growth hormone (GH) secretion is observed although the basic mechanism is not yet understood. A short-term hypocaloric diet is known to increase both spontaneous and GHRH-stimulated GH secretion in normal subjects. In order to gain further insight into the altered GH secretion in patients with Cushing's syndrome, we assessed the effect of a short-term hypocaloric diet on GH responses to GHRH in these patients. DESIGN: Two GHRH tests (1 microgram/kg i.v.) were performed, the first under basal conditions (normocaloric diet) and the second after a 3-day hypocaloric diet (650 cal/day). PATIENTS: Six female patients with untreated Cushing's disease. MEASUREMENTS: Plasma GH levels were measured by immunoradiometric assay. RESULTS: GHRH-induced GH release was impaired in patients with Cushing's disease on a normal diet (mean peak 12.4 +/- 6.4 mU/l, area under the curve (AUC) 744 +/- 332 mU/l/120 min). Following a hypocaloric diet, GH responses to GHRH were markedly enhanced in the same group of patients (mean peak 46.2 +/- 14.8 mU/l, AUC 3142 +/- 1032 mU/l/120 min, P < 0.05). CONCLUSIONS: This study demonstrates that in patients with Cushing's disease the somatotroph hyporesponsiveness to growth hormone releasing home is improved after a short-term hypocaloric diet. Therefore, blunted growth-hormone secretion in chronic hypercortisolism is a potentially reversible state and the secretory capacity of the somatotroph appears not to be severely compromised in patients with Cushing's disease.

Adolescent↗
PubMed1998

Conception after iodine-131 therapy for differentiated thyroid cancer.

We reviewed the medical history of 26 women with differentiated thyroid cancer who became pregnant after receiving therapeutic doses of radioactive iodine (131I) in order to document the possibility of a greater risk for disorders in these pregnancies. There were a total of 39 pregnancies, 6 of which occurred during the first year after therapy. In 3 cases the following anomalies were encountered: a male suffering Trisomy 18 (Edward's syndrome), a female with constitutional aplastic anemia, and a male with a congenital hip dysplasia. Of the 33 pregnancies that occurred after the first year post-therapy, there were 2 spontaneous abortions and a male effected by ureteral stenosis. Based on these data, although it cannot be confirmed that these congenital disorders are due to the 131I therapy, we recommend that pregnancy be avoided for the first year after therapy.

Abortion, Spontaneous↗
PubMed1998

Serum leptin levels in male marathon athletes before and after the marathon run.

Leptin is a hormone produced by the adipocytes to regulate food intake and energy expenditure at the hypothalamic level. It is commonly accepted that the main determinants of leptin secretion are the net amount of body fat and the mean size of adipocytes. On the contrary, important vectors of energy flux in the organism, such as food intake and energy expended on exercise, are not thought to be regulators of that secretion. To understand whether leptin is regulated by an acute energy expenditure such as strenuous exercise, 29 male athletes who had trained for marathon running were studied before and after a marathon run and compared with 22 nonobese, age-, sex-, and body mass index (BMI)-matched sedentary controls. Controls and marathon athletes showed no differences in BMI or fat-free mass. Marathon runners showed a strong reduction in total fat mass (6.2 +/- 0.4 kg; 9.1 +/- 0.5% of body fat) compared with controls (12.3 +/- 0.5 kg; 16.1 +/- 0.5% of body fat; P < 0.05). This difference in body composition was paralleled by a mean serum leptin level that in marathonians (2.9 +/- 0.2 micrograms/L) was significantly (P < 0.05) reduced compared with that in controls (5.1 +/- 0.6 micrograms/L). It is remarkable that the ratio of leptin per kg body fat, showed a very good agreement between the two groups, 0.40 +/- 0.04 microgram/L.kg for controls and 0.46 +/- 0.03 microgram/L.kg for marathonians. In the two groups, leptin was correlated with both body weight, BMI, and fat mass (P < 0.001). The marathon trajectory was the standard 42.195 km accomplished in an average time of 3 h, 17 min, 7 s, with a calculated energy expenditure of over 2800 Cal. After the marathon run, a water imbalance occurred, with a significant decrease in body weight and an increase in serum albumin. A significant (P < 0.05) reduction in leptin values was observed after the run (2.6 +/- 0.2 micrograms/L) compared with before (2.9 +/- 0.2 micrograms/L), which was more relevant considering the relative hemoconcentration. In conclusion, 1) compared with sedentary subjects, leptin levels are reduced in male marathon runners in parallel with the relevant reduction in total body fat; 2) expressed as a ratio of leptin per kg body fat, no differences were observed between marathonians and controls; and 3) after an energy expenditure of 2800 Cal in the marathon run, a reduction in leptin levels occurred. Strong changes in energy expenditure may regulate serum leptin levels in man.

Adult↗
PubMed1997

Urinary albumin excretion rate and cardiovascular disease in Spaniard type 2 diabetic patients.

To assess the prevalence of urinary albumin excretion abnormalities and their associations with cardiovascular disease or its classical risk factors in type 2 diabetes mellitus, 1348 clinic-proceeding patients have been studied retrospectively. The overnight urinary albumin excretion rate, blood pressure, smoking, ophthalmic and cardiovascular status, current therapies, estimates of glycemic control, plasma lipids, serum creatinine and uric acid have been ascertained. 767 (56.8%) patients were found normoalbuminuric, 461 (34.1%) microalbuminuric and 120 (8.9%) macroalbuminuric. In bivariate analyses, the urinary albumin excretion rate had statistically significant (P < 0.05) relationships with age, duration of diabetes, male sex, waist-to-hip ratio, systolic and diastolic pressure, coronary heart disease, cerebrovascular disease, peripheral vascular disease, hypertension, antihypertensive therapy, laser-treated retinopathy, kind of treatment, smoking habit, fasting glycaemia, HbA1c, creatinine, uric acid, triglycerides, high density lipoprotein (HDL)-cholesterol and apolipoprotein B. Borderline statistically significant (P < 0.1) relationships were found with hypolipidaemic therapy, insulin dose, non-HDL-cholesterol, apolipoprotein A1 and lipoprotein (a). In a multivariate stepwise logistic regression model, HbA1c, hypertension, male sex, age, diastolic blood pressure, coronary heart disease and body-mass index were sequentially selected as variables independently associated with microalbuminuria. Serum creatinine, HbA1c, male sex and hypertension were sequentially selected as independently associated with macroalbuminuria. Micro and macroalbuminuria are frequent abnormalities associated with poorly controlled and complicated disease, with overt cardiovascular disease and its classical risk factors as well as with the male sex.

Aged↗
PubMed1997

Relationships of C-peptide levels and the C-peptide/bloodsugar ratio with clinical/biochemical variables associated with insulin resistance in orally-treated, well-controlled type 2 diabetic patients.

The aim of the present study was to evaluate the relationship of C-peptide and the C-peptide/bloodsugar ratio with clinical/biochemical variables presenting a well-known association with insulin resistance in NIDDM patients in acceptable control, obtained without the use of exogenous insulin. A total of 118 non insulin dependent diabetes mellitus (NIDDM) patients treated with diet/oral drugs and having a HbA(1c) level < 7.5% have been studied. Non-stimulated C-peptide levels (RIA) and the C-peptide/bloodsugar ratio have been determined and their relationships with the blood pressure status, blood pressure figures, estimates of adiposity, age, known duration of diabetes, current therapies, plasma lipids, glycaemic control, urinary albumin excretion rate, uric acid and creatinine have been ascertained. C-peptide levels were significantly (P < 0.05) correlated with systolic (r = 0.21) and diastolic blood pressure (r = 0.19), BMI (r = 0.21), high density lipoprotein (HDL) (r = -0.22), non-HDL-cholesterol (r = 0.23), apolipoprotein B (r = 0.29), log of triglycerides (r = 0.39) and uric acid (r = 0.35). The C-peptide/bloodsugar ratio had statistically significant correlations with known duration of diabetes (r = -0.23), diastolic blood pressure (r = 0.21), body mass index (BMI) (r = 0.22), log of triglycerides (r = 0.23) and uric acid (r = 0.36). Hypertensives had higher C-peptide levels than normotensives (1.04 +/- 0.04 versus 0.88 +/- 0.04 nmol/ml, respectively (mean +/- S.E.), P < 0.05) and this statistically significant difference remained after adjustment for age and known duration of diabetes. In well-controlled NIDDM patients not receiving exogenous insulin, both C-peptide levels and the C-peptide/bloodsugar ratio have statistically significant relationships with clinical/biochemical variables presenting a well-known association with insulin resistance.

Administration, Oral↗
PubMed1997

Lack of association of lipoprotein (a) with coronary heart disease in Spaniard type 2 diabetic patients.

We tried to elucidate the possible relationship between lipoprotein (a) levels and coronary heart disease by assessing the presence of lipoprotein (a) covariates in NIDDM. We selected 41 type 2 diabetic patients with coronary heart disease and 82 type 2 diabetic patients free from cardiovascular disease. They were adjusted for age, sex and duration of diabetes. Routine chemical analysis was carried out using standard procedures, HbA1c by HPLC and lipoprotein (a) and urinary albumin excretion rate by immunonephelometry. No difference has been found in lipoprotein (a) levels between both groups of patients (18 [144.25] mg/dl in cases vs. 23 [197.25] mg/dl in controls (median [range]), Mann Whitney U-test, P > 0.1). No association has been found between coronary heart disease and lipoprotein (a) levels greater than 30 mg/dl (Pearson's chi 2, P > 0.1). Significant and independent linear relationships have been found between the square root of lipoprotein (a) levels, serum creatinine and total cholesterol (multiple r2: 0.15, P < 0.001). Patients treated with insulin had greater square root of lipoprotein (a) levels, even after adjusting for serum creatinine and total cholesterol (5.87 +/- 0.35 vs. 4.76 +/- 0.36 (mean +/- S.E.), ANCOVA, P < 0.05). These data do not show an association between symptomatic coronary heart disease and lipoprotein (a) in NIDDM. Significant and independent relationships have been found between this variable and serum creatinine, total cholesterol and insulin therapy.

Aged↗
PubMed1997

Acute pharmacological reduction of plasma free fatty acids enhances the growth hormone (GH)-releasing hormone-mediated GH secretion in patients with Cushing's syndrome.

In Cushing's syndrome, GH secretion is blocked with all the stimuli tested. It has been reported that the acute pharmacological reduction of free fatty acids (FFA) leads to an enhancement of GH secretion in normal subjects and in pathological conditions associated with reduced GH secretion. To understand if the elevated FFA levels of hypercortisolism may be responsible for the altered GH secretion, 14 patients with active Cushing's syndrome underwent 2 paired tests with 100 micrograms i.v. of GHRH on 2 different occasions. In one test, they were pretreated with placebo and in the other one, with acipimox 250 mg p.o. 4 h before, and 250 mg p.o. 1 h before GHRH. The basal FFA levels (799 +/- 57 mmol/L) were reduced by acipimox throughout the whole test (values under 240 +/- 28 mmol/L). In the placebo pretreated group, GHRH-induced GH secretion was severely impeded, with a mean GH peak of 1.8 +/- 0.3 micrograms/L and area under the curve of 121.3 +/- 21.6 micrograms/L-120 min. All the patients showed a GHRH-mediated GH peak under 4 micrograms/L. Acute reduction of FFA by acipimox enhanced the GHRH action, with a mean GH peak of 11.1 +/- 1.8 micrograms/L and area under the curve of 652.9 +/- 110.3 micrograms/L-120 min (both P < 0.005). Individually analyzed after acipimox, all 14 subjects presented an enhancement in the GHRH-mediated GH peak, and 8 patients showed a response over 10 micrograms/L. In conclusion, acute FFA reduction by acipimox increased the GH secretion elicited by GHRH in chronic hypercortisolism. Elevated FFA may be a contributing factor to the deranged GH secretion observed in Cushing's syndrome.

Adult↗
PubMed1996

Serum immunoreactive-leptin levels are increased in patients with Cushing's syndrome.

Leptin, the product of the ob gene, is a recently discovered hormone secreted by adipocytes. Cushing's syndrome is a disease state usually associated with weight gain due to the accumulation of adipose tissue. In order to study the effect of chronic glucocorticoid excess upon serum leptin levels; in the present work, four patients with recently diagnosed Cushing's syndrome and a group of control subjects matched for age, sex and body mass index (BMI) were studied. Serum leptin concentrations, measured by radioimmunoassay, were assessed in samples taken every 60 minutes over a 24 hour period. Assessment of leptin concentrations over 24 hours, by means of the area under curve showed a twofold increase in serum leptin levels in patients with Cushing's syndrome (mean+/-SEM 54.3+/-14) in comparison to control subjects (29.3+/-4.4; p<0.05). In conclusion, our data show that leptin levels are markedly increased in Cushing's syndrome patients. The relevance of this finding to the increased body fat present in patients with Cushing's syndrome merits further studies.

Adult↗
PubMed1996

[Medullary carcinoma of the thyroid gland. Prognostic factors].

OBJECTIVE: To analyze the clinical features and possible prognostic factors involved in the clinical course of a series of 26 patients with the diagnosis of thyroid medullar carcinoma (TMC). MATERIALS AND METHODS: An analysis was made of the variables age, sex, clinical course to diagnosis, paraneoplastic manifestations (flush, diarrhoea), clinical type (sporadic, non-associated, familial MEN IIa associated TMC, familial MEN IIb associated TMC), histologic uni or multicentricity, and stage of disease as possible predictive factors for the evolution. RESULTS: The most remarkable prognostic factor was tumoral stage. The likelihood of a patient diagnosed with stage I or II being free of metastatic disease was 1, 0.66 and 0.33 at 15, 16 and 17 years, respectively. In contrast, those patients in stage III at diagnosis had a likelihood of being free from metastasis 5 years after diagnosis and therapy of 0. With regard to sex, a better clinical course was observed among males than among females, statistically significant at 3 and 5, but not at 10 years. No statistical significance was reached with the other possible prognostic factors investigated. CONCLUSION: Given the obvious influence of tumoral stage of disease on prognosis, an early access to medical attention is desirable for diagnosis and treatment of TMC, as well as an early detection of family cases by a screening test.

Adolescent↗