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Biomedical subjects

F Valente

Publications and source records attributed to F Valente.

At least 37 records · Page 2Linked to original sources
PubMed1993

Prognostic factors of early fatal outcome and long-term survival in patients with Pneumocystis carinii pneumonia and acquired immunodeficiency syndrome.

Fifty-five episodes of Pneumocystis carinii pneumonia (PCP) in AIDS patients were evaluated to assess clinical and laboratory risk factors predicting the probability of surviving the acute episode of PCP and the long-term survival after PCP. Age > 45 yrs, PaO2 < 50 mmHg, AaPO2 > 50 mmHg, and LDH > 800 IU/L correlated strongly with early mortality; patients who needed mechanical ventilation had a significantly lower PaO2 and serum albumin, and higher AaPO2 and LDH compared to the patients who did not. Neither age nor PaO2, AaPO2, LDH, albumin, days from onset, time for recovery, CD4+ cell count correlated with long-term survival of AIDS patients with PCP. Informations obtained at initial presentation of PCP may predict early outcome and influence therapeutic approach, improving chances for survival.

AIDS-Related Opportunistic Infections↗
PubMed1993

Therapeutical doses of salbutamol inhibit the somatotropic responsiveness to growth hormone-releasing hormone in asthmatic children.

In humans beta-adrenergic receptors mediate an inhibitory effect on somatotropic function, likely via stimulation of hypothalamic somatostatin release. Accordingly, salbutamol (SAL), a beta 2-agonist, given iv abolishes the GH response to GH-releasing hormone (GHRH) in adults. Taking into account that in bronchial asthma an alteration in the beta-adrenergic neural control of airways has been hypothesized, we aimed to verify whether, in asthmatic children, beta-adrenergic activation inhibits or not GH secretion. To this goal, we studied the effect of therapeutical doses of SAL on GH response to GHRH in 15 asthmatic children (12 M and 3 F, 5.9-11.1 yr, pubertal stage I-II). All children underwent a GHRH test (1 microgram/kg iv). Moreover, in 7 children (group A), SAL was administered orally (0.125 mg/kg) 1 h before GHRH, while in 8 (group B) by inhaled aerosol (2 mg) 30 min before GHRH. Oral SAL (group A) abolished the GHRH-induced GH rise (AUC, mean +/- SE 165.1 +/- 33.3 vs 959.9 +/- 158.1 micrograms/L/h; p < 0.03). In group B, the GH response to GHRH was only blunted by inhaled SAL (938.6 +/- 284.6 vs 1378.8 +/- 315.6 micrograms/L/h; p < 0.02). In conclusion, our data show that in asthmatic children, therapeutical doses of SAL exert a marked inhibitory effect on GH secretion. Further studies are needed to exclude detrimental effects of chronic treatment with beta 2-agonists on GH secretion and growth velocity in asthmatic children.

Administration, Oral↗
PubMed1993

Evidence against depletion of the growth hormone (GH)-releasable pool in human primary hypothyroidism: studies with GH-releasing hormone, pyridostigmine, and arginine.

We investigated whether the impaired GH secretion of hypothyroid patients could be due to an increase in hypothalamic somatostatinergic tone. Twenty-four patients with primary hypothyroidism [20 females and 4 males; mean age (+/- SE), 47.5 +/- 2.7 yr] and 20 normal subjects (17 females and 3 males; age, 47.6 +/- 3.0 yr) were studied. In the first group of 12 hypothyroid patients, administration of pyridostigmine, a cholinergic agonist drug (120 mg, orally, at -60 min), notably increased GH responses to GH-releasing hormone (GHRH; 1 microgram/kg, iv, at 0 min; peak GH levels for pyridostigmine plus GHRH vs. placebo plus GHRH, 16.6 +/- 4.9 vs. 6.0 +/- 1.8 micrograms/L; P < 0.01). The GH responses to pyridostigmine plus GHRH, however, were considerably lower than those in 10 normal subjects (peak GH levels, 53.0 +/- 3.5 micrograms/L; P < 0.001). In the second group of 12 hypothyroid patients, arginine infusion (30 g, iv, from 0-30 min) markedly increased the GH responses induced by GHRH administration (1 microgram/kg, iv, at 0 min; peak GH levels for arginine plus GHRH vs. placebo plus GHRH, 30.6 +/- 4.7 vs. 5.3 +/- 1.0 micrograms/L; P < 0.001). However, GH release after GHRH plus arginine was greater in 10 normal subjects than in the hypothyroid patients (peak GH levels, 50.9 +/- 5.3 micrograms/L; P < 0.001). Pyridostigmine and arginine inhibit hypothalamic somatostatin tone. The stimulatory effect of both agents on GHRH-induced GH release indicates that reduced GH secretion in hypothyroidism can be reversed to a considerable extent by inhibiting hypothalamic somatostatinergic tone. The relatively greater potency of arginine compared to pyridostigmine suggests that hypothyroid patients may have an impairment of the cholinergic pathways. Furthermore, these data show that hypothyroid patients have a somatotrope secretory capacity much greater than previously thought.

Adult↗
PubMed1993

Comparison of the potentiating effect of pyridostigmine, arginine and propranolol on the GHRH-induced GH release in short children.

The effect of pyridostigmine (60 mg orally), arginine (0.5 g/kg iv) and propranolol (PROP, 40 mg orally) on GHRH (1 microgram/kg iv)-induced GH release was studied in seven short children. Pyridostigmine and arginine induced a similar potentiating effect on GHRH-induced GH rise (Peak, mean +/- SEM: 56.9 +/- 12.8 and 48.6 +/- 8.5 micrograms/L, respectively vs 12.3 +/- 1.6 micrograms/L; p < 0.05). Combination of GHRH with propranolol induced an increase of GH that was significant only with regard to peak (28.9 +/- 8.4 micrograms/L) but not to AUC. However, GH rises observed after GHRH combined with PD or ARG did not significantly differ from that recorded after coadministration of GHRH and PROP both for peak and AUC. Our results confirm that pyridostigmine and arginine have a striking potentiating effect on the GHRH-induced GH rise in children and show that the tests with GHRH + PD and GH + H + ARG are ore reliable than that with GHRH + PROP to explore the secretory capacity of somatotroph cells.

Adolescent↗
PubMed1992

Estimated incidence and prevalence of female breast cancer in Italian regions.

Female breast cancer incidence and prevalence in Italy have been estimated by region and vast areas from population-based survival data of breast cancer patients and 1970-1987 specific mortality data using a mathematical model. Italian age-standardized incidence rates (ASR) for 1987 range from 70 to 90 per 100,000 women-year in the Northern regions, 55 to 73 in the Center, and 45 to 72 in the South. Overall, the ASR is about 80 in the North, 70 in the Center and 60 in the South. In the absence of competitive mortality, breast cancer cumulative risk in the 0-74 years life span is about 7 women out of 100 in the North, 6 in the Center and 5 in the South. The decreasing risk pattern from North to Center then South appears less evident when under 45 age-specific rates are considered. Very high levels for young age-groups are present both in the North (Liguria and Emilia Romagna) and South (Sardinia and Apulia). The incidence pattern by age differs from region to region and over the considered period, suggesting that a birth-cohort effect is crossing the whole country. Using to model, it can be estimated that the risk by cohort increases from the generations born at the beginning of the century to those born in the 40s, after which, for subsequent generations, it has been decreasing in all the considered areas and is similar in the North and South. We can infer that for the whole country the incidence will increase up to the years 2000-2010 when those birth-cohorts at higher risk will also be at higher risk for age. In 1987, about 250,000 Italian women had a present or past history of breast cancer: for the 1970-1987 period, prevalence has increased by approximately 5,500 cases per year.

Age Factors↗
PubMed1992

Arginine abolishes the inhibitory effect of glucose on the growth hormone response to growth hormone-releasing hormone in man.

Acute hyperglycemia inhibits the growth hormone (GH) response to several stimuli including growth hormone-releasing hormone (GHRH), likely acting by stimulation of endogenous somatostatin release. The aim of our study was to verify whether arginine ([Arg] 30 g intravenously [IV] in 30 minutes), a well-known GH secretagogue likely acting via inhibition of hypothalamic somatostatin release, counteracts the inhibitory effect of oral glucose (OG) administration (100 mg orally) on the GH response to GHRH (1 micrograms/kg IV bolus) in seven normal subjects (aged 20 to 30 years). The GH response to GHRH (peak, 11.6 +/- 1.8 micrograms/L) was inhibited by previous OG load (peak, 7.4 +/- 0.8 micrograms/L; P less than .02 v GHRH alone) and potentiated by Arg coadministration (peak, 36.2 +/- 8.8 micrograms/L; P less than .03 v GHRH alone). The potentiating effect of Arg on the GHRH-induced GH increase was unaffected by previous OG load (peak, 30.4 +/- 6.9 micrograms/L). In conclusion, our results show that Arg abolishes the inhibitory effect of OG administration on the GHRH-induced GH response in man. These data, although indirect, suggest that both acute hyperglycemia and Arg act at the hypothalamic level, stimulating and inhibiting, respectively, the release of somatostatin.

Administration, Oral↗
PubMed1992

Interactions of galanin and arginine on growth hormone, prolactin, and insulin secretion in man.

Galanin (GAL), a 29 amino acid neuropeptide, is known to increase both basal and growth hormone-releasing hormone (GHRH)-induced growth hormone (GH) secretion while not significantly increasing prolactin (PRL) secretion in man. GAL is also endowed with an inhibiting effect on glucose-stimulated insulin release in animals, but not in man. We studied the effect of GAL (80 pmol/kg/min infused over 60 minutes) on the arginine- (ARG, 30 g infused over 30 minutes) stimulated GH, PRL, insulin, and C-peptide secretion in eight healthy volunteers (age, 20 to 30 years). GAL induced an increase of GH (GAL v saline, area under curve [AUC], mean +/- SEM: 316.5 +/- 73.9 v 93.2 +/- 20.9 micrograms/L/h, P less than .05), but failed to modify both PRL and insulin secretion. GAL enhanced the ARG-induced stimulation of both GH (1,634.1 +/- 293.1 v 566.9 +/- 144.0 micrograms/L/h, P less than .02) and PRL secretion (1,541.9 +/- 248.8 v 1,023.8 +/- 158.7 micrograms/L/h, P less than .02). On the contrary, GAL blunted the ARG-stimulated insulin (816.3 +/- 87.7 v 1,322.7 +/- 240.9 mU/L/h, P less than .05), as well as C-peptide secretion (105.1 +/- 9.8 v 132.8 +/- 17.3 micrograms/L/h, P less than .02). ARG administration induced a transient increase of glucose levels (P less than .01 v baseline) followed by a significant decrease (P less than .05 v baseline). This latter effect was prevented by the coadministration of GAL. In conclusion, these results show that in man GAL potentiates the GH response to ARG, suggesting that these drugs act at the hypothalamic level, at least in part, via different mechanisms.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Arginine potentiates but does not restore the blunted growth hormone response to growth hormone-releasing hormone in obesity.

A blunted growth hormone (GH) response to several stimuli, including growth hormone-releasing hormone (GHRH), has been shown in obesity. Arginine (ARG) has been demonstrated to potentiate the GHRH-induced GH increase in normal subjects, likely acting via inhibition of hypothalamic somatostatin release. To shed further light onto the mechanisms underlying the blunted GH secretion in obesity, we studied the effect of ARG (0.5 g/kg infused intravenously [IV] over 30 minutes) on both basal and GHRH (1 micron/kg IV)-stimulated GH secretion. Eight obese subjects (aged 26.4 +/- 3.9 years; body mass index, 39.0 +/- 1.9 kg/m2) and eight normal control volunteers (aged 27.0 +/- 1.7 years; body mass index, 22.3 +/- 0.5 kg/m2) were studied. In obese subjects, the GH response to both GHRH and ARG was lower (P less than .01 and P less than .002, respectively) than in controls. ARG potentiated the GH response to GHRH in obese patients (P less than .0003). However, in these patients, the GH secretion elicited by GHRH, even when coadministered with ARG, persisted at reduced levels (P less than .005) when compared with controls. Basal insulin-like growth factor-1 (IGF-1) levels did not significantly differ in obese subjects and in normal subjects (161.1 +/- 37.0 v 181.0 +/- 12.8 micrograms/L). In conclusion, ARG enhances the blunted GHRH-induced GH increase in obese patients, but the GH responses to ARG alone and to ARG + GHRH persist at lower levels than in normals. Thus, our results suggest the existence of a reduced pituitary GH pool in obesity.

Adolescent↗
PubMed1992

[Incidence and prevalence of respiratory tumors in Italy. Estimation from mortality data].

This study estimates the incidence and prevalence of larynx and lung cancers using a mathematical model based on available data on specific mortality and survival. In Italy, larynx and lung cancers account for more than 95% of respiratory cancers. In this paper, estimates of age/sex-specific and age-standardized incidence rates and prevalence are presented for the years 1970 and 1987. Age and birth-cohort effects on incidence are also presented by sex and broad geographical area. The procedure was firstly validated using data from four cancer registries: Varese (Northern Italy), Parma (North-Central Italy), Florence (Central Italy), and Ragusa (Southern Italy). Estimates were then carried out at the national level and for each major geographical area (i.e. North, Center and South). Larynx cancer age-standardized incidence rates increased for men by about 25% from 1970 to 1987. Age-specific rates increased for ages greater than 44 years, but decreased for younger ages. Cohort effects are low for older cohorts; they steeply increase and plateau for the 1900-1905 cohorts, and then peak for the 1930 cohort. The risk for cohorts born after 1930 systematically decreases. We estimated that the 1930 birth cohort has a risk five times higher than the 1890 cohort. For women, the incidence rates increased by about 30% from 1970 to 1987, for all age classes. Cohort effects steadily increase from the 1886 birth cohort to the 1960 cohort. The estimated prevalence between ages 30 and 84 increased from about 24,400 cases in 1970 (23,000 males and 1,400 females) to about 51,400 cases in 1987 (48,600 males and 2,800 females). For men, 42% of the increase can be attributed to an increase in the incidence of the disease; 45% can be attributed to population aging, and only 13% to an increase in the survival probability. Corresponding figures for women are 42%, 48%, and 10%. For lung cancer, we estimated 32,000 incident cases for 1987 (28,000 men and 4,000 women), two times the corresponding figures for 1970 (14,000 men and 2,000 women). Looking at age-adjusted rates, the overall risk of lung cancer increased by about 60% for men and 52% for women during a period of 17 years. Age-specific incidence rates increased proportionally with age for ages greater than 50 years. By contrast, there was a slight but systematic risk reduction in younger age classes.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1991

Arginine reinstates the somatotrope responsiveness to intermittent growth hormone-releasing hormone administration in normal adults.

It is well known that in normal adults the growth hormone (GH) response to GH-releasing hormone (GHRH) is inhibited by previous administration of the neurohormone. In 7 healthy volunteers (age 20-34 years) we studied the GH responses to two consecutive GHRH boluses (1 microgram/kg i.v. every 120 min) alone or coadministered with arginine (30 g i.v. over 30 min). The GH response to the first GHRH bolus (area under the curve, mean +/- SEM: 506.3 +/- 35.1 micrograms/l/h) was higher (p = 0.0001) than that to the second one (87.1 +/- 14.6 micrograms/l/h). The latter response was clearly increased (p = 0.0001) by coadministering arginine (980.5 +/- 257.5 micrograms/l/h). When every GHRH bolus was combined with arginine a marked potentiation of GH response to both boluses was found. However, the second combined administration of arginine and GHRH induced a GH increase which was lower compared to the first one (p = 0.016). In conclusion, our results show that arginine potentiates the GHRH-induced GH secretion preventing the lessening of somatotrope responsiveness to the neurohormone alone. As there is evidence that this phenomenon is due to an enhanced somatostatin release, these findings give further evidence of a somatostatin-suppressing effect of arginine.

Adult↗
PubMed1990

Arginine potentiates the GHRH- but not the pyridostigmine-induced GH secretion in normal short children. Further evidence for a somatostatin suppressing effect of arginine.

To investigate the mechanism underlying the GH-releasing effect of arginine (ARG), we studied the interactions of ARG (0.5 g/kg infused i.v. over 30 min) with GHRH (1 microgram/kg i.v.) and with pyridostigmine (PD, 60 mg orally) on GH secretion in 15 children and adolescents with familial short stature (5.1-15.4 years). In a group of eight subjects ARG induced a GH increase not statistically different to that observed after GHRH (peak, mean +/- SEM: 38.0 +/- 10.4 vs 64.0 +/- 14.4 mU/l). The combined administration of ARG and GHRH led to GH levels (101 +/- 15.2 mU/l) higher than those observed after GHRH (P less than 0.025) or ARG alone (P less than 0.001) and overlapping with those recorded after combined PD and GHRH administration (111 +/- 22.4 mU/l). In the other seven subjects, ARG and PD administration induced a similar GH response either when administered alone (25.2 +/- 13.6 and 27.8 +/- 4.0 mU/l, respectively) or in combination (33.8 +/- 5.4 mU/l). In conclusion, our results show that in children ARG administration potentiates GHRH- but not PD-induced GH increase. These findings agree with the hypothesis that the GH-releasing effect of both ARG and PD is mediated via the same mechanism, namely, by suppression of endogeneous somatostatin release. Combined administration of either ARG or PD with GHRH has a similar striking GH-releasing effect which is clearly higher than that of GHRH alone.

Adolescent↗
PubMed1990

Growth hormone (GH) responsiveness to combined administration of arginine and GH-releasing hormone does not vary with age in man.

At present, the mechanism(s) underlying the reduced spontaneous and stimulated GH secretion in aging is still unclear. To obtain new information on this mechanism(s), the GH responses to both single and combined administration of GH-releasing hormone (GHRH; 1 microgram/kg iv) and arginine (ARG; 30 g infused over 30 min), a well known GH secretagogue probably acting via inhibition of hypothalamic somatostatin release, were studied in seven elderly normal subjects and seven young healthy subjects. Basal GH levels were similar in both groups, while insulin-like growth factor-I levels were lower in elderly subjects (76.7 +/- 9.2 vs. 258.3 +/- 29.2 micrograms/L; P = 0.01). In aged subjects GHRH induced a GH increase (area under the curve, 314.9 +/- 91.9 micrograms/L.h) which was lower (P = 0.01) than that in young subjects (709.1 +/- 114.4 micrograms/L.h). On the other hand, the ARG-induced GH increase in the elderly was not significantly different from that in young subjects (372.8 +/- 81.8 vs. 470.6 +/- 126.5 micrograms/L.h). ARG potentiated GH responsiveness to GHRH in both elderly (1787.1 +/- 226.0 micrograms/L.h; P = 0.0001 vs. GHRH alone) and young subjects (2113.0 +/- 444.3 micrograms/L.h; P = 0.001 vs. GHRH alone). The potentiating effect of ARG on the GHRH-induced GH response was greater in elderly than in young subjects (1013.0 +/- 553.5% vs. 237.9 +/- 79.1%; P = 0.0001); thus, the GH increase induced by combined administration of ARG and GHRH overlapped in two groups. In conclusion, these results show that, differently from the GHRH-induced GH increase, the somatotroph response to combined administration of ARG and GHRH does not vary with age. Our finding suggests that an increased somatostatinergic activity may underlie the reduced GH secretion in normal aging.

Adult↗