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Biomedical subjects

A Giampietro

Publications and source records attributed to A Giampietro.

11 recordsLinked to original sources
PubMed2005

Coenzyme Q10 evaluation in pituitary-adrenal axis disease: preliminary data.

In previous works we have demonstrated plasma CoQ10 alterations in pituitary diseases, such as acromegaly or secondary hypothyroidism. However, pituitary lesions can induce complex clinical pictures due to alterations of different endocrine axes controlled by pituitary itself. A further rationale for studying CoQ10 in pituitary-adrenal diseases is related to the common biosynthetic pathway of cholesterol and ubiquinone. We have therefore assayed plasma CoQ10 levels in different conditions with increased or defective activity of pituitary-adrenal axis (3 subjects with ACTH-dependent adrenal hyperplasia, 2 cases of Cushing's disease and 1 case of 17-alpha-hydroxylase deficiency; 10 subjects with secondary hypoadrenalism, including three subjects with also secondary hypothyroidism). CoQ10 levels were significantly lower in isolated hypoadrenalism than in patients with adrenal hyperplasia and multiple pituitary deficiencies (mean +/- SEM: 0.57 +/- 0.04 vs 1.08 +/- 0.08 and 1.10 +/- 0.11 microg/ml, respectively); when corrected for cholesterol levels, the same trend was observed, but did not reach statistical significance. These preliminary data indicate that secretion of adrenal hormones is in some way related to CoQ10 levels, both in augmented and reduced conditions. However, since thyroid hormones have an important role in modulating CoQ10 levels and metabolism, when coexistent, thyroid deficiency seems to play a prevalent role in comparison with adrenal deficiency.

Adrenal Gland Diseases↗
PubMed2004

Growth hormone secretion and leptin in morbid obesity before and after biliopancreatic diversion: relationships with insulin and body composition.

Obesity is characterized by increased leptin levels and insulin resistance, whereas blunted GH secretion is paired with normal, low, or high plasma IGF-I levels. To investigate body composition in human obesity and the interactions among the GH-IGF-I axis, leptin, and insulin resistance [measured with the homeostasis model assessment (HOMA) score], we studied 15 obese females, aged 23-54 yr (mean age, 42.7 +/- 2.6), with a body mass index (BMI) of 44.02 +/- 1.45 kg/m(2), who underwent treatment by biliopancreatic diversion (BPD), before and after surgery (16-24 months; BMI, 28.29 +/- 0.89 kg/m(2)). Our controls were 15 normal females, aged 28-54 yr (mean age, 40.8 +/- 2.3 yr), with a BMI of 27.52 +/- 0.53 kg/m(2). Insulin and leptin levels and HOMA scores were higher pre-BPD than in the controls. The GH response to GHRH was blunted, with a GH peak and GH area under the curve (AUC) significantly lower than those in controls. IGF-I and IGF-binding protein-3 (IGFBP-3) were also lower than control values. After surgery, BMI, fat mass, lean body mass, HOMA, insulin, and leptin significantly decreased. Furthermore, the GH response to GHRH severely increased; IGF-I and IGFBP-3 levels did not significantly vary. Considering all subjects, correlation analysis showed a strong positive correlation between insulin and leptin, and a negative correlation between insulin and GH peak and between insulin and GH AUC. Regression analysis performed grouping pre- and post-BPD indicated that leptin and GH peak or AUC could best be predicted from insulin levels. The surgical treatment of severe obesity after stabilization of body weight decreases BMI and fat mass while preserving normal lean body mass as well as positively influencing insulin sensitivity and thus aiding the normalization of leptin levels. The insulin reduction may be mainly involved in the increase in the GH response to GHRH through various possible central and peripheral mechanisms while decreasing the peripheral sensitivity to GH itself, as shown by the stable nature of the IGF-I and IGFBP-3 values. Our findings suggest that the changes in insulin levels are the starting point for changes in both leptin levels and the somatotrope axis after BPD.

Adipose Tissue↗
PubMed2002

Preoperative growth hormone response to thyrotropin-releasing hormone and oral glucose tolerance test in acromegaly: a retrospective evaluation of 50 patients.

The objective of this study was to investigate the relationship between growth hormone (GH) dynamic tests (thyrotropin-releasing hormone [TRH] test and oral glucose tolerance test [OGTT]), insulin-like growth factor-I (IGF-I) plasma values, tumor size, and clinical outcome in patients with GH-secreting pituitary adenomas. Furthermore, we investigated the potential prognostic utility of the above biochemical parameters in the follow-up of patients with acromegaly. We studied 50 acromegalic patients (18 males and 32 females; mean age, 40 years; range, 16 to 69) who underwent trans-sphenoidal removal of a GH-secreting pituitary adenoma from 1990 to 1994. Preoperatively, we evaluated (1) GH plasmatic levels after an oral glucose load (OGTT) (blood samples were drawn at -15, 0, 30, 60, 90, 120, 150, and 180 minutes after oral administration of 0.75 g/kg body weight [BW] of glucose), (2) GH plasma levels after a TRH test (200 microg as an intravenous [IV] bolus), and (3) basal IGF-I plasma levels after an overnight fast. From 3 to 12 months after surgery we evaluated (1) GH plasma values after an OGTT, and (2) basal plasma IGF-I, free triiodothyronine (FT(3)), free thyroxine (FT(4)), thyroid-stimulating hormone (TSH), and urinary free cortisol. The same tests were performed every year for 5 years. All of the patients were classified into 4 subgroups according to the system of Hardy and Vezina. Preoperatively, "controlled" patients (n = 29) had a GH paradoxical response to TRH (n = 28) and an unresponsiveness to OGTT (n = 29); 23 of them belonged to the I and II classes. Only 5 poorly controlled patients (n = 21) showed a preoperative paradoxical response to TRH and 9 had a preoperative GH partial inhibition after OGTT; 19 of them belonged to the III and IV classes. Our data suggest that in the preoperative period in acromegalic patients the simultaneous presence of a GH paradoxical response to TRH and lack of GH inhibition after OGTT is inversely related to the tumor size and therefore more likely to be restored to normal by surgical treatment.

Acromegaly↗
PubMed2001

Opioid dysregulation after biliopancreatic diversion: effect of naloxone on preprandial and postprandial growth hormone (GH)-releasing hormone-induced GH release in surgically induced weight loss.

Previously, we have shown that in the opposite extremes of nutritional status (obesity and anorexia nervosa [AN]), the growth hormone (GH) response to GH-releasing hormone (GHRH) is not inhibited by the ingestion of a normal 800-kcal meal at noon. In obese subjects, GHRH-induced GH release is significantly increased (known as the "paradoxical response"). An opiate antagonist infusion (naloxone [NAL]) inhibited this postprandial meal-induced augmenting effect in obese subjects, suggesting opioid involvement in the paradoxical response. The paradoxical postprandial GH release persisted in obese subjects, who after biliopancreatic diversion (BPD) experienced a reduction in body weight, despite the elevation of fasting GH levels. We therefore tested a group of patients, before and after BPD, composed of 10 females, aged 23 to 54 years, who after surgery had experienced a significant reduction in body weight (mean body mass index [BMI], 25.78 +/- 1.01 kg/mg v 44.68 +/- 1.73 kg/mg). The subjects were studied 16 to 24 months after operation, in a phase of stabilized body weight. They underwent, in randomized order, the following tests: GHRH (1 microg/kg as an intravenous [IV] bolus) at 1:00 PM, in the fasting state; GHRH (1 microg/kg) at 1:00 PM, 45 minutes after a standard 800-kcal meal consumed between noon and 12:15 PM; and fasting state and postprandial GHRH (1 microg/kg) during NAL infusion (1.6 mg/h x 2.5 h, starting at noon). We found that NAL inhibited the paradoxical postprandial GH increase only in pre-BPD subjects (GH area under the concentration time curve [AUC] in microg/L/90 min)-before meal: after GHRH 237.54 +/- 62.28, after NAL + GHRH 699.2 +/- 271.57; after meal: after GHRH 575.46 +/- 109.68, after NAL + GHRH 156.17 +/- 24.96. On the other hand, NAL failed to have significant effects in post-BPD subjects (GH AUC in microg/L/90 min)-before meal: after GHRH 871.11 +/- 256.38, after NAL + GHRH 449.19 +/- 119.13; after meal: after GHRH 1,981.54 +/- 319.92, after NAL + GHRH 1,665.91 +/- 315.4. It could be hypothesized that the opioid system is radically modified by the surgical procedure, and that opioids are not the only mediators in the paradoxical response, which persists after BPD, despite the reversion of the hyposecretory GH state, which is a characteristic of obese subjects.

Adult↗
PubMed2000

Role of food intake in the modulation of hexarelin-induced growth hormone release in normal human subjects.

Hexarelin (HEX) is a new synthetic analog of the Growth Hormone releasing peptides and is stronger than GHRH in releasing GH in vivo. No information is available on the effect of food ingestion on HEX-induced GH secretion. On the other hand, we have previously demonstrated that food intake at lunchtime in normal subjects has an inhibitory effect on the GH response to GHRH. The aim of the present study was to investigate the effect of food ingestion on GH secretion induced by HEX as compared to GHRH in six normal men (aged 23-29 years) and six normal women (aged 24-29 years). The body weights for all subjects were within 120% of their ideal body weight, according to their sex and age. Our data confirm that HEX is much more powerful than GHRH in inducing GH release in humans, both in the fasting state (GH-AUC: 3010 +/- 695 after HEX, vs. 1339 +/- 281 after GHRH, microg/L/120 min; p<0.06) and after a meal (GH-AUC: 1523 +/- 121, after HEX, vs. 309 +/- 61, after GHRH, microg/L/120 min; p<0.06). Moreover, our study shows that food intake partially blunts the fasting GH response to HEX (GH-AUC: 3010 +/- 695 after HEX, in fasting state, vs. 1523 +/- 121 after HEX, after meal, microg/L/120 min; p<0.06; mean inhibition of AUC 41.02 +/- 7.96%), whereas it nearly abolishes the GH response to GHRH in the same subjects (GH-AUC: 1339 +/- 281 after GHRH, in fasting state, vs. 309 +/- 61 after GHRH, after meal, microg/L/120 min; p<0.06; mean inhibition of AUC 70.31 +/- 6.22%). In conclusion, our study confirms that HEX acts differently from GHRH; the GH releasing effect of HEX could be only partially influenced by the physiological metabolic or neuroendocrine food-related modifications.

Adult↗
PubMed2000

Inhibitory action on GHRH-induced GH secretion of chronic tamoxifen treatment in breast cancer.

OBJECTIVE: Previous in vitro and in vivo studies on animal models have demonstrated that tamoxifen (TAM) inhibits GH secretion. Studies in humans are conflicting. The aim of this study was to evaluate the effect of chronic TAM treatment on GH secretory dynamics in the presence of negligible endogenous oestrogens, in postmenopausal women with breast cancer. PATIENTS: Ten female patients were studied over a 6-12-month period after surgical therapy, before medical therapy, and during chronic treatment with TAM (20 mg/day p.o.). MEASUREMENTS: In all subjects we performed a standard GHRH-test (50 mg i.v. as a bolus) and compared the single time points, the peak response and the areas under the curves (AUC), before and during treatment. In basal samples, we evaluated the circulating levels of IGF-1, IGF-BP3 and their ratio, SHBG, FSH, LH, Oestradiol (E2) and PRL. GH was assayed by Immunoradiometric assay (IRMA). Insulin-like growth factor type I (IGF-I), Insulin-like growth factor-binding protein-3 (IGF-BP3), FSH, LH and PRL were measured by Radioimmunoassay (RIA). SHBG was measured by a noncompetitive liquid phase immunoradiometric assay, while E2 was measured directly in plasma by a liquid phase technique. RESULTS: TAM chronic treatment significantly reduced GH response to GHRH at single time point evaluations, GH peak response (mean decrease: 59.8 +/- 7.3%) and GH-AUC (mean decrease 53.8 +/- 8.9%). TAM also significantly reduced plasma IGF-1 levels. No significant variations were found in IGF-BP3 levels or in the IGF-1/IGF-BP3 ratio. A significant inverse correlation between SHBG and IGF-1 circulating levels was noticed during TAM treatment. CONCLUSIONS: Our data show that long-term tamoxifen treatment blocks the response of GH to exogenous GHRH and reduces IGF-1 levels, possibly by a central mechanism other than the demonstrated peripheral action. The results of this study, keeping in mind the demonstrated mitogenic role of IGF-1 in cancer proliferation, can contribute to clarify the mechanism by which TAM exerts its antiproliferative effect.

Aged↗
PubMed1991

Amplifications of multiple regions of the HTLV-I genome from DNA of an Italian spastic paraparesis patient but not from DNA of multiple sclerosis patients.

We searched for evidence of infection by the human T-cell lymphoma/leukemia virus type I (HTLV-I) in patients with multiple sclerosis (40 cases); brainstem encephalitis (1 case); Friedreich's ataxia (1 case); spastic paraparesis of unknown etiology (1 case). All patients were from the region of Abruzzo, Italy. Sera were all negative for anti-HTLV-I reactivity by the Western blotting (WB) analysis. DNAs from peripheral blood mononuclear cells were amplified using the polymerase chain reaction (PCR) technique with primers specific for the HTLV-I gag, pol, and env proviral regions. HTLV-I sequences were amplified only in the patient with spastic paraparesis of unknown etiology. In this case, HTLV-I infection might have been related to blood transfusions received 2 years prior to the onset of the neurologic symptoms. Members of the patient's family were negative for HTLV-I by PCR and WB. These data indicate that HTLV-I associated myelopathy is present also in Italy, but fail to substantiate an association of HTLV-I with multiple sclerosis.

Adolescent↗
PubMed1991

CD21+ (B2 antigen+) cell decrement and CD4+CD29+ (helper-inducer) cell increment suggest an activation of cell immune reactivity in multiple sclerosis.

Two-color flow cytometric analysis on peripheral blood lymphocytes of 35 untreated multiple sclerosis (MS) patients, 17 other medical disease (OMD) patients and 14 healthy control (HC) subjects was performed to evaluate the levels of different T and B cell subpopulations. In MS patients we observed an increase in CD4+CD29+ helper-inducer cells but this increase was not related to the different phases of the disease. We hypothesize that this change is related to the reduction of CD21+ cells expressing B2 antigen, a 140 kDa molecule disappearing after B cell activation. An increased level of CD4+CD45RA- (helper-inducer-like cells) and a reduction of CD4+CD29- (suppressor-inducer-like cells) were also present in our patients. These findings demonstrate an immune 'disequilibrium' in MS, which is linked with an increased level of CD25+ cells expressing the interleukin-2 (IL-2) receptor. IL-2, besides being a T cell growth factor, is also a B cell growth factor. These data let us hypothesize that an activation of the immune response is present in MS.

Adult↗
PubMed1991

Multiple sclerosis: an immune system activation disease.

Two-color flow-cytometric analysis on peripheral blood lymphocytes of 46 untreated multiple sclerosis patients (MS), 36 other medical disease patients (OMD) and 19 healthy control subjects (HC) was performed to know the relationships between T and B cell subpopulations. In MS patients we observed an increase of total lymphocyte count and an increase of CD4+CD29+ cells, which are adjuvant to B cell in antibody production. We hypothesized this change is related to the reduction of CD21+ cells, expressing B2 antigen which disappears after B cell activation. The unperfect balance of immune system in MS was also demonstrated by the increased level of CD25+ cells in relapsing-remitting patients and by the decreased level of CD4+ CD45RA+ (suppressor inducer) cells in progressive patients.

Adult↗