Pecori Giraldi F.,University of Milan |
Toja P.M.,University of Milan |
Filippini B.,University of Milan |
Michailidis J.,Ospedale San Luca IRCCS |
And 3 more authors.
International Journal of Andrology | Year: 2010
Symptoms and signs of male hypogonadism span all organ systems, including the cardiovascular apparatus. The electrocardiographic QT interval reflects cardiac ventricular repolarization and, if prolonged, increases the risk of malignant arrhythmias. QT interval duration is similar in boys and girls during childhood, but shortens in males after puberty and experimental studies suggest that testosterone is a major contributor to shortening of QT interval in men. The aim of the present pilot study was to assess the duration of ventricular repolarization in adult males with primary or secondary hypogonadism. Standard ECG recordings were performed in 26 men (mean age 39.2 ± 2.17 years) with pituitary or testicular hypogonadism and repeated in 15 patients during testosterone replacement. Twenty-six age-matched control men were also analysed. Measured QT intervals were corrected for heart rate according to Bazzett's formula (QTc = QT/√RR interval). The prevalence of prolonged QTc was considerably higher in hypogonadal patients (four of 26 men) than in control men (none, p < 0.05) and in the general, healthy population (<2.5%). QTc interval normalized on hormone replacement therapy in the four patients presenting prolonged QTc in the hypogonadal state. Heart rate and left ventricular mass did not differ among the two groups and no known QT-prolonging factor was apparent in patients with abnormal QTc interval. In conclusion, a high number prolonged QT interval measurements was observed in hypogonadal men who may therefore be at increased risk for cardiac arrhythmias. This observation reveals an additional feature of male hypogonadism, which may benefit from testosterone replacement therapy. © 2010 European Academy of Andrology. Source
Seravalle G.,Ospedale San Luca IRCCS |
Carzaniga C.,University of Milan |
Attanasio R.,Istituto Galeazzi |
Grassi G.,University of Milan Bicocca |
And 12 more authors.
Clinical Endocrinology | Year: 2012
Objective Sympathovagal imbalance has been shown in acromegaly by indirect measurements of adrenergic tone. Data regarding direct measurement of sympathetic activity are lacking as yet. Aim of this study was to assess the adrenergic tone through direct recording of muscle sympathetic nerve activity (MSNA) in acromegalic patients. Design Fifteen patients (age 26-66 years, eight women) with newly diagnosed active acromegaly without hyperprolactinaemia, pituitary hormone deficiencies, obstructive sleep apnoea and cardiac hypertrophy, and 15 healthy subjects matched for age, sex and body mass index were recruited. After evaluating anthropometric and echocardiographic parameters, anterior pituitary function, glucose and lipid metabolism, and measuring plasma leptin, direct recording of sympathetic outflow via the microneurographic technique was performed. Results For similar anthropometric and metabolic parameters in patients and controls, HOMA index was significantly increased in the former (4.2 ± 2.39 vs 1.6 ± 0.19, P < 0.001). Surprisingly, this finding of insulin resistance was accompanied by a marked sympathetic inhibition (MSNA 18.3 ± 8.10 vs 37.3 ± 6.48 bursts/min, P < 0.0001, respectively in patients and controls). A reduction in plasma leptin (1.6 ± 1.04 vs 6.5 ± 2.01 μg/l, P < 0.0001) was also recorded in the patients. MSNA was positively correlated with leptin (P < 0.0001). Conclusions Newly diagnosed acromegalic patients without cardiac hypertrophy display a decreased sympathetic outflow in spite of insulin resistance. This finding might be related to hypoleptinaemia. © 2012 Blackwell Publishing Ltd. Source
Scacchi M.,University of Milan |
Danesi L.,Ospedale San Luca IRCCS |
Cattaneo A.,University of Milan |
Sciortino G.,University of Milan |
And 16 more authors.
Endocrine | Year: 2016
Previous evidence supports a role for growth hormone (GH)–insulin-like growth factor (IGF)-I deficiency in the pathophysiology of osteopenia/osteoporosis in adult thalassemia. Moreover, serum IGF-II has never been studied in this clinical condition. Thus, we elected to study the GH secretory status and the levels of circulating somatomedins, correlating these parameters with bone mineral density (BMD) and biochemical markers of bone turnover. A hundred and thirty-nine normal weight adult thalassemic patients (72 men and 67 women) were studied. Lumbar and femoral neck BMD were measured in 106/139 patients. Sixty-eight patients underwent growth hormone releasing hormone plus arginine testing. Measurement of baseline IGF-I and IGF-II was performed in all patients, while osteocalcin, C-terminal telopeptide of type I collagen (CTx), and urinary cross-linked N-telopeptides of type I collagen (NTx) were assayed in 95 of them. Femoral and lumbar osteoporosis/Z score below the expected range for age were documented in 61.3 and in 56.6 % of patients, respectively. Severe GH deficiency (GHD) was demonstrated in 27.9 % of cases, whereas IGF-I SDS was low in 86.3 %. No thalassemic patients displayed circulating levels of IGF-II below the reference range. GH peaks were positively correlated with femoral, but not lumbar, Z score. No correlations were found between GH peaks and osteocalcin, CTx and NTx. GH peaks were positively correlated with IGF-I values, which in their turn displayed a positive correlation with osteocalcin, CTx, and NTx. No correlations emerged between IGF-I values and either femoral or lumbar Z scores. No correlations were found between IGF-II and any of the following parameters: GH peaks, osteocalcin, CTx, NTx, femoral Z score, and lumbar Z score. Our study, besides providing for the first time evidence of a normal IGF-II production in thalassemia, contributes to a better understanding of the involvement of the somatotropin-somatomedin axis in the pathophysiology of bone demineralization in this disease. In particular, the contribution of GHD to femoral osteoporosis appears to be likely mediated by locally produced rather than circulating IGF-I. © 2016 Springer Science+Business Media New York Source
Pecori Giraldi F.,University of Milan |
Toja P.M.,University of Milan |
Michailidis G.,Ospedale San Luca IRCCS |
Metinidou A.,Ospedale San Luca IRCCS |
And 4 more authors.
Experimental and Clinical Endocrinology and Diabetes | Year: 2011
Hypogonadal males have recently been shown to present prolonged QT interval, an electrocardiographic measure indicative of risk for fatal cardiac arrhythmias. Excess cortisol secretion induces low testosterone levels in male patients with Cushing's disease but no study has yet evaluated if this is accompanied by changes in QT interval duration. We therefore decided to evaluate whether male patients with Cushing's disease present changes in QT interval duration. QT interval was measured in electrocardiographic readings from 19 men and 35 women with Cushing's disease and age- and sex-matched controls were used for comparison. QT interval was corrected for heart rate according to Bazett's formula (QTc) and QTc >440 msec and >460 msec were taken as indicative of increased risk for torsade de pointes in men and women, respectively. Mean QTc was significantly longer in male patients compared with healthy controls (426.9±9.27 vs. 389.7±8.31, p<0.05) and 5 men with Cushing's disease presented prolonged QTc (prevalence 26%). By comparison, none of the women with Cushing's disease presented prolonged QTc. Hypokalemia and low testosterone appeared associated with long QTc. Conclusions: Male patients with Cushing's disease present prolongation of QT interval which may lead to measurements associated with high risk for ventricular arrhythmias. Both low testosterone levels and hypokalemia appear to contribute to long QT in men with Cushing's disease. © J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart · New York. Source