Background: Adipose tissue has been suggested to influence bone density and metabolism through the effect of some adipokines. However, whether adiponectin and visfatin may correlate with bone metabolism is still unclear. Aim: The aim of this study was to investigate the relationship of adiponectin and visfatin with bone density in patients with metabolic syndrome (MS). Subjects: We enroled 72 consecutive patients with MS (25 males, 47 females; mean age 58.14±11 yr) and 40 control subjects. Methods: Plasma adiponectin and visfatin levels were measured. Bone mineral density (BMD) was assessed by dual energy X-ray absorptiometry (DXA) at the level of lumbar spine L2–L4 (BMD L2–L4) and femoral neck (BMD-Fn). Results: MS patients had higher plasma visfatin and lower adiponectin levels than controls, (p<0.01 for both). Adiponectin was negatively correlated with BMD-Fn and BMD L2–L4 (r=−0.20, r=−0.24, respectively; p<0.05 for both) whereas plasma visfatin levels were positively correlated to BMD L2–L4 only in men (r=0.44; p<0.05). Conclusions: Our study shows that adiponectin and visfatin are oppositely associated with BMD. Although the mechanisms behind these correlations are unclear, a modulation of bone metabolism by these adipokines can be suggested.

Petramala, L.; Formicuccia, M. C.; Zinnamosca, L.; Cotesta, D.; Marinelli, C.; Sciomer, S.; Cavallaro, G.; De Toma, G.; Letizia, C.Author Information

A case of adrenal ganglioneuroma incidentally discovered during an abdominal ultrasound examination in a 26 year-old woman patient with recurrent episodes of dysuria. After a diagnostic work-up with laboratory and abdomen CT scan, the patient uderwent a laparotomic removal of the adrenal lesion. Histopathological examination of the adrenal mass confirmed the diagnosis.

Primary aldosteronism (PA) with synchronous carcinoid syndrome is extremely rare occurrence. In this article, we describe a case of PA due to adrenocortical adenoma (“aldosteronoma”) and concurrent malignant carcinoid tumor of ileum. The patient was treated with synchronous right adrenalectomy and resection of the ileum. This case is an example of concomitant presence of two types of tumors, effectively managed surgically. We report a case of a nonclassical form of multiple endocrine neoplasia type 1 (MEN 1) syndrome.

Obstructive sleep apnoea (OSA) is a sleep disorder characterized by recurrent episodes of oxygen desaturation during sleep, representing an independent risk factor for cardiovascular disease, such as myocardial infarction, stroke, congestive heart failure and resistant hypertension. Several neurohormonal mechanisms have been suggested to account for blood pressure increases, such as sympathetic nervous system hyperactivity, oxidative stress, renin—angiotensin—aldosterone system (RAAS) activation, endothelin system activation, and endothelial dysfunction. The aim of this study was to evaluate the behaviour of RAAS and the presence of primary aldosteronism (PA) in these patients and possible correlations between RAAS and the severity of OSA. From October 2007 to November 2008 we studied 325 consecutive newly diagnosed hypertensive patients; 71 patients (21.8%) presented with clinical signs of sleep disorders, evaluated also through a specific questionnaire (Epworth Sleepiness Scale). In hypertensive patients with sleep disorders, 53 patients were affected by OSA; in this group 18 patients were affected by PA (five with aldosterone-producing adenoma (APA) and 13 with bilateral hyperplasia (IHA)); obesity was also demonstrated (BMI >" xbd="961" xhg="938" ybd="2430" yhg="2403"/> 30 kg/m2). Overall, in patients with OSA PRA levels correlated positively with apnoea/hypopnoea index (AHI; r = 0.35; p<0.01), and in all groups the waist circumference and the neck circumference were correlated positively with AHI ( r = 0.3 p<0.02 and r = 0.3 p<0.03, respectively). We revealed a high prevalence of PA in patients with OSA, and we can conclude that patients with hypertension and OSA, especially those who are newly diagnosed, must be evaluated for PA.

BACKGROUND:Patients with primary hyperparathyroidism (pHPT) show an increased bioelectrical risk not related to cardiovascular complications, this risk seems to persist after surgery and this last finding is still controversial and probably related to follow-up length.METHODS:The aim of the study is to evaluate QT parameters in 11 patients with primary hyperparathyroidism (pHPT) 18 months after parathyroid surgery using computed standard 12-leads ECG compared to those of 29 healthy subjects (HS).RESULTS:In pHPT patients, 4 months after parathyroidectomy QT and QTc dispersion persist significantly higher than HS. 18 months after surgery, QT and QTc dispersion resulted comparable with HS. QT dispersion was found significantly higher in pHPT at 4 months respect 18 months after parathyroidectomy.CONCLUSIONS:ECG alteration after parathyroidectomy gradually return within normal limits and we can affirm that surgery erase bioelectrical risk in pHPT.

Background: Pheochromocytoma (pheo) and paraganglioma are rare tumours of neuroectodermal origin. Adipose tissue is considered an endocrine organ able to produce adipokines that plays a very important role in homeostasis of the tissue itself and regulation of several metabolic pathways and inflammation. Aim: to evaluate in a series of pts with pheo antropometric parameters and circulating levels of adipokines (visfatin and adiponectin) comparing these with those of a group of subjects with essential hypertension (EH) and healthy subjects (HS) matched for age and sex. Material and Methods: 11 pts with pheo (5M-6F age 55,6 ± 14 yrs), 25 EH (12M-13F, 53 ± 6 yrs), 20 HS (8M-12F, 55,7 ± 6 years). Anthropometrics data, fasting venous blood samples for medical routine and lipids profile, electrocardiogram, 2-D echocardiography, ABPM 24 hours were obtained from all subjects. In all patients were obtained samples to determine plasmatic levels of adiponectin and visfatin. Results: EH have higher (p <0,001) WC and BMI values respect to pheo and HS. Pheo and EH present higher blood pressure levels with statistical differences (p < 0,001) respect to HS. Adiponectin levels (12,6 ± 5,4 μg/ml) result lower in EH (p < 0,001) compared to those in pheo and HS (24,2 ± 16 and 22,4 ± 8 respectively) while visfatin levels were higher (p < 0,002) in EH (27 ± 16 μg/ml) respect those in pheo and HS (14 ± 10 and 12,2 ± 4,2 μg/ml respectively). The study of correlations show a negative correlation between adiponectin and glicemia, (r: -0,607; p < 0,0047), visfatin and LDL cholesterol (r: -0,652; p < 0,0028) in pheo pts, furthermore in this group we found a positive correlation between VMA and adiponectin (r:0,6; p < 0,0048). The echocardiografic study shows that both pheo pts and EH have cardiac remodeling due to hypertensive status.Study of correlations shows negative correlation between circulating levels adiponectin and left atrium diameter in pheo pts (r: -0,827; p < 0,0016). Conclusions: Activation of sympathetic nervous system via â 3 adrenoreceptors due to catecholamine overproduction in patients with pheo could explain modification in adipokines concentration, although further studies are requested to demonstrate this hypothesis.

PURPOSE:The aim of this study was to investigate the behaviour of plasma endothelin-1 (ET-1) levels in patients affected by retinitis pigmentosa (RP) and syndromic RP. METHODS:Blood samples were obtained from a group of 40 consecutive patients with RP matched with 35 healthy subjects (HS) as control. We carried out a complete ophthalmological examination. The study group included 26 patients with RP and 14 patients with syndromic RP. Plasma ET-1 levels were determined in duplicate with a specific radioimmunoassay method. RESULTS:In the HS plasma ET-1 levels were 7.48+/-2.58 pg/mL. The mean of plasma ET-1 concentrations in all patients with RP ( 16.2+/-5.6 pg/mL) was significantly (P<0.01) higher than that of HS. Moreover, in the syndromic RP patients, plasma ET-1 levels (18.9+/-6.8 pg/mL) were higher than those of HS and RP patients (P<0.01). CONCLUSION:The increase of plasma ET-1 levels in RP patients suggests that ET-1 may play a role in the pathophysiology of the diseases involving retinal pigment epithelial cells and the retinal vascular system such as RP.

CONTEXT:Primary aldosteronism (PA) has been recently associated with an unfavorable cardiometabolic profile. However, whether pro- and antiinflammatory adipokines levels can vary in PA is unknown.OBJECTIVE:We evaluated the circulating levels of resistin, leptin, and adiponectin, echocardiographic left ventricle (LV) parameters, and the prevalence of metabolic syndrome (SM) in subjects with PA.PATIENTS:Seventy-five subjects with established diagnosis of PA and 232 consecutive individuals with known or suspected hypertension were enrolled.MAIN OUTCOME MEASURES:Plasma adipokine levels and echocardiographic parameters were calculated. Prevalence of SM was also estimated.RESULTS:Among the 75 PA subjects, 37 patients were affected by aldosterone-producing adenoma and 38 by idiopathic hyperaldosteronism; 40 subjects were affected by essential hypertension (EH) and SM (EH SM+); 152 subjects were affected by EH without SM (EH SM-); and 40 subjects were normotensive (NT). Subjects with PA had the highest plasma resistin levels among the four groups (P < 0.01). Plasma resistin concentration was significantly higher in PA subjects when compared with EH SM+ individuals (P < 0.01) and EH SM- subjects (P < 0.01). PA subjects showed the higher LV mass and left atrium than EH individuals, irrespectively of the presence of SM (P < 0.01 for both). Plasma resistin levels was significantly correlated with ejection fraction and LV end-diastolic volume. The prevalence of SM was higher in PA subjects than in those with EH (25.4 vs. 20.3%).CONCLUSIONS:Our data suggest that elevated aldosterone levels is associated with elevated circulating resistin levels and cardiac morphological changes independently of the presence of SM.

The aim of the study was to test 1) whether chronic and stable coronary artery disease (CAD) could downregulate epicardial fat adrenomedullin synthesis and secretion, and decrease intracoronary plasma adrenomedullin levels, and 2) whether intracoronary plasma adrenomedullin levels could be related to epicardial adipose tissue adrenomedullin gene and protein expression in subjects with CAD. We examined 12 patients with CAD who required coronary artery bypass graft (CABG) and 10 patients with non-CAD who underwent cardiac surgery for valve replacement. Plasma levels of adrenomedullin were measured in peripheral vein circulation, in left coronary artery (LCA) and coronary sinus (CS) during coronary angiography. Epicardial adipose tissue biopsy for Reverse Transcription and Real-Time PCR (RT-PCR) adrenomedullin mRNA analysis and Western Blotting (WB) protein expression was performed during cardiac surgery in all subjects. Peripheral, LCA, and CS plasma adrenomedullin levels were significantly lower in CAD patients than in those with non-CAD (3.0+/-0.9 vs. 4.4+/-0.9 pg/ml p<0.01; 2.9+/-1 vs. 4.05+/-0.8 pg/ml, p<0.01, 3.1+/-0.9 vs. 3.98+/-0.9 pg/ml p=0.04, respectively). However, CS adrenomedullin levels were not statistically different than those in LCA suggesting that adrenomedullin was not secreted from epicardial fat into the coronary artery lumen. Epicardial fat adrenomedullin mRNA levels and protein expression were lower in patients with CAD than in those with non-CAD (p<0.01 for both). We conclude that 1) epicardial fat adrenomedullin gene and protein expression can be downregulated in CAD subjects, and 2) intracoronary adrenomedullin levels are lower in CAD. No evidence that epicardial adipose tissue really contributes intracoronary adrenomedullin can be provided at this time.

The aim of our study is to evaluate in Systemic Sclerosis (SSc) male patients the tadalafil effects on Raynaud's phenomenon and on AM and ET-1 plasma levels. In an open-label study 20 consecutive male patients with SSc were enrolled and received 10 mg of tadalafil daily for 12 weeks. The primary endpoint was the subjective reduction of frequency and duration of Raynaud's attacks measured with a 10-point Raynaud's Condition Score; the secondary aim was to modify Adrenomedullin (AM) and Endothelin-1 (ET-1) plasma levels. After the treatment Raynaud's phenomenon was improved by once-daily tadalafil (decrease of mean number of Raynaud's attacks and of Raynaud's Condition Score) and plasma AM and ET-1 levels decreased. The results of our study lead us to postulate the beneficial effect of adding long term inhibition of Phosphodiesterase type 5 to Systemic Sclerosis' therapy.

Introduction.Pheochromocytomas and paragangliomas are rare tumours with common embriogenetic origin, pheochromocytoma can be sporadic or syndromic.There are four different syndromes genetically determined (MEN 2, paraganglioma/pheochromocytoma syndrome, Von Hippel Lindau syndrome and neurofibromatosis type 1).Methods.We have evaluated in 93 patients with pheochromocytoma, the prevalence of syndromic forms and the prevalence of malignancy.Patients and methods: 93 patients with pheochromocytoma seen in the Day Hospital of Department of Clinical Sciences of "La Sapienza" University in Rome.A clinical story and a physical examination was made in all patients, a collection of 24 urine samples was obtained to determine metanephrine and acid vanylil mandelic (VMA).A CT scan of abdomen and/or a MR abdomen was performed to detect the presence of a mass and selected cases underwent a total body scintigraphy with I-131 MIBG.After an adequate medical preparation with alpha and betablockers patients underwent a surgical treatment with laparoscopic approach to remove the pheochromocytoma.A genetic analysis with study of susceptibility gene for pheochromocytoma (RET, VHL, NF1, SHDB/D) was performed in most of the patients.Results.Pheochromocyoma was sporadic in 77 cases (82%) (average age 45 years) and syndromic in 16 cases (18 %) (average age 38 years).MEN 2A was present in 5 cases (32% syndromic forms), VHL in 4 cases (25%), la NF1 in 4 cases (25%) and PGL 4 syndrome (SDHD) in 3 cases (18%).Pheocromocytoma was benign in 93% of cases, in 7% pheochromocytoma has a malignant nature.Conclusions.Our data are similar to those reported in literature and confirm the typical course of this disease.

The role of adiponectin and epicardial adipose tissue in coronary artery disease (CAD) is a subject of debate. Whether plasma adiponectin concentration in the coronary circulation is locally modulated by the epicardial fat is still unexplored. We evaluated the hypothesis whether intracoronary plasma adiponectin levels are related to adiponectin expression in epicardial adipose tissue in vivo in patients with CAD and without CAD (non-CAD). We examined 12 patients with CAD who required CABG and 10 patients with non-CAD who underwent cardiac surgery for valve replacement. Plasma levels of adiponectin were measured in peripheral vein circulation and in left coronary artery (LCA) during coronary angiography. Epicardial adipose tissue biopsy for adiponectin protein extraction was performed during cardiac surgery in both CAD and non-CAD subjects. Adiponectin protein expression in epicardial adipose tissue was lower in patients with CAD than in those with non-CAD (0.45+/-0.4 vs. 1.1+/-1.0, p<0.05). LCA plasma adiponectin levels significantly correlated with epicardial adipose tissue adiponectin protein expression (r=0.68, p=0.02) in all subjects. Peripheral adiponectin levels and epicardial fat adiponectin protein expression were the best correlates of LCA adiponectin, r (2)=0.49, p<0.01, p<0.05, respectively). Our study showed that intracoronary adiponectin levels reflect systemic adiponectin levels. Epicardial adipose tissue could partially contribute to adiponectin levels in the coronary circulation.

Aim.To evaluate the prevalence of metabolic syndrome (MS), according to ATP/NCEP 2001 criteria in patients with PA comparing to the prevalence of MS in patients with essential hypertension (EH), moreover the circulating levels of adipokines (leptin, adiponectin, resistin) have been evaluated in both groups.Methods.75 patients with PA (37 Males, 38 Females; age 52.9±11.4years, range 20-76 years), 40 healthy patients (HS) (24 M, 16 F, age 55.7 ± 6.1 years), 152 patients with EH without MS (80 M, 72 F, age 55.6 ± 12.4 years), 40 patients with EH and MS (22 M, 18 F, age 56.8±10.9years).Results.In 25.3% patients with PA was present MS, patients with PA and MS showed reduced levels of adiponectin (8.9±0.8 μg/ml) compared to patients with PA without MS (12±0.9μg/ml; p<0.05); in particular in the group of patients with idiopathic aldosteronism was found a correlation with the number of factors of MS and the levels of adiponectin (6.5±1.2 μg/ml 4 factors of MS vs 12.3±1.5 μg/ ml with 1 factor, p<0.05).In all the patients with PA and in the group of EH patients with MS have been found higher than those of HS (18.8±1.9 ng/ml, 16.9±2.4ng/ml, respectively vs 8.6±1.2 ng/ml; p<0.05).Circulating levels of resistin were higher in the group of PA patients respect to all the other groups (5.8±0.4 ng/ml vs 3.7±0.3ng/ml, 2.8±0.4 ng/ml, 2.1±0.5 ng/ml, respectively; p<0.05).In PA patients, was found a positive linear correlation between adiponectin and HDL cholesterol (r= 0.4; p<0.001).In the same group leptin was correlated with BMI (r=0.5;p<0.001) and with resistin (r=0.35;p<0.001).Conclusions.In patients with PA was found an high prevalence of MS, furthermore were found a significant reduction of adiponectin and elevated circulating levels of leptin and resistin.These metabolic alterations suggest a role of adipose tissue in the pathogenesis of metabolic syndrome in patients with primary aldosteronism.

Cushing's Syndrome (CS) may sometimes lead to dilated cardiomiopathy, even though this condition can be partially or completely reversed after treatment. In this article we report the case of a 28-yr-old woman with CS secondary to adrenal adenoma who exhibited congestive heart failure as an initial symptom. Two weeks before being admitted to our hospital, the patient started complaining of shortness of breath, orthopnea, paroxysmal nocturnal dyspnea and generalized edema. A physical examination did not reveal signs of hyper-cortisolism. Chest auscultation revealed bilateral diffused crepitation; blood pressure was 180/120 mmHg with heart rate of 90 beats/min. A chest Xray showed a cardiac shade enlargement due to congestive heart failure. Transthoracic echocardiography demonstrated a dilatated left ventricle and an impaired left ventricular systolic function. The patient's urinary cortisol excretion was elevated and circadian rhythm of cortisol was absent. ACTH level was low. In addition, plasma cortisol failed to decrease after administration of dexamethasone. An abdominal magnetic resonance imaging scan showed a 7-cm right adrenal mass. The patient was administered oxygen, spironolactone, ACE-inhibitor and the signs and symptoms of heart failure gradually improved. A laparoscopic right adrenalectomy was performed and pathological examination of the gland showed a benign adrenocortical adenoma. After the adrenalectomy the patient was started on hydrocortisone therapy and 5 months later the wall thickness of the left ventricle was within normal range and the patient's blood pressure was 130/80 mmHg. In conclusion we report the case of heart failure as the main clinical symptom in CS secondary to adrenal adenoma.