A rare case report of hypertrophic cardiomyopathy induced by catecholamine-producing tumor

RATIONALE: Catecholamine-producing tumors are rare, occurring in less than 0.2% of patients with hypertension, but can have relevant cardiovascular morbidity and mortality. PATIENT CONCERNS: A 37-year-old woman presented with a history of dyspnea, chest pain, palpitations, and paroxysmal hypertension. Electrocardiogram, echocardiogram, and cardiac magnetic resonance showed severe LVH with a prevalent involvement of the anterior portion of interventricular septum. Endomyocardial biopsy found severe hypertrophy with disarray of cardiomyocytes and ultrastructural evidence of contraction and necrosis of myocytes. Hormone investigations revealed high values of 24-hours urinary metanephrines. Abdominal computed tomography (CT) showed an enlarged left adrenal gland with a strong uptake of I-metaiodobenzylguanidine at scintigraphy scan. INTERVENTIONS:Thus, the adrenal tumor was surgically removed. OUTCOMES: At follow-up examination, the patient's metanephrines levels were normalized and the transthoracic echocardiogram showed a reduction of LVH. DIAGNOSIS AND LESSONS: We report a rare case of catecholamine-induced cardiomyopathy due to an adrenal adenoma mixed with nodules enriched in epinephrine-types secreting granules

Papilledema in patient with primary aldosteronism. an unusual case report

Primary Aldosteronism (PA) is the most frequent form of secondary hypertension [1]. Target treatment is important to reduce the risk of cardiovascular complications. Visual field defects and papilledema are reported in PA patients

Prevalence of peri-implant diseases among an Italian population of patients with metabolic syndrome: a cross-sectional study

Over the years, only few authors have studied the association of systemic conditions with peri-implantitis. The aim of this study is to detect frequency and severity of peri-implant diseases among an Italian population of patients affected by metabolic syndrome (MetS).METHODS: In this cross-sectional study, patients with at least one dental implant with >5 years of functional loading were screened to evaluate metabolic, periodontal and peri-implant status. MetS diagnosis was established in accordance with the NCEP ATP III criteria, while case definitions of the 2017 World Workshop were adopted for peri-implant diseases. For each implant, probing pocket depths, mucosal redness, bleeding on probing, suppuration, plaque index and marginal bone loss were recorded. Multinomial logistic regression analysed the relationship between gender, diagnosis of metabolic syndrome, presence of periodontitis, smoking, type of prosthesis and location of implants and peri-implant mucositis and peri-implantitis. RESULTS: 183 patients was enrolled: in MetS subjects, peri-implantitis was detected in 36.9% (n = 31) of implants, while mucositis in 60.7% (n = 51), with an OR of 10.01(p = 0.005) for mucositis and OR 15.26 (p = 0.001) for peri-implantitis, compared to subjects without MetS, where 26.3% of implants showed peri-implantitis and 55.5% mucositis. No differences were found for smoking, implant location, gender and type of prosthetic rehabilitation. Patients with periodontitis showed a higher association with peri-implant mucositis (OR = 4.33) and peri-implantitis (OR = 9.00). CONCLUSIONS: Based on the results of this study, patients affected by MetS showed a greater prevalence of peri-implant diseases, with further studies that need to confirm the possibility of this new possible risk indicator

Epicardial fat thickness in patients with autosomal dominant polycystic kidney disease.

Introduction: Autosomal dominant polycystic kidney disease (ADPKD) is associated with early organ damage such as left ventricular hypertrophy and higher cardiovascular risk when compared to essential hypertension (EH). Epicardial adipose tissue (EAT) is a new cardiovascular risk factor, but its role and correlation with left ventricular mass (LVM) in ADPKD is unknown. Aims: we sought to investigate whether EAT is higher and related to LVM indexed by body surface area (LVMi) in hypertensive patients with ADPKD compared to those with EH. Methods: We performed ultrasound measurement of EAT thickness, LVM, LVMi, and left atrium size (left atrial volume indexed for body surface, LAVI) in 41 consecutive hypertensive patients with ADPKD, compared to 89 EH patients. Results: EAT was significantly higher in the ADPKD group in comparison to EH subjects (9.2 ± 2.9 mm vs. 7.8 ± 1.6 mm, p < 0.001), and significantly correlated with LVM, LVMi, and LAVI in the ADPKD group (r = 0.56, p = 0.005; r = 0.424, p = 0.022; and r = 0.48, p = < 0.001, respectively). Comparing EAT against body mass index, systolic blood pressure, and age, we found that EAT was the strongest predictor of LVMi (β = 0.42, p = 0.007). Conclusion: Our data showed that EAT was higher in ADPKD patients than in EH subjects and independently correlated with LVMi. EAT measurement can be a useful marker for the cardiovascular risk stratification in ADPKD

Subclinical atherosclerosis due to increase of plasma aldosterone concentrations in essential hypertensive individuals

Background and aims: The adrenal mineralocorticoid system plays a key role in cardiovascular, metabolic and renal damage. This study aimed to assess the relationship between plasma aldosterone concentration (PAC) and some surrogate markers of subclinical atherosclerosis, such as carotid intima-media thickness (cIMT), ankle-brachial index (ABI) and biochemical parameters in patients with essential hypertension. Methods and results: From January 2014 to December 2017, we consecutively enrolled 804 essential hypertensive patients (407 men and 397 women, mean age 50 ± 14 years) without cardiovascular complications, distinguishing patients in quartiles according to PAC. Compared with the first quartile, the highest PAC quartile was associated with the highest levels of serum uric acid (SUA) (5.3 ± 1.3 vs. 5.0 ± 1.0 mg/dl; P = 0.01), triglycerides (117.5 ± 15.7 vs. 106.8 ± 10.5 mg/dl; P < 0.05), 24-h urinary albumin excretion (UAE) (38.8 ± vs. 7.6 ± mg/24 h; P < 0.05), cIMT (0.87 ± 0.22 vs. 0.80 ± 0.21 mm; P = 0.001) and increased prevalence of carotid plaques (26 vs. 16%; P < 0.005). Moreover, we found that in patients with PAC more than 150 pg/ml, the ABI was significantly lower than those with PAC < 150 pg/ml (1.01 ± 0.09 vs. 1.10 ± 0.09; P < 0.022). PAC was also found to be an independent predictor of the presence of carotid plaques and pathological ABI (<0.9) in essential hypertensive individuals. Conclusion: Our results revealed that higher PAC values are strongly associated with some metabolic variables, as triglycerides, UAE, cIMT, worse ABI and major prevalence of carotid plaques that, together with elevated blood pressure values, are strictly correlated with higher risk of atherosclerosis and cardiovascular complications

Three-dimensional environment sensitizes pancreatic cancer cells to the anti-proliferative effect of budesonide by reprogramming energy metabolism

Background Pancreatic ductal adenocarcinoma (PDAC) is the most lethal cancer with an aggressive metastatic phenotype and very poor clinical prognosis. Interestingly, a lower occurrence of PDAC has been described in individuals with severe and long-standing asthma. Here we explored the potential link between PDAC and the glucocorticoid (GC) budesonide, a first-line therapy to treat asthma.Methods We tested the effect of budesonide and the classical GCs on the morphology, proliferation, migration and invasiveness of patient-derived PDAC cells and pancreatic cancer cell lines, using 2D and 3D cultures in vitro. Furthermore, a xenograft model was used to investigate the effect of budesonide on PDAC tumor growth in vivo. Finally, we combined genome-wide transcriptome analysis with genetic and pharmacological approaches to explore the mechanisms underlying budesonide activities in the different environmental conditions.Results We found that in 2D culture settings, high micromolar concentrations of budesonide reduced the mesenchymal invasive/migrating features of PDAC cells, without affecting proliferation or survival. This activity was specific and independent of the Glucocorticoid Receptor (GR). Conversely, in a more physiological 3D environment, low nanomolar concentrations of budesonide strongly reduced PDAC cell proliferation in a GR-dependent manner. Accordingly, we found that budesonide reduced PDAC tumor growth in vivo. Mechanistically, we demonstrated that the 3D environment drives the cells towards a general metabolic reprogramming involving protein, lipid, and energy metabolism (e.g., increased glycolysis dependency). This metabolic change sensitizes PDAC cells to the anti-proliferative effect of budesonide, which instead induces opposite changes (e.g., increased mitochondrial oxidative phosphorylation). Finally, we provide evidence that budesonide inhibits PDAC growth, at least in part, through the tumor suppressor CDKN1C/p57Kip2.Conclusions Collectively, our study reveals that the microenvironment influences the susceptibility of PDAC cells to GCs and provides unprecedented evidence for the anti-proliferative activity of budesonide on PDAC cells in 3D conditions, in vitro and in vivo. Our findings may explain, at least in part, the reason for the lower occurrence of pancreatic cancer in asthmatic patients and suggest a potential suitability of budesonide for clinical trials as a therapeutic approach to fight pancreatic cancer