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Farahnak P.,Section of Surgery | Farahnak P.,Karolinska Institutet | Larfars G.,Section of Internal Medicine | Larfars G.,Karolinska Institutet | And 4 more authors.
Journal of Clinical Endocrinology and Metabolism | Year: 2011

Context: The extent and clinical significance of cardiovascular (CV) abnormalities associated with mild primary hyperparathyroidism (PHPT) are still matters for discussion. Objective: The main objective of the present study was to evaluate biochemical CV risk markers in PHPT patients before and after parathyroidectomy (PTX) in comparison with controls. Design and Subjects: In a prospective case-control design, 49 patients with PHPT and 49 healthy matched controls were included. Methods: Blood pressure (BP), 25-OH-D, plasminogen activator inhibitor-1 activity, von Willebrand factor antigen, homocysteine, high-sensitivity C-reactive protein, IGF-I, and lipid profile were evaluated at baseline and 15 ± 4 months after PTX. Results: At baseline, the level of 25-OH-D was significantly lower in patients compared with controls (40.1 ± 16.5 vs. 64.6 ± 20.8 nmol/liter, P < 0.001) and increased after PTX (58.9 ± 19.5, P < 0.001). Postoperatively, 25-OH-D was inversely correlated to the PTH level (r = -0.34; P < 0.05). Systolic BP (127.2 ± 17.4 vs. 119.3 ± 12.5mmHg, P < 0.05) and triglyceride (TG; 1.04 ± 0.60 vs. 0.86 ± 0.43 mmol/liter, P < 0.05) were higher in patients compared with controls and decreased slightly in patients after PTX (BP, 124.4 ± 16.8mmHg, and TG, 0.94 ± 0.50 mmol/liter, P < 0.05). Otherwise, there were no intergroup differences in coagulation, inflammatory, metabolic, and lipid status. Conclusions: Except for a lower 25-OH-D level and slightly higher systolic BP and TG levels, patients with mild PHPT without other CV risk factors did not differ from healthy controls as regards biomarkers predicting CV diseases. PTX had an overall positive effect on TG level, BP, and vitamin D status. Copyright © 2011 by The Endocrine Society.

Rehman H.U.,Section of Internal Medicine
Endocrinologist | Year: 2010

A case of primary hyperparathyroidism masked by coexistent vitamin D deficiency is described. The case illustrates the difficulties in the diagnosis and treatment of such patients. Copyright © 2010 by Lippincott Williams & Wilkins.

Franceschini A.,University of Ferrara | Capece M.,University of Ferrara | Chiozzi P.,University of Ferrara | Falzoni S.,University of Ferrara | And 5 more authors.
FASEB Journal | Year: 2015

The P2X7 receptor (P2X7R) is a known and powerful activator of the NOD-like receptor (NLR)P3 inflammasome; however, the underlying pathways are poorly understood. Thus, we investigated the molecular mechanisms involved. The effect of P2X7R expression and activation on NLRP3 expression and recruitment was investigated by Western blot, RT-PCR, coimmunoprecipitation, and confocal microscopy in microglial mouse cell lines selected for reduced P2X7R expression and in primary cells from P2X7R-/- C57BL/6 mice. We show here that P2X7R activation by ATP (EC50 = 1 mM) or benzoyl-ATP (EC50 = 300 μM) and P2X7R down-modulation caused a 2- to 8-fold up-regulation of NLRP3 mRNA in mouseN13microglial cells. Moreover, NLRP3 mRNA was also up-regulated in primary microglial and macrophage cells from P2X7R-/- mice. Confocal microscopy and immunoprecipitation assays showed that P2X7R and NLRP3 closely interacted at discrete subplasmalemmal sites. Finally, P2X7R stimulation caused a transient (3-4 min) cytoplasmic Ca2+ increase localized to small (2-3 mm wide) discrete subplasmalemmal regions. The Ca2+ increase drove P2X7R recruitment and a 4-fold increase in P2X7R/NLRP3 association within 1-2 min. These data show a close P2X7R and NLRP3 interaction and highlight the role of P2X7R in the localized cytoplasmic ion changes responsible for bothNLRP3 recruitment and activation. © FASEB.

Trotta F.,University of Ferrara | Colina M.,Section of Internal Medicine
Best Practice and Research: Clinical Rheumatology | Year: 2012

Multicentric reticulohistiocytosis (MRH) and fibroblastic rheumatism (FR) are uncommon disorders with similar joint and skin manifestations. They are usually included among the non-Langerhans histiocytoses, but recent insights drive some criticism. The diagnosis is often challenging and must be confirmed by the histological typical features. If the skin manifestations are missing, the arthritic complaints may be confused with those of other rheumatic disorders. In these cases, only a careful clinical and radiological evaluation leads to the correct diagnosis. The natural course of the diseases may rapidly develop into disabling manifestations, making an aggressive treatment strongly recommendable. There is emerging evidence that anti-tumour necrosis factor-α agents and bisphosphonates are promising drugs for MRH, while a course of methotrexate and steroids seems to be the best option for FR. Finally, the clinician should be aware that in many cases MRH, but not FR, is associated with a large number of systemic manifestations and with malignancy. This eventuality must be accurately ruled out. © 2012 Elsevier Ltd. All rights reserved.

Murdolo G.,Assisi Hospital | Bartolini D.,University of Perugia | Tortoioli C.,Section of Internal Medicine | Piroddi M.,University of Perugia | And 2 more authors.
Free Radical Biology and Medicine | Year: 2013

The expansion of adipose tissue (AT) is, by definition, a hallmark of obesity. However, not all increases in fat mass are associated with pathophysiological cues. Indeed, whereas a "healthy" fat mass accrual, mainly in the subcutaneous depots, preserves metabolic homeostasis, explaining the occurrence of the metabolically healthy obese phenotype, "unhealthy" AT expansion is importantly associated with insulin resistance/type 2 diabetes and the metabolic syndrome. The development of a dysfunctional adipose organ may find mechanistic explanation in a reduced ability to recruit new and functional (pre)adipocytes from undifferentiated precursor cells. Such a failure of the adipogenic process underlies the "AT expandability" paradigm. The inability of AT to expand further to store excess nutrients, rather than obesity per se, induces a diabetogenic milieu by promoting the overflow and the ectopic deposition of fatty acids in insulin-dependent organs (i.e., lipotoxicity), the secretion of various metabolically detrimental adipose-derived hormones (i.e., adipokines and lipokines), and the occurrence of local and systemic inflammation and oxidative stress. Hitherto, fatty acids (i.e., lipokines) and the oxidation by-products of cholesterol and polyunsaturated fatty acids, such as nonenzymatic oxysterols and reactive aldehyde species, respectively, emerge as key modulators of (pre)adipocyte signaling through Wnt/β-catenin and MAPK pathways and potential regulators of glucose homeostasis. These and other mechanistic insights linking adipose dysfunction, oxidative stress, and impairment of glucose homeostasis are discussed in this review article, which focuses on adipose peroxidation as a potential instigator of, and a putative therapeutic target for, obesity-associated metabolic dysfunctions. © 2013 Elsevier Inc.

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