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1.  Total percutaneous femoral vessels cannulation for minimally invasive mitral valve surgery 
Annals of Cardiothoracic Surgery  2013;2(6):739-743.
Background
Minimally invasive mitral valve surgery (MIMVS) has experienced several technological changes in the last two decades. Our aim was to describe one of the most recent improvements, the utilization of a total percutaneous femoral vessels cannulation technique during MIMVS.
Methods
We performed a retrospective observational analysis of this technique among 300 consecutive MIMVS patients, with particular focus on cannulation aspects of MIMVS, its success rate and potential complications.
Results
From October 2008 to December 2012, 300 patients (60% males) were operated on. Mean age was 62.9±16.4 years. Indications for operation included mitral valve repair (93%) and mitral valve replacement (7%). Two femoral arterial catheterizations failed and required conversion to sternotomy. The complications on the arterial side were: 5 (1.6%) cases of bleeding during the introduction of Prostar leading to a preoperative surgical hemostasis; 2 (0.6%) retroperitoneal bleeds during cardiopulmonary bypass requiring difficult surgical control but with an uneventful follow-up; 6 (2%) bleeding episodes after removal of the arterial cannula easily controlled by direct surgical revision; 1 (0.3%) arterio-venous fistula requiring a surgical correction on postoperative day 32; 1 (0.3%) patient had a transitory claudication due to a superficial femoral artery thrombosis progressively compensated by the collateral circulation. There were no postoperative bleeding complications. There were no other complications linked to the femoral cannulations or to the groin occurred during the follow-up. The percentage of uneventful arterial cannulations was 80% among the first 50 patients (N=10 out of 50) and 98.8% thereafter (N=3 out of 250).
Conclusions
Total percutaneous femoral vessels cannulation technique is particularly suitable for MIMVS with a high success rate and few complications after a short learning curve. With the advent of the percutaneous approach, the traditional complications of the groin incision have completely disappeared in modern operations with no groin infection, hematoma or lymphocele.
doi:10.3978/j.issn.2225-319X.2013.08.02
PMCID: PMC3856992  PMID: 24349975
Complications; femoral artery; mitral valve; minimally invasive; percutaneous
2.  Hepcidin Expression in Iron Overload Diseases Is Variably Modulated by Circulating Factors 
PLoS ONE  2012;7(5):e36425.
Hepcidin is a regulatory hormone that plays a major role in controlling body iron homeostasis. Circulating factors (holotransferrin, cytokines, erythroid regulators) might variably contribute to hepcidin modulation in different pathological conditions. There are few studies analysing the relationship between hepcidin transcript and related protein expression profiles in humans. Our aims were: a. to measure hepcidin expression at either hepatic, serum and urinary level in three paradigmatic iron overload conditions (hemochromatosis, thalassemia and dysmetabolic iron overload syndrome) and in controls; b. to measure mRNA hepcidin expression in two different hepatic cell lines (HepG2 and Huh-7) exposed to patients and controls sera to assess whether circulating factors could influence hepcidin transcription in different pathological conditions. Our findings suggest that hepcidin assays reflect hepatic hepcidin production, but also indicate that correlation is not ideal, likely due to methodological limits and to several post-trascriptional events. In vitro study showed that THAL sera down-regulated, HFE-HH and C-NAFLD sera up-regulated hepcidin synthesis. HAMP mRNA expression in Huh-7 cells exposed to sera form C-Donors, HFE-HH and THAL reproduced, at lower level, the results observed in HepG2, suggesting the important but not critical role of HFE in hepcidin regulation.
doi:10.1371/journal.pone.0036425
PMCID: PMC3346721  PMID: 22586470
3.  Iron Metabolism in Thalassemia and Sickle Cell Disease. 
There are two main mechanisms by which iron overload develops in thalassemias: increased iron absorption due to ineffective erythropoiesis and blood transfusions. In nontransfused patients with severe thalassemia, abnormal dietary iron absorption increases body iron burden between 2 and 5 g per year. If regular transfusions are required, this doubles the rate of iron accumulation leading to earlier massive iron overload and iron-related damage. Iron metabolism largely differs between thalassemias and sickle cell disease, but chronic transfusion therapy partially normalize many of the disparities between the diseases, making iron overload an important issue to be considered in the management of patients with sickle cell disease too. The present review summarizes the actual knowledge on the regulatory pathways of iron homeostasis. In particular, the data presented indicate the inextricably link between erythropoiesis and iron metabolism and the key role of hepcidin in coordinating iron procurement according to erythropoietic requirement. The role of erythropoietin, hypoxia, erythroid-dependent soluble factors and iron in regulating hepcidin transcription are discussed as well as differences and similarities in iron homeostasis between thalassemia syndromes and sickle cell disease.
doi:10.4084/MJHID.2009.006
PMCID: PMC3033158  PMID: 21415988
4.  Revaluation of clinical and histological criteria for diagnosis of dysmetabolic iron overload syndrome 
AIM: To re-evaluate the diagnostic criteria of insulin resistance hepatic iron overload based on clinical, biochemical and histopathological findings.
METHODS: We studied 81 patients with hepatic iron overload not explained by known genetic and acquired causes. The metabolic syndrome (MS) was defined according to ATPIII criteria. Iron overload was assessed by liver biopsy. Liver histology was evaluated by Ishak’s score and iron accumulation by Deugnier’s score; steatosis was diagnosed when present in ≥ 5% of hepatocytes.
RESULTS: According to transferrin saturation levels, we observed significant differences in the amount of hepatic iron overload and iron distribution, as well as the number of metabolic abnormalities. Using Receiving Operating Curve analysis, we found that the presence of two components of the MS differentiated two groups with a statistically significant different hepatic iron overload (P < 0.0001). Patients with ≥ 2 metabolic alterations and steatosis had lower amount of hepatic iron, lower transferrin saturation and higher sinusoidal iron than patients with < 2 MS components and absence of steatosis.
CONCLUSION: In our patients, the presence of ≥ 2 alterations of the MS and hepatic steatosis was associated with a moderate form of iron overload with a prevalent sinusoidal distribution and a normal transferrin saturation, suggesting the existence of a peculiar pathogenetic mechanism of iron accumulation. These patients may have the typical dysmetabolic iron overload syndrome. By contrast, patients with transferrin saturation ≥ 60% had more severe iron overload, few or no metabolic abnormalities and a hemochromatosis-like pattern of iron overload.
doi:10.3748/wjg.14.4745
PMCID: PMC2739335  PMID: 18720534
Iron overload; Hepatic iron distribution; Transferrin saturation; Metabolic syndrome; Hepatic steatosis

Results 1-4 (4)