Early Hypocalcemia is the most frequent complication after thyroid surgery. Several studies have tried to identify factors (patient caracteristics or surgical technique variations) affecting hypocalcemia following thyroid surgery. This studiy evaluates the role of several factors in postoperative hypocalcemia development. A retrospective study conducted on 2108 patients that underwent thyroid surgery in a single center (1669 women and 439 men). Postoperative early hypocalcemia was defined as serum calcium levels lower than 8,0 mg/dl measured 24 h after surgery. Following factors were evaluated in the study: sex, age, glandular hyperfunction, preoperative diagnosis, preoperative serum calcium levels, preoperative serum PTH levels, type of surgery performed (total thyroidectomy vs. lobectomy); minimally invasive video assisted thyroidectomy (MIVAT); number of parathyroid preserved in situ, postoperative serum calcium levels, changes in perioperative calcium levels (difference between preoperative values ​​and postoperative calcium levels), presence of carcinoma in the surgical specimen, presence of thyroiditis based on histopatology reports. Among evaluated factors only gender and surgical procedure revealed to be significantly correlated to early hypocalcemia development. In fact female patients experienced postoperative hypocalcemia in 42% (701/1669) of cases, which was signicantly higher than the 21.4% (94/439) identified in men. We also noticed a greater hypocalcemia incidence in patient undergoing total thyroidectomy (38.8%) than in patient undergoing lobectomy group (13.8%). Early hypocalcemia development didn’t appear to be related to preoperative serum calcium levels but it showed a statistically significant correlation with perioperative serum calcium level drop. This findings suggest that sex (female gender is a strong risk factor),surgical procedure and perioperative changes in serum calcium are the only factors (among all variables examined) that influence early hypocalcemia development.

Background: Since the early 1980s, epidemiological evidence has suggested a connection between low calcium intake and preeclampsia The purpose of this meta-analysis is to summarize current evidence regarding calcium supplementation during pregnancy in predicting preeclampsia and associated maternal–fetal complications. Methods: Literature revision of all RCT (random allocation of calcium versus placebo) available in MEDLINE/PUBMED up to 2/29/2012 regarding calcium supplementation during pregnancy for preventing preeclampsia. We used the Mantel-Haenszel’s Method for four subgroup of patients: Adequate calcium intake; Low calcium intake; Low risk of preeclampsia; High risk of preeclampsia. We considered p < 0.05 as significant. Results: There is no consensus in Literature about: (1) the efficacy of calcium supplementation in the prevention of preeclampsia, (2) other/adverse/long-term effects of calcium supplementation in pregnancy. Conclusions: Preeclampsia is likely to be a multifactorial disease. However, inadequate calcium intake represents a factor associated with an increased incidence of hypertensive disease. The results of our meta-analysis demonstrate that the additional intake of calcium during pregnancy is an effective measure to reduce the incidence of preeclampsia, especially in populations at high risk of preeclampsia due to ethnicity, gender, age, high BMI and in those with low baseline calcium intake.

Hepatitis C virus infection (HCV) represents a unique model to characterize, from early to late stages of infection, the T cell differentiation process leading to exhaustion of human CD8+ T cells. Here we show that in early HCV infection, exhaustion-committed virus-specific CD8+ T cells display a marked upregulation of transcription associated with impaired glycolytic and mitochondrial functions, that are linked to enhanced ataxia-telangiectasia mutated (ATM) and p53 signaling. After evolution to chronic infection, exhaustion of HCV-specific T cell responses is instead characterized by a broad gene downregulation associated with a wide metabolic and anti-viral function impairment, which can be rescued by histone methyltransferase inhibitors. These results have implications not only for treatment of HCV-positive patients not responding to last-generation antivirals, but also for other chronic pathologies associated with T cell dysfunction, including cancer.

Background: Methods: Results: Conclusion: