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Screening programs (SC) have been proven to reduce both incidence and mortality of CRC. We retrospectively analyzed patients who underwent surgical treatment for CRC between 01/2011 and 01/2017. The current screening program in our region collects patients aged from 50 to 69. For this reason, out of a total of 600 patients, we compared 125 patients with CRC founded during the SC to 162 patients who presented with symptoms and were diagnosed between 50-69 years old (NO-SC). 45% patients in the SC group were diagnosed as AJCC stage I vs 27% patients in the NO-SC group; 14% vs 20% were stage II, 14% vs 26% were stage III, and 3% vs 14% were stage IV (p 0.002). We found a significant difference in surgical approach: 89% SC vs 56% NO-SC patients had laparoscopic surgery (p 0.002). In the NO-SC group, 16% patients underwent resection in an emergency setting. Only 5% patients in the SC group had postoperative complications vs 14% patients in the NO-SC group (p 0.03). We had a 2-year OS of 86%, being 95% in the SC group and 80% in the NO-SC group (p 0.002). Likewise, the whole 2-year DFS was 77%, whereas it was 90% in the SC group and 66% in the NO-SC group (p 0.002). Screening significantly improves early diagnosis and accelerated surgical treatment. We obtained earlier stages at diagnosis, a less invasive surgical approach, and lower rates of complications and emergency surgery, all this leading to an improvement in both OS and DFS.

Altered glucose metabolism negatively modulates outcome in acute coronary syndromes (ACS). Insulin resistance is commonly associated with increasing BMI in the general population and these associations may involve obesity-related changes in circulating ghrelin and adipokines. We aimed at investigating interactions between BMI, insulin resistance and ACS and their associations with plasma ghrelin and adipokine concentrations. Homeostasis model assessment of insulin resistance (HOMA(IR))-insulin resistance index, plasma adiponectin, leptin, total (T-Ghrelin), acylated (Acyl-Ghrelin), and desacylated ghrelin (Desacyl-Ghrelin) were measured in 60 nondiabetic ACS patients and 44 subjects without ACS matched for age, sex, and BMI. Compared with non-ACS, ACS patients had similar HOMA(IR) and plasma adipokines, but lower T- and Desacyl-Ghrelin and higher Acyl-Ghrelin. Obesity (BMI > 30) was associated with higher HOMA(IR), lower adiponectin, and higher leptin (P < 0.05) similarly in ACS and non-ACS subjects. In ACS (n = 60) HOMA(IR) remained associated negatively with adiponectin and positively with leptin independently of BMI and c-reactive protein (CRP) (P < 0.05). On the other hand, low T- and Desacyl-Ghrelin with high Acyl-Ghrelin characterized both obese and non-obese ACS patients and were not associated with HOMA(IR). In conclusion, in ACS patients, obesity and obesity-related changes in plasma leptin and adiponectin are associated with and likely contribute to negatively modulate insulin resistance. ACS per se does not however enhance the negative impact of obesity on insulin sensitivity. High acylated and low desacylated ghrelin characterize ACS patients independently of obesity, but are not associated with insulin sensitivity.

Objective: The renin-angiotensin-aldosterone system (RAAS) plays an important role in the control of renal function both in physiological and pathological conditions. The aim of the present study was to evaluate the relation between four genetic polymorphisms of the RAAS and renal insufficiency in a population of patients with essential hypertension living in north-east Italy., Design and Methods: Eighty-six hypertensive patients with renal insufficiency and 172 hypertensive patients without renal damage matched for age and hypertension duration to within 2 years were evaluated. Genotyping for insertion/deletion of angiotensin-converting enzyme (ACE I/D), angiotensinogen (AGT) M235T, angiotensin II type 1 receptor (AT1R) A1166C and aldosterone synthase (CYP11B2) -344C/T polymorphisms were performed using polymerase chain reaction, with further restriction analysis when required., Results: Each of the genetic polymorphisms of the RAAS genes was associated with renal failure; the adjusted odds ratios were 1.47 and 1.89 for ACE D allele, assuming a co dominant and a recessive mode of inheritance, respectively; 1.51 for AGT T235 allele assuming a co dominant, and 1.98 assuming a recessive, pattern of inheritance; 1.79 for AT1R C1166 allele considering a dominant pattern; and 3.89 for CYP11B2 -344C allele as a recessive effect. However, CYP11B2 genotypes were not in Hardy-Weinberg equilibrium among controls. The associations AGT TT-AT1R AC and CYP11B2 CC-ACE DD showed a possible positive interaction in the development of renal insufficiency among hypertensive subjects. The association AGT MM-AT1R AA and AGT MM-AT1R AA-CYP11B2 TT or TC combinations were associated with a reduced risk for renal failure., Conclusions: Our findings suggest that in patients with essential hypertension an unfavorable genetic pattern of RAAS may contribute to the increased risk for the development of renal failure.

Background: Since a large fraction of patients affected by chronic hepatitis C do not respond to alpha-interferon therapy, we planned a pilot study of intravenous beta-interferon therapy in Italian patients non responsive to several courses of alpha-interferon., Methods: Ten Italian patients with chronic hepatitis C were treated intravenously with beta-interferon to assess the biochemical and virological responses. Each patient received intravenously 6 MU of beta-interferon daily for 7 days a week for a period of 2 months; in responders, this treatment was followed by intramuscular beta-interferon administration 6 MU three times a week for an additional 8 weeks., Results: All the patients were infected by the genotype 1b of hepatitis C virus and had a high serum concentration of HCV-RNA (4.1 +/- 3.3 x 10(7) copies/ml). During intravenous therapy, 4 patients (40%) showed a complete return to normal of alanino-aminotransferase and 3 cases became HCV-RNA negative. During intramuscular beta-interferon administration, two patients breakthrough. At the end of the follow-up (six months after the end of the treatment) two patients only showed return to normal of alanino-aminotransferase, but one of them remained HCV-RNA positive., Conclusions: These results indicate that even genotype 1b of hepatitis C virus can be suppressed by intravenous beta-interferon therapy, as previously described in similar cases in Japan. The rate of sustained biochemical and virologic response was, however, low, suggesting that further studies are needed to define the best regimen to achieve eradication of hepatitis C virus infection.

Idiopathic dilated cardiomyopathy (IDC) is a heart disease of unknown aetiology characterised by impaired ventricular function usually associated with dilatation of the cardiac chambers. In order to test the hypothesis of an immunological cause for the disease at the genetic level, we performed linkage analysis between the putative disease locus and some of the potential candidate genes involved in the immune response or coding for the targets for autoantibodies in a large multigeneration family (63 members) from southern Italy with autosomal dominant transmission of the disease. Twenty-nine polymorphic markers on 18 different chromosomal locations were investigated, including markers linked to the genes coding for the HLA antigens, the immunoglobulin heavy and light chains, the receptors for the immunoglobulin Fc fragments, the subunits of the T cell receptor and the associated CD3, CD4, CD8, and CD45 antigens, interleukins 1, 3, 4, 5, 6, 9, and 11, the interleukin 1 and 2 receptors, and the genes coding for the beta 1 adrenoreceptor, the adenine nucleotide translocator-1, and the cardiac alpha and beta myosin heavy chains. No evidence for genetic linkage to IDC was found at any of these candidate loci. These results indicate that the still unidentified IDC gene maps outside several loci involved in the regulation of immune reactivity.

The authors evaluated the 2956 blood cultures performed in a multispecialist hospital in Trieste (Italy) during a whole year. A computer assisted analysis of the data pointed out that a single blood culture performed in a bacteremic patient could reveal 93% of positivities, two blood cultures in the same day at least 96.6% and three at least 98.3%. Furthermore, in suspected bacteremic patients who received several blood cultures in subsequent days, the chance for a second day culture to reveal a bacteremia not pointed out in the first day was less than 4%, while it was 0% for the following days. These results assess the importance of a correct approach to the suspected bacteremic patient, and point out the usefulness of performing at most three blood cultures in the first day of clinical suspicion of bacteremia.