27 research outputs found
Efficacy and durability of multifactorial intervention on mortality and MACEs:a randomized clinical trial in type-2 diabetic kidney disease
Background: Multiple modifiable risk factors for late complications in patients with diabetic kidney disease (DKD), including hyperglycemia, hypertension and dyslipidemia, increase the risk of a poor outcome. DKD is associated with a very high cardiovascular risk, which requires simultaneous treatment of these risk factors by implementing an intensified multifactorial treatment approach. However, the efficacy of a multifactorial intervention on major fatal/non-fatal cardiovascular events (MACEs) in DKD patients has been poorly investigated. Methods: Nephropathy in Diabetes type 2 (NID-2) study is a multicentre, cluster-randomized, open-label clinical trial enrolling 395 DKD patients with albuminuria, diabetic retinopathy (DR) and negative history of CV events in 14 Italian diabetology clinics. Centres were randomly assigned to either Standard-of-Care (SoC) (n = 188) or multifactorial intensive therapy (MT, n = 207) of main cardiovascular risk factors (blood pressure 40/50Â mg/dL for men/women and < 175Â mg/dL, respectively). Primary endpoint was MACEs occurrence by end of follow-up phase. Secondary endpoints included single components of primary endpoint and all-cause death. Results: At the end of intervention period (median 3.84 and 3.40Â years in MT and SoC group, respectively), targets achievement was significantly higher in MT. During 13.0Â years (IQR 12.4â13.3) of follow-up, 262 MACEs were recorded (116 in MT vs. 146 in SoC). The adjusted Cox shared-frailty model demonstrated 53% lower risk of MACEs in MT arm (adjusted HR 0.47, 95%CI 0.30â0.74, P = 0.001). Similarly, all-cause death risk was 47% lower (adjusted HR 0.53, 95%CI 0.29â0.93, P = 0.027). Conclusion: MT induces a remarkable benefit on the risk of MACEs and mortality in high-risk DKD patients. Clinical Trial Registration ClinicalTrials.gov number, NCT00535925. https://clinicaltrials.gov/ct2/show/NCT0053592
Colorectal Cancer Stage at Diagnosis Before vs During the COVID-19 Pandemic in Italy
IMPORTANCE Delays in screening programs and the reluctance of patients to seek medical
attention because of the outbreak of SARS-CoV-2 could be associated with the risk of more advanced
colorectal cancers at diagnosis.
OBJECTIVE To evaluate whether the SARS-CoV-2 pandemic was associated with more advanced
oncologic stage and change in clinical presentation for patients with colorectal cancer.
DESIGN, SETTING, AND PARTICIPANTS This retrospective, multicenter cohort study included all
17 938 adult patients who underwent surgery for colorectal cancer from March 1, 2020, to December
31, 2021 (pandemic period), and from January 1, 2018, to February 29, 2020 (prepandemic period),
in 81 participating centers in Italy, including tertiary centers and community hospitals. Follow-up was
30 days from surgery.
EXPOSURES Any type of surgical procedure for colorectal cancer, including explorative surgery,
palliative procedures, and atypical or segmental resections.
MAIN OUTCOMES AND MEASURES The primary outcome was advanced stage of colorectal cancer
at diagnosis. Secondary outcomes were distant metastasis, T4 stage, aggressive biology (defined as
cancer with at least 1 of the following characteristics: signet ring cells, mucinous tumor, budding,
lymphovascular invasion, perineural invasion, and lymphangitis), stenotic lesion, emergency surgery,
and palliative surgery. The independent association between the pandemic period and the outcomes
was assessed using multivariate random-effects logistic regression, with hospital as the cluster
variable.
RESULTS A total of 17 938 patients (10 007 men [55.8%]; mean [SD] age, 70.6 [12.2] years)
underwent surgery for colorectal cancer: 7796 (43.5%) during the pandemic period and 10 142
(56.5%) during the prepandemic period. Logistic regression indicated that the pandemic period was
significantly associated with an increased rate of advanced-stage colorectal cancer (odds ratio [OR],
1.07; 95%CI, 1.01-1.13; P = .03), aggressive biology (OR, 1.32; 95%CI, 1.15-1.53; P < .001), and stenotic
lesions (OR, 1.15; 95%CI, 1.01-1.31; P = .03).
CONCLUSIONS AND RELEVANCE This cohort study suggests a significant association between the
SARS-CoV-2 pandemic and the risk of a more advanced oncologic stage at diagnosis among patients
undergoing surgery for colorectal cancer and might indicate a potential reduction of survival for
these patients
Hepatic steatosis and necro-inflammatory activity overestimated liver stiffness by transient elastography in staging liver fibrosis in chronic hepatitis C
Serum sodium correction rate and the outcome in severe hyponatremia.
Study objective We investigated the serum sodium correction rate on length of hospitalization and survival rate, in severe chronic hyponatremic patients at the Emergency Department (ED). Design An observational study using clinical chart review. Setting The ED of the University Hospital of Marcianise, Caserta, Italy with approximately 30,000 patients visits a year. Type of participants We reviewed sixty-seven patients with severe hyponatremia subdivided in 2 subgroups: group A consisting of 35 patients with serum sodium correction rate < 0.3 mmol/h and group B consisting of 32 patients with serum sodium correction rate between < 0.5 and ⼠0.3 mmol/h. Intervention Emergency patients were evaluated for serum sodium correction rate for hyponatremia by clinical chart review. Measurements and main results Severe hyponatremia was defined as a serum sodium level < 120 mmol/l. Mean serum sodium correction rate of hyponatremia was of 0.17 ¹ 0.09% in group A and 0.41 ¹ 0.05% in group B (p < 0.001 vs group A). The length of hospital stay was 10.7 ¹ 3.7 days for group A, and it was significantly decreased to 3.8 ¹ 0.4 days for group B (p < 0.005 vs group A). In addition we observed that correction rate of hyponatremia in group A was associated with a significantly lower survival rate (25%) in comparison to group B (60%) (p < 0.001 vs group A). Conclusion: We observed that serum sodium correction rate ⼠0.3 and < 0.5 mmol/h was associated with a shorter length of hospital stay and a major survival rate. Š 2017 Elsevier In
Hepatic steatosis and insulin resistance are associated with serum imbalance of adiponectin/tumour necrosis factor-alpha in chronic hepatitis C patients
Background Steatosis and insulin resistance (IR) have a pathogenic role in chronic hepatitis C (HCV). Adipocytokines balance modulates hepatic lipid content and IR. Aim To evaluate serum adipocytokines and relationship with virological, histological and metabolic parameters in chronic HCV. Methods Adiponectin and tumour necrosis factor-alpha (TNF-alpha) levels, HCV genotypes, HCV-RNA, IR (HOMA-IR), body mass index and liver steatosis and fibrosis were assessed in 161 non-diabetic chronic HCV patients. Results Chronic HCV patients with steatosis showed lower serum adiponectin levels and higher levels of TNF-alpha, HOMA, alanine aminotransferase, gamma-glutamiltransferase and Histological Activity Index (HAI) and fibrosis scores. Low adiponectin levels were independently associated with grades of steatosis and HOMA-IR. Higher tumour necrosis factor-alpha levels were observed in patients with low adiponectin levels. The extension of steatosis was inversely correlated with adiponectin levels. A correlation between grade of steatosis with HOMA-IR and fibrosis was observed. HCV genotype 3-infected patients showed lower adiponectin levels than those with other genotypes. An independent predictor of low adiponectin levels in genotype 3 infection was the extension of steatosis. Liver fibrosis score was associated with steatosis, HAI and age. Conclusions Chronic HCV patients with steatosis showed a serum adiponectin/TNF-alpha imbalance that is associated with IR. Reduced adiponectin levels may be involved in the pathogenesis of steatosis, which in turn accelerates progression of fibrosis in chronic HCV
Epstein Barr virus infection reactivation as a possible trigger of primary biliary cirrhosis-like syndrome in a patient with multiple sclerosis in the course of fingolimod treatment.
Primary biliary cirrhosis (PBC) and multiple sclerosis (MS) are considered autoimmune diseases with a multifactorial aetiology which is thought to be due to a combination of genetic predisposition and environmental triggers. An association of both diseases has been previously described in sporadic case reports. Fingolimod, an antagonist of the sphingosine 1 phosphate receptor family (S1P1/3/4/5), is a promising and effective drug in the treatment of MS. Here we describe a case of PBC like syndrome that was unmasked, concomitantly or consequently to Epstein Barr virus (EBV) infection reactivation, in a 34 year old male patient with relapsing remitting multiple sclerosis who was receiving fingolimod treatment
Chronic HCV infection is a risk factor of ischemic stroke
Objectives: Cerebrovascular diseases are leading cause of death worldwide. Plaque rupture and embo- lization account for one-third of ischemic stroke. The causes are not fully known, but inflammation plays a pathogenic role. Recently, HCV infection has been identify as risk of atherosclerosis. HCV replicates within carotid plaques and brain endothelia cells; moreover, HCV patients showed higher levels of inflammation. Thus, we hypothesized that subjects carrying HCV are at higher risk of stroke. Accordingly, we evaluated prevalence and role of HCV infection in patients with stroke.
Methods: A priori sample size was calculated. Overall, 820 consecutive patients were enrolled, 123 with stroke and, as control, 697 age- and gender-matched (295 with COPD; 402 with diseases other than HCV- associated). Patients were evaluated for HCV and conventional risk of stroke.
Results: Prevalence of HCV was higher in patients with stroke than that observed in control (26.8% vs. 6.6%, p 1â4 0.0001). An analysis of stroke patients showed that those HCV positive were younger (p 1â4 0.017) had lower serum levels of cholesterol (p 1â4 0.001), triglycerides (p 1â4 0.045), and higher serum levels of inflammation markers (ESR, p 1â4 0.001; CRP, p 1â4 0.0001; fibrinogen, p 1â4 0.012). A multivariate analysis showed that HCV infection was an independent risk factor of stroke (O.R. 2.04, 95% C.I. 1.69 e2.46; p 1â4 0.0001). A secondary analysis showed that HCV patients had higher (p 1â4 0.031) prevalence of past ischemic heart disease.
Conclusions: HCV infected patients are at higher and earlier risk of stroke. Inflammation is a key mediator. Clinicians in clinical practice and researchers in future trials should take into account these new findings