Cardiovascular autonomic testing in the work-up of cerebellar ataxia: insight from an observational single center study

Journal of Neurology - Cerebellar ataxias are a heterogeneous group of disorders of both genetic and non-genetic origin. In sporadic cases, two entities are recognized: multiple system atrophy of...     

Cardiac troponin I as prognostic marker in heart failure patients discharged from emergency department

Despite evidence that cardiac troponin I (cTnI) identifies patients with advanced heart failure (HF) at risk of death, data on heterogeneous HF populations are scarce. Our purpose was to verify and analyze the prognostic role of cTnI in acute HF patients admitted to the emergency department. This was an observational longitudinal prospective study carried out in an urban hospital. We studied 99 patients discharged from the department between March and December 2002 with a HF diagnosis and samples of cTnI. Patients with acute coronary syndromes, myocarditis or renal failure were excluded. The main outcome was death from any cause. The detection level of the cTnI assay was 0.05 ng/ml. cTnI was detected in 45.5% of HF patients. These patients had a higher NYHA class (P < 0.001) at initial presentation and longer hospitalization (P = 0.004) than cTnI-negative patients. Nineteen deaths occurred during the study: 17 for HF and 2 for acute coronary syndrome. Finally, detectable cTnI was associated with increased mortality risk (RR 4.7; 95% CI 1.3–17.1; P = 0.021) also after adjustment for other adverse prognosis factors (age, NYHA class and presence of relapses). Our HF cTnI-positive patients had a worse clinical presentation and longer hospitalization. cTnI is a significant independent predictor of death and of longer hospitalization. It could be used for the early identification of HF patients at an increased risk of death in the long term, and of longer hospitalization. Thus, cTnI can aid decision-making and clinical management in the emergency department. A short abstract of the paper was presented at the A.C.E.P. Scientific Assembly-Research Forum in Boston U.S.A. October 2003.     

Is There Anything to the Reported Association Between <Emphasis Type="Italic">Helicobacter pylori</Emphasis> Infection and Autoimmune Thyroiditis?

Higher serological prevalence rates of Helicobacter pylori (Hp) infection have been reported in patients with autoimmune thyroiditis (AT), and it has been suggested that monoclonal antibodies against Cag-A positive Hp strains can cross-react with follicular cells of the thyroid gland. We studied the prevalence of AT and thyroid functional status in patients who underwent gastroscopy for dyspeptic symptoms. Patients were tested for TSH, free thyroid hormones, and antithyroglobulin and antithyroperoxidase antibodies (ATPO). Hp positivity was determined using urea breath test (UBT). Serum samples from 302 patients (59.9% women) were evaluated. One hundred ninety-one subjects (63.2%) were Hp-negative, and 111 of 302 (36.8%) were Hp-positive. Forty-three of 191 Hp-negative patients (22.5%; 95% CI, 17.1–29.0%) had an increase of either antibody, compared to 30 of 111 (27.0%; 95% CI, 19.6–36.0%) Hp-positive patients (P = 0.40). Similar results were obtained using positivity for both antibodies (7.3 vs. 7.2%; P = 1) or for ATPO (18.8 vs. 21.6%; P = 0.54). The prevalences of hypothyroidism (4.7 vs. 5.5%) or hyperthyroidism (5.8 vs. 5.5%) were also similar (P = 0.95). Hormonal levels were not different in the two groups (P > 0.22 in all cases). The previously reported association between AT and Hp infection was not observed in our study. Infection by Hp does not appear to increase the risk of AT in individuals with dyspeptic symptoms, and screening for this condition in patients with a positive UBT is not indicated.     

Candida tropicalis fungaemia: incidence,risk factors and mortality in a general hospital

The risk factors and clinical features of patients with Candida tropicalis fungaemia have not been fully defined. We performed a case–control study comparing 59 cases of C. tropicalis fungaemia with 177 episodes of fungaemia caused by other species of Candida in our hospital over a 24-year period (January 1985 to December 2008). Patients with C. tropicalis fungaemia were more likely to be older (median age, 67 vs. 56 years; p 0.01), to have cancer (45.5% vs. 31.6%, p 0.04), and to have the abdomen as the portal of entry (32.2% vs. 11.9%, p 0.001), and had a higher in-hospital mortality rate (61% vs. 44%, p 0.03). Multivariate analysis showed that the independent risk factors for C. tropicalis fungaemia were cancer (OR 4.5; 95% CI 1.05–3.83; p 0.03) and the abdomen as the portal of entry (OR 13.6; 95% CI 1.9–8.2; p <0.001). When survivors were compared with non-survivors, the risk factors associated with a poor outcome were neutropenia (19.4% vs. 0; p 0.03), corticosteroid treatment (36% vs. 13%; p 0.07), and septic shock (50% vs. 17.4%; p 0.01). The independent risk factors for mortality in the multivariate analysis were corticosteroid treatment (OR 8.2; 95% CI 0.9–27.7; p 0.04) and septic shock (OR 14.6; 95% CI 2.4–90.2; p 0.004), whereas urinary tract infection (OR 0.07; 95% CI 0.01–0.8; p 0.03) and catheter removal (OR 0.06; 95% CI 0.01–0.4; p 0.002) were protective factors. C. tropicalis is the fourth most common cause of fungaemia in our hospital. It is associated with underlying malignancy, the abdomen as the portal of entry, and poor outcome.     

From microbiota toward gastro-enteropancreatic neuroendocrine neoplasms: Are we on the highway to hell?

Gut microbiota is represented by different microorganisms that colonize the intestinal tract, mostly the large intestine, such as bacteria, fungi, archaea and viruses. The gut microbial balance has a key role in several functions. It modulates the host’s metabolism, maintains the gut barrier integrity, participates in the xenobiotics and drug metabolism, and acts as protection against gastro-intestinal pathogens through the host’s immune system modulation. The impaired gut microbiota, called dysbiosis, may be the result of an imbalance in this equilibrium and is linked with different diseases, including cancer. While most of the studies have focused on the association between microbiota and gastrointestinal adenocarcinomas, very little is known about gastroenteropancreatic (GEP) neuroendocrine neoplasms (NENs). In this review, we provide an overview concerning the complex interplay between gut microbiota and GEP NENs, focusing on the potential role in tumorigenesis and progression in these tumors.