IL-18 stimulates B-type natriuretic peptide synthesis by cardiomyocytes in vitro and its plasma levels correlate with B-type natriuretic peptide in non-overloaded acute heart failure patients.

Background: An altered IL-18 pathway in heart failure (HF) has recently been described and this cytokine was shown to be of clinical and prognostic utility. Cardiomyocytes are a target of this cytokine which exerts inflammatory, hypertrophic, and profibrotic activities. B-type natriuretic peptide is a cardiac hormone produced in response to cardiac filling to regulate cardiovascular homeostasis.

In-hospital percentage BNP reduction is highly predictive for adverse events in patients admitted for acute heart failure: the Italian RED Study.

Introduction: Our aim was to evaluate the role of B-type natriuretic peptide (BNP) percentage variations at 24 hours and at discharge compared to its value at admission in order to demonstrate its predictive value for outcomes in patients with acute decompensated heart failure (ADHF).

Methods: This was a multicenter Italian (8 centers) observational study (Italian Research Emergency Department: RED). 287 patients with ADHF were studied through physical exams, lab tests, chest X Ray, electrocardiograms (ECGs) and BNP measurements, performed at admission, at 24 hours, and at discharge.

Brain natriuretic peptide and N-terminal pro-B-type natriuretic peptide show a different profile in response to acute decompensated heart failure treatment.

Brain natriuretic peptide (BNP) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) are currently used for the diagnosis, prognosis, and therapeutic decision making in heart failure patients. The aim of the study was to compare BNP and NT-proBNP plasma concentration profiles in 42 patients with decompensated heart failure who underwent treatment in the emergency department. A significant decrease in both peptide concentrations fell beyond 24 hours of therapy.

Usefulness of serial assessment of natriuretic peptides in the emergency department for patients with acute decompensated heart failure.

The value of natriuretic peptides, both B-type natriuretic peptide (BNP) and N-terminal prohormone brain natriuretic peptide (NTproBNP), for determining diagnosis, severity, and prognosis of emergency department (ED) patients with acute decompensated heart failure (ADHF) has been well documented. Emerging data support the hypothesis that repeated natriuretic peptide determinations in the acute phase of ADHF may assist in confirming the diagnosis, monitoring drug therapy, and evaluating the adequacy of patient stabilization. Data from the authors' group demonstrate that in patients admitted to the ED for acute dyspnea, serial NTproBNP measurement at admission and 4, 12, and 24 hours later was useful in confirming the diagnosis of ADHF compared with patients with chronic obstructive pulmonary disease.

Decrease in NTproBNP plasma levels indicates clinical improvement of acute decompensated heart failure.

Thirty-seven consecutive patients with acute decompensated heart failure (ADHF) admitted to emergency departments for acute dyspnea were investigated. Ten patients with acute exacerbation of chronic obstructive pulmonary disease and 10 patients with hypertension crisis were also included as controls. For each patient, a plasma amino-terminal pro-B-type natriuretic peptide (NTproBNP) concentration measurement was performed at admission, 4, 12, and 24 hours later, and on the day of discharge.

Increased circulating levels and salivary gland expression of interleukin-18 in patients with Sjögren's syndrome: relationship with autoantibody production and lymphoid organization of the periductal inflammatory infiltrate.

IL-18, an immunoregulatory and proinflammatory cytokine, has been shown to play an important pathogenic role in Th1-driven autoimmune disorders. In this study, we evaluated the circulating levels and salivary-gland expression of IL-18 in patients with Sjögren's syndrome (SS), a mainly Th1-mediated disease. IL-18 serum levels were measured by ELISA in 37 patients with primary SS, 42 with rheumatoid arthritis, and 21 normal controls.

The clearance of apoptotic cells: implications for autoimmunity.

Apoptosis has been clearly characterised by the ability to limit the activation of inflammatory responses through the disposal of the apoptotic cell by rapid uptake by phagocytes. The exposure of phosphatidylserine deriving from the loss of plasma lipid asymmetry is the early membrane signal which alerts the phagocyte about the imminent apoptotic death of the cell. Also modifications of membrane carbohydrate groups on apoptotic cells contribute to phagocyte recognition.