B-Type Natriuretic Peptide in the Diagnosis of Heart Failure

B-type natriuretic peptide is released from the ventricles of the heart in response to hemodynamic stress, and blood levels of B-type natriuretic peptide may be useful in the diagnosis of heart failure. In this study, a rapid, bedside immunoassay for B-type natriuretic peptide was used to make or exclude the diagnosis of heart failure in patients with acute dyspnea from various causes. The assay was found to have good sensitivity and excellent specificity in the diagnosis of heart failure.

Measurement of B-type natriuretic peptide levels is not a stand-alone test for heart failure. It will be of most value when used in conjunction with clinical observations, especially when the cause of acute dyspnea is unclear. The finding of a low level of B-type natriuretic peptide (less than 50 pg per milliliter) is good evidence of the absence of heart failure.

Related Perspective

Hepatitis B e Antigen and Hepatocellular Carcinoma

This prospective cohort study of 11,893 men in Taiwan examined the relation between the base-line prevalence of hepatitis B surface antigen (HBsAg) and hepatitis B e antigen (HBeAg) and the subsequent development of hepatocellular carcinoma. There were 39 cases of hepatocellular carcinoma per 100,000 person-years of follow-up among men who were negative for both antigens at enrollment, 324 cases per 100,000 person-years among men who were positive for HBsAg but negative for HBeAg, and 1169 cases per 100,000 person-years among those who were positive for both HBsAg and HBeAg.

Chronic hepatitis B virus infection is known to be associated with an increased risk of hepatocellular carcinoma. This study demonstrates a strong association between the presence of HBeAg and the subsequent development of hepatocellular carcinoma and suggests a potential role for HBeAg testing to identify high-risk patients who would be candidates for antiviral drug therapy and close monitoring for early detection of liver cancer.

Related Editorial

Osteoprotegerin Deficiency and Juvenile Paget's Disease

Juvenile Paget's disease is an autosomal recessive osteopathy characterized by rapidly remodeling woven bone, osteopenia, fractures, and progressive skeletal deformity. Its molecular basis is not known. Since osteoprotegerin suppresses bone turnover, functioning as a decoy receptor for osteoclast differentiation factor, the authors sought to identify mutations in the gene for this protein (TNFRSF11B) in two unrelated Navajo patients. Studies that included polymerase-chain-reaction amplification followed by direct sequencing, as well as Southern blotting of genomic DNA, revealed a homozygous deletion of TNFRSF11B in both patients.

Juvenile Paget's disease results from osteoprotegerin deficiency induced by the homozygous deletion of TNFRSF11B. Consequently, circulating levels of soluble osteoclast differentiation factor are elevated.

Related Editorial

Toll-like Receptor 4 Polymorphisms and Atherogenesis

Toll-like receptor 4 (TLR4) mediates the innate immune response to gram-negative bacteria and other pathogens. This study found that a common polymorphism of TLR4 (Asp299Gly), which attenuates receptor signaling, is associated with an increased risk of systemic infection, lower circulating levels of certain inflammatory markers, and a reduced risk of atherosclerosis.

The findings support the concept that inflammation is involved in the pathogenesis of atherosclerosis and that genetic factors that attenuate the inflammatory response may reduce the risk of atherosclerosis.

Clinical Practice: Postpartum Depression

A woman visits the doctor for her six-week postpartum evaluation. She reports that she cannot sleep even if her baby sleeps. She cries daily and worries constantly. She does not feel hungry and is not eating regularly. Making decisions is overwhelming. How should she be evaluated and treated?

This article reviews ways of identifying and managing postpartum depression.

Clinical Implications of Basic Research: Early Genetic Influences on Behavior

In a recently published study, investigators at Columbia University reported on a mouse model in which the forebrain serotonin-1A receptor was knocked out. The mice demonstrated inhibition of certain aspects of behavior. For example, when placed in an open area the affected mice were less likely to explore than normal mice. In this commentary, Dr. Freedman discusses the implications of this provocative research for the genetic control of human behavior.

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