DESTIN, FLA. — The benefits of tumor necrosis factor blockade extend beyond the joints to the hearts and minds of rheumatoid arthritis patients, Dr. Iain McInnes reported at the Congress of Clinical Rheumatology.
Findings from two new studies suggest that anti-TNF treatment can inhibit the cytokine-induced chain of events that leads to the increased risk of cardiovascular disease and clinical depression in RA.
Along with lead investigator Dr. Mike J.L. Peters of VU University Medical Center in Amsterdam, Dr. McInnes and colleagues at the University of Glasgow (Scotland) have shown, for the first time, that anti-TNF-alpha therapy decreased circulating levels of the cardiac neurohormone N-terminal prohormone brain natriuretic peptide (NT-proBNP) in patients with rheumatoid arthritis (RA) who do not have evident heart failure.
Previously identified as a clinically relevant biomarker for heart failure, NT-proBNP is independently associated with cardiovascular risk in individuals with and without preexisting cardiovascular disease. Thus, the observed reduction in NT-proBNP suggests a “potential beneficial effect of [TNF-alpha] blockers with respect to vascular risk and ventricular function in rheumatoid arthritis,” he said.
The study measured serum NT-proBNP at baseline and after 16 weeks of biweekly adalimumab treatment in 171 consecutive RA patients without heart failure (Ann. Rheum. Dis. 2010 April 7 [doi:10.1136/ard.2009.119412]). After week 16, the investigators observed an approximately 18% reduction in NT-proBNP levels, providing biological evidence that TNF-alpha blockade does not worsen ventricular function in patients with RA who do not have prevalent heart failure, and supporting epidemiologic findings that indicate it may reduce overall cardiovascular risks in these patients, said Dr. McInnes. The results also add weight to the accumulating evidence that implicates TNF-alpha in the cardiovascular events associated with RA, and support the beneficial effect that blocking TNF-alpha has on surrogate vascular markers, he said.
In a separate study, Dr. McInnes and colleagues sought to assess the functional effects of anti-TNF-alpha therapy on the brains of depressed patients with RA. They determined that TNF-alpha blockade mediates altered serotonin transporter availability and induces an improvement in depression measures.
“I think we as rheumatologists underappreciate the prevalence and impact of depression on our patients,” he said, referring to a 2006 report suggesting that the prevalence of major depressive disorder exceeds 40% and that of suicidal ideation is up to 11% in RA patients (Rheumatology 2006;45:1,325-7).
Dr. McInnes and his associates measured SERT density using SPECT (single-photon emission CT) in six patients with seropositive RA 2 weeks before the initiation of adalimumab therapy and 4 days after the last treatment, he said.
After anti-TNF-alpha therapy, “there was a significant decrease in the [SERT] density in all of the patients.” Along with that came overall improvements in physical and mental functioning, as measured by the Hamilton Rating Scale for Depression, the Social Functioning 36-item scale, the Hospital Anxiety and Depression Scale, and the composite 28 joint count Disease Activity Score, Dr. McInnes reported.
http://www.rheumatologynews.com/article/S1541-9800(10)70284-2/fulltext
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