TNF and Herpes Risk; Lupus Presenting as Heart Failure

Last week's articles on rheumatology in the major nonspecialty journals

TNF InhibitorsAssociation Between the Initiation of Anti–Tumor Necrosis Factor Therapy and the Risk of Herpes Zoster
JAMA (2013) 309:887-895. doi:10.1001/jama.2013.1099. Free full text.

Compared to patients who started on non-biologic DMARDs, there was no increased risk of herpes zoster in patients who started anti-TNF medications for rheumatoid arthritis (RA), inflammatory bowel disease, psoriasis, psoriatic arthritis or ankylosing spondylitis in the largest retrospective cohort study yet, involving 35,000 subjects. There was, however, an increased risk among patients who used corticosteroids. Designed to resolve conflicting conclusions from earlier studies, this analysis involved patients who had taken adalimumab, etanercept, or infliximab.  The annual overall incidence of herpes zoster increases from 4/1,000 at age 50 to 11/1,000 at age 80. In this study, the annual incidence in RA was about 12/1,000, and 20/1,000 with high doses of glucorticoids. The authors support widespread vaccination of RA patients age ≥50, although they also support a trial of the live vaccine among anti-TNF users.
 

Systemic Lupus Erythematosus

Clinical Problem-Solving: The Heart of the MatterN Engl J Med, (2013) 368:944-950. Full text $15

Transesophageal echocardiography screening detects Libman–Sacks endocarditis in close to half of SLE patients. In most cases it is insignificant, but about 10% of those cases develop severe valvular regurgitation and heart failure. This case report involved a 22-year-old woman with systemic lupus erythematosus (SLE) who presented initially with heart failure. The heart failure was caused by an extremely invasive Libman–Sacks endocarditis (sterile valvular vegetations), which had infiltrated the mitral valve. The patient was treated with glucorticoids, mycophenolate mofetil, an ACE inhibitor, diuretics and warfarin, and she improved. However, several longitudinal cohort studies have found that immunosuppressive treatments had no effect on valvular lesions, and glucorticoid therapy may make it worse.