Friday, 15 Feb 2019

You are here

Does RA kill you? Let me count the ways….and what you can do about it

There were many presentations at EULAR 2018 in Amsterdam about the mortality of RA.

Excess mortality seems to start after 6 years of RA with an excess of approximately 13 to 14% over 10 years (0P0344). This was observed in two large administrative (billing) databases from the provinces of Ontario (27,405 people with RA) and British Columbia (13,834 with RA), Canada and showed the same results matched to age and sex matched general population. Others have found that most deaths are from cardiovascular events and then cancer and less often infection (but more common than the general population). The Oslo RA register showed that over time the excessive mortality gap in RA is decreasing (FRI0043) where 10 year mortality was less in the patients studied (from 2004-2008) vs from 1994-1998 and 1999-2003.

So it is interesting that plaquenil (HCQ) prolongs survival (OP091). Incident RA pts from Denmark from 2004-14 compared users of HCQ to matched non-users. The author stated that mostly HCQ is prescribed in combination with MTX and not as monotherapy but the proportion with HCQ monotherapy was not provided so there could be imbalance (confounding) where perhaps HCQ users had less severe disease if many had monotherapy. The all-cause mortality was 17% reduced and CV deaths decreased by 22%. Interestingly there was no reduction in diabetes which other studies have shown.

Mortality was increased in seropositive RA patients (ACPA and/or RF) in an administrative database (HUMANA) that was linked with a lab database. Interestingly mortality was less if using bDMARDs compared to csDMARDs (OP0195). Even more interesting, MTX with a bDMARDs had less cardiovascular events than use of a bDMARD alone (from Medicare database) (OP0192).  

So, what should we do? I don’t know the full answer but will continue to use HCQ (as I often start ERA pts on triple therapy) and may consider less likely to stop it and when using a bDMARD I have reasons beyond better disease control and retention to try to encourage concomitant MTX use if tolerated. Finally, we can’t forget about the identification and treatment of modifiable CV risk factors in our patients!

 

Disclosures: 
The author has no conflicts of interest to disclose related to this subject

Add new comment

More Like This

No Added Benefit to MRI-Guided Therapy in Rheumatoid Arthritis

A treat-to-target (T2T) strategy to manage rheumatoid arthritis hinges on clinical metrics to optimize therapy. But investigators from Denmark have shown that using magnetic resonance imaging–guided T2T failed to improve disease activity remission rates or reduce radiographic progression.

Differing Effects of Smoking and HLA-DRB1 in Seropositive Rheumatoids

Analyses from the Swedish EIRA incident rheumatoid arthritis cohort study shows that smoking and HLA-DRB1 exert differential effects on serologically defined RA subsets - but that the strongest influence was seen in double positive (CCP+, RF+) individuals.

Update on Pregnancy Management in RA

Two recent reports offer good news to rheumatoid arthritis (RA) women who are planning to become pregnant. 

The first studies, RA women experiencing fertility issues who turn to assisted reproductive technology (ART) shows that live births were significantly lower in women with rheumatoid arthritis receiving ART treatment compared to usual rates in women without rheumatoid arthritis.

Multidisciplinary Recommendations for Rheumatoid Foot Problems

Approximately 90% of patients with rheumatoid arthritis (RA) have foot problems. A multidisciplinary panel (including 2 patients, 22 professionals (rheumatologists, rehabilitation physicians, orthopaedic surgeons, specialized nurses, podiatrists, orthopaedic shoe technicians, pedicurists, researchers) in the Netherlands set out to develop recommendations for those who treat RA foot problems. 

Does Seropositivity Change with Therapy?

A subanalysis of the early rheumatoid arthritis (RA) "IMPROVED" study has shown that changes in RA-autoantibody levels are not associated with disease activity or or long-term drug response, but instead reflect intensity of immunosuppression. Thus while autoantibody levels may be modifiable by our best therapies, modifying CCP or RF levels appears to have limited clinical relevance.