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Daniel Aletaha
Researcher at Medical University of Vienna
Publications - 398
Citations - 51111
Daniel Aletaha is an academic researcher from Medical University of Vienna. The author has contributed to research in topics: Rheumatoid arthritis & Medicine. The author has an hindex of 74, co-authored 298 publications receiving 43215 citations. Previous affiliations of Daniel Aletaha include National Institutes of Health & University of Vienna.
Papers
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Journal ArticleDOI
Developments in the clinical understanding of rheumatoid arthritis
Josef S Smolen,Daniel Aletaha +1 more
TL;DR: It has been shown that composite disease activity indices have special merits in following patients, that disease activity governs the evolution of joint damage, and that disability can be dissected into several components – among them disease activity and joint damage.
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Rheumatoid factor, not antibodies against citrullinated proteins, is associated with baseline disease activity in rheumatoid arthritis clinical trials
TL;DR: The data presented suggest that the presence of RF has a clear association with higher levels of disease activity but that the existence of ACPAs has not and even appears to be associated with lower disease activity.
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Response of elderly patients with rheumatoid arthritis to methotrexate or TNF inhibitors compared with younger patients
TL;DR: Responsiveness of elderly patients with RA to MTX or TNFi+MTX is similar to that observed in patients of younger age, and the effects of the combination were more profound than those of MTX monotherapy.
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Perception of improvement in patients with rheumatoid arthritis varies with disease activity levels at baseline
TL;DR: The perception of improvement of disease activity of patients with RA is considerably different depending on the disease activity level at which they start, and much higher changes in disease activity were needed to achieve MCII according to patient judgment.
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Forget personalised medicine and focus on abating disease activity
Josef S Smolen,Daniel Aletaha +1 more
TL;DR: Three different lines of evidence are summarized suggesting that current biological therapies directed at different molecules or cells have similar efficacy in rheumatoid arthritis and target similar populations of patients; therefore, distinct biological effects of targeted therapies may not account for differences in response.