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Has the Mathematization of Rheumatoid Arthritis Gone Too Far?

Carlos Antonio Moura, MD, Ana Luísa Cerqueira de Sant’Ana Costa, MD, & Carlos Geraldo Moura, MD  |  Issue: November 2020  |  November 12, 2020

The search for knowledge has shaped Western culture and is based on Greek philosophy, especially Aristotelian metaphysics. During the Middle Ages, this knowledge was matured by dialectical scholasticism, culminating, in its later stages, in the amalgam between Islamic science and the neo-Aristotelianism of St. Thomas Aquinas.1 In this way, the foundations of the future scientific method were established, keeping faith and reason intertwined and interdependent.

From the 16th century onward, Western science started to reach a progressive protagonism in society, especially through Bacon’s empiricism, Cartesianism, Newtonian mechanics and Darwin’s evolutionism.2 The whole process pointed to the emergence of a new religion, which was baptized by Auguste Comte as positivism. Entering the 20th century, modern science, a lover of mathematical calculations, has received pertinent criticism. When Karl Popper suggested falsifiability theory, instead of verifiability, as the best way for science to obtain evidence, the foundation of evidence-based medicine was laid.

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This scientific evidence poses a dilemma: Should all of this knowledge culminate in the art of individualizing the understanding of patients, diseases and their treatments, or should it result in mathematical simplification of samples?

Recognition of RA

In rheumatology, rheumatoid arthritis (RA) is emblematic of this evolution. In 1800, French surgeon Augustin Jacob Landré-Beauvais identified a rheumatism with a phenotype distinct from gout, a previously known disease. British rheumatologist Alfred Baring Garrod called the disease rheumatoid gout in 1859, and his son, Archibald Garrod, in 1890, coined the term rheumatoid arthritis in his book, A Treatise on Rheumatism and Rheumatoid Arthritis.3 Recognition of this new disease made it possible to develop diagnostic strategies, serological research and therapeutic proposals.

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In 1937, Erik Waaler discovered that serum of patients with RA caused agglutination in sheep’s blood; this work was replicated in 1948 by Harry Rose, and culminated in the Waaler-Rose test. In 1949, H.C. Coggeshall and colleagues coined the term rheumatoid factor.3,4

The scientific process demands physicians use their expertise to phenotype & individualize the management of our patients instead of mathematizing them.

Also in 1949, the first RA therapeutic criteria were proposed, even though the first diagnostic criteria weren’t developed until 1956.5,6 The criteria were focused on staging, functionality and post-treatment disease activity, including erythrocyte sedimentation rate, signs and symptoms, radiographic progression, etc. They laid the foundation for the first RA clinical remission criteria, established in 1982.7 Following advances in research and statistical methodologies, these criteria would be refined in the 1990s, with the determination of funcional status and DAS28 score, both calculable like many algebraic equations.8,9

At the beginning of the 21st century, the treat-to-target strategy was established in RA and was adopted for other rheumatic diseases.10 Although we know a specific target should exist, the question remains: What is the best way to measure success in reaching the target?

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