Rheumatoid arthritis is an inflammatory disease characterized by chronic joint erosive processes, affecting approximately 1% of the population. [1] The pathogenic mechanisms processes involve the activation of pro-inflammatory cytokines, including TNF alpha. [2]
The purpose of this case presentation is to elucidate a possible correlation between the high level of blood TNF alpha and the apparent lack of response to biologic therapy directed against this molecule.
A female patient, aged 55 years, diagnosed with rheumatoid arthritis in 2006, presents an increased inflammatory biological syndrome. The patient was being treated biologically (adalimumab, and two years of etanercept previously. One year ago, the patient presents the elevation values of the blood tests commonly used to monitor the status of patients with inflammatory rheumatoid arthritis up to 2.5-3 x than normal values. Initially, this increase is considered to be due to a respiratory seasonal condition. We continued monitoring the status, after subsequent remission of these respiratory disorders, and we observed the persistence of those elevated test, this time without an obvious possible causing comorbidity.
We decided to evaluate the current patient status and we obtained the following information:
Biological syndrome currently moderately exceeds the maximum normal values. ESR was 47 mm/h and CRP 1.5 than the normal value.
TNF alpha value determined by immunochemical methods with detection by chemiluminescence (CLIA) is 67.2 pg / mL
Biological confirmation by determining serum TNF alpha and increased observation that the current level may be one explanation for the possible reactivation of the disease prompted us to continue the study in patients receiving anti-TNF alpha biologic. This study is ongoing. We can imagine this correlation between the level of TNF alpha and the degree of disease activity at least in the case of a group of patients treated with biological drugs. If this could be demonstrated, then perhaps we can expect a change in the curative approach of these patients, meaning that dose adjustment can be considered depending on the level of TNF alpha, and why not, depending on other cytokines that may be included in future studies.