From the Research
Rinvoq (upadacitinib) would not typically be expected to cause a decrease in complement proteins C3 and C4. Rinvoq is a Janus kinase (JAK) inhibitor that works by blocking specific enzymes involved in inflammatory signaling pathways, primarily affecting cytokine production and immune cell activation. It does not directly target or deplete complement proteins like C3 and C4, which are part of the innate immune system's complement cascade. If a patient taking Rinvoq shows decreased C3/C4 levels, this is more likely related to an underlying autoimmune condition such as systemic lupus erythematosus or active inflammatory disease rather than a direct medication effect. The complement system functions independently of the JAK-STAT pathway that Rinvoq targets. During routine monitoring of patients on Rinvoq, any unexpected decrease in complement proteins should prompt investigation for other causes, including disease flares or concurrent conditions, rather than assuming it's a medication side effect, as supported by the mechanism of action described in studies such as 1. Key points to consider include:
- The mechanism of action of upadacitinib, which involves the inhibition of JAK enzymes and their subsequent effects on cytokine signaling pathways 1, 2
- The lack of direct interaction between upadacitinib and the complement system, suggesting that any changes in C3/C4 levels are unlikely to be a direct result of the medication 1
- The importance of monitoring patients for underlying conditions or disease flares that could affect complement protein levels, as highlighted in various studies on the use of upadacitinib in different diseases 3, 4, 5