<p>Current plaque psoriasis treatments aim to control symptoms, minimize disease impact, and enhance patient quality of life. Identifying potential biomarkers remains a crucial goal, as they may aid in predicting outcomes and monitoring the disease in clinical settings and may offer new therapeutic targets or strategies.</p>

When we think about biomarkers, especially in the therapeutic landscape for plaque psoriasis, it is like a “hunt for the white whale.” Biomarkers could be used for many different things, such as diagnosis, drug monitoring, and disease prognosis. Also, in terms of systemic comorbidities of the chronic inflammatory burden of psoriasis, could we identify a biomarker that predicts whether someone is more likely to develop psoriatic arthritis or cardiovascular disease?

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The most commonly discussed potential use of biomarkers in psoriasis is for determining which drug is right for a specific patient. Even though the efficacies may appear similar within each drug class, the drugs all behave a little differently. Sometimes it can be overwhelming to decide what is the best choice for an individual patient. This is where a biomarker can potentially be useful, but I do not think that we are there yet.

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There is good work being done to identify systemic biomarkers for more severe disease or disease activity. It would be helpful to have something quantifiable that gives us a sense of the patient’s disease severity in that moment. Currently, when it comes to predicting response to therapy, biomarkers such as HBD-2 can potentially be helpful in following disease activity. There may be other serum analyses that can be useful, but my impression is that they are not yet ready for clinical use. Hopefully, we get to the point where some biomarkers can be reproducibly used to better help our patients with psoriasis.

This is certainly a hot topic in plaque psoriasis. There are some emerging technologies, such as tape strips that supposedly indicate what might be the best mechanism of action for an individual patient. However, we know that our current therapies work well. If a patient with psoriasis already has a very good chance of responding to an IL-23 or IL-17 inhibitor, and we learn that they have a “very, very good chance” or a “slightly very good chance,” the technology is not clinically critical, in my mind. Now, if that technology were to become available for drugs that target different pathways, such as apremilast or deucravacitinib, that could be really valuable. They are good drugs, but not everyone responds.

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There are emerging data on drug monitoring in patients who are being treated with biologics. It has been suggested that if a patient is not responding or is losing response to a biologic therapy, it might be because their drug levels are low rather than because the drug is not working. Knowing the drug level may also allow you to increase the dose or decrease the frequency to optimize response. There is pharmacokinetic variability from person to person, and trials are ongoing to evaluate this approach. This is promising and would be fairly accessible if it proves to be useful going forward.

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Another area where a biomarker would be useful is psoriatic arthritis because it currently remains a diagnosis of exclusion. If I suspect that a patient might have inflammatory arthritis, I will first want to make sure that they do not have rheumatoid arthritis (RA). RA does not respond to IL-17 or IL-23 inhibitors, and a patient could become disabled from their RA if they are prescribed the wrong agent. These are complicated diagnoses. Osteoarthritis, fibromyalgia, and psoriatic arthritis can comingle. For now, blood work can be helpful. Even though the laboratory tests are not perfect, they give us some insights.

Our use of biomarkers for prognostication, treatment determination, and disease monitoring is still in its infancy. As my colleagues have explained, it is an area of active interest and research. Can biomarkers help us personalize treatment decisions or confirm disease control? For example, if a patient’s plaque psoriasis is very well controlled, might that patient be able to receive medication less frequently? The ability to find a biomarker to determine which drug would fit which patient opens a lot of doors. Rational prescribing would allow us to reduce waste from using the wrong medicine, potentially improve patient compliance and adherence, and have much better quality-of-life outcomes for patients with psoriasis.

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We would also like to be able to use biomarkers to determine which patients might go on to develop comorbidities. Right now, there are a number of different papers that are out and several approaches that are being used to try to understand this. However, nothing has been widely validated for use in clinical practice.

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Part of the challenge, I think, is that there are a few different ways to potentially harvest biomarkers for this disease. One way is to take patients’ blood and look at biomarkers. It turns out that what is happening in the serum may not always correlate well with what is going on in the skin. Other methods look at the skin itself. Can you take a skin biopsy or tape strip and look for protein or gene expression? There are many studies investigating this, and different approaches have been tried. However, none of them have been completely successful or have been introduced broadly into the treatment paradigm for psoriasis in the clinical environment at this point.