The pharmaceutical world has seen remarkable developments in terms of treatments and medications. One such development involves a medication named Upadacitinib which is used to treat a number of inflammatory conditions, including atopic dermatitis, psoriatic arthritis, Crohn disease, rheumatoid arthritis, ankylosing spondylitis and ulcerative colitis. Upadacitinib, being a Janus kinase (JAK) inhibitor, modulates immune responses and effectively controls inflammation.
For cases of atopic dermatitis, a skin condition that results in itchy rashes that cannot be controlled by topical medications alone, upadacitinib has proven to be quite useful. Approved by health regulators in January 2022 specifically for atopic dermatitis, the drug operates by blocking immune signals and inhibiting the inflammatory effects of key cytokines involved in the condition. It selectively prevents JAK1s from evoking inflammation symptoms and itch that are associated with several cytokines and other pathways.
Clinical research has substantiated the benefits of upadacitinib in patients with moderate to severe atopic dermatitis who have undergone more than a year of continuous treatment. Although it presents certain side effects like cutaneous or infectious diseases, changes in blood tests and infections, the advantages outweigh the negatives in most scenarios.
Interestingly, upadacitinib has been linked to potentially inducing alopecia areata, a hair loss disorder. This finding was based on a case study of a 55-year-old female patient with severe atopic dermatitis who was administered the drug. Nearly a year after the treatment, the patient reported two round patches of hair loss on her scalp with no prior history of alopecia areata.
This relationship between alopecia development and upadacitinib is of critical importance as JAK inhibitors are FDA-approved treatments for the condition. Moreover, 16% of patients with alopecia also have other autoimmune diseases such as thyroid disease, vitiligo and lupus erythematosus that are associated with the hair loss disorder. Additionally, nearly 39% alopecia areata cases also have atopic dermatitis, a subtype of eczema.
The mechanism involved in inducing alopecia areata with upadacitinib has not been clearly delineated yet. Scientists have postulated that it could be attributed to the modulation of JAK1 not being sufficient and it being necessary for multiple JAK pathways to be modulated to prevent the autoimmune symptoms seen in alopecia areata. Drug-induced alopecia areata usually occurs within a year of treatment initiation, further supporting a connection between the onset of hair loss and treatment commencement.
There is also a theory suggesting that the emergence of alopecia could partially be due to autoimmune complication. The possibility of alopecia areata being caused by upadacitinib defies the conventional thought process that hair loss is solely tied to having an underlying atopic dermatitis condition.
The complexity and contrasting arguments surrounding upadacitinib’s role in treating alopecia areata point towards the need for additional research, particularly into the possibility that only inhibiting JAK1 may not be sufficient. Until we gain a more comprehensive understanding, patients and medical professionals need to be aware of these potential complications. It’s a marked reminder that while we make forward strides in medical science, there are always new challenges and facets to discover, understand, and address.
