What makes a patient suspect that they may have alopecia?
Patients may suspect they have alopecia when they notice sudden patchy hair loss or more-than-usual hair loss. For example, it is very common to hear patients say, "I got up one morning, and there were clumps of hair on my pillow," or "When I was washing my hair, I saw clumps of hair on my bathroom floor." Others may have been told by a family member, a friend, or their hairdresser that they have bald patches on their scalp. It is important to note here that the onset of hair loss is sudden, distinguishing AA from other types of hair loss with a slow onset.
How does alopecia areata impact patients?
Alopecia areata has a profound negative impact on many aspects of patients' lives, including their social and family lives, intimate relationships and sex lives, and work or school performance; all of which exert a massive toll on their emotional and mental well-being.1,7,8 Coping with AA is a daily challenge. In our patient survey, 70% of patients reported AA having a large or very large impact on their emotional and mental well-being. More worryingly, AA may lead to depression and anxiety. A recent study reported that one-third of patients have symptoms of depression and anxiety, while up to one-fifth of patients have depressive or anxiety disorders that require psychiatric care.2 The significant psychological toll of AA does not appear to lessen over time.1 Even during times of complete hair regrowth, patients live with the fear and anxiety of a relapse.
Coping with the disorder, specifically concealing the bald patches, takes a considerable time investment for patients, which may have been previously underrecognized.1 On average, patients spend about 10 hours per week concealing hair loss. The time investment and the disease burden extend beyond the patient to include caregivers as well, as exemplified in this narrative from one patient’s mother:
"Helping my girl to survive the disease has been extremely difficult because as she got worse, we had to go shopping for weeks to try and find things to cover the patches, eyebrows, and eyelashes, and find somebody to tattoo the eyebrows."
Aside from hair growth, "not using or having to consider using a head covering or wig" was what the patients we surveyed most wanted from treatment, followed by "feeling more confident."
Is there an underappreciation of the burden of alopecia areata on patients?
Based on responses to our clinician survey, dermatologists and primary care physicians appear to underestimate - to some degree - the impact of AA on patients. This is reflected in patient anecdotes about interactions with clinicians where they hear statements such as:
"This is not cancer. So, don't get so nervous. It's going to go away" or "It's just stress. Try to relax," which is terrible for patients because they feel like, "Oh, it's my fault. It's because I'm stressed that I'm getting this disease that's not going away."
Patients with AA often feel that they are to blame for their condition. And historically, there has been poor education about disease burden in medical school curricula and residencies, which may partly explain the underappreciation of the disease burden seen in our survey.
Why is it important to understand the pathogenesis of alopecia areata?
Most clinicians know that AA is an autoimmune disorder but may be less familiar with its pathogenesis. Knowledge of AA pathogenesis is important to understand the targets and mechanism of action of immunotherapies for AA. However, there is a level of complexity surrounding AA's pathogenesis that can be off-putting. Explaining the pathogenesis in a simplistic way may be helpful.
Central to the pathogenesis of AA is loss of immune privilege of the hair follicle (HF).9,10 Immune privilege is the suppres-sion of an immune response to antigens in a localized area. In a healthy HF, immune privilege is localized to the hair bulge and anagen phase of the hair bulb, where it protects the HF from inflammatory processes and promotes immune toler-ance (Figure 1a). Several mechanisms are in place to maintain the integrity of immune privilege: (1) secretion of immune inhibitors by the HF epithelium, such as interleukin (IL)-10, somatostatin, transforming growth factor beta-1 (TGF-beta1), melanocyte-stimulating hormone alpha (alphaMSH), and macro-phage migration inhibitory factor (MIF), which are referred to as "immune privilege guardians"; (2) downregulation of major histocompatibility complex I (MHC-I), preventing self-antigen presentation to CD8+ T cells; and (3) prevention of immune cells entering and exiting the HF through the HF extracellular matrix that serves as a barrier10 (Figure 1b).
