1 Start 2 Complete Please select your profession: * Physician Nurse Nurse Practitioner Pharmacist Dentist Physician Assistant Other... Please select your profession: Other... How would you best describe your practice setting? * Private physician office/practice Private NP office/practice Nurse Managed clinic Retail-based clinic Urgent care clinic Hospital inpatient unit Hospital outpatient clinic (not an ED) Long-term care facility Average years in practice: * <5 5-10 11-15 6-20 21-25 >25 Average number of patients seen per week with disease targeted in the education: * <5 5-10 11-15 16-20 21-25 >25 Melanocytes in non-segmental vitiligo can die through several regulated pathways, including apoptosis, ferroptosis, pyroptosis, and necroptosis. Why does the mode of melanocyte death matter for disease progression? * Apoptosis is the most immunogenic form of cell death and the main driver of T-cell recruitment Immunogenic forms of cell death release damage-associated molecular patterns (DAMPs) that propagate immune activation, whereas apoptosis is comparatively immunologically silent The mode of cell death determines which JAK isoform is activated in neighboring keratinocytes Only melanocytes lost through anoikis cause permanent depigmentation, because detached melanocytes cannot be replaced Which mechanism best explains why vitiligo often recurs at previously affected sites after JAK inhibitor therapy is stopped? * JAK inhibition permanently depletes the melanocyte stem cell reservoir in the hair follicle Autoreactive CD8⁺ tissue-resident memory T cells (TRM) remain in previously lesional skin, sustained by IL-15 signaling. JAK inhibition suppresses their signaling but does not eliminate them. Prolonged JAK inhibition selects for keratinocytes carrying activating JAK2 mutations Patients develop neutralizing antidrug antibodies against small-molecule JAK inhibitors Which agent in development for vitiligo does not directly inhibit IFN-γ receptor signaling? Its activity shows that more than one node in the cytokine network may be therapeutically relevant. * Ruxolitinib Upadacitinib Ritlecitinib Brepocitinib Which next step is most consistent with the disease mechanisms discussed in this activity? * A 46-year-old man with Fitzpatrick skin type IV has generalized non-segmental vitiligo covering about 15% of his body surface area (BSA), involving the face, trunk, and forearms. Eight months ago he presented with rapidly spreading disease and confetti-like macules. He was treated with a 12-week oral dexamethasone minipulse, full-body narrowband UVB (NB-UVB) twice weekly, and tacrolimus 0.1% ointment. His disease stabilized, and early perifollicular repigmentation appeared on his face. Ten weeks after the steroid course ended, new macules with trichrome borders have appeared on his trunk. His adherence to NB-UVB and tacrolimus is documented. Stop NB-UVB and start an oral JAK inhibitor as monotherapy, since suppressing IFN-γ signaling alone is enough to restore pigment Add an oral JAK inhibitor for sustained systemic immunomodulation, and continue NB-UVB to supply the melanocyte stimulus Replace tacrolimus with ruxolitinib 1.5% cream on all affected areas and stop NB-UVB Stop all therapy, because recurrence after steroid withdrawal shows the disease is refractory to immune-directed treatment Leave this field blank
