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After completing this case study, students should be able to:
Describe the pathophysiology and clinical presentation of plaque psoriasis.
Discuss the appropriate use of topical, photochemical, and systemic treatment modalities including biologic agents for psoriasis, based on disease severity.
Compare the efficacy and adverse effects of systemic therapies for psoriasis, including first-line standard therapies (methotrexate, acitretin, cyclosporine), second-line therapies (azathioprine, hydroxyurea, sulfasalazine), and the biologic agents (TNF-alpha inhibitors, ustekinumab, IL-17 inhibitors, and IL-23 inhibitors).
Select appropriate therapeutic regimens for patients with plaque psoriasis based on disease severity and patient-specific considerations such as organ dysfunction.
Educate patients with psoriasis about proper use of pharmacotherapy, potential adverse effects, and necessary precautions.
“Nothing is helping my psoriasis.”
Gerald Kent is a 50-year-old man with a 27-year history of psoriasis who presented to the outpatient dermatology clinic 2 days ago with another flare-up of his psoriasis. He was admitted to the inpatient dermatology service for a severe flare of plaque psoriasis involving his arms, legs, elbows, knees, palms, abdomen, back, and scalp (Fig. 110-1).
Plaque psoriasis. This papulosquamous skin disease is characterized by small and large erythematous papules and plaques with overlying adherent silvery scale. (Adapted with permission from: Yancey KB, Lawley, TJ. Approach to the patient with a skin disorder. In: Jameson J, Fauci AS, Kasper DL, et al, eds. Harrison’s Principles of Internal Medicine. 20th ed. 2018. New York, NY: McGraw-Hill Education; 2018. https://accesspharmacy.com. Accessed April 12, 2019.)
The patient was diagnosed with plaque psoriasis at age 23. He initially responded to topical therapy with medium-potency topical corticosteroids, later to calcipotriol. He subsequently required photo-chemotherapy using psoralens with UVA phototherapy (PUVA) to control the condition. PUVA eventually became ineffective, and about 10 years ago he was started on oral methotrexate 5 mg once weekly. Dosage escalations kept the condition under fairly good control for about 5 years. Flare-ups during that period were initially managed with SCAT (short-contact anthralin therapy), but they eventually became more frequent and lesions were more widespread despite increasing the methotrexate dose. A liver biopsy performed about 5 years ago showed no evidence of fibrosis, hepatitis, or cirrhosis.
After requiring two SCAT treatments in a 4-month period, along with methotrexate 25 mg once weekly orally (given as two doses of 12.5 mg 12 hours apart), a change in therapy was considered necessary at that time. Because he was receiving the maximum recommended methotrexate dose and had already reached a lifetime cumulative methotrexate dose of 2.2 grams, he was changed to a cyclic regimen of cyclosporine ...