Serious Infections: Patients treated with HUMIRA are at increased risk for developing serious infections that may lead to hospitalization or death.These infections include active tuberculosis (TB), reactivation of latent TB, invasive fungal infections, and bacterial, viral, and other infections due to opportunistic pathogens. Most patients who developed these infections were taking concomitant immunosuppressants such as methotrexate or corticosteroids.
Malignancies: Lymphoma, including a rare type of T-cell lymphoma, and other malignancies, some fatal, have been reported in patients treated with TNF blockers, including HUMIRA.
Other Serious Adverse Reactions: Patients treated with HUMIRA also may be at risk for other serious adverse reactions, including anaphylaxis, hepatitis B virus reactivation, demyelinating disease, cytopenias, pancytopenia, heart failure, and a lupus-like syndrome.
Plaque Psoriasis: HUMIRA is indicated for the treatment of adult patients with moderate to severe chronic plaque psoriasis who are candidates for systemic therapy or phototherapy, and when other systemic therapies are medically less appropriate. HUMIRA should only be administered to patients who will be closely monitored and have regular follow-up visits with a physician.
Hidradenitis Suppurativa: HUMIRA is indicated for the treatment of adult patients with moderate to severe hidradenitis suppurativa.
Psoriatic Arthritis: HUMIRA is indicated, alone or in combination with non-biologic DMARDs, for reducing signs and symptoms, inhibiting the progression of structural damage, and improving physical function in adult patients with active psoriatic arthritis.
HUMIRA specifically targets and blocks a key driver of systemic inflammation, TNF-α, which can contribute to skin disease on the outside and joint damage on the inside. The relationship between these pharmacodynamic activities and the mechanism(s) by which HUMIRA exerts its clinical effects is unknown.1
Watch this brief video to get an overview of the inflammatory cytokines, including TNF-α, that underlie psoriatic diseases, and how HUMIRA works.
The American Academy of Dermatology recognizes the role of TNF-α in the pathophysiology of psoriasis based on the observation that there are elevated levels of TNF-α in both the affected skin and serum of patients with psoriasis.5Explaining HUMIRA’s mechanism of action to your patients Visit HUMIRA.com to see patient-friendly educational materials developed to do just that Visit HUMIRA.com
— Menter et al. J Am Acad Dermatol. 2008
HS is a severe immune-mediated skin disease: chronic, progressive, inflammatory—and debilitating.6-10 It is characterized by recurrent nodules, abscesses, and fistulas in the apocrine gland-bearing regions of the body.8,11
Watch the video below exploring HUMIRA’s mechanism of action in relation to HS.
Review the role TNF-α plays in HS and see how HUMIRA's mechanism of action works to reduce inflammation.
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One study found that HS lesions expressed 5 times more TNF-α than normal skin.12
The symptomatic lesions of moderate to severe HS can start at any time between puberty and middle age—one study states the average age of onset is age 21.11
The typical presentation of moderate to severe HS symptoms include8:
gluteal cleft 14%
gluteal cleft 13%
The 2nd International Conference on HS offers these diagnostic criteria for HS16:
All three criteria must be met before establishing a diagnosis.
HUMIRA is indicated for moderate to severe HS, which can be progressive and debilitating.1,6,9-11
HS severity may be determined using the Hurley staging system, a widely used classification.17
See how the PIONEER Trials
to HUMIRA’s clinical
Patients treated with HUMIRA are at increased risk for developing serious infections that may lead to hospitalization or death. Most patients who developed these infections were taking concomitant immunosuppressants such as methotrexate or corticosteroids.
Discontinue HUMIRA if a patient develops a serious infection or sepsis.
Reported infections include:
Carefully consider the risks and benefits of treatment with HUMIRA prior to initiating therapy in patients: 1. with chronic or recurrent infection, 2. who have been exposed to TB, 3. with a history of opportunistic infection, 4. who resided in or traveled in regions where mycoses are endemic, 5. with underlying conditions that may predispose them to infection. Monitor patients closely for the development of signs and symptoms of infection during and after treatment with HUMIRA, including the possible development of TB in patients who tested negative for latent TB infection prior to initiating therapy.
Lymphoma and other malignancies, some fatal, have been reported in children and adolescent patients treated with TNF blockers, including HUMIRA. Postmarketing cases of hepatosplenic T-cell lymphoma (HSTCL), a rare type of T-cell lymphoma, have been reported in patients treated with TNF blockers, including HUMIRA. These cases have had a very aggressive disease course and have been fatal. The majority of reported TNF blocker cases have occurred in patients with Crohn’s disease or ulcerative colitis and the majority were in adolescent and young adult males. Almost all of these patients had received treatment with azathioprine or 6-mercaptopurine concomitantly with a TNF blocker at or prior to diagnosis. It is uncertain whether the occurrence of HSTCL is related to use of a TNF blocker or a TNF blocker in combination with these other immunosuppressants.
For full Prescribing Information, visit rxabbvie.com/pdf/humira.pdf
References: 1. HUMIRA Injection [package insert]. North Chicago, IL: AbbVie Inc. 2. Tracey D, Klareskog L, Sasso EH, Salfeld JG, Tak PP. Tumor necrosis factor antagonist mechanisms of action: a comprehensive review. Pharmacol Ther. 2008;117(2):244-279. 3. Data on File ABVRRTI61639. 4. Data on File ABVRRTI61723. 5. Menter A, Gottlieb A, Feldman SR, et al. Guidelines of care for the management of psoriasis and psoriatic arthritis: Section 1. Overview of psoriasis and guidelines of care for the treatment of psoriasis with biologics. J Am Acad Dermatol. 2008;58(5):826-850. 6. Nazary M, van der Zee HH, Prens EP, Folkerts G, Boer J. Pathogenesis and pharmacotherapy of Hidradenitis suppurativa. Euro J Pharm. 2011;672(1-3):1-8. 7. Matusiak L, Bieniek A, Szepietowski JC. Psychophysical aspects of hidradenitis suppurativa. Acta Derm Venereol. 2010;90(3):264-268. 8. Alikhan A, Lynch PJ, Eisen DB. Hidradenitis suppurativa: a comprehensive review. J Am Acad Dermatol. 2009;60(4):539-561. 9. Micheletti RG. Natural history, presentation, and diagnosis of hidradenitis suppurativa. Semin Cutan Med Surg. 2014;33(suppl 3):S51-S53. 10. Poli F, Jemec GBE, Revuz J. Clinical presentation. In: Jemec GBE, Revuz J, Leyden JJ, eds. Hidradenitis suppurativa. Berlin Heidelberg, Germany; Springer-Verlag; 2006:11-24. 11. Collier F, Smith RC, Morton CA. Diagnosis and management of hidradenitis suppurativa. BMJ. 2013;346:f2121. 12. van der Zee HH, de Ruiter L, van der Broecke DG, Dik WA, Laman JD, Prens EP. Elevated levels of tumour necrosis factor (TNF)-α, interleukin (IL)-1B and IL-10 in hidradenitis suppurativa skin: a rationale for targeting TNF-α and IL-B. Br J Dermatol. 2011;164(6):1292-1298. 13. Kurzen H, Kurokawa I, Jemec GBE, et al. What causes hidradenitis suppurativa? Exp Dermatol. 2008;17(5):455-456; discussion 457-472. 14. van der Zee HH, Laman JD, Prens EP. Hidradenitis suppurativa: viewpoint on clinical phenotyping, pathogenesis and novel treatments. Exp Dermatol. 2012;21(10):735-739. 15. Vazquez BG, Alikhan A, Weaver AL, et al. Incidence of hidradenitis suppurativa and associated factors: a population-based study of Olmsted County, Minnesota. J Invest Dermatol. 2013;13(1):97-103. 16. Fimmel S, Zouboulis CC. Comorbidities of hidradenitis suppurativa (acne inversa). Dermatoendocrinol. 2010;2(1):9-16. 17. Jemec GBE. Clinical practice. Hidradenitis suppurativa. N Engl J Med. 2012;366(2):158-164.