Atopic Dermatitis vs Psoriasis

Why Barrier dysfunction with Th2 inflammation is correct

• Atopic dermatitis arises from an impaired epidermal barrier (often filaggrin-related) layered with Th2-skewed immune inflammation.
• The chronic pruritic flexural plaques, dry skin, and personal history of asthma place this squarely in the atopic march.
• Barrier loss drives water loss and allergen entry, perpetuating the itch-scratch cycle and secondary infection risk.

Why the others are wrong

• IgE-mediated contact hypersensitivity — Right-immunology-wrong-mechanism trap: allergic contact dermatitis is a delayed T-cell reaction at the contact site, not the barrier-plus-Th2 atopic process.
• IL-23/IL-17 keratinocyte hyperproliferation — Wrong-pathway trap: the IL-23/Th17 axis drives psoriasis, which typically forms well-demarcated plaques with silvery scale on extensor surfaces, not intensely pruritic flexural eczema with xerosis in an atopic child.
• Dermatophyte fungal invasion of the skin — Mimic trap: tinea produces annular scaly plaques with central clearing, not chronic atopic flexural disease.

Why Infliximab is correct

• Infliximab is a tumor necrosis factor (TNF)-alpha inhibitor, and TNF inhibitors can cause new-onset or worsening heart failure (a class labeling warning)
• In the ATTACH trial of patients with NYHA class III-IV heart failure, infliximab at 10 mg/kg increased deaths and heart-failure hospitalizations; the label contraindicates doses above 5 mg/kg in moderate-to-severe heart failure
• The 2019 AAD-NPF joint psoriasis guidelines advise avoiding TNF inhibitors in NYHA class III-IV heart failure, and the 2021 ACR rheumatoid arthritis guideline likewise favors non-TNF agents in that setting
• This patient's NYHA class III ischemic cardiomyopathy with LVEF 30% is exactly that setting, so an IL-17 or IL-23 pathway agent is the safer choice for his psoriasis
• He has no joint symptoms, so there is no psoriatic arthritis to weigh in the choice; even when psoriatic arthritis is present, secukinumab, ustekinumab, and guselkumab are also approved for it, so a TNF inhibitor's joint benefit would not offset its heart-failure risk

Why the others are wrong

• Secukinumab - an IL-17A inhibitor with no heart-failure warning; its class caution is new or worsening inflammatory bowel disease, which he does not have, so it is a reasonable option for him (the trap is carrying the IL-17 bowel caution over to the heart)
• Ustekinumab - an IL-12/23 p40 inhibitor with no heart-failure warning; its label warns mainly of infection and, rarely, posterior reversible encephalopathy syndrome, so it is an appropriate non-TNF choice in moderate-to-severe heart failure
• Guselkumab - an IL-23 p19 inhibitor with no heart-failure warning, so it is a guideline-supported alternative for severe plaque psoriasis in a patient with NYHA class III heart failure

Additional high-yield points

• The heart-failure warning applies to the whole TNF inhibitor class (adalimumab, etanercept, certolizumab pegol, golimumab), not only infliximab; etanercept showed no benefit in heart-failure trials (RENAISSANCE, RECOVER)
• Other reasons to avoid TNF inhibitors: demyelinating disease such as multiple sclerosis or optic neuritis, and untreated latent tuberculosis or active hepatitis B
• Screen for latent tuberculosis (IGRA or tuberculin skin test) before starting any biologic for psoriasis; hepatitis B screening is required before TNF inhibitors and is routinely done before other biologics