Psoriasis in children — branching viva

Opening question

Examiner: Take me through this child. What is the diagnosis, and what is your frame for managing it? [1]

Candidate: The most likely diagnosis is chronic plaque psoriasis — the thick, well-demarcated, scaly patches on the extensor elbows, knees and scalp, with nail pitting and a father with psoriasis, are the classic picture of the commonest form of childhood psoriasis. My frame is three-layered: match the treatment to the severity and quality-of-life impact, screen the comorbidities that travel with psoriasis, and build a long-term partnership with the family because this is a chronic relapsing disease. Because she is otherwise well with limited sites, this begins with topical therapy and a comorbidity screen, with escalation if the disease or its impact grows. [1] [2]

Examiner: How do you classify paediatric psoriasis, and how does it differ from the adult disease? [2]

Candidate: By lesion shape and site. Chronic plaque psoriasis is the commonest — well-demarcated erythematous plaques with silvery-white scale on the extensor surfaces and scalp, with the Auspitz sign of pinpoint bleeding and Koebner phenomenon where plaques arise in lines of trauma. Acute guttate psoriasis is the other classic form — small droplet papules across the trunk one to two weeks after streptococcal pharyngitis. Children differ from adults: the face is involved more often, the scalp is a frequent first site, and infants can present with napkin or diaper-area psoriasis. Nail and scalp involvement are common, and I would examine all of these. [2] [3]

Branch 1 — pathophysiology

Examiner: Explain the immune mechanism that drives the psoriasis plaque. [2]

Candidate: The core loop is IL-23 driving Th17 T-cells to release IL-17 and IL-22, which act on keratinocytes to drive excessive proliferation and abnormal differentiation. Dendritic cells in the skin release IL-23 and tumour necrosis factor alpha, the Th17 cells amplify the loop, and the keratinocyte response — acanthosis, parakeratosis and neutrophil recruitment — produces the visible plaque. This IL-23 and Th17 and IL-17 axis is exactly what the modern biologics interrupt, each at a defined point. [2] [1]

Examiner: What is the genetic basis, and what ignites the loop in a susceptible child? [2]

Candidate: Psoriasis is polygenic, and the strongest single association is the HLA-Cw6 allele within the PSORS1 locus, linked to early-onset and guttate disease — which fits this child, with her father affected and her childhood onset. The genetics set the stage, but the triggers ignite the loop: streptococcal infection for guttate disease, skin trauma for the Koebner phenomenon, stress, obesity and certain drugs. Identifying and managing these triggers is part of the treatment. [2] [3]

Branch 2 — diagnosis and assessment

Examiner: How will you confirm psoriasis here, and how do you measure severity? [1]

Candidate: The diagnosis is clinical — the well-demarcated, silvery-scaled plaques with Auspitz and Koebner signs, scalp and nail involvement and a family history need no investigation to confirm. I reserve a skin biopsy for the genuinely atypical or non-responsive case. I measure severity by estimating the body surface area involved, recording a Physician Global Assessment or PASI, and capturing quality of life with the Children's Dermatology Life Quality Index. The CDLQI matters because a child with limited skin disease but a devastated quality of life may warrant more aggressive therapy than the surface area alone suggests. [1] [2]

Examiner: What is your differential for a scaly plaque on the elbow? [2]

Candidate: Atopic dermatitis is flexural, poorly demarcated and intensely itchy with an atopy history, whereas psoriasis is extensor, sharply demarcated and thick-scaled. Seborrhoeic dermatitis gives greasy yellowish scale on the scalp and nasolabial folds, and tinea is annular with an advancing edge and confirms with potassium hydroxide examination of skin scrapings. In a child with a non-responsive plaque I would reconsider the diagnosis before escalating. [2] [3]

Branch 3 — treatment and the stepwise pathway

Examiner: What treatment will you give this child? [1]

Candidate: The foundation is emollients, fragrance-free washes, trigger identification and a written management plan. For her limited plaque disease, first-line is a potency-matched topical corticosteroid combined with a vitamin-D analogue such as calcipotriol — a potent corticosteroid such as betamethasone or mometasone for the trunk and limb plaques for a limited course, and a mild corticosteroid such as hydrocortisone 1 per cent on any facial involvement to avoid atrophy. Calcipotriol is steroid-sparing, and after control I step down to calcipotriol or weekend proactive maintenance to reduce flare. [1] [2]

Examiner: When would you escalate, and to what? [1]

Candidate: If the disease becomes moderate or widespread, the first-line second step is narrowband UVB phototherapy at 311 nm, two to three sessions weekly in dermatology. For severe, refractory or quality-of-life-destroying disease, systemic therapy steps in: methotrexate once weekly with folic acid and monitoring is the usual first choice, cyclosporin gives rapid short-course control, and acitretin is avoided in girls of childbearing potential for teratogenicity. If conventional systemic therapy fails or is unsuitable, a biologic follows — etanercept, ustekinumab or the IL-17 and IL-23 inhibitors — after a baseline tuberculosis and infection screen. [1] [10]

Branch 4 — comorbidities and the whole child

Examiner: What comorbidities must you screen for? [11]

Candidate: Three domains. First, obesity and metabolic risk — children with psoriasis are more likely to be overweight, and the excess weight clusters with dyslipidaemia, hypertension and insulin resistance, so I measure body mass index and blood pressure, and arrange lipids and glucose in severe disease. Second, juvenile psoriatic arthritis — I ask about morning stiffness, joint swelling and dactylitis, because nail disease predicts arthritis and missed disease risks permanent joint damage and uveitis. Third, the psychosocial burden — I screen mood and ask about bullying and school refusal, because the visible, chronic nature of psoriasis carries a real depression and quality-of-life burden in children. [11] [2]

Examiner: The family has heard about biologics. What is the paediatric evidence? [9]

Candidate: The landmark trial is Paller's etanercept study in the New England Journal of Medicine in 2008, in which subcutaneous etanercept at 0.8 mg/kg weekly significantly improved plaque psoriasis in children and adolescents over placebo and established the paediatric evidence base. Ustekinumab, which blocks IL-12 and IL-23, and the IL-17 inhibitors secukinumab and ixekizumab extend the options, and several now have age-specific paediatric approvals. The recent biologics network meta-analysis ranks the classes by efficacy and tolerability. A biologic is reserved for severe or refractory disease or where conventional systemic therapy fails, within a specialist service. [9] [10]

Branch 5 — guttate and the emergencies

Examiner: Suppose her younger brother breaks out in teardrop spots after a sore throat. What is that, and what is the prognosis? [7]

Candidate: That is acute guttate psoriasis — the post-streptococcal pattern in which streptococcal superantigens ignite the IL-23 and Th17 and IL-17 loop in many small lesions at once in a genetically susceptible child. I would confirm the streptococcal trigger with a throat swab and antistreptolysin-O titre and treat the infection, manage the eruption with emollients and a mild topical steroid, and add a short course of narrowband UVB for extensive disease. The prognosis is relatively favourable — guttate psoriasis often remits spontaneously over weeks to months — though it can evolve into chronic plaque disease, so I would review him over time. [7] [2]

Examiner: What are the emergencies in paediatric psoriasis? [1]

Candidate: Erythrodermic psoriasis — erythema and scaling over most of the body with temperature and fluid disturbance — and generalised pustular psoriasis — widespread sterile pustules on fiery erythema with fever and skin pain. Both need admission, temperature fluid and electrolyte support, exclusion of sepsis and urgent dermatology involvement for systemic therapy. The other emergency is psychological — severe depression, self-harm or school refusal — which needs immediate psychosocial assessment and support. [1] [3]

Wrap

Examiner: Summarise the paediatric psoriasis stance in one sentence. [1]

Candidate: Recognise the form — chronic plaque, guttate, scalp, nail, face or napkin — make a clinical diagnosis and measure severity with body surface area and the CDLQI, treat limited disease with a potency-matched topical corticosteroid plus calcipotriol and widespread disease with narrowband UVB, reserve methotrexate, cyclosporin and the biologics for severe or refractory disease, and never forget the whole child — because the obesity, the joints and the mood are what turn a skin disease into a childhood that struggles. [1] [11]