Lucan · Conditions

Plaque psoriasis

dermatology10 free questions

Australian guidance: eTG Dermatology — Psoriasis + Australasian College of Dermatologists

1. Definition and epidemiology

Plaque psoriasis is a chronic, immune-mediated inflammatory skin disease characterised by well-demarcated erythematous plaques with silvery scale, driven by keratinocyte hyperproliferation. It affects approximately 2 to 3 percent of the Australian population, with around 500,000 Australians living with the condition at any given time. Peak onset occurs in two bimodal clusters: the second to third decade (Type I, HLA-Cw6 associated, more familial and severe) and the fifth to sixth decade (Type II, less genetic loading).

2. Pathophysiology

Plaque psoriasis is fundamentally a T-cell driven inflammatory loop. Dendritic cells in the dermis are activated by self-antigens, possibly triggered by streptococcal superantigens, trauma (Koebner phenomenon), or medications such as lithium and beta-blockers. These dendritic cells drive naive T cells toward a Th1 and Th17 phenotype, releasing tumour necrosis factor-alpha (TNF-alpha), interferon-gamma, interleukin-17 (IL-17), and IL-22. IL-17 and IL-22 act on keratinocytes to produce massive epidermal hyperplasia: the normal 28-day transit time from basal layer to skin surface is compressed to as little as 3 to 4 days. This results in parakeratosis (retention of keratinocyte nuclei in the stratum corneum), loss of the granular layer, and the characteristic silvery scale. Neutrophils accumulate beneath the parakeratotic scale to form Munro microabscesses. Dermal vasculature is dilated and tortuous, which accounts for the erythema and the Auspitz sign (pinpoint bleeding on scale removal as thin suprapapillary dermis is disrupted).

3. Clinical presentation and diagnostic criteria

The classic lesion is a well-defined, salmon-pink or erythematous plaque with overlying silvery-white adherent scale, distributed symmetrically on extensor surfaces: elbows, knees, scalp, and the lumbosacral region are the most commonly affected sites. Nail involvement occurs in 50 percent of patients with skin disease, manifesting as pitting (the most common), onycholysis, oil-drop discolouration, and subungual hyperkeratosis. Scalp psoriasis typically presents as thick adherent scale beyond the hairline. Psoriasis is a clinical diagnosis; no formal diagnostic criteria are required. The Auspitz sign and Koebner phenomenon support the diagnosis. Skin biopsy is reserved for atypical presentations. Psoriatic arthritis (PsA) affects up to 30 percent of patients and may precede, coincide with, or follow skin disease; the most common pattern is asymmetric oligoarthritis. Genital and flexural (inverse) psoriasis lack scale due to moisture and require separate consideration.

4. Investigations and AU-specific cutoffs

Psoriasis is a clinical diagnosis and routine investigations are not required to confirm it. The following are indicated when initiating systemic therapy or monitoring for comorbidities:

Full blood count and liver function tests are baseline prior to methotrexate or acitretin. Renal function (eGFR and creatinine) is required before cyclosporin, with cyclosporin contraindicated if eGFR is persistently below 60 mL/min/1.73m2. Fasting lipid profile and liver enzymes are required before acitretin given teratogenicity and dyslipidaemia risk. HbA1c and fasting glucose screen for the metabolic syndrome, which is significantly more prevalent in patients with moderate to severe psoriasis. Prior to commencing a biologic agent, the following are required per Australasian College of Dermatologists and PBS authority criteria: hepatitis B surface antigen and core antibody, hepatitis C antibody, HIV serology, tuberculosis screening (quantiferon-TB gold or Mantoux), and a current chest X-ray. BSA (body surface area) involvement of 10 percent or greater, or PASI (Psoriasis Area and Severity Index) of 10 or greater, or DLQI (Dermatology Life Quality Index) above 10, defines moderate to severe disease and is required to qualify for PBS-subsidised biologic therapy.

5. Management

Management is stratified by disease severity. Mild disease (BSA less than 10 percent, PASI below 10, DLQI 10 or below) is managed with topical agents. Moderate to severe disease qualifies for phototherapy or systemic agents.

Topical first-line agents include potent to very potent topical corticosteroids (e.g. betamethasone dipropionate) used on body plaques, with a lower-potency agent reserved for the face and flexures. Vitamin D analogues (calcipotriol) are used in combination with corticosteroids; the fixed-dose combination calcipotriol/betamethasone dipropionate (Enstilar foam or Daivobet gel, PBS listed) improves adherence and efficacy over monotherapy. Coal tar preparations remain useful adjuncts for scalp disease.

Phototherapy with narrowband ultraviolet B (NBUVB) is the preferred second-line option for widespread disease unsuitable for topicals, especially in pregnancy. PUVA (psoralen plus ultraviolet A) is now less commonly used due to carcinogenic risk.

Conventional systemic agents include methotrexate (first-line systemic, PBS listed), cyclosporin (rapid onset, used for short courses or flares), and acitretin (useful for palmoplantar or pustular variants but requires strict contraception for three years post-cessation in women of childbearing age due to teratogenicity).

Biologic agents are approved for moderate to severe plaque psoriasis in adults who have failed or are contraindicated to at least one conventional systemic agent. PBS Authority criteria require PASI 10 or greater (or BSA 10 or greater) plus DLQI above 10. Approved classes include TNF-alpha inhibitors (adalimumab, etanercept), IL-17 inhibitors (secukinumab, ixekizumab), IL-12/23 inhibitor (ustekinumab), and IL-23 inhibitors (guselkumab, risankizumab, tildrakizumab). For PBS continuation, PASI 75 response (at least 75 percent reduction from baseline PASI) is required at week 16 to 28.

Patient education should address trigger avoidance: streptococcal throat infections, stress, smoking, alcohol, and offending medications. A shared care model involving the GP and dermatologist is the AU standard of care.

6. Pharmacology and AU PBS notes

Calcipotriol/betamethasone dipropionate (Daivobet gel, Enstilar foam): PBS item 8875M/8876N for moderate to severe plaque psoriasis on the body. Limit of one tube per prescription; not for the face.

Methotrexate: PBS streamlined authority for moderate to severe psoriasis. Initiated at 5 to 10 mg weekly, titrated to 15 to 25 mg weekly. Folic acid 5 mg weekly (not on methotrexate day) is co-prescribed to reduce mucositis and hepatotoxicity. Contraindicated in pregnancy (category X), significant hepatic fibrosis, or renal impairment. Baseline and annual liver biopsy replaced by FIB-4 score or elastography per current Australian practice.

Cyclosporin: not for long-term use; maximum 1 to 2 years. Monitor blood pressure and renal function fortnightly initially. AU brand: Neoral.

Acitretin: PBS listed for severe recalcitrant psoriasis. Teratogenicity mandates contraception for 3 years post-cessation. No alcohol during treatment (forms etretinate).

Adalimumab (Humira, Hadlima): PBS Authority Item for severe plaque psoriasis failing conventional systemics. 80 mg SC at week 0, 40 mg at week 1, then 40 mg fortnightly.

Secukinumab (Cosentyx): IL-17A inhibitor. 300 mg SC weekly for 5 doses (induction), then monthly. PBS listed for severe plaque psoriasis. Caution in inflammatory bowel disease (may worsen).

Guselkumab (Tremfya): IL-23 inhibitor. 100 mg SC at weeks 0 and 4, then every 8 weeks. PBS listed.

7. Complications and monitoring

Psoriatic arthritis affects up to 30 percent of patients; annual PEST (Psoriasis Epidemiology Screening Tool) or PASE screening is recommended in primary care to facilitate early rheumatology referral, as joint damage is preventable with early treatment.

Metabolic syndrome (obesity, hypertension, dyslipidaemia, insulin resistance) is 1.5 to 2 times more prevalent in patients with psoriasis compared to the general population; annual fasting lipids, blood pressure, and HbA1c monitoring is standard AU practice.

Cardiovascular disease risk is elevated independently of traditional risk factors; absolute cardiovascular risk assessment (AusCVDRisk calculator) should be performed annually in patients with moderate to severe disease.

Lymphoma risk is modestly elevated, particularly with long-term PUVA use (T-cell lymphoma) and possibly with biologic use; no specific surveillance beyond standard cancer screening is currently recommended in Australia.

Depression and anxiety are highly prevalent comorbidities, with quality of life impairment comparable to ischaemic heart disease; DLQI and PHQ-9 screening at each review is best practice.

Monitoring on biologic therapy: full blood count and liver function tests every 6 to 12 months; annual tuberculosis and hepatitis B re-screening is not routinely required after baseline unless new risk factors emerge.

Skin cancer surveillance: annual skin check recommended for patients on long-term cyclosporin, PUVA, or biologic therapy given increased susceptibility.

Practise this in Lucan

Written for Australian practice and grounded in the guidance named above. Study material only — not medical advice. Always check against current guidelines.