Psoriasis

Psoriasis is a chronic, immune-mediated skin disease driven by dysregulated interleukin-23/interleukin-17 (IL-23/IL-17) axis signalling, producing markedly increased epidermal cell turnover.^[1] Plaque psoriasis (also called psoriasis vulgaris) is the most common subtype and the focus of this chapter, presenting as inflamed, thickened, well-demarcated plaques with overlying silvery scale, classically on the scalp, extensor elbows and knees, sacral area, and nails. Erythrodermic, guttate, and generalized pustular psoriasis are distinct, less common subtypes with their own presentations and, for the latter two, dermatologic-emergency potential (see Red Flags & Refer) — they are not covered in depth here. Psoriasis is a systemic disease, not just a skin disease: up to one-third of patients develop psoriatic arthritis, and cardiovascular disease, metabolic syndrome, dyslipidemia, diabetes, hypertension, inflammatory bowel disease, and depression/anxiety all occur more often alongside it, which is why comorbidity screening is a standing part of every visit, not an afterthought.^[1] Correct diagnosis matters before any treatment decision is made — several common conditions mimic psoriasis at each affected site, and the wrong diagnosis leads to the wrong treatment (see the differential tables in Assessment & Diagnosis).

Core lesion morphology

Classic plaque psoriasis presents as well-demarcated, inflamed plaques with overlying silvery-white scale. Plaques appear pink-to-red in lightly pigmented skin and purple, dark brown, or grey in darkly pigmented skin, where the erythema and scale can both be far less obvious — a real cause of diagnostic delay if the exam is anchored to the classic light-skin description. Postinflammatory pigmentary change can persist for months after plaques have cleared, particularly in darkly pigmented skin, and should not be mistaken for active disease. The Koebner phenomenon — new psoriatic plaques forming at sites of skin trauma (scratches, surgical scars, sunburn, tattoos) — is characteristic and is a practical reason to counsel patients to minimize skin trauma.

Up to one-third of patients with psoriasis develop psoriatic arthritis, which can affect peripheral joints, the axial spine, entheses (tendon/ligament insertion points), and produce dactylitis ("sausage digit") — new joint symptoms in a patient with psoriasis should always be actively asked about (see Assessment & Diagnosis and Red Flags & Refer).^[2]

• Family history of psoriasis — almost half of patients report an affected relative; genetic predisposition plays a major role.
• Smoking — associated with increased psoriasis severity; ask about smoking status in every patient and offer cessation support.
• Excessive alcohol consumption — associated with increased severity, and relevant to treatment selection given the hepatotoxicity of methotrexate and acitretin.
• Obesity — associated with increased disease severity and with reduced response to some systemic therapies; weight management is a genuine adjunct to disease control, not just general health advice.
• Physical trauma to the skin (Koebner phenomenon) — scratches, sunburn, tattoos, and surgical scars can trigger new plaques at the trauma site.
• Certain medications can trigger or worsen psoriasis, including lithium, beta-blockers, antimalarials, interferon, and, on withdrawal, systemic corticosteroids — ask about new or changed medications when a patient's psoriasis unexpectedly worsens.
• Streptococcal pharyngitis is a recognized trigger specifically for guttate psoriasis (not covered in depth in this chapter).
• Psychological stress is commonly reported by patients as a trigger for flares, though the evidence base for this association is less rigorous than for the factors above.

Face: differentiating psoriasis from its mimics

Hands and feet: differentiating psoriasis from its mimics

Fold (intertriginous) areas: differentiating psoriasis from its mimics

Trunk and extremities: differentiating psoriasis from its mimics

History

• Onset, duration, and pattern of skin lesions; personal or family history of psoriasis or psoriatic arthritis.
• Joint symptoms — pain, swelling, stiffness (especially morning stiffness over 30 minutes), a swollen digit, or heel pain — at every visit, using a structured screen (see PEST below) rather than only asking generally.
• Triggers: recent infection (especially streptococcal pharyngitis for guttate psoriasis), new medications (lithium, beta-blockers, antimalarials, interferon), skin trauma, and psychosocial stress.
• Impact on quality of life, sleep, work/school, and mental health — depression and anxiety are more common in psoriasis and should be actively screened for, not assumed absent.
• Cardiovascular risk factors and other comorbidities (obesity, diabetes, hypertension, dyslipidemia, inflammatory bowel disease) — screen for these directly, particularly in moderate-to-severe disease, and refer for management as needed.^[1]

Examination and severity assessment

Examine the scalp, nails, and typical extensor/flexural sites even if the patient's chief complaint is a single area, since involvement elsewhere supports the diagnosis and informs severity. Estimate body surface area (BSA) involvement using the patient's own palm (including fingers) as a rough guide to 1% BSA. A widely used practical classification: mild disease is under 3% BSA, moderate disease is 3-10% BSA, and severe disease is over 10% BSA — though involvement of a special site (face, scalp, palms/soles, genitals, nails) or a significant quality-of-life impact can make even a lower-BSA case a candidate for systemic therapy regardless of the percentage (see Choose Initial Treatment).^[3] Formal severity indices (PASI — Psoriasis Area and Severity Index; BSA percentage) are clinician-assessed composite ratings used mainly in dermatology practice and clinical trials to track treatment response over time, rather than a simple point-sum screening score — they are not reproduced here as a self-scoring tool.

Screening for psoriatic arthritis: the Psoriasis Epidemiology Screening Tool (PEST)

Ask every psoriasis patient without an existing psoriatic arthritis diagnosis about joint symptoms at least annually, using a structured tool rather than relying on the patient to volunteer joint complaints — many patients do not connect joint pain with their skin disease. The PEST questionnaire is a simple 5-question, 1-point-each screening tool.^[4]

A total score of 3 or more (out of 5) is a positive screen and warrants referral to rheumatology for further assessment — a positive PEST does not by itself confirm psoriatic arthritis, since it can also flag other inflammatory arthritides or fibromyalgia, but it identifies patients who need specialist evaluation rather than reassurance.^[4]

When testing is not needed

Classic plaque psoriasis at typical sites is a clinical diagnosis — skin biopsy is not routinely needed and should be reserved for atypical presentations or when a mimic (see the tables above) cannot be excluded clinically. A KOH scraping or fungal culture is worthwhile whenever tinea is a realistic possibility (fold areas, palms/soles, face), since treating tinea as psoriasis with a topical corticosteroid can worsen a fungal infection.

• Achieve clear or almost-clear skin and durable, long-term disease control — not just partial improvement.
• Relieve itch, pain, and physical discomfort from active plaques.
• Improve health-related quality of life, including the psychosocial and occupational impact of visible skin disease.
• Select therapy that also controls joint disease whenever psoriatic arthritis is present, rather than treating skin and joints as separate problems.
• Minimize treatment-related adverse effects, matching therapy intensity to disease severity and to the individual patient's risk profile and preferences.
• Screen for and manage the comorbidities associated with psoriasis (cardiovascular risk factors, metabolic syndrome, depression/anxiety, inflammatory bowel disease), particularly in moderate-to-severe disease.
• Promptly identify and refer patients with severe, treatment-resistant, or emergency-pattern psoriasis (erythrodermic, generalized pustular) to a dermatologist.

• Regular use of a nonirritating, fragrance-free moisturizer hydrates plaques and reduces itching and scaling; thicker vehicles (ointments and creams) are more effective than lotions at hydrating skin and providing a barrier against irritants. Apply the medicated topical product first, then the moisturizer.
• Wash the scalp at least 2 to 3 times weekly with a nonirritating, fragrance-free shampoo to help moisturize and remove scale debris; applying shampoo to dry hair and scalp before adding water can improve removal of oil-based medicated scalp preparations.
• Minimize skin trauma (scratching, aggressive manicures/pedicures, tight or occlusive clothing) to reduce Koebnerization; keep nails trimmed short.
• In fold areas specifically, minimize friction and occlusion, wear loose-fitting clothing, and use moisture-wicking fabrics to reduce irritation, maceration, and Koebnerization.
• Support smoking cessation and moderation of alcohol intake — both are associated with increased disease severity.
• Encourage a healthy weight — obesity is associated with increased severity and reduced treatment response.
• Address the substantial nonadherence problem with topical therapy directly: ask about cost, inconvenience, time burden, and cosmetic acceptability of the specific vehicle prescribed, and adjust the regimen (e.g., switching a cream to an ointment for better efficacy on thick plaques, or to a lotion/foam for easier application to hair-bearing areas) rather than assuming nonadherence reflects poor motivation.
• Phototherapy: narrow-band UVB (NB-UVB) is the established, most commonly used phototherapy modality for psoriasis inadequately controlled by topical therapy, given its convenience (no photosensitizing agent needed) and favourable safety profile relative to PUVA (psoralen plus UVA), which carries an increased long-term skin-malignancy risk. Administered under dermatology supervision, typically 3 to 5 sessions weekly; can be combined with topical agents. Requires a substantial ongoing time commitment, which is the main practical barrier to its use.^[8]

Pregnancy

• Topical corticosteroids remain a core option throughout pregnancy — low- and moderate-potency agents are preferred over higher-potency agents where adequate.
• Topical vitamin D analogues (calcipotriol, calcitriol) have not been formally established as safe in pregnancy, but systemic absorption of topical calcipotriol is low and clinically significant effects are considered unlikely.
• Topical tazarotene is not recommended in pregnancy given its retinoid class.
• Coal tar and anthralin have measurable systemic absorption; no adverse fetal effects have been consistently reported, but avoid extensive use given limited safety data.
• NB-UVB phototherapy is considered the safest option for widespread psoriasis in pregnancy that is not controlled by topical therapy alone.^[8]
• Methotrexate and acitretin are contraindicated in pregnancy — both are teratogenic (see Pre-Pregnancy Planning below).
• Cyclosporine is not associated with adverse outcomes in the transplant-patient literature; reserve for severe disease in pregnancy, at the minimal effective dose.
• Apremilast and deucravacitinib have limited human pregnancy data, and risk is difficult to assess — avoid unless no adequate alternative exists.
• TNF-alpha inhibitors have the most reassuring pregnancy safety data among the biologics; certolizumab pegol has minimal to no placental transfer in the third trimester and is generally preferred when a biologic is needed close to delivery, while adalimumab, etanercept, and infliximab do cross the placenta (increasingly in the third trimester), with a theoretical concern for neonatal immunosuppression — discuss live-vaccine timing for the infant with the treating team when one of these was used in pregnancy.^[5]
• IL-17, IL-23, and IL-12/23 inhibitors have limited pregnancy data, and risk is difficult to assess — weigh the benefit of disease control carefully against this uncertainty with the patient.

Pre-pregnancy planning

• Methotrexate must be stopped at least 3 months before attempting conception, by both the person who will carry the pregnancy and their partner if also taking methotrexate — though limited evidence suggests paternal low-dose methotrexate exposure near conception has not been associated with adverse pregnancy or fetal outcomes.
• Acitretin requires effective contraception starting 1 month before treatment, continuing throughout treatment, and for at least 3 years after stopping, in anyone who could become pregnant — avoid alcohol during treatment and for a similar interval afterward, since alcohol promotes conversion of acitretin to etretinate, a longer-acting teratogen that can persist in the body for years. No waiting period is required before conception in a person who takes acitretin and produces sperm.

Breastfeeding

• Avoid direct contact between an infant's skin or mouth and any body area treated with a topical product.
• Avoid coal tar given infant absorption risk via skin-to-skin or skin-to-mouth contact.
• Topical corticosteroids carry low risk to a breastfeeding infant except with extensive use of the most potent agents.
• Topical calcineurin inhibitors (tacrolimus, pimecrolimus) have minimal systemic absorption and can be used.
• Methotrexate and acitretin are avoided while breastfeeding given their inherent toxicity, despite low transfer into breast milk.
• Cyclosporine transfers into breast milk in small amounts; use is generally avoided while breastfeeding.
• Apremilast and deucravacitinib transfer into breast milk is unknown; use is not recommended while nursing.
• Certolizumab pegol shows minimal to no transfer into breast milk and is considered acceptable while breastfeeding by most experts. Other biologics are large molecules with low expected transfer, but caution is advised, especially with a newborn or preterm infant, until more data accumulate.

Pediatrics

This chapter focuses on adult plaque psoriasis. Topical therapy remains first-line in children, generally using lower-potency corticosteroids and shorter courses given a higher skin-surface-to-body-mass ratio and greater systemic absorption risk. Several biologics carry a Health Canada-approved pediatric indication for moderate-to-severe plaque psoriasis (including etanercept, ustekinumab, secukinumab, and ixekizumab, subject to age-specific approval) — a child or adolescent who is a candidate for phototherapy or a systemic/biologic agent should be managed together with a pediatric dermatologist rather than dosed by extrapolation from adult regimens.

Renal and hepatic impairment

• Methotrexate is contraindicated in significant renal impairment and active liver disease, and requires more frequent monitoring in mild-moderate impairment.
• Cyclosporine is nephrotoxic — avoid in pre-existing significant renal impairment and monitor renal function closely during use.
• Acitretin requires monitoring of liver enzymes given hepatotoxicity risk; use with caution in hepatic impairment.
• Apremilast requires a reduced dose (10 mg once daily) in severe renal impairment (creatinine clearance under 30 mL/min).
• Deucravacitinib should be avoided in severe hepatic impairment; active infection is also a reason to avoid starting it.
• Most biologics are not renally or hepatically dose-adjusted, but active infection and organ function should be reconfirmed before every dose.

Response assessment

Reassess topical therapy for adequate response after 4 to 8 weeks; question the diagnosis, rather than simply escalating potency again, if there has been no meaningful improvement within 1 to 2 months of an optimally applied regimen.^[6] For systemic and biologic agents, assess response at the interval standard for that agent — most biologics show a meaningful response by 12 to 16 weeks, and a lack of any response by that point should prompt a switch rather than an extended trial.

Baseline and ongoing labs by drug class

• Methotrexate: baseline CBC, liver enzymes, renal function, and hepatitis B/C serology; repeat CBC and liver enzymes periodically (commonly every 2 to 4 weeks initially, then every 8 to 12 weeks once stable) for the duration of therapy.
• Acitretin: baseline and periodic fasting lipid profile, liver enzymes, and renal function.
• Cyclosporine: baseline and regular blood pressure and renal function — do not let serum creatinine rise more than about 30% above baseline without dose reduction or discontinuation; monitor lipids periodically. Not recommended for continuous use beyond about 1 year given cumulative nephrotoxicity risk; intermittent courses are preferred.^[3]
• Apremilast: no routine bloodwork monitoring is required.
• Deucravacitinib: no routine bloodwork monitoring is specifically mandated, though standard infection vigilance applies.
• Biologics (all classes): baseline tuberculosis screening (TST or IGRA, with chest x-ray if positive), hepatitis B and C serology, and confirmation that vaccinations are current before starting; ongoing vigilance for infection at every visit rather than routine repeat bloodwork for most agents.^[5]

Vaccination

Confirm vaccinations are up to date before starting an immunosuppressive or biologic agent wherever possible. Inactivated vaccines (including recombinant zoster vaccine) can be given safely during immunosuppressive or biologic therapy, though the immune response may be somewhat reduced. Avoid live-attenuated vaccines (MMR, varicella, live zoster, yellow fever, live oral typhoid, live intranasal influenza) during methotrexate, cyclosporine, apremilast, deucravacitinib, or biologic therapy.^[10]

Psoriatic arthritis screening

Screen every psoriasis patient without a known psoriatic arthritis diagnosis at least annually using the PEST questionnaire (see Assessment & Diagnosis) — refer to rheumatology for a score of 3 or more, or for any new, persistent joint symptoms regardless of score.^[2]

Comorbidity screening

Screen for cardiovascular risk factors, metabolic syndrome, diabetes, and depression/anxiety, particularly in moderate-to-severe disease — consider earlier and more frequent screening in this group given the higher comorbidity burden.^[1]

1. Confirm adherence and correct application technique before assuming a topical agent has failed — ask specifically about frequency, amount used, and vehicle acceptability, since poor adherence is a well-documented, common, and reversible cause of apparent topical failure.
2. Reconfirm the diagnosis — reconsider the differential-diagnosis tables in Assessment & Diagnosis if response is genuinely inadequate despite confirmed adherence to an appropriate regimen.
3. Increase topical corticosteroid potency, or add/switch to a second topical class (vitamin D analogue, tazarotene, coal tar, or roflumilast) if response remains inadequate after 4 to 8 weeks of an appropriately potent agent.
4. If topical therapy at maximal reasonable intensity is still inadequate, or the disease has crossed the systemic-therapy threshold (over 10% BSA, an inadequately controlled special site, or significant quality-of-life impact), refer for phototherapy if accessible, or start a conventional systemic agent or biologic.
5. If a conventional nonbiologic systemic agent (methotrexate, acitretin, cyclosporine, apremilast, deucravacitinib) is inadequate at an appropriate dose and duration, move to a biologic.
6. If a first biologic is inadequate after an appropriate trial (commonly 12 to 16 weeks), switch to a biologic with a different mechanism of action rather than cycling within the same class, particularly after failure of a TNF-alpha inhibitor.^[9]
7. At any point, actively ask about new joint symptoms — inadequate skin response combined with new joint complaints may mean the current agent, however good for skin, is not adequately controlling the joint domain, and a switch to an agent with established efficacy across both domains (TNF-alpha or IL-17 inhibitor) should be considered.^[2]
8. Refer to dermatology for any patient with recalcitrant disease despite an adequate systemic or biologic trial, disease at a cosmetically or functionally sensitive site not responding to standard measures, or a presentation raising concern for erythrodermic or generalized pustular psoriasis.

• Stopping a long course of a potent topical corticosteroid, or systemic corticosteroid therapy for another condition, abruptly in a patient with psoriasis — can precipitate a rebound flare or generalized pustular psoriasis.
• Using an ultra-high- or high-potency topical corticosteroid long-term on the face or in skin folds — these sites are the most prone to atrophic change, and a lower-potency agent or a non-steroid topical (roflumilast, tacrolimus, pimecrolimus) should be used for anything beyond a short flare.
• Never screening for psoriatic arthritis, or only asking generally about joint pain instead of using a structured tool — many patients do not spontaneously report joint symptoms or connect them to their skin disease.
• Starting a biologic, or apremilast/deucravacitinib/cyclosporine in a patient with infection risk factors, without completing tuberculosis and hepatitis B/C screening first.
• Giving a live vaccine to a patient on methotrexate, cyclosporine, apremilast, deucravacitinib, or a biologic, instead of confirming vaccination status before starting therapy.
• Treating fold-area or facial psoriasis as if it were trunk/extremity psoriasis — these sites need lower topical corticosteroid potency and different adjuncts (see Choose Initial Treatment) given their higher atrophy risk.
• Missing tinea or candidiasis at a fold or palmoplantar site and treating it as psoriasis with a topical corticosteroid, which can worsen an untreated fungal infection — confirm with a KOH scraping or fungal culture when there is any doubt.
• Choosing a TNF-alpha inhibitor in a patient with multiple sclerosis, another demyelinating disease, or significant heart failure — both are relative contraindications for this class.
• Choosing an IL-17 inhibitor in a patient with active or a strong history of inflammatory bowel disease — this class can trigger new-onset or worsen existing IBD; an IL-23 inhibitor or TNF-alpha inhibitor is generally preferred in this situation.
• Exceeding the weekly maximum dose of an ultra-high-potency topical corticosteroid (commonly 50 g/week in adults), or continuing it well beyond the 4-to-8-week window it was intended for.
• Forgetting comorbidity screening (cardiovascular risk factors, metabolic syndrome, depression/anxiety) in a patient with moderate-to-severe disease — psoriasis is a systemic disease, not just a skin disease.
• Assuming a topical calcineurin inhibitor (tacrolimus, pimecrolimus) is on-label for psoriasis — it is Health Canada-approved for atopic dermatitis, and its use in psoriasis (most often at the face and folds) is an established but off-label practice; counsel and document accordingly.

How to use this table: doses are adult doses and require patient-specific confirmation, including renal/hepatic adjustment. Select any drug name to open its complete Pharmasist Drug Database page.

Phototherapy (non-drug)

Narrow-band UVB (NB-UVB) is the established, most commonly used phototherapy modality for psoriasis inadequately controlled by topical therapy — preferred over psoralen-plus-UVA (PUVA) given greater convenience and a more favourable long-term safety profile; PUVA carries an increased skin-malignancy risk with cumulative use. Administered under dermatology supervision, typically 3 to 5 sessions weekly, and can be combined with topical agents such as coal tar, anthralin, a vitamin D analogue, a topical corticosteroid, or tazarotene. Length of remission is longest with phototherapy among available options, though it is not a cure.

Topical corticosteroids, by potency

The mainstay of therapy for localized disease. Use the lowest potency that controls the site being treated; step down or stop once control is achieved rather than continuing indefinitely.

Vitamin D analogues

A nonsteroidal option for the trunk and extremities; not for the face or folds.

Vitamin D analogue / corticosteroid combination

Topical retinoid, and retinoid/corticosteroid combination

Topical phosphodiesterase-4 (PDE4) inhibitor

Topical calcineurin inhibitors

Health Canada-approved for atopic dermatitis; use in psoriasis is an established but off-label practice, particularly at the face and folds given no atrophy risk with extended use.

Keratolytic agents, and corticosteroid/keratolytic combination

Adjuncts that remove scale and improve penetration of a co-applied corticosteroid or vitamin D analogue — not stand-alone treatments for the inflammatory component of psoriasis.

Tars and anthracene derivatives

Older, effective, inexpensive options whose use has declined mainly due to odour, staining, and the resulting adherence problems with the chronic treatment psoriasis needs.

Intralesional corticosteroid

Adjunct topical antifungals (secondary candidiasis in fold areas)

Not psoriasis treatments themselves — added when a macerated or malodorous fold-area plaque suggests secondary candidal infection.

Systemic nonbiologic agents

For moderate-to-severe disease inadequately controlled by topical therapy and phototherapy, or when phototherapy is inaccessible.

Biologic agents — TNF-alpha inhibitors

Effective across all 6 psoriatic arthritis domains including axial disease, with the most reassuring pregnancy safety data among the biologic classes. Relative contraindications: multiple sclerosis or other demyelinating disease; significant heart failure. Complete tuberculosis and hepatitis B/C screening and confirm vaccinations are current before starting any agent in this class; avoid live vaccines during therapy.

Biologic agents — IL-17 inhibitors

Among the most effective classes for skin clearance in current comparative evidence, and effective across all 6 psoriatic arthritis domains including axial disease. Relative contraindication: active or strongly suspected inflammatory bowel disease, which this class can trigger or worsen. Mucocutaneous candidiasis is a class-associated adverse effect. Complete tuberculosis and hepatitis B/C screening and confirm vaccinations are current before starting; avoid live vaccines during therapy.

Biologic agents — IL-23 inhibitors

Strong skin-clearance efficacy with an infrequent maintenance schedule. Effective for peripheral arthritis, enthesitis, dactylitis, and nail disease, but weaker evidence for the axial-spine domain of psoriatic arthritis than TNF-alpha or IL-17 inhibitors. Guselkumab and risankizumab also have inflammatory bowel disease indications. Complete tuberculosis and hepatitis B/C screening and confirm vaccinations are current before starting; avoid live vaccines during therapy.

Biologic agents — IL-12/23 inhibitor

The longest real-world safety experience among current biologics, with quarterly maintenance dosing. Generally less effective on average for skin clearance than the IL-17 and IL-23 inhibitor classes in current comparative evidence. Complete tuberculosis and hepatitis B/C screening and confirm vaccinations are current before starting; avoid live vaccines during therapy.