Types of Psoriasis
| Type | Appearance | Where | % of Cases |
|---|---|---|---|
| Plaque (vulgaris) | Thick silvery-white scale on red plaques | Elbows, knees, scalp, lower back | ~80–90% |
| Guttate | Teardrop-shaped, smaller lesions | Trunk, limbs | ~10% |
| Inverse | Smooth red plaques, no scale | Flexures (armpits, groin, under breasts) | ~3–5% |
| Pustular | White pustules on red skin | Palms, soles (palmoplantar) or generalised | Rare |
| Erythrodermic | Whole body redness and scaling | Generalised | Rare: emergency |
Treatment Ladder
- Emollients + topical corticosteroids (mild-moderate)
- Topical vitamin D analogues (calcipotriol/betamethasone combination)
- Topical coal tar or dithranol (effective but messy)
- Phototherapy (UVB narrowband, 2–3 sessions/week for 6–8 weeks)
- Systemic: methotrexate, ciclosporin, or acitretin (PUVA/UVB failures)
- Biologics (TNF-α blockers, IL-17 inhibitors, IL-23 inhibitors): for moderate-severe disease; PASI score >10
Psoriasis is more than a skin condition
Psoriasis is a systemic inflammatory disease that happens to be visible on the skin, and treating it as purely dermatological misses much of what matters. Up to a third of people with psoriasis develop psoriatic arthritis, which can begin years after the skin disease and, unlike the rash, causes irreversible joint damage if untreated. Any new joint pain, morning stiffness, swollen fingers or toes, or heel pain in someone with psoriasis should prompt assessment rather than being attributed to unrelated wear and tear.
Psoriasis also carries an increased burden of cardiovascular disease, metabolic syndrome, fatty liver, inflammatory bowel disease and depression. Severe disease is associated with the greatest excess risk. This is why blood pressure, lipids, glucose and weight are checked periodically rather than only when symptoms arise.
Common triggers and aggravating factors
- Streptococcal throat infection, a classic trigger for guttate psoriasis, particularly in younger people.
- Skin trauma, including scratches, sunburn and tattoos, which can seed new plaques along the injury.
- Medication: lithium, beta blockers, antimalarials, and abrupt withdrawal of oral corticosteroids, which can precipitate severe flares.
- Smoking and alcohol, both of which worsen disease and reduce treatment response.
- Stress and infection, and in some people, cold dry weather.
Monitoring required by treatment
Topical treatments need little monitoring, but systemic therapies do. Methotrexate requires regular full blood count, liver function and kidney function, since marrow suppression and hepatotoxicity are the main risks. Ciclosporin requires blood pressure and kidney function monitoring and is used for limited periods. Acitretin is teratogenic for years after stopping and requires strict contraception alongside lipid and liver monitoring. Biologic therapies require screening for tuberculosis and hepatitis before starting. Knowing which tests belong to your treatment, and roughly when they are due, is a practical way to avoid gaps.
References
The clinical information on this page is drawn from peer-reviewed sources indexed by the US National Library of Medicine. Links go to the source so you can read it yourself.
- Psoriatic Arthritis. In: StatPearls. Treasure Island (FL): StatPearls Publishing. NCBI Bookshelf NBK547710
- Oliveira Mde F, Rocha Bde O, Duarte GV. Psoriasis: classical and emerging comorbidities. An Bras Dermatol. 2015;90(1):9-20. doi:10.1590/abd1806-4841.20153038 · PMID 25672294
References
Sources cited on this page. PubMed links open the original abstract.
- Griffiths CEM, Armstrong AW, Gudjonsson JE, Barker JNWN. Psoriasis. Lancet. 2021;397(10281):1301–1315. PMID 34270920 · doi:10.1016/S0140-6736(20)32549-6
Psoriasis and Systemic Inflammation: What Blood Tests Reveal
Psoriasis is not confined to the skin. In moderate-to-severe disease, systemic inflammation is measurable in the blood. C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) are frequently elevated during flares, reflecting the same cytokine cascade – particularly tumour necrosis factor-alpha (TNF-α), interleukin-17 (IL-17), and interleukin-23 (IL-23) – that drives keratinocyte hyperproliferation. A 2021 review in the Journal of the American Academy of Dermatology confirmed that CRP correlates with disease severity scores (PASI), making it a useful objective marker when clinical assessment is uncertain.1
Psoriatic arthritis (PsA) develops in approximately 30% of people with psoriasis, and blood tests help both confirm suspicion and monitor disease. Rheumatoid factor (RF) and anti-CCP antibodies are typically negative in PsA – distinguishing it from rheumatoid arthritis – while uric acid may be elevated. HLA-B27 positivity supports an inflammatory spondyloarthropathy pattern, particularly when axial or sacroiliac joint involvement is present. Full blood count abnormalities, including mild anaemia of chronic disease, can occur in long-standing psoriatic arthritis and warrant monitoring.
Metabolic Comorbidities: The Hidden Risk Beyond Skin
Psoriasis is an independent risk factor for cardiovascular disease, metabolic syndrome, and type 2 diabetes. Fasting glucose, HbA1c, and a full fasting lipid profile are recommended at diagnosis and periodically thereafter, particularly in moderate-to-severe disease. A large prospective study published in JAMA Dermatology found that patients with severe psoriasis had a 58% higher risk of major cardiovascular events compared with controls, independent of traditional risk factors – an association mediated in part by shared inflammatory pathways.2
Thyroid function testing (TSH) is relevant because both hypothyroidism and hyperthyroidism can exacerbate psoriasis, and thyroid autoimmunity occurs at higher rates in psoriasis patients than in the general population. Vitamin D deficiency – measured as 25-hydroxyvitamin D – is also common and clinically meaningful: low vitamin D impairs the regulatory T-cell responses that normally dampen the inflammatory cascade underlying plaque formation.
Monitoring During Biologic and Systemic Therapy
Systemic and biologic treatments for psoriasis require structured blood monitoring. Methotrexate – still widely used – requires baseline and regular liver function tests (ALT, AST, albumin), full blood count (for cytopenias), and renal function (creatinine, eGFR), as it is renally cleared and hepatotoxic with cumulative dosing. Acitretin (a retinoid) necessitates fasting lipid monitoring, as it can raise triglycerides significantly. Ciclosporin requires creatinine, urea, and blood pressure monitoring due to nephrotoxicity risk.
Biologic agents targeting TNF-α, IL-17, or IL-23 require pre-treatment screening for latent tuberculosis (interferon-gamma release assay or Mantoux test) and hepatitis B surface antigen, as immunosuppression can reactivate both. Routine blood monitoring intervals during biologic therapy vary by agent and are set by prescribing guidelines, but typically include full blood count and liver function every three to six months. Your dermatologist or rheumatologist will establish a monitoring schedule specific to your treatment.
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