Psoriasis is a chronic, immune-mediate skin disorder that is characterised by the rapid proliferation of keratinocytes which subsequently leads to the formation of thick, scaly plaques. These plaques commonly appear on the elbows, knees, scalp and lower back (although any body part may be affected). There are different forms of psoriasis which we will discuss in this article, namely:
- Chronic plaque psoriasis - this is also known as psoriasis vulgaris. It is the most common form and makes up 80-90% of cases.
- Localised pustular psoriasis - it is the second most common form of psoriasis and occurs on the palms and soles typically.
- Flexural psoriasis - it is also known as inverse psoriasis.
- Guttate psoriasis - it is also known as droplet psoriasis and is commonly seen on the arms, legs and trunk.
- Erythrodermic psoriasis - it is a rare but potentially fatal medical emergency that presents with widespread, severe psoriasis along with systemic illness.
- Generalised pustular psoriasis - it is also a rare but potentially fatal medical emergency.
- Nail psoriasis - seen In most patients with psoriasis (about 50% will present with nail psoriasis). 10% of psoriasis patients will have only nail manifestations
🏘️ Epidemiology
It is estimated that 1-3% of the population has psoriasis. However, the incidence may be under-estimated due to patients with mild psoriasis not seeking medical assistance.
Most individuals with psoriasis have a family history of the condition.
Psoriasis has a bimodal distribution of 20-30 years old and then again at 50-60 years old. These are sometimes referred to as type I and type II psoriasis.
It affects men and women equally (although localised pustular psoriasis is more common in women).
Ethnic variation is seen with Caucasian groups being more likely to develop the condition as compared with other ethnic groups.
Pathophysiology
The aetiology of psoriasis involves genetic predisposition, environmental triggers and immune dysregulation:
- Genetic predisposition - the heritability of psoriasis lies between 60-90%. Several loci have been associated with psoriasis, the most notable being the PSORS1 locus which is found on chromosome 6. The region includes genes that encode for HLA-Cw6. HLA-Cw6 encodes an antigen that is involved in activation of T-cells. It is strongly linked to an increased susceptibility of psoriasis.
- Environmental triggers - these factors may trigger the onset or exacerbation of psoriasis:
- Streptococcal infections - guttate psoriasis is often seen following an upper respiratory tract infection (such as strep throat). It is not only guttate psoriasis that may be precipitated, but chronic plaque psoriasis, generalised pustular psoriasis and erythrodermic psoriasis too.
- Drugs - medications such as lithium, antimalarials, ß-blockers, NSAIDs, ACEIs, tetracycline and penicillin antibiotics all may lead to the onset of psoriasis. Patients who are on potent oral or topical corticosteroids who have sudden cessation of the medication may develop generalised pustular psoriasis, or severe erythrodermic psoriasis.
- Ultraviolet exposure - sunlight may exacerbate psoriasis in certain individuals, but for most it is usually beneficial.
- Trauma - damage to the skin that was previously uninvolved in psoriasis may subsequently develop psoriatic lesions 1-2 weeks later. This is known as the Koebner phenomenon.
- Hormones - disease activity increases during puberty, post-partum and also during the menopause. In pregnancy the disease improves in 80-90% of patients while in 10-20% it actually worsens. These periods suggest a hormonal influence on disease activity.
- Stress - periods of high psychological stress are shown to exacerbate psoriasis and also may lead to the onset of the disease.
- Smoking - localised pustular psoriasis is almost exclusive to smokers.
- Alcohol - alcohol impairs skin barrier function and alters immune function which can trigger the disease.
- Obesity - adipose tissue may result in a pro-inflammatory state which increases disease activity.
- Immune dysregulation - activation of dendritic cells in the skin (triggered by environmental factors or skin/cell damage) results in presentation of antigens to naïve T-cells in lymph nodes. These naïve T-cells differentiate in to Th1 and Th17 cells. These differentiated Th1 and Th17 cells migrate to the skin and release pro-inflammatory cytokines (such as TNF-alpha, interferon gamma, IL-17 and IL-23). IL-17 in particular drives hyperproliferation of keratinocytes and amplification of the immune response. Recruitment of immune cells to the region perpetuates a cycle of inflammation and keratinocyte hyperproliferation. This is what leads to the characteristic psoriatic plaques made up of hyperkeratotic epidermis with neutrophils and other immune cells. Angiogenesis occurs too which leads to the erythematous nature of the plaques.
🔢 😷 Classification and presentation
- Erythematous plaques with silvery-white scale. Sometimes the scale may be yellow or orange-brown in colour.
- The plaques are typically found on the scalp, post-auricular area, trunk, buttocks, periumbilical area and extensor surfaces (forearms, elbows, shins, knees). If the plaque is found on a joint line, or on the palm/sole it may form a fissure.
- The plaques are usually symmetrically distributed and may coalesce to form larger lesions.
- The lesions can range in size from 1cm upwards. They are usually oval or irregularly shaped.
- Removal of the scale presents a glossy red membrane with pinpoint bleeding. This is known as Auspitz’s sign.
- A halo may present around the plaque (due to vasoconstriction). This is known as Woronoff’s ring.
Pustular psoriasis may be localised or may be generalised:
- Localised pustular psoriasis
- Generalised pustular psoriasis
It is also known as palmoplantar pustular psoriasis as it almost exclusively affects the palms and soles. It may affect the tips of fingers and toes too.
It presents with yellow-brown pustules within an existing psoriatic plaque.
It is associated with thyroid disease.
Generalised pustular psoriasis is a potentially life-threatening emergency. It usually follows a history of chronic plaque psoriasis but may occur independently without a history of psoriasis.
It presents as a widespread erythema, followed by non-follicular pustule formation. These pustules may coalesce to form “lakes of pus”.
Patients may have systemic upset such as fever, malaise, tachycardia, arthralgia and weight loss.
It is the most severe variant of psoriasis and is characterised by intermittent flares with complete/partial remission in between.
The lesions are the same as those seen in chronic plaque psoriasis but often there may be little to no scaling due to the friction at the affected sites.
The sites it affects include the groin, axilla, inframammary folds, abdominal folds, sacrum and gluteal cleft.
The lesions appear red and glossy. A fissure may be present too.
This is a subset of psoriasis that mainly occurs in children, teenagers and adolescents although it can sometimes occur in older adults. It may present independently after an upper respiratory streptococcal infection, or it may present as an acute exacerbation of chronic plaque psoriasis.
It presents with small, round or oval lesions ranging from 2mm-1cm in diameter. The lesions are scaly and may be pink/red.
The lesions are found all over the body over 1-7 days, especially on the trunk and proximal limbs. It may also be seen on the ears, scalp and face (but rarely on the soles).
Erythrodermic psoriasis is a potentially life-threatening emergency. It may develop gradually from chronic plaque psoriasis or it may appear suddenly. It is precipitated by things such as systemic infection, tar, ciclosporin, phototherapy or sudden cessation of corticosteroids.
It presents with diffuse and severe psoriasis (>90% of the total body surface area).
The lesions may be warm. Systemic illness is also present typically (fever, malaise, tachycardia, lymphadenopathy, peripheral oedema).
Nail psoriasis can occur with any type of psoriasis, especially in individuals who develop psoriatic arthritis. It more commonly affects fingernails but toenails are also commonly affected. The entire nail and surrounding structure may be affected.
Manifestations of nail psoriasis are as follows:
- Nail pitting
- Discolouration - an orange-yellow tint may be seen on the nail bed (oil drop sign).
- Subungual hyperkeratosis - this is when there is “plaque” formation under the nail bed.
- Onycholysis - detachment of the nail from the nail bed. This predisposes individuals to infections.
- Nail dystrophy - deformed, thickened, discoloured nails.
🔍 Investigations
Psoriasis is a clinical diagnosis. A skin biopsy may be done if the presentation is atypical.
Patients should be asked of articular symptoms to assess for psoriatic arthritis. This can be done using a Psoriasis Epidemiology Screening Tool (PEST). If the patient score ≥3 out of 5 → refer to rheumatology. There is also another scoring system known as the Dermatology Life Quality Index (DLQI) which helps with understanding the effect it is having on the patient’s quality of life.
🧰 Management
First of all, patients should be offered lifestyle advice that helps to control the psoriasis:
- Smoking cessation
- Limiting alcohol intake
- Weight loss
🥇 Topical therapies
If there are thick plaques present, then we may want to “de-scale” the plaques with coconut oil arachus oil or salicylic acid prior to starting topical therapies. Topical therapies are offered as the first-line option for most types of psoriasis. Patients who are offered topical therapies should be reviewed within four weeks. The therapies can be offered as:
- Creams, lotions or gels - suitable for widespread psoriasis or regions that are hair-bearing.
- Ointments - suitable for areas with thick scale.
Topical therapies include:
- 🥇 Moisturising emollients - these should always be used regularly. They should preferably have no active ingredients within them.
- 🥇 Potent topical corticsteroid (betnovate 0.1%) + topical vitamin D (calciopotriol) - they should both be used once daily, but applied at different times in the day. Topical corticosteroids should not be used for longer than 8 weeks on one site. A four-week treatment break would be needed in between if the skin is not clear.
- Review after 4 weeks
- Good initial response → continue treatment until the skin is clear/nearly clear.
- 🥈 Poor initial response → check adherence and tolerability of topical treatments. Continue topical steroid + vitamin D for another 4 weeks OR use topical vitamin D twice a day and stop the topical corticosteroid.
- Review after another 4 weeks
- 🥉 Poor response to vitamin D alone → use topical corticosteroid twice a day for 4 weeks OR use coal tar once/twice a day.
- If there is treatment-resistant psoriasis
- Dithranol - may be applied for short periods of time (10-30 minutes) before being rinsed off. It works by inhibiting keratinocyte proliferation.
🥈 Phototherapy
Phototherapy is generally considered as a second-line therapy after exhausting topical therapies. Except in guttate psoriasis or moderate-severe psoriasis where it becomes the first-line option.
- Ultraviolet B (UV-B) therapy
- Psoralen plus ultraviolet-A (PUVA) therapy - this is a form of photochemotherpay that uses UV-A along with psoralen which is a photosensitising drug. It is the preferred therapy in palmoplanter psoriasis as it is difficult to treat. However, it is rarely used due to the adverse effects of nausea, pigmentation changes and increased risk of skin cancer.
🥉 Systemic therapies
- 🥇 Methotrexate - methotrexate is a conventional synthetic disease-modifying anti-rheumatic drug (csDMARD) which works by inhibiting dihydrofolate reductase which in turn inhibits DNA synthesis within keratinocytes to control psoriasis. If used in individuals of child-bearing age, contraceptives must be advised during treatment and for 6 months after finishing treatment. This is due to the risk of teratogenicity. It is also contra-indicated during breastfeeding.
- 🥈 Ciclosporin - ciclosporin is a calcineurin inhibitor that is used when rapid control is needed. It is used in palmplantar pustulosis and when patients are considering pregnancy as it is not teratogenic. Other calcineurin inhibitors, such as tacrolimus, may be used for flexural psoriasis.
- 🥉 Acitretin - acitretin is a retinoid. Its use is reserved for those who have failed other systemic options or who are contra-indicated the alternative systemic options. Pregnancy must be avoided during therapy and for 3 years after cessation of treatment.
- Biological agents:
- TNF-alpha inhibitors (infliximab, etanercept, adalimumab) - these are generally reserved for severe and treatment-resistant disease.
- IL-17 and IL-23 inhibitors - these monoclonal antibodies have been licensed for use recently. They have improved efficacy as compared to TNF-alpha inhibiting agents.
- IL-17 ihibitors - secukinumab
- IL-23 inhibitors - ustekinumab
🚨 Complications
- Cardiovascular complications - psoriasis patients have an increased risk of cardiovascular disease (such as myocardial infarction and stroke). As such it is imperative to advise patients on managing risk factors such as smoking, hypertension and obesity need to be managed properly.
- Psoriatic arthritis - this shall be discussed in more detail here.
- Psychosocial effects
- Inflammatory bowel disease - psoriatic patients are at higher risk.