Psoriasis is a common, chronic, often disfiguring skin condition affecting 2-to-3 per cent of the Irish population. Males and females are equally affected. Initial presentation is usually in the late teens to early 20s. Around 75 per cent of cases occur before the age of 40. There is a second peak in presentation, involving a smaller group of patients, over the age of 50.

Over the years, it has become increasingly evident that psoriasis is not only a skin disease. Systemic comorbidities include arthritis, cardiovascular disease, obesity, fatty liver disease, anxiety, and depression. Recent therapeutic advances with targeted biological drugs have revolutionised the management of severe psoriasis. Unfortunately for the two-thirds of affected individuals with mild psoriasis, we have not witnessed similar advances in topical therapies. Nevertheless, primary care has much to contribute to the ongoing care of psoriasis patients.

Disease activity fluctuates unpredictably over the years – 10-to-15 per cent of patients get a period of remission of five years or more. While we do not have a cure, there is much that can be done to help control the condition. Even though treatment regimens may be messy and give variable results, a cautiously optimistic approach should be adopted when managing individuals with mild psoriasis presenting in primary care.

It follows that GPs need to have a good understanding of psoriasis, the treatment options available in primary care, possible comorbidities, and recognise when it is appropriate to refer to secondary care.

Symptoms and signs

In the past psoriasis was considered a non-pruritic condition. In fact, itch is common although generally it is less marked than in eczema.

As psoriasis is a clinical diagnosis, careful examination of the presenting lesions is most important. Chronic plaque psoriasis is the most common form of psoriasis, accounting for up to 90 per cent of cases. Individual lesions are sharply demarcated, thickened, salmon-pink plaques that are covered in scales, which can be fine and silvery, or thick, yellow, and adherent. Plaques are symmetrically distributed, most commonly over the elbows, knees, lower back, umbilicus, and natal cleft. Plaques range from small, guttate type (<1cm) lesions to extensive confluent plaques. The extent of skin disease can fluctuate over months or years. After clearance there can be post-inflammatory erythema that persists for several months. Post-inflammatory hypo- and hyper-pigmentation are common in patients with skin of colour (Image 9).

Auspitz sign helps distinguish psoriasis from other rashes (Image 4 and Image 5). Scratching a plaque lifts the silvery scale, making it more apparent. Lifting large scales may cause capillary bleeding.

Plaques in body flexures (inverse pattern psoriasis) such as the axilla, gluteal fold, or under the breasts, have little or no scale and the plaques are thinner. These changes in clinical presentation are due to occlusion where skin meets skin. Plaques have a glazed appearance, a sharply defined margin, and an exudate may be present (Image 2).

Classification of psoriasis can be confusing. All plaques are essentially similar, involving inflammation and hyperproliferation of the skin. The classification in Figure 1 is based on the body area involved. Clinical features vary accordingly, eg, plaques in flexural sites, where skin meets skin, do not show scale, and are thinner than plaques over the knees, elbows, etc (Image 1).

The site of skin involvement will also affect our choice of treatment, eg, potent topical steroids may be used for psoriasis over the elbows, trunk, or knees, but only mild or moderate steroids should be used in flexural
areas such as the axilla and groin.

TRAUMA 

Psoriatic plaques may develop at sites of skin injury – the Koebner phenomenon.

INFECTION 

Streptococcal throat infection triggers 60 percent of guttate psoriasis. It may also cause flare-ups of chronic plaque disease. Tonsillectomy may be considered if the problem recurs. HIV infection may trigger or exacerbate psoriasis.

SUNLIGHT 

Most psoriasis improves on exposure to sunlight, but in 10 per cent sunlight can cause a flare of disease. Patients should be warned that psoriasis may spread to sunburned areas ( Koebner phenomenon ).

STRESS 

In surveys, patients repeatedly report that they find that stress exacerbates their psoriasis. As it is such a stressful condition, it is often not clear which came first.

ALCOHOL EXCESS AND SMOKING 

Psoriasis patients consume more alcohol and smoke more than their peers. Whether they have a causal role, or just reflect increased stress, is not clear. Smoking does increase the risk of developing palmoplantar pustulosis and stopping smoking may resolve the problem.

DRUGS 

Lithium, anti-TNF drugs, and chloroquine may trigger exacerbations of psoriasis, although most patients can take these medications without effect on their disease. Withdrawal of systemic or super-potent TCS may cause a flare of psoriasis, especially if patients have been on them for some time.

Aetiology

The exact cause of psoriasis is not fully understood, but involves a complex interplay between genetic and environmental factors. Lymphocytes release cytokines, interferon alpha, interleukin, and tumour necrosis factor (TNF) that result in overgrowth of the epidermis (resulting in thick, silvery scaled plaques), capillary proliferation, and inflammation (giving a red colour). There has been a steady increase in the number of effective biological therapies targeting the body’s immune response available in secondary care. While they are expensive, they can give dramatic improvement in disease control.

A family history of psoriasis occurs in about 30 per cent of patients. Monozygotic twins have a two-to-three-fold increased risk of psoriasis compared with dizygotic twins. If one parent has psoriasis, there is a 14 per cent risk of their child developing it. If both parents are affected the risk is 41 per cent. If one sibling has psoriasis the risk is 6 per cent. Various triggers may trigger or exacerbate psoriasis (see Figure 2).

Differentiating psoriasis from eczema

• The well-demarcated edge is probably the most distinguishing feature of psoriasis (Image 5). The edge of a patch of eczema is more diffuse.
• Scratching a plaque of psoriasis makes the silvery scale more obvious.
• Patches of chronic eczema show lichenification; ie, skin thickening with exaggeration of skin markings.
• Psoriasis has a characteristic distribution pattern on the extensor surfaces, especially on the elbows and knees, and on the scalp. Atopic eczema favours the flexural surfaces of elbows and knees.
• The Koebner phenomenon, that may be seen in psoriasis, does not occur in eczema.

Management of psoriasis in primary care

Advances in biological therapies have revolutionised management in secondary care. Huge resources have been invested in the development of these targeted therapies. No such effort is apparent to find new, effective, and acceptable treatments for the majority of patients with milder disease. Psoriasis therefore remains a difficult-to-treat condition in the primary care setting. What constitutes an acceptable level of control is very subjective. Many find topical therapies burdensome and results may be limited.

Before making a shared decision on a treatment plan, explore the patient’s knowledge, hopes, and expectations, and to what extent psoriasis impacts their daily life. There is much that we can do to help our patients deal with their disease and a positive, realistic attitude should be maintained. All patients need time to discuss the condition. Information can be supplemented by patient information leaflets.

Patients need to accept that they have a chronic condition that cannot be cured and will require long-term management. The effects of psoriasis on work, personal relationships, and social life should be explored. Many patients need to hear that psoriasis is not infectious. In recent years the Psoriasis Association has been very active in providing advice, education, and support to patients. All patients should consider joining the association.

Primary care treatments

Emollients

Emollients are often forgotten when treating psoriasis. All patients should
be advised to use emollients liberally, daily. Emollients help moisturise plaques and reduce scaling. They may make it more comfortable and less obvious. Many patients are happy with this level of improvement. Patients need to try a few different emollients to find which one combines acceptability with effectiveness for them. All patients suffering from psoriasis should be prescribed sufficient emollient to allow frequent, generous application.

Tar

Tar has long been used to treat psoriasis and still has a place today. It can be used as crude coal tar or tar extracts. Crude coal tar is messy, inconvenient, and smelly. There are several commercial preparations of tar extracts available as creams, lotions, and shampoos. These are less effective than crude coal tar, but more convenient and pleasant to use. There is no evidence that therapeutic use of tar products causes skin or internal cancer.

Dithranol

Like tar, dithranol is a long established, effective, and safe topical therapy for psoriasis. With short contact dithranol therapy, it is left on the skin for 20-to-30 minutes before being washed off. It is effective in 50-to-60 per cent of patients and some achieve a prolonged remission. It can cause skin irritation and pigmentation. It stains any surface it comes in contact with. In the past it was available in various strengths (dithrocream 0.1 per cent, 0.25 per cent, 0.5 per cent, 1 per cent, and 2 per cent). Recently a 15 per cent non-licensed preparation has been available.

Topical Treatments for Psoriasis

TREATMENT	ADVANTAGES	PROBLEMS
Emollients	Low side-effect rate, cheap	Limited efficacy when used alone
Tar	Effective. Tar extracts less effective, but easier to use	Messy, smelly. Irritation
Dithranol	Short contact is effective and safe	Stains skin and anything it comes in contact with. Skin irritation
Corticosteroids (TCSs)	Effective, easy to use	Skin atrophy, bruising, striae. Rebound of psoriasis on stopping
Vitamin D analogues	Effective, easy to use	Skin irritation
Tacrolimus	Very effective on thin plaques only	Need sun protection and avoidance. Burning sensation for first five days of application. Not a licensed psoriasis treatment

Topical corticosteroids

Topical steroids are easy to prescribe and pleasant to use. Their use in treating plaque psoriasis was controversial up to recent years and indeed their use was once frowned upon. NICE guidelines in the UK give the use of topical corticosteroid (TCSs) in psoriasis a favourable recommendation.

Problems with their use include:

• Side-effects on the skin – atrophy, telangiectasia, bruising (Image 7).

• Steroids sometimes seem to change the nature of the disease making it unstable. Unstable psoriasis looks red and angry. In this state it is difficult to treat. If calcipotriol, tar, or dithranol are applied they may exacerbate the irritation. The risk is greatest when a potent or very potent topical steroid has been applied for some time and then suddenly stopped. In extreme cases generalised pustular psoriasis may be precipitated. When plaques of psoriasis are irritated and acutely inflamed it is best to apply generous amounts of emollient until the disease again stabilises (the plaques regain their pink colour and are covered with silvery scales). Patients with more widespread unstable disease and those with generalised pustular psoriasis require urgent referral.

• Tachyphylaxis – extended use of TCSs give less and less of a therapeutic response. This happens with all potencies of steroid. To avoid this phenomenon continuous application of TCSs should not be continued for longer than one month.

TCSs are best used in combination with other topical therapies to bring about a speedy clinical improvement. There is evidence that the best results when treating plaque psoriasis are with a combination of a vitamin D analogue with betamethasone (dovobet). Combining a topical steroid with tar or dithranol gives better results than either used alone. Combination therapy is continued for one month at which point the topical steroid should be stopped or used only intermittently.

Vitamin D analogues

Vitamin D analogues are usually combined with a potent TCS in fixed-dose combination products. The fixed combination products containing calcipotriol plus betamethasone (enstilar foam, dovobet gel, dovobet ointment) are often used as a first-line option for chronic plaque psoriasis. Another fixed-combination product more recently available in Ireland combines calcipotriene and betamethasone dipropionate (wynzora cream). It is an option if the patient prefers a less greasy preparation. These applications do not stain, are easy to use, and are usually well tolerated. Because of their ease of use they are the treatment of choice when managing chronic plaque psoriasis in primary care, involving less than 30 per cent of the body surface. When the psoriasis plaques are flat, and the skin feels smooth to touch, these products should be stopped. Some patients may need to continue applying them once or twice weekly to maintain response. As they each contain a potent topical steroid, they should not be applied to the face, flexures, or genitalia.

Calcineurin inhibitors

Tacrolimus (protopic) is the only calcineurin inhibitor available in Ireland. It is very effective on thin plaques of psoriasis. Best results are with the 0.1 per cent ointment preparation. Such plaques are found on facial, genital, and flexural areas. Calcineurin inhibitors are immunosuppressant and, in theory, might interfere with skin repair after ultraviolet light damage. Although photoprotection and sun avoidance are advised, long-term studies have shown no increase in either skin or internal cancer with tacrolimus. A burning sensation at the site of application for the first five days of treatment is common, but settles if treatment is persevered with. Using tacrolimus to treat psoriasis is off label. Patients should be advised of this.

Flexural psoriasis

Essentially flexures are areas of the body where skin meets skin. This creates an occlusive effect that affects both the presentation and the management of psoriasis. Flexures that may be involved in psoriasis include the axilla, gluteal cleft, umbilicus, under the breasts, retro auricular fold, skin folds, and the inguinal crease. This pattern is also referred to as inverse pattern psoriasis. Plaques are sharply demarcated, thin, and have little or no scale. They are pink-to-red in colour and have a shiny, glazed appearance. An exudate may be present.

Facial and genital skin is thin and the treatment regimen for both areas is similar to that for flexural psoriasis. Patients should be asked if they have flexural or genital involvement as very often, they will not volunteer this information. Great psychosocial distress may ensue when such areas are involved.

Emollients are always advised. Potent and very potent corticosteroids risk skin atrophy on flexures, the face, and genitalia, and should be avoided. Hydrocortisone is generally not very effective. The moderate potency clobetasone butyrate (eumovate) is the best choice, combining efficacy with safety. The ointment formulation is favoured. It can be combined with calcipotriol ointment (dovonex). One can be applied in the morning with the other at night.

Tacrolimus (protopic) is ineffective on the thick lesions of chronic plaque psoriasis. In contrast, the thin plaques and the occlusive effect in flexures enhance drug penetration and effectiveness. Studies have shown a response rate of 90 per cent, far better than many of our other treatment options. They remain unlicensed for use in psoriasis.

Scalp psoriasis

Scalp involvement (Image 6) is common and may sometimes be the only manifestation of the disease. Up to 80 per cent of psoriasis patients have scalp involvement. In 40 per cent of these it involves more than half of the scalp surface. The prevalence of scalp involvement increases with duration of the disease.

Treatment requires getting through a thick coverage of scalp hair necessitating non-messy solutions. This is difficult to achieve with creams, ointments, and especially pomades. Patient compliance and tolerability can play a crucial role in successful management. Patients prefer gels, lotions, and foams. Oils and creams are less acceptable, with ointments the least attractive option. Therefore, when it comes to treatment, choice of vehicle can be as important as the choice of therapy itself.

Two approaches have been adopted in an attempt to improve acceptability and effectiveness of topical treatment:

1) Reduce messiness of treatment
Cocois contains tar and salicylic acid. It has a bit of a smell, but is generally well-tolerated. It can be applied at night and washed out in the morning, longer than recommended by the manufacturers.
2) Combine treatments
Combine TCS and tar – Cocois can be applied as above. After washing it out in the morning a steroid scalp application is applied.

Combine TCS and a vitamin D analogue; eg, Dovobet gel. It is applied at night to the scalp and washed out in the morning.

If the scalp disease is hyperkeratotic the thick scales need to be softened and removed. Arachis oil, coconut oil, or olive oil may help. Coconut oil is easy to apply to scalp plaques and can be left on for 30 minutes or overnight. A comb can then be used to gently lift off the softened plaques. The hair is then washed with tar-based shampoo.

Pregnancy and psoriasis

Psoriasis generally tends to improve during pregnancy, but may sometimes flare. Exacerbations often improve after delivery. Topical vitamin D analogues and TCSs are safe in pregnancy. Use the least potent TCS application.

Comorbidity in psoriasis

Psoriasis is now established as a systemic, inflammatory disease not just involving the skin. Common systemic manifestations include:

• Cardiovascular disease;
• Depression;
• Psoriatic arthritis (PsA).

GPs are ideally placed to assess and manage multimorbidity and are best placed to provide and co-ordinate care for this group of patients.

Treatment of Chronic Plaque Psoriasis

TREATMENT OF CHRONIC PLAQUE PSORIASIS

First-line – Once daily calcipotriol plus betamethasone (enstilar foam, dovobet gel, dovobet ointment) or calcipotriene plus betamethasone dipropionate (wynzora cream)

Second-line – Betamethasone ointment am + tar preparation

(exorex lotion) pm

(dovonex) pm

Third-line – Betamethasone ointment am + short contact dithranol therapy pm

FACE, FLEXURES, GENITALIA

First-line – Clobetasone butyrate (eumovate) ointment am + calcipotriol ointment

Second-line Tacrolimus 0.1 per cent (protopic) once daily

SCALP

First choice – dovobet gel pm Second-line– Cocois pm plus betamethasone scalp application am

FIGURE 4: Treatment algorithm for topical treatment of chronic plaque psoriasis

When to Consider Referral to Secondary Care

• Inadequate response to topical therapy – emollients, vitamin D analogues, and TCSs
• Psoriasis covering more than 15-to-20 per cent of the body surface
• Widespread unstable or erythrodermic psoriasis
• Generalised pustular psoriasis
• PsA
• Disease severity causing unemployment
• Marked psychosocial impact

Cardiovascular disease

In recent years repeated studies have confirmed that there is an association between psoriasis and the metabolic syndrome diabetes mellitus, obesity, heart failure, and hypertension. As a consequence, psoriasis patients are at increased risk of type 2 diabetes mellitus (five-fold), myocardial infarction (two-to-three-fold), and have a life expectancy four years shorter than healthy controls. Psoriasis is now established as an independent risk factor for cardiovascular disease. Risk factors for cardiovascular disease should be addressed. The level of risk correlates with the severity of psoriasis.

All psoriasis patients should have:

• Advice on a healthy diet and maintaining a healthy weight. Obesity seems to increase the risk of psoriasis and reduce the effectiveness of treatment. Losing weight seems to increase treatment effectiveness.
• Regular blood pressure checks.
• Waist measurement.
• Body mass index (BMI) measurement.
• Advice on smoking cessation.
• A random HbA1C (or fasting glucose) and fasting lipids should be checked if the BMI is greater than >25 or the waist circumference is greater than 80cm or there is a first-degree relative with type 2 diabetes mellitus.

Depression

There is a significant psychiatric and psychosocial morbidity risk in psoriasis patients. It has been shown that there is a 6 per cent prevalence of active suicidal ideation (versus 2.4-to-3.3 per cent in general medical patients). Psoriasis is a systemic inflammatory disease. Inflammatory mediators such as TNF mediate depression. It is of interest that anti-TNF therapies have shown promising antidepressant activity in clinical trials. Patients’ mood, and their feelings regarding their disease and its management, should regularly be discussed.

Psoriatic arthritis

PsA (Image 8) develops in up to 30 per cent of patients with psoriasis, presenting as a range of destructive inflammatory arthropathies. Up to 50 per cent of patients who develop PsA develop persistent inflammation. If untreated, progressive joint damage results in severe physical limitations and disability. Early signs include joint pain, morning stiffness, enthesitis (inflammation of the tendon and ligament attachments to bones), and dactylitis (swollen, sausage-like swelling of digits). Prevalence increases with more extensive disease.

As it is a seronegative, PsA is difficult to diagnose. Always ask patients about joint pains and morning stiffness when reviewing them. Early diagnosis and referral for consideration of disease-modifying anti-rheumatic drugs is essential if PsA is suspected.

Five patterns of PsA:

• Distal interphalangeal arthropathy – 5-to-10 per cent – primarily in men;
• Symmetric polyarthritis resembling rheumatoid arthritis – often relatively asymmetrical and may involve distal interphalangeal joints;
• Asymmetric oligoarthritis – 30 per cent – (typically involvement of a large joint, eg, knee, plus a few small joints of the hands or feet);
• Spondyloarthropathy (± sacroiliitis);
• Arthritis mutilans – destructive arthritis affecting the hands and feet.

Unfortunately, in recent years the availability of some topical therapies has not been reliable and all prescribers need to be aware of what is available when writing their prescriptions (see Figure 4).

The exact cause of psoriasis is not fully understood, but involves a complex interplay between genetic and environmental factors

Acne vulgaris, commonly known as acne, is a chronic inflammatory skin condition affecting millions of people worldwide, particularly adolescents and young adults. Acne presents primarily on the face, chest, and back, and is characterised by various lesions including comedones, papules, pustules, nodules, and cysts. It affects approximately 9.4 per cent of the global population, ranking it eighth among skin diseases. Prevalence rates are estimated to range from 35-to-90 per cent among adolescents. While prevalence decreases with age, acne can remain a significant dermatological concern for adults. Adolescent acne occurs more frequently in males, however, post adolescent acne predominantly affects females.^1,2,3

Aetiology

Acne is a multifactorial skin disorder that arises from the complex interplay of genetic, hormonal, microbial, and environmental factors. Genetics play an important role in acne development, with studies indicating a higher prevalence in individuals with a family history of the condition. Genes influence several aspects of acne pathogenesis, including sebum production, keratinisation processes, and the immune system’s response to Cutibacterium acnes (C. acnes). Environmental factors include diet, climate, pollution, and lifestyle. Dietary habits, particularly the consumption of high-glycaemic-index foods and dairy products, have been linked to acne severity, possibly due to their role in insulin-like growth factor 1 (IGF-1) signalling, which can exacerbate sebum production and inflammation.^1,2,3

Acne is profoundly influenced by hormonal factors, particularly those that alter sebaceous gland function. Androgens are pivotal in stimulating sebocyte proliferation, increasing intracellular lipid droplets, and inducing hyperkeratinisation of the follicular infrainfundibulum, leading to increased sebum production and acne severity. In addition to local hormonal effects on sebaceous glands, systemic hormonal disorders play a role in triggering adult acne. Additionally, stress has been recognised to exacerbate acne through hormonal fluctuations that increase sebum production. The skin microbiome, including C. acnes, coagulase-negative Staphylococcus, and fungal species, plays a role in maintaining skin health by balancing homeostatic relationships. While the proliferation of C. acnes has been associated with acne, it is the diversity and specific phylotypes of C. acnes that are more directly implicated in development of the condition.^1,2,3

Pathophysiology

The pathophysiology of acne is a complex interplay of hyperkeratinisation, sebum overproduction, bacterial proliferation, and inflammation, which interact and amplify each other, leading to the formation of various acne lesions.^1,3

Follicular hyperkeratinisation: This is the initial step in acne development. This process involves an abnormal increase in the production and desquamation of keratinocytes within the hair follicle. Under normal circumstances, keratinocytes are shed from the follicular epithelium in a controlled manner. In acne, there is increased proliferation of keratinocytes, leading to a higher turnover rate. Instead of being shed, the keratinocytes stick together, forming a cohesive plug. This results in the blockage of the follicular ostium, creating a microcomedo. Androgens, particularly dihydrotestosterone (DHT), play a significant role in stimulating follicular keratinocyte proliferation. Other factors such as local cytokine milieu and genetic predisposition also contribute to this process.^1,3,4

Sebaceous gland hyperactivity: Sebum production is primarily regulated by androgens, and individuals with acne typically have enlarged sebaceous glands and increased sebum secretion. Androgens, especially during puberty, stimulate the sebaceous glands to produce more sebum. This effect is mediated by androgen receptors on sebaceous gland cells. In acne patients, the composition of sebum may also be altered, with increased levels of squalene and decreased linoleic acid. This change in lipid composition can promote comedogenesis and inflammation. Conditions such as polycystic ovary syndrome (PCOS), which is characterised by hyperandrogenism, can exacerbate acne by further increasing sebum production.^1,3,4

C. acnes proliferation: The anaerobic bacterium C. acnes colonises the follicle, contributing to inflammation. C. acnes is a gram-positive anaerobic bacterium that resides within the pilosebaceous unit. It plays a central role in the inflammatory phase of acne. The blocked follicle provides an anaerobic environment conducive to C. acnes proliferation. C. acnes forms biofilms within the follicle, protecting it from the host immune response and antibiotics. C. acnes produces lipases that hydrolyse triglycerides in sebum into free fatty acids, which are pro-inflammatory and comedogenic. C. acnes stimulates toll-like receptor 2 (TLR2) on keratinocytes and immune cells, triggering the release of pro-inflammatory cytokines (eg, interleukin (IL)-1, IL-8, tumour necrosing factor (TNF)-α, and chemokines, leading to an influx of inflammatory cells production. The immune response to C. acnes and its metabolic products leads to inflammation, resulting in the clinical manifestations of acne.^1,3,4

Inflammation: Inflammation is both a consequence of and a contributing factor to the other pathogenic processes in acne. The activation of TLR2 by C. acnes results in the production of inflammatory mediators, including IL-1, IL-8, and TNF-α. These mediators recruit neutrophils and other immune cells to the site, leading to the formation of papules and pustules. Neutrophils release enzymes and reactive oxygen species that contribute to follicular wall rupture and the spilling of follicular contents into the dermis, exacerbating inflammation. T-helper (Th)-1 and Th17 cells are also involved in the inflammatory response, producing additional cytokines such as interferon gamma (IFN-γ) and IL-17, which sustain inflammation. As inflammation resolves, the healing process can result in scarring, especially in cases of severe or nodulocystic acne. Atrophic scars form due to tissue loss, while hypertrophic scars and keloids result from excessive collagen deposition.^1,3,4

The interactions among these four pathogenic factors create a cycle that sustains and exacerbates acne lesions. Environmental and lifestyle factors also play a significant role in modulating acne severity.

Clinical presentation

Acne affects the pilosebaceous units, predominantly on the face, chest, back, and shoulders. Severity and types of lesions vary widely, influencing the approach to diagnosis and treatment. Lesions are broadly categorised into non-inflammatory and inflammatory types.⁵

Non-inflammatory lesions: Comedones:

Open comedones^3,5 or blackheads occur when the follicle is partially blocked by keratin and sebum. The open nature of the follicle allows the material to be oxidised by air, giving it a black appearance. Closed comedones or whiteheads are formed when the follicle is completely blocked, preventing oxidation and maintaining a white or flesh-coloured appearance.

Inflammatory lesions:

• Papules are small, raised, red bumps that may be tender to the touch. They indicate inflammation lesions^3,5 within the follicle.

• Pustules are like papules, but contain visible pus at their tips, indicating a more intense inflammatory response.

• Nodules are large, solid, painful lesions that are deeper within the skin. They result from severe inflammation and often involve the rupture of the follicle wall, leading to a more extensive inflammatory reaction.

• Cysts are deep, painful, pus-filled lesions that can lead to significant scarring. They represent the most severe form of acne and are often associated with nodules (nodulocystic acne).

Acne typically affects areas with a high density of sebaceous glands. The face is the most common site, with lesions frequently appearing on the forehead, nose, cheeks, and chin. Acne on the chest and back can be more challenging to treat due to the thicker skin and larger sebaceous glands. The shoulders and upper arms are less commonly affected, but can still present with significant lesions.^1,3,5 The severity of acne can be classified based on the number, type, and distribution of lesions.

Mild acne is predominantly comedonal with a few inflammatory lesions, limited to small areas on the face or trunk, with minimal risk of scarring.^1,3,5

Moderate acne comprises an increased number of inflammatory lesions, including papules and pustules, greater involvement of the face, and may extend to the chest and back. There is potential for post-inflammatory hyperpigmentation and mild scarring.^1,3,5

Severe acne displays numerous inflammatory lesions, including nodules and cysts, with extensive involvement of the face, chest, and back. There is a high risk of significant scarring and potential for psychological impact.^1,3,5

Acne vulgaris is the most common type, making up 99 per cent of all acne cases, however, certain forms of acne present unique clinical features, including:^1,3,5

• Acne conglobata is a severe form of nodulocystic acne characterised by interconnected abscesses and sinus tracts, leading to extensive scarring.

• Acne fulminans is an acute, severe form presenting with sudden onset
  of ulcerative acne, systemic symptoms like fever, and elevated inflammatory markers. It often
  requires systemic treatment.

• Mechanical acne is caused by physical factors such as friction, pressure, or occlusion. It is common
  in athletes or individuals wearing tight clothing or equipment.

• Cosmetic acne is triggered by using certain skincare or cosmetic products that are comedogenic.

• Drug-induced acne is linked to medications such as corticosteroids, lithium, and certain antiepileptics. The distribution is typically monomorphic, with uniform lesion types.

Additional clinical considerations include:^1,3,5

• Post-inflammatory hyperpigmentation (PIH): Dark spots that remain after the resolution of inflammatory lesions. PIH is more common in individuals with darker skin tones.

• Scarring, which can be atrophic (ice pick, boxcar, and rolling scars) or hypertrophic/keloidal. The risk increases with the severity and duration of acne.

• The psychological impact of acne can significantly affect an individual’s self-esteem and quality-of-life, leading to social withdrawal, anxiety, and depression.

Diagnosis

Diagnosing acne vulgaris involves a comprehensive approach that includes patient history, physical examination, and, in some cases, laboratory investigations. The goal is to accurately identify the type and severity of acne, differentiate it from other dermatological conditions, and determine any underlying factors that may contribute to its occurrence.^1,6,7

A thorough patient history is important for diagnosing acne and identifying potential exacerbating factors. This includes documenting when the acne started and its progression over time. Noting the distribution and types of lesions, such as comedones, papules, pustules, nodules, and cysts, is important. Reviewing treatments previously used, their effectiveness, and any side-effects experienced helps in understanding the patient’s treatment history. Assessing whether there is a family history of acne or related conditions can provide insights into genetic predispositions. Considering lifestyle factors such as diet, skincare routines, cosmetic use, stress levels, and exposure to potential triggers like occupational or environmental factors is important. For female patients, noting any correlation between acne flare-ups and menstrual cycles can help identify hormonal influences. Identifying any medications that may contribute to acne, such as corticosteroids, lithium, or antiepileptics, is necessary for a comprehensive evaluation.^1,6,7

A detailed physical examination is important to assess the type, distribution, and severity of acne lesions. This involves identifying the presence of non-inflammatory lesions, such as open and closed comedones, as well as inflammatory lesions, including papules, pustules, nodules, and cysts. Mapping the affected areas is necessary to understand the distribution of acne. The severity of acne should be graded using standardised scales such as the Global Acne Grading System (GAGS) or the Leeds acne grading technique. Evaluating for signs of scarring, including post-inflammatory hyperpigmentation, atrophic scars, and hypertrophic or keloidal scars, is important.^1,6,7

Acne vulgaris is diagnosed based on clinical criteria, which include the presence of characteristic lesions and their distribution. Key diagnostic features are:^1,6,7

• Presence of comedones – open and closed comedones are hallmark features.

• Inflammatory lesions like papules, pustules, nodules, and cysts.

• Seborrheic areas – lesions predominantly occur in areas with a high density of sebaceous glands.

Laboratory tests are not typically required for diagnosing acne vulgaris, but may be considered in certain scenarios. Hormonal evaluation may be carried out in female patients with signs of hyperandrogenism (eg, hirsutism, irregular menstrual cycles), and assessing levels of androgens, luteinising hormone (LH), follicle-stimulating hormone (FSH), and prolactin can help identify underlying conditions like PCOS. Microbiological tests are rarely indicated, but may be used to rule out bacterial folliculitis or fungal infections if the diagnosis is unclear. Skin biopsy is not routinely performed for acne, but may be indicated to exclude other diagnoses if the presentation is atypical.^1,6,7

Differentiating acne from other skin conditions like rosacea, folliculitis, perioral dermatitis, seborrheic dermatitis, keratosis pilaris, and hidradenitis suppurativa is important for an accurate diagnosis.^1,6,7

Treatment and management

The treatment and management of acne involves a multifaceted approach tailored to the type and severity of the condition, individual patient characteristics, and potential underlying factors.

Topical treatments are often the first-line of therapy for mild-to-moderate acne and can be used in combination with systemic treatments for more severe cases.^8,9,10

• Topical retinoids are effective in normalising follicular keratinisation, promoting cell turnover, and reducing comedone formation. They are beneficial for both inflammatory and non-inflammatory lesions.

• Benzoyl peroxide, an antimicrobial agent, reduces C. acnes colonisation and has anti-inflammatory properties. It is often used in combination with topical antibiotics or retinoids to reduce the risk of antibiotic resistance.

• Topical antibiotics are commonly used to reduce bacterial load and inflammation. They are most effective when combined with benzoyl peroxide to mitigate resistance.

• Azelaic acid has antibacterial, anti-inflammatory, and comedolytic properties, making it useful for treating mild-to-moderate acne, particularly in patients with sensitive skin.

• Salicylic acid as a beta-hydroxy acid helps to exfoliate the skin and clear clogged pores, making it effective for comedonal acne.^8,9,10

Systemic treatments are indicated for moderate-to-severe acne or when topical treatments have failed.^8,9,10

• Oral antibiotics: Tetracyclines and macrolides are commonly used for their antibacterial and anti-inflammatory effects. They are typically prescribed for three-to-six months to reduce bacterial load and inflammation.

• Hormonal therapies: Oral contraceptives and anti-androgens are effective for female patients with hormonal acne. These therapies help regulate hormone levels, reduce sebum production, and decrease androgen-mediated skin effects.

• Oral isotretinoin: A potent retinoid, is reserved for severe, recalcitrant acne. It reduces sebaceous gland size and sebum production, normalises keratinisation, and has anti-inflammatory properties. It requires careful monitoring due to potential side-effects, including teratogenicity.

• Other systemic agents: In certain cases, systemic corticosteroids or dapsone may be used for specific forms of severe or refractory acne, such as acne fulminans or acne conglobata.^8,9,12

The HSE treatment guidelines for acne are outlined in Table 1.¹¹

Drug	Dose	Duration	+/- Notes
First-line treatment:
Benzoyl peroxide 5% w/w gel (Acnecide)	Apply twice weekly to affected areas, slowly increase frequency as tolerated	Can take up to 2 months to take effect. If effective, consider ongoing treatment	May bleach hair, fabrics. Can cause photosensitivity
Predominantly comedones:
Adapalene 0.1% w/w cream or gel (Differin)	Apply twice weekly to affected areas, slowly increase frequency as tolerated	Review after 3 months. If effective, consider ongoing treatment	Contraindicated in pregnancy. Apply after washing to dry skin. Can cause photosensitivity
Adapalene + Benzoyl Peroxide combination:
Adapalene 0.1%/benzoyl peroxide 2.5% gel (Epiduo)	Apply twice weekly to affected areas, slowly increase frequency as tolerated	Review after 3 months. If effective, consider ongoing treatment	Contraindicated in pregnancy. Apply after washing to dry skin. May bleach hair, fabrics. Can cause photosensitivity
Inflammatory lesions (pustules):
Clindamycin/benzoyl peroxide 10mg/g + 50mg/g Gel (Duac)	Apply twice weekly to affected areas, slowly increase frequency as tolerated	Review and limit use to 3 months if possible (max 6 months)	Topical antibiotics should not be used alone or with oral antibiotics due to resistance risk. May bleach hair, fabrics. Can cause photosensitivity
Combination of lesions and comedones:
Adapalene 0.1%/benzoyl peroxide 2.5% gel (Epiduo)	Apply twice weekly to affected areas, slowly increase frequency as tolerated	Review after 3 months. If effective, consider ongoing treatment	Contraindicated in pregnancy. Apply after washing to dry skin. May bleach hair, fabrics. Can cause photosensitivity
2nd line option for irritation or hyperpigmentation:
Azelaic acid 15% gel (Skinoren)	Apply every 12 hours	Review after 3 months. If effective, consider ongoing treatment

Adjunctive treatments can enhance the effectiveness of pharmacologic therapies and address residual issues such as scarring. Superficial chemical peels using glycolic acid or salicylic acid can help improve comedonal acne and post-inflammatory hyperpigmentation. Laser and light therapy options such as pulsed dye laser, intense pulsed light, and blue light therapy target C. acnes and reduce inflammation. Fractional lasers can improve scarring. Photodynamic therapy involves the application of a photosensitising agent followed by light activation to reduce sebaceous gland activity and bacterial load. Micro needling stimulates collagen production and can improve atrophic acne scars.^3,8,9

MODERATE ACNE NOT RESPONDING TO TOPICAL TREATMENT

(Seek specialist advice in pregnancy)

Oral antibiotics should be reviewed if no response is seen after 12 weeks of therapy

*Oral and topical antibiotics should not be used in combination, as there is an increased risk of antibiotic resistance

DRUG	DOSE	DURATION	+/- NOTES
1st choice options
Lymecycline PLUS Topical agent from table above (except Duac*)	408mg every 24 hours As above	Review and limit use to 3 months if possible (max 6 months). To be continued during and after for maintenance.	Contraindicated for children <12 years old and pregnancy. Can cause photosensitivity. Lymecycline 408mg equivalent to 300mg of tetracycline base.
2nd choice options
Doxycycline PLUS Topical agent from table above (except Duac*)	100mg every 24 hours As above	Review and limit use to 3 months if possible (max 6 months). To be continued during and after for maintenance.	Not suitable for children <12 years old and pregnancy. Can cause photosensitivity.
OR
Trimethoprim PLUS Topical agent from table above (except Duac*)	200mg every 12 hours for 1 month then 300mg every 12 hours for 3 months As above	As above, to continue during and after oral antibiotic to prevent recurrence	Not suitable in pregnancy. Caution re Stevens-Johnson syndrome/ toxic epidermal necrolysis. Monitor full blood count when on trimethoprim long-term.

Please note:

• Repeat treatment, if necessary, should be with a previously effective antibiotic
• Minocycline is not routinely used for management of acne vulgaris, but if prescribing from secondary care advise patient of, and monitor for, abnormal LFTs, irreversible cutaneous pigmentation, and reversible drug-induced lupus. Minocycline can cause a blue-grey discoloration of inflamed skin.

SEVERE ACNE

Treatment as per moderate acne, but refer for specialist advice. Consider referral for isotretinoin in the following instances:

• Presence of nodulocystic acne
• Failure of two different oral antibiotic courses (two 3-to-6 month courses) with appropriate topical agent
• Presence of scarring

TABLE 1: HSE treatment guidelines for acne

Lifestyle and dietary modifications

While the role of diet in acne is still debated, certain dietary modifications may help some individuals. Reducing the intake of high glycaemic index foods may improve acne in some patients by decreasing insulin and IGF-1 levels. Limiting dairy products, particularly skimmed milk, has been suggested to reduce acne severity in some studies. Stress can exacerbate acne, so incorporating stress-reducing activities such as exercise, meditation, or yoga may be beneficial.^3,8,9

Patient education and support

Educating patients about their condition and treatment is important for adherence and success. Advising on gentle, non-comedogenic skincare products and the importance of regular cleansing can help manage acne. Realistic expectations about the timeframe for seeing improvements and the importance of adherence to prescribed treatments should be discussed with the patient. Addressing the emotional and psychological impact of acne is important, as is providing resources or referrals for counselling if needed.^3,8,9

Emerging therapies and outlook

Acne is a multifactorial skin disease that requires long-term treatment. A wide range of topical and systemic treatment options have been introduced over the years, however, many patients do not see satisfactory treatment results and experience difficulties adhering to treatment recommendations. 

Research into new treatments for acne continues to evolve. Procedural treatments such as laser devices, photodynamic therapy, chemical peels, and intralesional injections present viable alternatives for reducing acne symptoms and scarring. Emerging therapies focus on novel biologics, bacteriophages, probiotics, and peptides, providing promising future options. The main aim is to create more individualised, effective, and sustainable acne management strategies that tackle the root causes of acne rather than just addressing its symptoms. ^12,13