Skin Diseases

TL;DR. Skin disease is the fourth leading cause of non-fatal disease burden worldwide, and almost all of it is either a barrier problem, an inflammation problem, an infection, or a growth. Eczema is a broken barrier that lets irritants and allergens in and water out, which is why moisturiser is a treatment rather than a cosmetic. Acne is a blocked, inflamed oil gland, affects around 85 percent of adolescents, and has genuinely effective treatments that people are frequently too embarrassed to ask for. Psoriasis is an immune disease that happens to show on the skin and carries cardiovascular risk with it. And the most important thing on your skin is the one you should be looking for: a mole that has changed.

Key takeaways

• Eczema is a barrier disease first. A gene called filaggrin, which builds the outer skin barrier, is faulty in a substantial share of people with eczema, and the leaky barrier is also the route through which food allergies develop.
• Topical steroid phobia causes more harm than topical steroids do. Under-treatment of eczema from fear of steroids is a documented and common problem.
• Acne is not caused by dirt, chocolate, or poor washing, and over-washing makes it worse.
• Psoriasis is a systemic inflammatory disease. It is associated with arthritis in 20 to 30 percent, and with cardiovascular disease, so it is treated as more than a skin problem.
• Skin cancer is the most common cancer in fair-skinned populations, and change in a lesion matters more than its appearance (Chapter 25).
• Skin disease presents differently in darker skin, redness is harder to see, and this contributes to documented delays in diagnosis.

Eczema (atopic dermatitis)

In short: A broken barrier plus an over-reactive immune response, in a self-perpetuating itch-scratch loop.

What it is. Chronic, relapsing, intensely itchy inflammation of the skin, affecting roughly 15 to 20 percent of children and 2 to 10 percent of adults, with rates that rose sharply through the twentieth century.

What actually goes wrong. Two things at once:

1. A defective barrier. The outer skin layer is dead cells embedded in a lipid matrix (Chapter 7). Loss-of-function mutations in filaggrin, a protein essential to building that layer, are present in a substantial minority of people with eczema and are the strongest known genetic risk factor. A leaky barrier means water escapes (dry skin) and irritants, allergens, and microbes get in.
2. An over-reactive type 2 immune response to what gets in, driven by interleukin-4 and interleukin-13, producing inflammation and, importantly, itch signalling directly.

The itch-scratch cycle is the engine. Itching leads to scratching, scratching damages the barrier further and releases more inflammatory mediators, which causes more itch. Breaking the cycle is most of what treatment does.

Why it matters beyond the skin. Infant eczema is the entry point of the atopic march: eczema, then food allergy, then asthma and hay fever. The current best explanation is that allergens crossing inflamed skin sensitise the immune system, while the same protein eaten by mouth would induce tolerance. That is why early peanut introduction prevents peanut allergy (Chapter 46) and why treating infant eczema properly is being tested as an allergy prevention strategy.

Treatment, in order:

Don't be confused: topical steroid phobia causes more harm than topical steroids. Surveys consistently find that a large majority of patients and carers are anxious about using them and that many under-use or refuse them, leading to prolonged uncontrolled eczema, more infection, more sleep loss, and more scarring. Used at the right strength, on the right site, for flares, topical steroids are safe. The genuine risks (skin thinning, and a rare withdrawal reaction after prolonged potent use) come from long-term continuous use of strong preparations on thin skin, not from treating a flare properly.

Acne

In short: A blocked, inflamed oil gland, affecting almost everyone at some point, with treatments that work and are frequently not asked for.

What it is. Affects roughly 85 percent of people aged 12 to 24, and persists into adulthood in a substantial minority, particularly women.

What actually goes wrong, in four steps:

1. Androgens increase oil (sebum) production at puberty, which is why acne starts then and why hormonal conditions such as PCOS worsen it.
2. The pore lining cells become sticky and fail to shed properly, blocking the duct. A blocked pore is a comedone: a whitehead if closed, a blackhead if open. Blackheads are oxidised pigment, not dirt, which is why scrubbing does not remove them.
3. A bacterium, Cutibacterium acnes, thrives in the blocked, oil-rich pore.
4. Inflammation produces the red papules, pustules, and, in severe cases, nodules and cysts that scar.

Myths worth dispatching:

• It is not caused by poor hygiene. The blockage is inside the pore.
• Over-washing and scrubbing make it worse, by damaging the barrier and increasing inflammation.
• Chocolate has never been convincingly implicated. There is modest evidence linking high glycaemic-load diets and possibly skimmed milk to acne, and it is far weaker than folk wisdom assumes.

Treatment ladder:

Isotretinoin deserves its own note because it is both remarkably effective and heavily regulated. It causes severe birth defects, so pregnancy prevention programmes with mandatory contraception and testing are required. It causes dryness of skin, lips, and eyes in nearly everyone. A possible association with depression and suicide has been extensively studied; large studies have not established a causal link and severe acne itself is strongly associated with depression, but monitoring mood remains standard practice.

The point most worth making about acne is that scarring is preventable and permanent. Treating early and adequately prevents scars that no later treatment fully removes, and the psychological burden of acne is substantial and consistently underestimated by clinicians.

Psoriasis

In short: An immune disease that shows on the skin, comes with arthritis in a fifth to a third of patients, and carries cardiovascular risk.

What it is. Well-demarcated, red (or, in darker skin, violet or grey-brown), scaly plaques, classically on elbows, knees, scalp, and lower back. Affects roughly 2 to 3 percent of people.

What actually goes wrong. An immune response driven by the IL-23 and IL-17 axis activates keratinocytes, which then multiply roughly ten times faster than normal. Skin cells that should take a month to reach the surface arrive in a few days, unable to mature properly, producing the characteristic thick silvery scale.

Why it is more than skin:

• Psoriatic arthritis develops in roughly 20 to 30 percent, and it is erosive, so early detection matters (Chapter 47).
• Cardiovascular disease risk is raised, plausibly through systemic inflammation, so cardiovascular risk factors should be assessed.
• Metabolic syndrome, depression, and inflammatory bowel disease are all associated.

Treatment: topical steroids and vitamin D analogues, coal tar, phototherapy, then systemic agents (methotrexate, ciclosporin), then biologics targeting TNF, IL-17, or IL-23, which have produced complete or near-complete skin clearance rates that were inconceivable two decades ago.

Skin infections

In short: Bacterial, fungal, and viral, and the important skill is distinguishing the ones that need urgent treatment.

Other common conditions

In short: Six more that account for a large share of dermatology visits.

Rosacea. Persistent facial redness, flushing, visible vessels, and acne-like bumps, mainly in adults. Triggers include heat, alcohol, spicy food, sun, and stress. Treated with topical metronidazole or ivermectin, oral doxycycline at anti-inflammatory doses, and laser for the vessels. Its ocular form causes gritty, inflamed eyes and is frequently missed.

Urticaria (hives). Raised, intensely itchy weals that come and go within hours, from histamine release (Chapter 46). Acute urticaria usually follows an infection or a drug; chronic urticaria lasting over six weeks is usually not allergic at all and is treated with high-dose antihistamines, then omalizumab.

Seborrhoeic dermatitis. Greasy scaling on scalp, eyebrows, and nasal folds, associated with a yeast. Dandruff is its mild form. Treated with antifungal shampoos and mild topical steroids.

Vitiligo. Autoimmune destruction of pigment cells producing sharply defined white patches. Not dangerous and often profoundly distressing, with a psychological impact that varies enormously by culture and skin tone. Treatments include topical steroids and calcineurin inhibitors, phototherapy, and newer JAK inhibitors.

Alopecia areata. Autoimmune hair loss in discrete round patches. Can progress to complete scalp or body hair loss. JAK inhibitors are the first genuinely effective systemic treatment.

Pressure ulcers. Skin and underlying tissue death from sustained pressure over a bony prominence, in people who cannot reposition themselves. Almost entirely preventable with repositioning, appropriate surfaces, nutrition, and skin care, and a recognised marker of care quality.

Skin cancer, and what to look for

In short: The most common cancer in fair-skinned populations, and change matters more than appearance.

Covered in Chapter 25. The practical version:

The ABCDE of melanoma:

Also worth acting on: the ugly duckling sign (a mole that looks different from your others), any lesion that bleeds repeatedly, and any sore that has not healed in a month.

Non-melanoma skin cancers are far more common and rarely fatal. Basal cell carcinoma appears as a pearly, sometimes ulcerated nodule that grows slowly and almost never spreads, but destroys local tissue if neglected. Squamous cell carcinoma is a scaly, tender, growing lesion that can spread.

Skin cancer in darker skin is less common, diagnosed later, and has worse outcomes. It appears in less sun-exposed sites (palms, soles, under nails, mucous membranes), it is not looked for, and awareness is lower among both patients and clinicians. Any new or changing pigmented lesion on a palm, sole, or nail bed deserves attention regardless of skin tone.

Skin of colour

In short: The same diseases look different, and standard teaching materials have historically shown almost only white skin.

Several practical differences matter:

• Redness is harder to see. Inflammation appears violet, grey, or dark brown rather than red, which means cellulitis, eczema, and drug reactions are all more easily missed.
• Post-inflammatory pigment change is far more prominent and longer-lasting, so the marks left after acne or eczema are often the patient's main concern and should be treated as such.
• Keloid scarring is considerably more common, which affects decisions about elective surgery and piercing.
• Specific conditions are more common, including central centrifugal cicatricial alopecia and pseudofolliculitis barbae.
• Vitamin D synthesis is slower in more pigmented skin at high latitudes, raising deficiency risk.

Audits of dermatology textbooks and online resources have repeatedly found that images of darker skin are a small minority of those shown, and this has measurable consequences for diagnostic accuracy. It is a straightforwardly fixable gap.

What the person can do

In short: Protect the barrier, protect from UV, and know the three things that mean see someone today.

• Moisturise if your skin is dry or eczematous, generously, and keep going when it looks better.
• Use soap substitutes and avoid hot, long showers, which strip lipids.
• Use sun protection: shade in the middle of the day, clothing and hats, and sunscreen at the quantity actually needed (most people apply a quarter to a half of the tested amount). Reapply.
• Do not use sunbeds. They are classified as a group 1 carcinogen.
• Check your skin periodically, including soles, between toes, and the scalp, and ask someone to check your back.
• Treat acne early and properly rather than waiting for it to resolve, because scars are permanent.
• Do not stop a topical steroid your clinician prescribed out of fear. Ask about the right strength, site, and duration instead.
• See someone the same day for: rapidly spreading redness with fever, pain out of proportion to the appearance of a skin infection, or a widespread blistering rash with mouth involvement, which can indicate a severe drug reaction.

Sources and notes

Skin disease burden ranking: Hay et al., Journal of Investigative Dermatology, 2014, and Global Burden of Disease analyses. Filaggrin mutations in eczema: Palmer et al., Nature Genetics, 2006. Topical steroid phobia prevalence: multiple international surveys, reviewed in Li et al., JAMA Dermatology, 2017. Atopic march and dual-allergen exposure hypothesis: Lack, Journal of Allergy and Clinical Immunology, 2008. Acne prevalence: Bhate and Williams, British Journal of Dermatology, 2013. Diet and acne evidence: systematic reviews finding modest associations with glycaemic load and skimmed milk. Isotretinoin and psychiatric outcomes: large registry and cohort studies finding no clear causal association. Psoriasis and psoriatic arthritis prevalence, and cardiovascular association: Griffiths, Armstrong, Gudjonsson, and Barker, The Lancet, 2021. Diversity of images in dermatology teaching resources: Adelekun, Onyekaba, and Lipoff, Journal of the American Academy of Dermatology, 2021. Sunbed classification: IARC.

Open questions. Whether aggressive early treatment of infant eczema prevents food allergy is under trial and not yet established. The cause of the twentieth-century rise in eczema prevalence is unresolved. The relative contribution of diet to acne remains modest and contested.

Next: what happens when blood clots where it should not, or fails to return from where it went. 👉