Last reviewed: 20 Dec 2021
Last updated: 16 Oct 2018



Dry, pruritic skin, typically with erythema, scaling, or vesicles; lichenification in skin flexures when there is chronic inflammation.[1] In infants the extensor surfaces, cheeks, and forehead are preferentially affected.[2] Patients often have a personal or family history of other atopic diseases such as asthma or allergic rhinitis.[2]

Atopic dermatitis is a chronic, relapsing disease, and educating patients and their families is necessary so that they develop an understanding of basic skin care and how to avoid trigger factors.[3][4][5] First-line treatment is with emollients and topical corticosteroids. Other options that may be used in patients unresponsive to first-line therapy include topical calcineurin inhibitors, phototherapy, or immunosuppressive agents. [ Cochrane Clinical Answers logo ] com.bmj.content.model.overview.Caption@7097952e[Figure caption and citation for the preceding image starts]: Acute atopic dermatitis on the face of an infantPersonal collection of Dr A. Hebert [Citation ends].

Irritant contact dermatitis (ICD) is caused by direct toxicity and can occur in any person without prior sensitisation. Allergic contact dermatitis (ACD) is a delayed hypersensitivity reaction, which requires prior sensitisation.

Both result in localised burning, stinging, itching, blistering, erythema, and swelling after contact with an allergen or irritant. Eruption is often clearly delineated with sharp borders. Hyperpigmentation, fissuring, and scaling may also occur.[6]

After an allergen or irritant is identified, the main goals of treatment are avoidance of future exposure and resolution of existing dermatitis. ICD is treated with exposure reduction and moisturisers.[7] [ Cochrane Clinical Answers logo ] ACD is treated with exposure elimination, and topical corticosteroids or topical calcineurin inhibitors. Severe ACD may require treatment with oral[Figure caption and citation for the preceding image starts]: Allergic contact dermatitis to nickel in watchbandPersonal collection of Dr Snehal Desai [Citation ends].

Recurrent crops of 1- to 2-mm vesicles, with pruritus on the palms, soles, and/or lateral aspects of the fingers. Pompholyx is more acute, severe eruptions of large bullae on the hands and feet.[8] The common exacerbating factor is irritation, as seen in frequent hand washing, hyperhidrosis, and stress. However, the underlying aetiology is unknown.

The foremost objective in treatment is identification and avoidance of exacerbating factors. All patients should be instructed on strategies to maintain effective skin barrier mechanisms, such as frequent use of emollients and avoidance of irritants.[9] In patients unresponsive to lifestyle measures, topical corticosteroids[10][11] or immunomodulators are used.[12][13] For severe cases of eruptive bullae on the palms and soles (pompholyx), oral corticosteroids are helpful. Recalcitrant cases of dyshidrotic conditions are treated with a wide variety of therapeutic options, including phototherapy, oral immunosuppressants, or nickel-directed[Figure caption and citation for the preceding image starts]: Dyshidrotic eczemaPhotograph courtesy of Dr Spencer Holmes [Citation ends].

Erythematous and greasy scaly patches on the scalp, glabella, nasolabial fold, posterior auricular skin, and anterior chest.[14] It is a chronic condition that includes dandruff (pityriasis capitis) in adults and cradle cap in infants. An explosive, often generalised onset of seborrhoeic dermatitis may be a marker for HIV infection, regardless of age.

Variable course that seldom completely subsides. An infant form (cradle cap) usually resolves within the first few months of life. Symptom control is the mainstay of treatment. Topical agents such as corticosteroids, coal tar, calcineurin inhibitors, and antifungals are used for treatment.[15][16][17] Shampoos and scalp preparations are appropriate treatments when seborrhoeic dermatitis is confined to the scalp.[18] Cradle cap in infants can usually be managed using emollients such as topical olive oil. Systemic antifungals should be reserved for severe cases and avoided in infants and[Figure caption and citation for the preceding image starts]: Seborrhoeic dermatitis, glabella, with scaling and mild erythemaPersonal collection of Dr Robert A. Schwartz [Citation ends].

Primarily an irritant contact dermatitis, nappy rash is inflammation of the skin in the area of the body covered by a nappy. It is most common in the first 1 to 2 years of life, but can occur in any person who routinely wears nappies. Recalcitrant nappy rash may signal secondary infection or underlying systemic or dermatological disorders, and requires further evaluation.

Initial treatment involves re-enforcing good nappy practices, such as frequent nappy changes, use of super-absorbent disposable nappies, cleansing the nappy area of potential irritants by using commercial cleansing wipes or using water on cotton cloth, periods of nappy-free time, and application of barrier cream, ointment, or paste.[19]

Circumscribed lichenified erythematous, often hyperpigmented, cutaneous plaques occurring most commonly on the scalp, neck, forearms, ankles, and genitalia as a result of chronic scratching and rubbing. One or multiple LSC patches or plaques can arise on skin affected by an underlying dermatosis such as atopic dermatitis, allergic contact dermatitis, stasis dermatitis, superficial fungal (tinea and candidiasis) and dermatophyte infections, lichen sclerosis, viral warts, scabies, lice, arthropod bite, or cutaneous neoplasia.[20][21]

LSC can be a difficult condition to treat, causing frustration in both the patient and physician.[20] The main goals of treatment are to remove any triggering and exacerbating environmental factors, repair the barrier function of the skin, identify and treat any underlying dermatological or systemic condition that could be driving the condition in secondary LSC, and disrupt the itch-scratch cycle characteristic of LSC through reduction in the degree of skin inflammation and control of nocturnal pruritus.[21] Treatment of LSC should be individualised and may include topical corticosteroid, emollients, and lifestyle modification. Nocturnal pruritus may be treated with an older-generation sedating[Figure caption and citation for the preceding image starts]: Secondary lichen simplex chronicus in the setting of atopic dermatitisPersonal collection of Dr Swick [Citation ends].

Sunburn is an acute inflammatory reaction of the skin induced by overexposure to ultraviolet (UV) radiation. Skin findings include erythema and oedema, with or without vesiculation, followed by desquamation. Symptoms include pain and/or pruritus. Acute sunburn is a self-limited condition and typically requires only supportive care. No current treatments can reverse UV-induced skin damage.[22] Primary prevention via sun avoidance, physical protection, and the appropriate use of sunscreen is key to managing the condition, as cellular damage caused by UV radiation is irreversible and may, with time, accelerate photo-ageing and increase the risk of skin cancer.

The most common symptom in dermatology is itching, which may occur with or without visible skin lesions. A thorough history and complete physical examination are central to the evaluation of pruritus. During medical examination it is important to identify a possible cause/disease responsible for itching as well as determining the intensity and time frame of the pruritus.

The aetiology can often be a dermatitis but may also include infections and urticaria. Of the inflammatory dermatoses, atopic dermatitis is the most common diagnosis for patients seen in paediatric dermatologists' clinics.[23] Seborrhoeic dermatitis occurs in 2 age groups: infants (beginning before age 2 months) and adolescents. In adolescents, sebaceous secretions are altered by the normal skin flora, which induces dermatitis in the affected areas.[24] The most common agents causing allergic contact dermatitis in children are species of Toxicodendron (poison ivy, poison oak, or poison sumac) and the metal nickel.[25][26]

The dermatological manifestations of HIV are protean and often multiple in patients with HIV infection.

Some skin diseases are fairly specific to HIV. HIV-specific dermatoses include HIV-related lipodystrophy, eosinophilic folliculitis, oral hairy leukoplakia, papular pruritic eruption of HIV, and HIV photodermatitis.

Other skin diseases may appear in non-HIV-infected populations but have altered presentation with HIV, presenting more commonly or in a more severe form in HIV-infected people. Seborrhoeic dermatitis is occurring with strikingly increased prevalence.[27][28] Prevalence increases with increased immunosuppression. Atopic dermatitis has a high prevalence in adult as well as paediatric patient populations with HIV.[29]



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