The daily dose of steroids depends on the severity of the disease and on the clinical parameters of the patient. A typical initial dose for most moderate to severe dermatologic conditions is 1.0 mg/kg of prednisone or prednisone-equivalent per day [4]. Short courses (less than 4 weeks) of corticosteroid therapy are usually safe and effective in treating acute skin diseases. In long-term treatments, adjuvant or steroid-sparing agents such as other immunosuppressive drugs, antimalarials, and sulfones are often used in an attempt to reduce the dose of corticosteroids required to control the disease. Very short courses (2–3 weeks or less) of corticosteroids do not necessitate tapering, although most clinicians do not stop the treatment abruptly so as to eliminate the risk of disease recurrence and of steroid withdrawal symptoms.

In pediatric dermatology, the most common route of systemic administration is the oral route, with a steroid molecule of intermediate anti-inflammatory potency, such as prednisone, usually given in an early morning single dose [5]. General recommendations for corticosteroid use are valid in dermatological practice as well. The therapeutic dosage of systemic corticosteroids used in skin disorders, most often ranging from 0.5 to 1.5 mg/kg/day, may cause suppression of the hypothalamic–pituitary–adrenal axis and growth suppression in the long-term treatment of pediatric patients. Because long-acting agents such as dexamethasone are highly effective in suppression of the hypothalamic–pituitary–adrenal axis, and because hydrocortisone and cortisone acetate are too short-acting for a lasting therapeutic effect, most dermatologists are likely to use prednisone or methylprednisolone [6]. While the latter is an excellent choice for minimizing the mineralocorticoid effects, prednisone is cheap, widely available, and marketed in many dosage forms.

Systemic corticosteroid therapy produces cutaneous side effects similar to those of Cushing’s syndrome, which are well known to dermatologists, including striae distensae, purpura, telangiectasia, atrophy, steroid acne, hirsutism, alopecia, hyperpigmentation, and wound healing impairment. Of these, striae distensae are permanent, while the others may be reversible.

In acute self-limited steroid-sensitive skin disorders, such as severe contact dermatitis, a short (1–2 weeks) course of oral prednisone is usually started and rapidly tapered. In acute allergic or anaphylactic reactions, for example, following insect bites or drug reactions, hydrocortisone is usually given intravenously accompanied by antihistamines [7].

Autoimmune bullous diseases such as pemphigus, pemphigoid, dermatitis herpetiformis, and linear immunoglobulin A dermatitis are rare in children but they require vigorous corticosteroid therapy when diagnosed [8]. Childhood bullous pemphigoid is usually responsive to moderate prednisone doses (0.5–1 mg/kg/day), while pemphigus vulgaris is more difficult to control and requires larger doses to achieve remission. The use of corticosteroid-sparing agents is often necessary to reduce corticosteroid side effects in the treatment of pemphigus vulgaris. Dapsone is possibly a better therapeutic option for dermatitis herpetiformis and linear immunoglobulin A dermatitis, but concomitant use of corticosteroids is required, at least initially, to achieve better results.

A wide spectrum of therapeutic agents with anti-inflammatory and immunosuppressive action are available in the treatment of juvenile-onset systemic lupus erythematosus. Among these, low doses of systemic corticosteroids are useful in controlling minor manifestations of the disease, while higher doses are still used to manage major manifestations that can endanger the patient’s life [9].

Aggressive management with high-dose oral systemic corticosteroids, with or without other drugs, is the traditional treatment for juvenile dermatomyositis. Aggressive treatment directed at achieving a rapid and complete control of muscle inflammation is highly successful in minimizing the long-term sequelae of the disorder, including calcinosis. High oral doses of prednisone (1.5–2 mg/kg daily) or pulse intravenous methylprednisone therapy (30 mg/kg) are used [10]. Pulse intravenous corticosteroid therapy is usually preferred to maintain efficacy while lowering the side effects [11], although this treatment may lead to muscle strength deterioration and no long-term changes in the outcome [12]. Some authors suggest that early intervention with additional immunomodulatory agents allows for a faster recovery, with less medication and fewer disease sequelae [13].

Pulsed intravenous corticosteroid therapy is often used in connective tissue disorders (dermatomyositis, scleroderma) allowing for a shorter course of therapy with fewer long-term side effects. Usually, a single high daily dose of methylprednisolone is given intravenously over 2 h 1–5 (but usually 3) consecutive days per month. Children seem to tolerate this regimen exceedingly well. Sudden death of cardiac arrest, possibly due to a sudden electrolyte shift, has been described in adults, so that appropriate cardiologic monitoring is mandatory during treatment.

High-dose intravenous methylprednisolone on 3 consecutive days given monthly and accompanied by a low weekly dose of methotrexate (0.3–0.6 mg/kg) is standard treatment for children with localized severe forms of cutaneous scleroderma [14]. Although consensus on specific regimens is lacking [15], the dose of the drug in the literature is 30 mg/kg/day (not exceeding 500 mg) for 3 days monthly for 3 months. This regimen appears to be effective and is generally well tolerated by children [16]. Problems of renal, cardiac, and endocrine nature must be carefully assessed before starting the procedure, while blood pressure, urinalysis, full blood count, renal and liver function, and electrolytes should be monitored during treatment.

Systemic steroids have represented the mainstay of treatment for problematic infantile hemangiomas for many years thanks to their well-known antiproliferative and antiangiogenic properties [17]. Usually, a prednisone-equivalent daily dose of 1–3 mg/kg is administered for weeks to months in the proliferating phase of the hemangioma [18]. Although systemic propranolol has currently become the first-line treatment for infantile hemangiomas worldwide, systemic steroids are still used if β-blockers are contraindicated.

Alopecia areata is a common disorder affecting the scalp and body hair. It may occur at any age, but usually appears before the age of 20 years. Although the exact etiology of the disorder is still unclear, corticosteroids are widely used in both topical and systemic administration. Topical clobetasol propionate has been proven effective in inducing hair regrowth as a result of a local effect [19]. The usefulness of systemic corticosteroids as a therapeutic modality for severe forms of alopecia areata remains a matter of debate. Oral daily prednisone intake of 0.5–1 mg/kg/day may induce satisfactory regrowth in 40 % of patients, but this result is often not maintained after treatment. In children with widespread alopecia areata, intravenous methylprednisolone pulses on 3 consecutive days in 1-month intervals [20] or single high oral doses of prednisolone in 1-month intervals [21] have also been used. Short disease duration, younger age at onset, and multifocal as opposed to severe diffuse alopecia are positive prognostic factors in alopecia areata. Unfortunately, in patients with alopecia totalis and universalis, even pulse therapy is often disappointing.

Vitiligo is a common chronic and often progressive disorder of possible autoimmune origin causing disfiguring depigmentation in children and adults. Systemic corticosteroids have been used to arrest disease progression and to induce repigmentation. The effectiveness of low-dose oral corticosteroids in preventing the progression of the disease has been reported and represents a therapeutic option in patients difficult to treat, with spreading disease, or not responding to other treatments (e.g., topical corticosteroids and photochemotherapy) [22]. Treatment schedules include the use of an oral mini-pulse with 2.5, 5, or 10 mg of betamethasone or dexamethasone on 2 consecutive days per week after breakfast [23, 24]. Although children have been included in some of the published studies, conclusions on long-term efficacy are lacking, especially in the pediatric population.

In a subset of patients affected by severe or recalcitrant psoriasis, including arthropathic, pustular, and erythrodermic forms, systemic treatment is needed. Although systemic steroids are rapidly effective in psoriasis at the beginning of treatment, tachyphylaxis also ensues quickly. Worsening with possible induction of severe, often generalized, pustular psoriasis may be observed as a treatment outcome. Hence, systemic steroids are not an option in these patients, who should receive other treatment (e.g., phototherapy, acitretin, methotrexate, cyclosporine, or tumor necrosis factor-α inhibitors) [25].

Intramuscular administration of corticosteroids for dermatological disorders is seldom required in pediatric practice. Advantages include close physician control over therapy, guaranteed compliance, and assured absorption [5]. Sterile abscesses, hypopigmentation, and local atrophy at the injection site are well-known side effects of both intramuscular and intralesional corticosteroid therapy.

Intramuscular injection of corticosteroids remains the most common cause of postinjectional atrophy. Antibiotics, insulin, human growth hormone, and vasopressin are other possible causative drugs. Steroids act by increasing lipolysis while inhibiting lipogenesis and fibroblast activity. Reports on this topic are mainly focused on triamcinolone and on steroids in poorly soluble forms, such as triamcinolone acetonide. The occurrence of atrophy is related to the power, the quantity, the concentration, and the solubility of the drug as well as to the anatomical level of the injection. The deeper the injection, the lower the atrophy, which is likely to occur when the needle fails to reach the muscular tissue. Subcutaneous atrophy after corticosteroid injection is usually self-healing in the pediatric patient, although it may take many months for the damaged skin to go back to normal.