Eczema, also known as atopic dermatitis, usually develops in early childhood and often runs in families. Scaly, itchy rashes are the main symptoms. The condition can be treated using moisturizers, avoiding certain soaps and other irritants and with prescription creams and ointments containing corticosteroids to relieve itching. For the study, researchers examined results from 16 previously published studies and found as many as four in five people were afraid to use corticosteroids for eczema.
Common side effects of corticosteroids can include stretch marks as well as thinning, thickening or darkening of the skin. Less often, these steroids can cause acne or infected hair follicles or more serious side effects in the eyes like glaucoma and cataracts.
When this happens, the skin can degenerate and become lax, wrinkled, and shiny. Affected areas can be noticeably thinner than surrounding skin with visible spider veining telangiectasias , hypopigmentation, and the sudden prominence of underlying veins. Atrophy is usually reversible once steroid use is stopped, but it may take months for the skin to thicken to normal.
Repeated use of topical steroids in areas where skin touches skin, such as the groin and armpits, can result in stretch marks striae. Stretch marks from topical steroid use are permanent and irreversible. They can be very itchy and may require a lower strength steroid to treat the underlying itch. A typical example of this is seen when someone applies a topical steroid to an itchy groin rash. If the cause is fungal, the rash will get redder and itchier and spread more extensively than a typical fungal infection.
This can lead to a condition called tinea incognito wherein the rash is inflamed with visible pustules. Some people are allergic to the non-active component of a topical steroid also known as the vehicle. People who have a chronic skin condition and use multiple prescriptions including over-the-counter topical steroids are at higher risk of developing these allergies. Glaucoma is a disease in which the pressure inside the eye increases to the point of damaging the optic nerve. There are isolated reports of people developing glaucoma after long-term use of topical steroids around the eyes.
How this happens is not completely understood, but it is believed that enough of the steroid can be absorbed in the surrounding tissue to leech into the eye itself. Sign up for our Health Tip of the Day newsletter, and receive daily tips that will help you live your healthiest life. Abraham A, Roga G. Topical steroid-damaged skin. Indian J Dermatol. Side-effects of topical steroids: A long overdue revisit. Indian Dermatol Online J ; Rathi SK, D'souza P. Rational and ethical use of topical corticosteroids based on safety and efficacy.
Misuse of topical corticosteroids over face: A clinical study. Indian Dermatol Online J. Dey VK. Misuse of topical corticosteroids: A clinical study of adverse effects. Contact allergy in the population of patients with chronic inflammatory dermatoses and contact hypersensitivity to corticosteroids. Postepy Dermatol Alergol.
Systemic adverse effects from TS have also been described and they are more likely to develop when highly potent TS are used for prolonged periods on thin skin e. Hypothalamic-pituitary adrenal axis suppression is known to occur with all TS. Factors responsible for HPA axis suppression include:. Increase in the steroid penetration increases HPA suppression potential, especially in atopic children.
Betamethasone dipropionate and diflorasone diacetate have an increased ability to suppress adrenal function. Temporary reversible suppression is seen with 49 g of superpotent TS used for 2 weeks. Children and babies have a high ratio of surface area to body volume hence are more likely develop HPA axis due to systemic absorption. Iatrogenic Cushing syndrome, corticosteroid-related Addison crises, growth retardation and death are also reported.
The reactivity of the HPA axis can be assessed with the adrenocorticotropin hormone test. Recovery is time-dependent and occurs spontaneously. Hypergylcemia and the unmasking of latent diabetes mellitus can occur after prolonged application and high percutaneous absorption of TS; also systemically absorbed TS may precipitate or exacerbate hyperglycemia, especially in patients with preexisting hepatic disease. Topical steroids have minimal or no mineralocorticoid activities, but hydrocortisone and 9-a-fluoroprednisolone, have measurable mineralocorticoid activity.
Prolonged treatment may lead to edema and hypocalcemia. Rare systemic adverse effects of topical steroids[ 8 ]. Hypopigmentation and skin atrophy can occur when TS are applied topically or injected locally. However, the mechanism by which hyopigmentation occurs is not clear. Linear extension of the hypopigmentation is due to lymphatic uptake of steroid crystals. Venkatesan and Fangman demonstrated that melanocytes are intact in steroid-induced hypopigmentation, which indicates that TS may impair melanocyte function.
Triamcinolone is more likely to cause depigmentation due to its larger size, the higher tendency to aggregate and higher density. Hence for lesions close to the skin surface, especially in hyperpigmented patient triamcinolone should be avoided, instead TS with smaller particles and less tendency to aggregate should be preferred. Koushik Lahiri, b Telangiectasia overlying vitiligo patch on eyelid.
Kaushik Lahiri, b Telangiectasia with bacterial infection. Shyam Verma, b Perilesional diffuse hypopigmentation Courtesy Dr. Shyam Verma. Skin atrophy is the commonest side effect, reported to be caused by all topical TS. Epstein et al. Microscopic degenerative changes in epidermis are evident following days of treatment. Initially epidermis becomes thin due to reduction in epidermal cell size, which reflects a decreased metabolic activity. After prolonged exposure there is a reduction in cell layers, that is, stratum granulosum disappears and stratum corneum becomes thin.
Synthesis of stratum corneum lipids and keratohyalin granules and formation of corneodesmosomes required for structural integrity of stratum corneum are suppressed. Inhibition of the function of melanocytes may occur, giving rise to localized hypopigmentation.
Topical steroids induce resorption of mucopolysaccharide ground substance in the dermis. Repeated use in the same area causes epidermal thinning and changes in connective tissue of dermis leading to lax, transparent, wrinkled and shiny skin along with striae, fragility, hypopigmentation and prominence of underlying veins. The loss of connective tissue support for dermal vasculature results in erythema, telangiectasia and purpura. Degree of skin atrophy is influenced by age, body site, potency and presence of occlusion.
It is caused by suppressive action on cell proliferation and inhibition of collagen synthesis. Dermal atrophy is caused by decreased fibroblast growth and reduced synthesis of collagen, acid mucopolysaccharides and stimulation of human dermal microvascular endothelial cells.
Intertriginous areas are particularly susceptible due to thinner skin, increased moisture, elevated temperature and partial occlusion provided by the skin in these sites. Striae due to TS use need to be distinguished from those that occur due to excessive weight gain and pregnancy.
Contact hypersensitivity to TS may cause persistence or worsening of skin diseases. It is rare, but its risk increases with prolonged exposure. Nonfluorinated TS e. Binding to the amino acid arginine is probably required for development of contact allergy. Contact sensitivity can develop not only to constituents e. Sensitivity to more than one TS is common. Risk factors for development of contact sensitivity include history of multiple patch test positivity to non-TS allergen, treatment resistant eczema, leg ulcers, stasis dermatitis, perineal dermatitis and chronic actinic dermatitis.
It presents as chronic dermatitis not responding to locally applied steroids or rarely, as acute eczema, urticaria, acute local edema, immediate-type reaction, or id eruption like spread over the body. Mucocutaneous infections tinea versicolor, onychomycosis due to Trichophyton and Candida species, dermatophytosis are common during treatment with TS, occurring early in the therapy. When dermatophyte infections are treated with TS, the symptoms and signs improve transiently, giving rise to tinea incognito.
TS suppress the normal cutaneous immune response to dermatophytes leading to enchantment of fungal infections. Granuloma gluteale infantum a persistent reddish-purple, granulomatous, papulonodular eruption seen on buttocks, thighs or inguinal fold in children, is a well-known consequence of diaper dermatitis being treated with TS, caused by impairment of immune response to Candida by TS.
Similar effects on mitigation or prolongation of herpes simplex, molluscum contagiosum and scabies infection have also been reported; hence TS should not be used in presence of these infections. TS also facilitate proliferation of Propionibacterium acnes and Demodex folliculoroum leading to acne-rosacea like condition. Reactivation of Kaposi sarcoma has also been reported. Systemic corticosteroid therapy, in some cases intravenous or inhaled TS are known to induce acneiform lesions.
The eruption consists of small and uniformly sized monomorphic inflammatory papules and pustules with few or no comedones, located predominantly on trunk and extremities, with less involvement of the face. In the case of inhaled steroids, lesions occur in and around nose or mouth. Anti-inflammatory effects of TS may initially suppress inflammatory lesions and erythema, but flare-ups occur on stopping TS.
The eruption subsequently resolves after discontinuation of the TS. Topical steroids induce comedone formation by rendering follicular epithelium more responsive to comedogenesis. They also lead to increased concentration of free fatty acids in skin surface lipids and increased numbers of bacteria in the pilosebaceous duct. Free fatty acids, formed in pilosebaceous ducts by breakdown of triglycerides in the sebaceous secretion, may contribute to comedogenesis.
Topical steroids induced rosacea is seen in middle-aged woman, presenting with papules and pustules. These are initially controlled with low potency TS, but lesions may reappear and require continued use of higher potency TS.
Perioral dermatitis occurs in females on the face and is caused by long term use of potent TS on face. It presents as follicular papules and pustules on an erythematous base seen in a perioral distribution, with sparing of skin adjacent to the vermilion border. It is also seen in men and children. Steroids promote vellus hair growth by unknown mechanism. Local and disseminated hypertrichosis due to TS is rare, seen commonly with systemic steroids. Even months after withdrawal of TS the darker hairs may persist.
Hypopigmentation after topical use is quite common, but not noticed frequently in very light skinned individuals. TS probably interfere with the melanin synthesis by smaller melanocytes, causing patchy areas of hypopigmentation which are reversible after discontinuation of steroids. Hyperpigmentation after intralesional steroids has been well-documented. These develop after severe steroid induced dermal atrophy and loss of intercellular substance, causing blood vessels to lose their dermal matrix support.
The resulting fragility of dermal vessels leads to purpuric, irregularly shaped, hypopigmented, depressed pseudoscars over extremities. Continued misuse of TS can also lead to ulceration. Tachyphylaxis is characterized by decreasing efficacy of TS during continued treatment.
It occurs commonly in psoriasis patients. Withdrawal of TS is followed by a disease flare. As the tissue becomes less sensitive tachyphylaxis , increasingly potent preparations are required to achieve comparable effects, leading to more severe side effects.
Withdrawal of potent TS applied to the extensive area of psoriasis for a prolonged period may result in a relapse or a papulopustular flare and may even precipitate unstable or severe generalized pustular psoriasis. This is especially likely when steroids are used in large quantities or applied under occlusion.
Similarly, abrupt withdrawal can cause eczema flares. Steroid addiction is known to occur after inadvertent application of potent TS usually on the face. Three phases have been described: 1 Initial treatment improves pustulation, pruritus, erythema and scaling; 2 with continued use, local immunosuppression increases microbial growth and 3 on treatment withdrawal, rebound flares of itching, redness, postulation and scaling are seen.
Misuse of TS on the face is seen all over India and its incidence appears to be increasing rapidly. TSDF has also been described under various names like steroid addiction, dermatitis rosaceaformis steroidica and red face syndrome. In this condition after long term application of TS on the face, there is severe rebound erythema, burning and scaling on the face on attempting to stop the application of TS. Side effects caused by steroid eye drops are listed in Table 1.
But there are few reports of such ocular complications due to TS. Blindness due to glaucoma following extended TS use on the face is reported. Topical steroids have demonstrated to impair wound healing and re-epithelialization in animal and human models. Topical steroids are known to decrease skin elasticity. This can be assessed by pulling the skin and observing incomplete retraction on mechanical stress cessation.
Skin aging pathophysiology is similar to the one that follows TS application. Marked skin thickness decrease, especially in light-exposed areas and delayed skin recovery are reported. Topical steroids application can lead to subtle changes in the epidermal barrier as observed by decreased formation of lipid lamellar bodies and delayed barrier recovery. This effect, theoretically may worsen barrier impairment in atopic dermatitis and psoriasis, but it seems to be outweighed by reducing inflammation and permitting barrier repair.
Vehicle of TS can potentiate the side effects of TS and cause local side effects of its own. Table 3 lists the components of the vehicle that cause side effect. British National Formulary states that skin of children is sensitive so they are likely to be susceptible to side effects of TS, hence they should be avoided in children or, if necessary, used with care and for short periods.
Food and Drug Administrations center for drug evaluations and research have reported TS side effects similar to those seen in adults. Some side effects not reported in adults but seen in children include local irritation, mood change, gynecomastia, genital hypertrichosis and staphylococcal infection. Guidelines regarding TS use are available to prevent their misuse. General measures to prevent TS induced side effects are mentioned in Table 4 while Table 5 mentions measures to prevent site specific side effects.
Topical corticosteroids misuse occurs at various levels. Abraham A, Roga G. Topical steroid-damaged skin. Indian J Dermatol. Side-effects of topical steroids: A long overdue revisit. Indian Dermatol Online J ; Rathi SK, D'souza P. Rational and ethical use of topical corticosteroids based on safety and efficacy. Misuse of topical corticosteroids over face: A clinical study.
Indian Dermatol Online J. Dey VK. Misuse of topical corticosteroids: A clinical study of adverse effects. Contact allergy in the population of patients with chronic inflammatory dermatoses and contact hypersensitivity to corticosteroids. Postepy Dermatol Alergol.
Steroid-induced glaucoma: An avoidable irreversible blindness. J Curr Glaucoma Pract. Table of Contents View All. Table of Contents. Steroid Rosacea. Skin Atrophy. Stretch Marks. Alteration of Infection. Topical Steroid Allergy. Was this page helpful? Thanks for your feedback! Sign Up. What are your concerns? Article Sources. Verywell Health uses only high-quality sources, including peer-reviewed studies, to support the facts within our articles.