Salep Kortikosteroid Untuk Dermatitis

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    Dermatitis Atopik by Vidya Sutanto on Prezi

    salep kortikosteroid untuk dermatitis

    The introduction of topical steroids TS of varying potency have rendered the therapy of inflammatory cutaneous disorders more effective and less time-consuming. However the usefulness of these has become a double edged sword with constantly rising instances of abuse and misuse leading to serious local, systemic and psychological side effects.

    These side effects occur more with TS of higher potency and on particular areas of the body like face and genitalia. The article reviews the side effects of TS with special mention about peadiatric age group, also includes the measures for preventing the side effects.

    The introduction of topical corticosteroids TC by Sulzberger and Witten in is considered to be the most significant landmark in the history of therapy of dermatological disorders. Although, it is this very usefulness of the drug which has become a double edged sword and made it vulnerable to now an alarming proportion with constantly rising instances of abuse and misuse leading to serious local, systemic, and psychological side effects.

    Such misuse occurs more with TC of higher potency and on softer areas of the body particularly the face and genitalia. The end-users of TC are hapless patients. They tend to overuse TCs beyond the time limit set by clinicians by repeating prescriptions. Of more concern is the mass use of TCs as fairness creams. Vast sections of the Indian society have willingly or unknowingly become victims to the craze of beautification leading to a virtual epidemic of monomorphic acne, steroid atrophy, steroid rosacea, telangiectasia, perioral dermatitis, striae and other manifestations of a condition which has been collectively described as topical steroid damaged facies TSDF.

    At the opposite end of the spectrum lies the danger of steroid addiction. The most common side effects are localized to sites of application. These tend to occur with prolonged treatment and depend on potency of TS, its vehicle and site of application. The most common include atrophy, striae, rosacea, perioral dermatitis, acne and purpura. Hypertrichosis, pigment alteration, delayed wound healing and exacerbation of skin infections are less frequent.

    In the infection column, put comma between Granuloma gluteale infantum and genital ulceration. 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:.

    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. Skin atrophy is the commonest side effect, reported to be caused by all topical TS.

    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. 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: Misuse of TS on the face is seen all over India and its incidence appears to be increasing rapidly.

    Side-effects of topical steroids: A long overdue revisit

    salep kortikosteroid untuk dermatitis

    salep kortikosteroid untuk dermatitis

    salep kortikosteroid untuk dermatitis