Medium potency topical corticosteroids

The doctor may suggest hospitalization simply because it may be necessary to break the cycle of chronic inflammation, or other problems that are exacerbating the illness. Frequently, five or six days of vigorous in-hospital treatment care can result in a dramatic clearing of the eczema. Food tests, allergy skin testing, and the development of an outpatient therapy plan can all be done during the hospitalization. Unfortunately, getting approval from insurers is often difficult. During an acute flare the number of 15-20 minute baths must be increased to three or four per day. Besides hydrating the skin, baths also increase the penetration of topical medication up to ten-fold if the medicine is applied immediately after the bath. Wet wraps after baths may also help hydration and medicinal penetration. Bedtime wet wraps are most practical, and can be done with elasticized gauze followed by ace bandages or double pajamas. (The first pair of pajamas is worn damp but not soaking wet, and a second pair of dry pajamas is worn over them. For a tighter fit, sometimes a plastic sauna suit is used instead of the dry pajamas.) For feet and hands, socks can be used. Additional blankets or increased room heat may be necessary during this three to seven days to prevent chilling.

The rationale for the use of vitamin D derivatives in the treatment of psoriasis is based on the observation that patients with hypocalcemia often develop various forms of psoriasis, most notably the pustular form. In one case, a patient who had undergone thyroidectomy developed repeated flares of pustular psoriasis after decreases were made in her dosage of ergocalciferol (Vitamin D 2 ); each episode was related to severe hypocalcemia and resolved after her serum calcium levels normalized. 14 Another patient with osteoporosis experienced dramatic improvement in severe psoriasis after receiving an oral form of vitamin D. 15 This finding, along with the discovery that the bioactive form of 1,25-dihydroxycholecalciferol has been shown to inhibit keratinocyte proliferation and promote keratinocyte differentiation, 16 has led to the development of vitamin D analogs for the treatment of psoriasis.

Drug Release from the Semi Solid Dosage Forms and Drug Deposition Studies: Drug release from the semi solid dosage forms are performed by the Franz- type static diffusion cells. In this epidermal side of the skin was exposed to ambient condition. While dermal side was kept facing the receptor solution. Receptor compartment containing 20mL phosphate buffer pH was thermo stated at 32±°C and stirred at 600 rpm. Skin was saturated with diffusion medium for 1 h before the application of sample. A 200-mg of sample was applied on the donor compartment. For determination of drug deposited in the skin, the diffusion cell was dismantled after a period of 4, 8, 16, and 24 h. The skin was carefully removed, and drug present on the skin surface was cleaned with distilled water 28 .

Like other topical corticosteroids, hydrocortisone valerate has anti-inflammatory, antipruritic and vasoconstrictive properties. The mechanism of the anti-inflammatory activity of the topical steroids, in general, is unclear. However, corticosteroids are thought to act by the induction of phospholipase A 2 inhibitory proteins , collectively called lipocortins. It is postulated that these proteins control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes by inhibiting the release of their common precursor arachidonic acid. Arachidonic acid is released from membrane phospholipids by phospholipase A 2 .

Medium potency topical corticosteroids

medium potency topical corticosteroids

Like other topical corticosteroids, hydrocortisone valerate has anti-inflammatory, antipruritic and vasoconstrictive properties. The mechanism of the anti-inflammatory activity of the topical steroids, in general, is unclear. However, corticosteroids are thought to act by the induction of phospholipase A 2 inhibitory proteins , collectively called lipocortins. It is postulated that these proteins control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes by inhibiting the release of their common precursor arachidonic acid. Arachidonic acid is released from membrane phospholipids by phospholipase A 2 .

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