Prednisolone topical

If patients have a severe subepithelial infiltration, a topical steroid may be required. However, topical steroids may cause serious ocular complications and may worsen herpetic conjunctivitis, which has symptoms similar to viral conjunctivitis. Additionally, the period of virus shedding may be prolonged by up to 50% by topical prednisolone. Only ophthalmologists should prescribe topical steroids.10... 

Suspension. If the drug is not sufficiently soluble, it can be formulated as a suspension. A suspension may also be desired to improve stability, bioavailability, or efficacy. The major topical ophthalmic suspensions are the steroid anti-inflammatory agents prednisolone acetate, dexamethasone, fluorometholone, and rimex-olone. Water-soluble salts of prednisolone phosphate and dexamethasone phosphate are available however, they have a lower steroid potency and are poorly absorbed. 

A Kupferman, HM Leibowitz. (1974). Topically applied steroids in comeal disease. IV. The role of drug concentration in stromal absorption of prednisolone acetate. Arch Ophthalmol 91 377-380. 

Examples of group I, i.e. weak or low efficacy topical steroids, are hydrocortisone acetate in various concentrations, methylprednisolone 1.0% and prednisolone 0.5%. Group II, the moderately potent steroids, includes alclometasone dipropionate 0.05%, hydrocortisone butyrate 0.1%, triamcinolone acetonide 0.025% and fluocinolone ace-tonide 0.01%. Group III, the potent steroids, contains among others betamethasone valerate 0.1%, betamethasone dipropionate 0.05%, budesonide 0.025%, desoximetasone 0.05%, fluticasone propionate 0.05%, amcinonide 0.1%, fluocinonide 0.05% and mometasone furoate 0.1%. Group IV comprises the very potent agents such as clobetasol propionate 0.05% and halobetasol propionate 0.05%. 

Prednisolone (EMSOLONE) 5-60 mg/day oral, 10-40 mg intramuscular/intra articular inj. and 0.25% topical (skin, eye)... 

An ester derived from prednisolone has found use as a topical ophthalmic antiinflammatory dmg. Cleavage of the side chain in prednisolone (31-1) with sodium periodate affords the corresponding carboxylic acid (30-2). Treatment of that product with propionyl chloride affords initially the ester at 17 along with some of the mixed anhydride. The anhydride is then hydrolyzed with a mild base to afford the 17-ester (31-3). Alkylation of the carboxylic acid with chloromethylchlorosufonyl chloride (from bromochloromethane and sulfonyl chloride) leads to the chloromethyl ester (31-4) and thus loteprednol [26]. 

Synthetic glucocorticoids are prednisolone, prednisone, methylprednisolone, dexamethasone, betamethasone and triamcinolone (Table 13.2). Hydrocortisone is available as either succinate or phosphate salts for oral and intravenous administration. It is the drug of choice when a rapid effect is required, e.g. acute adrenal insufficiency, or as peri-operative replacement therapy. Prednisolone can also be given intravenously. It has about 0.8 of the mineralocorticoid activity of hydrocortisone. Prednisone is a prodrug that is converted to prednisolone in the body. For chronic therapy, synthetic steroids without mineralocorticoid activity are preferred, such as dexamethasone, betamethasone or triamcinalone. Beclo-metasone passes membranes poorly and is more active topically than when given orally. It is used as an aerosol for chronic rhinitis and asthma, and topically in severe eczema. Fludrocortisone is a synthetic halogenated derivate of cortisol that is used for its mineralocorticoid effect. 

Acute-onset calcific band keratopathy has been reported in a woman using topical prednisolone (SEDA-20, 372 75). 

An 11-year-old boy with iridocyclitis developed Cushing s syndrome, a posterior subcapsular cataract, and increased intraocular pressure in both eyes after the topical administration of prednisolone acetate 1% eye-drops bilaterally for 6 months. The Cushing s syndrome was aggravated when periocular methylpredni-solone acetate was started while bilateral posterior subtenon injections of 80 mg of suspension were continued every 6 weeks for 6 months. He had not used systemic glucocorticoids before. 

A 58-year-old woman, who had been involved in the manufacturing of glucocorticoid creams and ointments for over 10 years, developed occupational contact sensitization to topical glucocorticoids (472). Patch tests were positive to hydrocortisone, hydrocortisone butyrate, and tixocortol pivalate. Intradermal tests were positive to hydrocortisone succinate, methylpredniso-lone, and prednisolone. An oral challenge with betamethasone 0.75 mg, 2.5 mg, and 8 mg on three consecutive days resulted in no adverse reactions. 

Sawusch, M.R., T.P. O Brien, and S.A. Updegraff. 1989. Collagen corneal shields enhance penetration of topical prednisolone acetate. J Cataract Refract Surg 15 625. 

In rats and mice the topical application of a 20 to 40% vitamin E ointment suppressed chemical-induced allergic or irritant contact dermatitis comparable to the effects of a 0.5% prednisolone... 

The introduction of a 16a-hydroxy group into 6a,9-difluoro-prednisolone led to a compound (fluocinolone) with the anticipated favorable biological spectrum, namely high anti-inflammatory activity (35-fold that of hydrocortisone, seven-fold that of triamcinolone) and - in contrast to the C-16 unsubstituted compound - no retention of sodium. The corresponding 16,17-acetonide (fluocinolone acetonide) exhibited 100-fold the anti-inflammatory activity of hydrocortisone, with no sodium retention. In clinical trials, 6a,9-difluoro-16a-hydroxyprednisolone was found to be a potent suppressor of inflammatory conditions such as rheumatoid arthritis, as well as allergic conditions such as asthma, whilst its acetonide proved to be highly effective as topical corticoid. 

The introduction of a 16a-hydroxy-group into 9a-fluoro-prednisolone leads to a compound which is devoid of sodium retention but has anti-inflammatory activity considerably lower than that of the parent compound. The 16a- and 16/7-rnelhyl-9a-fluoro-prednisolones, on the other hand, are more potent than the parent compound yet free of sodium retention. Peculiarly, the conversion of 16a-hydroxy-9a-fluoro-prednisolone to the 16a, 17-acetonide markedly increases topical activity, without significantly affecting oral anti-inflammatory activity. 

Introduction of the 16a-methyl group into 6a,9-difluoro-prednisolone led to flu-methasone, which is used topically in the treatment of various skin disorders. 

Abuse of topically administered drugs by practitioners or patients can cause significant ocular toxicity. Infiltrative keratitis has occurred from long-term use of anesthetic eyedrops for relief of pain associated with corneal abrasions. Bilateral posterior subcapsular cataracts have developed after the topical administration of prednisolone acetate 0.12% twice daily over long durations. Practitioners should closely monitor patients treated with drugs known to have potentially significant ocular or systemic side effects. 

A placebo-controUed study of patients with stromal keratitis receiving topical prednisolone and trifluridine showed no benefit to adding oral acyclovir in terms of time to healing or treatment failure, likelihood of resolution, or 6-month best corrected acuity (HEDS). 

Prednisolone acetate is available in 0.125% and 1.0% concentrations. Kinetic studies have shown that raising the concentration of prednisolone acetate from 1.0% to 1.5% or 3.0% does not enhance its anti-inflammatory effects. In severe inflammatory reactions, topical dosing of prednisolone acetate 1% at 1-minute intervals for 5 minutes each hour may provide the best clinical suppression of inflammation (Table 12-5). As compared with other topical ocular steroids, 1% prednisolone acetate is generally considered the most effective anti-inflammatory agent fiar anterior segment ocular inflammation. 

Anti-Inflammatory Effect of Different Dosage Schedules for Topical Administration of Prednisolone Acetate 1%... 

After topical application to the eye, fluorometholone alcohol penetrates and is rapidly metabolized within the aqueous humor. Comparative anti-inflammatory studies indicate that the efficacy of fluorometholone alcohol is somewhat less than dexamethasone alcohol and prednisolone acetate (see Table 12-1). Increasing the concentration of fluorometholone alcohol from 0.1% to 0.25% does not significantly increase its anti-inflammatory activity but does enhance its tendency to raise lOP. The 17-acetate derivative of fluorometholone has demonstrated greater anti-inflammatory activity in the experimental rabbit keratitis model than has fluorometholone alcohol. However, studies with fluorometholone acetate show that it is metabolized slowly as compared with the alcohol derivative (Figure 12-1). Thus it is possible that the 17-acetate substitution to the fluorometholone base not only enhances its anti-inflammatory effects, but also impedes its metabolism. 

Associated toxic epithelial keratitis should respond to blepharitis treatment. Topical steroids are generally not required imless the cornea is significantly involved or a phlyctenule is present. In this case prednisolone 0.12% used two or three times a day for a few days may be used. Combination steroid-antibiotic ointments, such as tobramycin-dexamethasone or the topical combination drop tobramycin-loteprednol, may prove to be useful for those patients complaining of excessive itching and burning. Steroids control the hypersensitivity component that is often present and reduce the congestion and irritation that often provoke the patient to rub the eye and aggravate the blepharitis. 

Management of the ocular aspects of Reiter s syndrome is directed toward control of inflammation.The uveitis can be fairly severe and resistant to therapy. In most instances such topical steroids as 1% prednisolone acetate or 0.1% dexamethasone are recommended. Dosage is variable but in severe cases should be administered initially every 1 to 2 hours and accompanied by such cycloplegic agents as 5% homatropine or 0.25% scopolamine two to three times daily. Aggressive treatment reduces formation of synechiae and subsequent secondary glaucoma. In patients who have severe uveitis, either sub-Tenon s capsule or oral steroids may be used in conjimction with topical management. 

Therapy depends on etiology. In individuals who are suspected of having tuberculosis, diagnosis should make use of a purified protein derivative skin test, chest radiograph, and sputum cultures if necessary. These individuals should be referred for comanagement to their primary physician or to an infectious disease specialist. Though antituberculin agents are systemically administered, the ocular lesions are appropriately treated with topical steroids. In most instances, patients respond to 1% prednisolone acetate every 3 to 4 hours for the first day, subsequently tapered rapidly on the basis of the clinical response. 

More severe forms of toxic keratitis may require prophylactic antibiotic therapy to protect the inflamed cornea. The use of topical aminoglycosides should be avoided, however, as they tend to exacerbate the condi-tion.The use of a mild steroid, such as 0.12% prednisolone drops four times a day, aids the resolution of more advanced cases. Any allergic component involving the eyelids or conjunctiva should be treated appropriately. 

---