What is hydrocortisone valerate cream 0.2 used for

John Decker (Part II)

Alice Fay Jackson (Part I)

Mrs. Jackson, a 58-year-old black elementary school teacher, complains of a 4-day history of skin sensitivity and aching of the area on the left side of her back extending to her axilla, which has prevented her from wearing her bra. Yesterday she noticed a patch of small painful blisters on her upper left abdomen (Plate 12). She has been applying calamine lotion to the area since the blisters appeared and taking ibuprofenMotrin) without relief. She had an injection of cortisone a week ago in her family doctor's office to help relieve her back pain resulting from osteoarthritis. She sleeps with a heating pad under her back at night when her back pain flares.

Her prescribed medications include famotidine (Pepcid) for indigestion and hormone replacement therapy after a hysterectomy for uterine fibroids and menorrhagia.

On physical examination, you note some conjunctival pallor, but her skin is finely textured and relatively free of wrinkles. She has a sprinkling of 2-mm black papules across her nose and cheeks (Plate 13).

Erythematous papules and vesicles arising just lateral to her spine trace the T5 dermatome around to the anterior axillary line on the left, and the area is tender to palpation. Her sacral area appears hyperpigmented and mottled with a reticular erythematous pattern, fairly well demarcated in an oval shape approximately 8 × 10 cm.

Topical and Systemic Medications

The first-line medication for AD is a topical corticosteroid (TCS). For mild AD, a TCS with group VI and VII potency (Table 2) may suffice. However, for moderate to severe AD, a TCS with at least group III to V potency is chosen to increase efficacy and to shorten the duration of need for these medications.

The use of TCS is confronted with various obstacles, including rare side effects such as skin atrophy, but mostly patients’ or parents’ misunderstanding of TCS. Studies have shown that twice-daily use of fluticasone propionate (Cutivate) 0.05% cream (group V) and desonide (DesOwen, Tridesilon) 0.05% ointment or aqueous gel (group V and VI, respectively) continuously up to 1 month in young children with AD results in no significant adverse effect. It is therefore important to clarify for patients or parents the safety and side effects based on the potency of the TCS.

Topical calcineurin inhibitors (TCI) (pimecrolimus [Elidel] 1% cream and Protopic/tacrolimus ointment) are alternative nonsteroidal antiinflammatory medications for AD. Elidel is indicated for mild to moderate AD in patients older than 2 years, whereas 0.03% and 0.1% Protopic are indicated for moderate to severe AD in patients 2 to 15 years old and in patients 16 years old or older, respectively. Both Elidel and Protopic have an FDA black box warning saying that their long-term use may be associated with cancer risk. However, a recent large longitudinal study has failed to confirm this risk. These medications continue to be useful alternatives for skin areas that are prone to atrophy, including the face, axillae, and groins.

A third class of topical medication, phosphodiesterase 4 inhibitor (crisaborole [Eucrisa] 2% ointment), has been approved by the FDA for patients 2 years and older with mild to moderate AD. A biologic dupilumab (Dupixent), which targets IL-4 and IL-13, has also been approved by the FDA for patients 12 years and older with moderate to severe AD.

Wet-wrap treatment, phototherapy, and systemic immunosuppressive therapies (e.g., cyclosporine [Sandimmune, Neoral],1 azathioprine [Imuran],1 methotrexate [Trexall],1 and mycophenolate mofetil [CellCept])1 are alternatives, but not approved by FDA, for severe AD patients. Because of the potential serious adverseeffects associated with these treatments, referral to an allergist or dermatologist is recommended before their initiation.

Systemic corticosteroids usually are not recommended for AD because of their known adverse effects, including stunted growth in children, adrenal suppression, osteoporosis, and cataracts. A rebound of AD symptoms is common after the medication is stopped. If a systemic corticosteroid is used, it should be tapered over a short period (e.g., a week) while topical antiinflammatory treatment is intensified.

The efficacy and side effects of the following medications have not been established in AD: intravenous immunoglobulin (IVIG),1 anti-IgE (omalizumab [Xolair]),1 probiotics,7 montelukast (Singulair),1 Chinese medicinal herbs, and fish oils.1

Basic Chemistry

Chemical StructureStructureCommentsOne-hundred twelve milligrams of hydrocortisone acetate is approximately equivalent to 100 mg of hydrocortisone. One-hundred nineteen milligrams of hydrocortisone butyrate is approximately equivalent to 100 mg of hydrocortisone. One-hundred twenty-eight milligrams of hydrocortisone hydrogen succinate is approximately equivalent to 100 mg of hydrocortisone. One-hundred thirty-four milligrams of hydrocortisone sodium phosphate is approximately equivalent to 100 mg of hydrocortisone. One-hundred thirty-four milligrams of hydrocortisone sodium succinate is approximately equivalent to 100 mg of hydrocortisone. One-hundred twenty-three milligrams of hydrocortisone valerate is approximately equivalent to 100 mg of hydrocortisone The Complete Drug Reference (2003).Chemical FormulaC21H30O5PropertiesPhysical PropertiesHydrocortisone, hydrocortisone acetate, and hydrocortisone butyrate are white, crystalline powders The Complete Drug Reference (2003).Hydrocortisone hydrogen succinate and hydrocortisone sodium phosphate are white, or almost white, hygroscopic powders The Complete Drug Reference (2003).Hydrocortisone sodium succinate is a white or nearly white, odorless, hygroscopic, amorphous solid The Complete Drug Reference (2003) The Merck Index (2001).Molecular Weight362.463SolubilityHydrocortisone is practically insoluble in water, sparingly soluble in alcohol and in acetone, and slightly soluble in dichloromethane. Hydrocortisone acetate is practically insoluble in water, slightly soluble in dehydrated alcohol and in dichloromethane. Hydrocortisone butyrate is practically insoluble in water, soluble in alcohol, in acetone, and in methyl alcohol, freely soluble in chloroform, and slightly soluble in ether. Hydrocortisone hydrogen succinate is practically insoluble in water, freely soluble in dehydrated alcohol and in acetone. It dissolves in dilute solutions of alkali carbonates and alkali hydroxides. Hydrocortisone sodium phosphate is freely soluble in water, practically insoluble in dehydrated alcohol and in chloroform. A 0.5% aqueous solution has a pH of 7.5–9.0. Hydrocortisone sodium succinate is very soluble in water and in alcohol, very slightly soluble in acetone, and insoluble in chloroform.

Corticosteroids.

Corticosteroids reduce inflammation and pruritus and are effective for both the acute and chronic components of AD. They affect multiple resident and infiltrating cells primarily through suppression of inflammatory genes, reducing inflammation and pruritus. Topical corticosteroids are available in a wide variety of formulations, ranging from extremely high-potency (group 1) to low-potency (group 7) preparations (Table 33.2). The vehicle in which the product is formulated can alter the potency of the corticosteroid and move it up or down in this classification. Generic formulations of topical corticosteroids are required to have the same active ingredient and the same concentration as the original product. However, many generics do not have the same vehicle formulation, and the bioequivalence of the product can vary significantly.

Choice of a particular product depends on the severity and distribution of skin lesions. In general, an effective topical corticosteroid of the lowest potency should be used. However, choosing a preparation that is too weak may result in persistent or worsening AD. Resistant lesions may respond to a potent topical corticosteroid under occlusion, although this needs to be used cautiously to prevent irreversible atrophic changes. When treating pediatric patients, clinicians should be aware of age-appropriate indications (e.g., fluticasone 0.05% cream, up to 28 days in children age ≥3 months; fluticasone lotion, ≥12 months of age; mometasone cream/ointment, ≥2 years of age).

With appropriately used low- to medium-potency topical corticosteroids, side effects are infrequent. Thinning of the skin with telangiectasias, bruising, hypopigmentation, acne, striae, and secondary infections may occur. The face, particularly the eyelids, and the intertriginous areas are especially sensitive to these adverse effects, and only low-potency preparations should be used routinely on these areas. Perioral dermatitis, characterized by erythema, scaling, and follicular papules and pustules that occur around the mouth, in the alar creases, and sometimes on the upper lateral eyelids, can occur with the use of topical corticosteroids on the face. “Steroid addiction” describes an adverse effect primarily of the face of adult women treated with topical corticosteroids, who complain of a burning sensation. Patients improve with total discontinuation of the corticosteroid therapy.177 High-potency topical corticosteroids must be used cautiously, especially under occlusion, because they may lead to significant atrophic changes and systemic side effects.

Topical corticosteroids are available in a variety of bases, including ointments, creams, lotions, solutions, gels, sprays, oil, and even tape (Table 33.2). Therefore no need exists to compound these medications. Ointments are most occlusive and as a rule provide better delivery of the medication while preventing evaporative losses. In addition, ointments spread more evenly than other creams or solutions. In a humid environment, creams may be better tolerated than ointments, because the increased occlusion can cause itching or even folliculitis. In general, however, creams and lotions, although easier to spread, are less effective and can contribute to skin dryness and irritation. Solutions can be used on the scalp and hirsute areas, although the alcohol content can be irritating, especially if used on inflamed or open lesions, and additives used to formulate the different bases can cause sensitization. Furthermore, allergic contact dermatitis to the corticosteroid molecule is being recognized with increasing frequency.61 This diagnosis is often difficult to establish clinically, because it can present as acute or chronic eczema.

hydrocortisone

(hye-droe-kor'-ti-sone)

▪ Brand Name(s): Acticort 100, Aeroseb-HC, A-Hydrocort, Ala-Cort, Ala-Scalp HP, Anucort-HC, Anumed-HC, Anusol-HC, Anutone-HC, Caldecort, Cetacort, Colocort, Cortane, Cortaid, Cort-Dome High Potency, Cortef, Cortenema, Cortifoam, Cortizone-5, Cortizone-10, Cotacort, Emcort, Gly-Cort, Hemorrhoidal HC, Hemril-30, Hemril-HC Uniserts, Hydrocortone, Hydrocortone Phosphate, Hytone, Instacort 10, Lacticare-HC, Locoid, Locoid Lipocream, Nupercainal Hydrocortisone Cream, Nutracort, Orabase HCA, Pandel, Penecort, Preparation H Hydrocortisone, Proctocort, Proctocream-HC, Procto-Kit 1%, Procto-Kit 2.5%, Proctosert HC, Proctosol-HC, Proctozone-HC, Rectasol-HC, Rederm, Scalp-Aid, Solu-Cortef, Texacort, WestCort

OTC: Cortaid, Cortizone, Dermolate, Gynecort Female Creme, Lanacort-5, Tegrin-HC

Combinations

Rx: with chloramphenicol (Chloromycetin/HC suspension—ophthalmic); with neomycin and polymyxin B (Cortisporin Otic, Drotic, Otocort—otic); with neomycin, polymyxin B, and bacitracin (Cortisporin Ointment, Neotricin HC—ophthalmic); with oxytetracycline (Terra-Cortril—ophthalmic); with urea (Carmol HC)

Chemical Class: Glucocorticoid

▪ Clinical Pharmacology:

Mechanism of Action: An adrenocortical steroid that inhibits accumulation of inflammatory cells at inflammation sites, phagocytosis, lysosomal enzyme release and synthesis, and release of mediators of inflammation. Therapeutic Effect: Prevents or suppresses cell-mediated immune reactions. Decreases or prevents tissue response to inflammatory process.

Pharmacokinetics:

RouteOnsetPeakDurationIVN/A4-6 hr8-12 hr

Well absorbed after IM administration. Widely distributed. Metabolized in the liver. Half-life: Plasma, 1.5-2 hr; biologic, 8-12 hr.

▪ Available Forms:

Tablets (Cortef): 5 mg, 10 mg, 20 mg.

Oral Suspension, cypionate (Cortef): 10 mg/5 ml

Cream (Rectal): 1% (Nupercainal Hydrocortisone Cream, Cortizone-10, Preparation H Hydrocortisone, Proctocort, Procto-Kit 1%), 2.5% (Anusol-HC, Hemorrhoidal HC, Procto-Kit 2.5%, Proctosol-HC, Proctozone-HC).

Cream, butyrate (Topical [Locoid, Locoid Lipocream]): 0.1%.

Cream, probutate (Topical [Pandel]): 0.1%.

Cream, valerate (Topical [WestCort]): 0.2%.

Cream (Topical): 0.5% (Cortizone-5), 1% (Ala-Cort, Caldecort, Cortizone-10, Hycort, Hytone, Penecort), 2.5% (Hytone, Proctocream-HC).

Foam (Rectal [Cortifoam]): 10%.

Gel (Topical [Instacort 1%): 1%.

Lotion: 0.5% (Cetacort), 1% (Ala-Cort, Cetacort, Cortone, Lacticare-HC, Nutracort), 2.5% (Hytone, Lacticare-HC, Nutracort).

Ointment, butyrate (Topical [Locoid]): 0.1%.

Ointment, valerate (Topical [WestCort]): 0.2%.

Ointment (Topical): 0.5% (Cortizone-5), 1% (Anusol-HC, Cortaid, Cortizone-10, Hydrocortisone 1%, Hytone), 2.5% (Hytone).

Paste (Topical [Orabase HCA]): 0.5%.

Solution (Topical): 1% (Acticort 100, Gly-Cort, Penecort, Rederm, Scalp-Aid, Texacort), 2.5% (Texacort).

Solution, butyrate (Topical [Locoid]): 0.1%.

Spray (Topical [Aeroseb-HC]): 0.5%.

Suppositories: 25 mg (Anucort-HC, Anumed-HC, Anusol-HC, Anutone-HC, Cort-Dome High Potency, Hemorrhoidal HC, Hemril-HC, Proctosol-HC, Rectasol-HC), 30 mg (Emcort, Hemril-30, Proctocort, Proctosert HC).

Suppositories (Rectal [Colocort, Cortenema]): 100 mg/60 ml.

Injection (A-Hydrocort, Solu-Cortef): 100 mg, 250 mg, 500 mg, 1 g.

Injectable Solution, sodium phosphate (Hydrocortone Phosphate): 50 mg/ml.

Injectable Suspension, acetate: 25 mg/ml, 50 mg/ml.

▪ Indications and Dosages:

Acute adrenal insufficiency: IV 100 mg IV bolus; then 300 mg/day in divided doses q8h.

Anti-inflammation, immunosuppression: IV, IM 15-240 mg q12h. PO 15-240 mg q12h.

Status asthmaticus: IV 100-500 mg q6h.

Shock: IV 500 mg-2g q2-6h.

Adjunctive treatment of ulcerative colitis: Rectal 100 mg at bedtime for 21 nights or until clinical and proctologic remission occurs (may require 2-3 mo of therapy). Rectal (Cortifoam) 1 applicator 1-2 times a day for 2-3 wk, then every second day until therapy ends. Topical Apply sparingly 2-4 times a day.

▪ Contraindications: Fungal, tuberculosis, or viral skin lesions; serious infections

Pruritus and Inflammation

Children with AD often require topical anti-inflammatory agents to reduce pruritus and inflammation. When selecting topical agents, the choice of vehicle is important in terms of both efficacy and compliance. Ointments are more occlusive and tend to contain fewer ingredients and less alcohol and therefore cause less stinging and burning; however, they may leave the patient feeling greasy. Ointments are best tolerated by infants and young children. Creams are less occlusive, have a greater propensity to cause stinging and burning, but may be better tolerated by older children and adults. Lotions and solutions are generally less effective emollients and contain higher concentrations of alcohol, but these may be better tolerated in hair-bearing areas such as the scalp.

Topical antiinflammatory medications

Topical corticosteroids have been the mainstay of treatment for AD (Table 3.2), and are available in a wide range of potencies from the weakest class VII corticosteroids (e.g., hydrocortisone acetate) to the ultrapotent class I steroids (Table 3.3). The use of more potent topical corticosteroids, particularly when applied to large surface areas, under occlusion or for long periods of time, may lead to adverse effects (Table 3.4). The face and intertriginous areas are the most susceptible sites, and may show local effects, even when weaker steroids are used for prolonged periods (Fig. 3.28). Because of their increased body surface area-to-weight ratio, small children have the greatest risk of systemic absorption of topically applied steroids. Concern about the use of topical steroids has led to ‘steroid phobia’ among families and even physicians.99 As a result, compliance may be decreased and weak topical steroids insufficient for adequate control may be used.

In general, group I corticosteroids are not recommended for patients younger than the age of 12 years, should not be used in intertriginous areas or under occlusion, and require a rest period after 14 days of use. Use of this group of ultrapotent steroids is usually reserved for lichenified plaques and recalcitrant dermatitis of the hands and feet, and should be limited. Considering the widespread use of topical corticosteroids, few local adverse reactions occur when topical steroids are carefully chosen and used appropriately based on site of application and severity of the dermatitis.100 As such, even potent topical corticosteroids may safely be used in small areas for short periods of time.

The choice of treatment will depend on the severity and localization of the dermatitis, the age of the pediatric patient, and the history of use of topical antiinflammatory agents. The least potent preparation that adequately controls the disease process should be used. For children with mild to moderate disease, intermittent use of a low strength topical steroid with emollient application to maintain clearance usually suffices. However, children with moderate to severe disease often show a cycle of rapid recurrent flaring when topical antiinflammatory suppression is discontinued. A commonly used regimen to maintain control in these children while minimizing the risk of chronic steroid application is to apply mid-potency to potent topical steroids for acute flares (e.g., for a few days to up to 2 weeks twice daily) followed by intermittent therapy with topical steroid101 or, to avoid continuing steroid altogether, with a topical calcineurin inhibitor (see below). Studies have suggested that topical calcineurin inhibitors can be applied three times weekly to recurrently affected sites to retain control of the dermatitis once improved with the use of topical steroids.102,103

The potency of a topical corticosteroid is largely determined by vasoconstrictor assay, and is related to its vehicle as well as to its chemical formulation. Vasoconstrictor assays reveal that generic formulations tend to vary in their clinical activity and their vehicles may at times contain agents differing from those of brand name formulations. Thus, care must be taken in considering substitution of brand name corticosteroids by generic formulations. The concentration of each topical corticosteroid is only significant with respect to potency relative to other corticosteroids of the same chemical formulation. Accordingly, hydrocortisone acetate 2.5% is much weaker than triamcinolone acetonide 0.1%, which in turn is weaker than clobetasol propionate 0.05%, even though the concentrations would suggest the opposite. It also should be recognized that hydrocortisone acetate differs chemically from hydrocortisone butyrate, hydrocortisone probutate, and hydrocortisone valerate, which as mid-potency steroids are stronger than hydrocortisone acetate. Halogenated steroids are usually stronger than non-halogenated steroids.

Corticosteroid ointments afford the advantage of occlusion, more effective penetration, and in general greater efficacy than equivalent cream or lotion formulations. Ointments are particularly effective in the management of dry, lichenified, or plaque-like areas of dermatitis. Ointment formulations, however, may occlude eccrine ducts, inducing sweat retention and pruritus, and hair follicles, leading to folliculitis. As with emollients, formulations in ointments may not be as well tolerated during the summer months of increased heat, perspiration, and high humidity. On the other hand, creams often contain additives that may be irritating or sensitizing. Creams and lotions, however, are more cosmetically elegant, and afford the advantages of greater convenience and acceptability during hot weather and in intertriginous areas. Traditional gels and foams are not well tolerated in individuals with AD, but may be most effective in the management of acute weeping or vesicular lesions. Topical corticosteroids in emollient-based foam formulations and hydrocolloid gels (in contrast to the alcohol-containing foams and gels) are particularly useful for hairy areas, to avoid occlusion, and for cosmesis. Oil preparations are most commonly used for scalp dermatitis. Best applied to a wet scalp, oil formulations can be shampooed out after at least 1 hour to overnight. A fluocinolone acetonide oil preparation, however, has been shown to be helpful after the bath for children with extensive AD.104

Occlusion of treated areas with polyethylene film, such as Saran wrap, or the use of corticosteroid-impregnated polyethylene film (Cordran tape) enhances the penetration of corticosteroids up to 100-fold. This mode of therapy is particularly effective for short periods of time (8–12 h a day on successive days) for patients with chronic lichenified or recalcitrant plaques of dermatitic skin. Occlusive techniques, however, are contraindicated for prolonged periods of time, and are not recommended in infected or intertriginous areas. Given that the diaper is an occlusive dressing, application of steroids in the diaper area of infants should be avoided or limited to short-term use of low-strength topical steroids.

For sites of severely lichenified dermatitis, salicylic acid can be compounded into preparations with steroids to improve penetration. Tar (liquor carbonis detergens or crude coal tar) can be also be used as an adjunctive therapy in patients with chronic dermatitis in the form of tar baths (e.g., Cutar) or compounded with topical corticosteroids (e.g., compounding triamcinolone 0.1% with 6% salicyclic acid and 5–10% liquor carbonis detergens in Aquaphor ointment). The objectionable odor, staining properties, potential for irritation, risk of causing folliculitis, and low potential risk of later carcinogenesis make tar a choice only for only selected patients.

Where should you not use hydrocortisone cream?

Is hydrocortisone valerate 0.2% strong?

How long does it take for hydrocortisone cream to start working?

What does hydrocortisone cream do to the skin?