1 Name of Medicine

Hydrocortisone acetate.

2 Qualitative and Quantitative Composition

Chemists' Own Skin Irritation Cream contains 1.0% w/w hydrocortisone acetate: 30 g tube.
Hydrocortisone acetate is an odourless, white or almost white, crystalline powder. Hydrocortisone acetate 112 mg is approximately equivalent to 100 mg of hydrocortisone.
Practically insoluble in water and in ether, soluble in ethanol (1 in 230) and in chloroform (1 in 200).

3 Pharmaceutical Form

Chemists' Own Skin Irritation Cream is a soft white cream with a faint odour of chlorocresol. It contains 1.0% w/w microfine hydrocortisone acetate in a water miscible, lanolin free cetomacrogol base. Chlorocresol 0.1% w/w is used as a preservative.

4 Clinical Particulars

4.1 Therapeutic Indications

Topical corticosteroid therapy for the temporary relief of symptoms of non-infected inflammatory conditions of the skin (e.g. minor skin irritations, itching and rashes due to eczema, dermatitis, contact dermatitis [such as rashes due to soap, detergent, cosmetics and jewellery], insect bites, itching anal and genital areas and sunburn).

4.2 Dose and Method of Administration

Adults and children from 2 years of age: apply a thin layer to affected areas 2-4 times daily. Reduce the number of applications as the disorder subsides. The cream should not be used under occlusive dressings or waterproof bandages unless advised to by a doctor. This preparation should not be used for more than 7 days except on the advice of a doctor. Rub in gently.

4.3 Contraindications

Tuberculous and fungal conditions of the skin, acute Herpes simplex, vaccinia, varicella and all viral infections.
Untreated bacterial infections.
Parasitic infestations (e.g. scabies).
In patients with markedly impaired circulations since skin ulceration has occurred in these patients following the use of corticosteroids.
Hypersensitivity to any component of the cream.
Not to be used in the eyes.
Not to be used for acne or rosacea.
The cream should not be used under occlusive dressings or waterproof bandages unless advised to by a doctor.
Hydrocortisone may mask signs of infection. If any infection is present, an appropriate anti-infective agent should be used first. Chemists' Own Skin Irritation Cream may be used to reduce inflammation but if a favourable response does not occur promptly then use of the product should be discontinued until the infection has been adequately controlled.
If any skin irritation develops, discontinue use and treat appropriately. If extensive areas are treated, or if occlusive dressings are used, the possibility also exists for increased systemic absorption and this could in turn lead to depression of the hypothalamic pituitary adrenal axis. In all such patients it is essential to monitor adrenal function at regular intervals.

4.4 Special Warnings and Precautions for Use

For external use only. Avoid contact with eyes.
This medicine should not be used in the eyes. Use of the cream near the eyes should be avoided. This is due to the risk of corticosteroid-induced open-angle glaucoma.
As with other topical corticosteroids, when extensive areas are treated, sufficient systemic absorption may occur to produce the features of hypercorticalism. Rarely, local atrophy or striae may occur after prolonged treatment. This must be borne in mind when treating conditions such as severe eczema and seborrheic dermatitis. Appropriate antimicrobial therapy should be used whenever treating inflammatory lesions that have become infected.
If irritation develops Chemists' Own Skin Irritation Cream should be discontinued and alternative therapy instituted. Prolonged and heavy doses of hydrocortisone may have an immunosuppressant effect and thus decrease resistance to infection as well as mask signs of it. If infection of the skin is present suitable antifungal or antibacterial agents should be used first. Any occlusive dressings should be discontinued. If the infection does not respond promptly to therapy, corticosteroid therapy should be discontinued until the infection has been controlled.
Where very large areas are treated for long periods (e.g. atopic dermatitis), the possibility of systemic absorption exists, particularly if an occlusive dressing is applied. Prolonged use of large quantities of topical corticosteroids may also result in atrophic striae or acne eruptions.
Due to the possible systemic absorption of topical steroids, there may be a need for periodic evaluation of hypothalamo-pituitary-adrenal (HPA)-axis suppression by using the urinary free cortisol test or the corticotrophin stimulation test. If the HPA-axis suppression is evident, withdrawal should be attempted and the frequency of application reduced.
Manifestations of adrenal suppression in children include retardation of linear growth, delayed weight gain, low plasma cortisol concentrations and lack of response to corticotrophin stimulation (see Section 5.2 Pharmacokinetic Properties). Manifestations of intracranial hypertension include bulging fontanelles, headache, and bilateral papilloedema. Topical corticosteroid therapy in children should be limited to the minimum amount necessary for therapeutic efficacy; chronic topical corticosteroid therapy may interfere with growth and development. Parents should be advised not to use tight-fitting nappies or plastic pants on a child being treated in the diaper area, since such garments may constitute occlusive dressings.
Children have a greater surface to mass ratio than adults, and so may be at greater risk of adverse events from increased dosages.
Any corticosteroid therapy tends to elevate blood glucose levels in diabetic patients, and this should be monitored during treatment.
Corticosteroids should be used cautiously in patients with non-specific ulcerative colitis, diverticulitis, colon abscess or other pyogenic infection, colon obstruction, or extensive fistulas and sinus tracts, fresh intestinal anastomoses, active or latent peptic ulcers, renal insufficiency, hypertension, osteoporosis and myasthenia gravis.
Topical corticosteroids should be used with caution in the management of psoriasis, as exacerbation of the disease or pustular psoriasis may occur during or on withdrawal of topical corticosteroid therapy.
Topical corticosteroids should also be used with caution in patients with impaired T cell function or in those patients receiving other immunosuppressive therapy. The immunosuppressive effects of corticosteroids may be associated with impairment of the normal function of T cells and macrophages. The result of this impairment may be the activation of latent infection or exacerbation of intercurrent infections, including those caused by Candida, Mycobacterium, Toxoplasma, Strongyloides, Pneumocystis, Cryptococcus, Nocardia and Amoeba.
Patients on long term therapy, if there is a risk of immunosuppression, should not be given any live attenuated vaccines.
If hypersensitivity occurs, stop application and institute appropriate therapy.

Visual disturbance.

Use in hepatic impairment.

Use in renal impairment.

Use in the elderly.

Paediatric use.

Effects on laboratory tests.

4.5 Interactions with Other Medicines and Other Forms of Interactions

There are many potential drug interactions with hydrocortisone, however most are quite unlikely with topical therapy, occurring mainly with prolonged or over-use.
Carbamazepine, phenytoin and rifampicin all induce hepatic enzymes and thus lead to increased metabolism of hydrocortisone.
Concomitant use of diuretics, which also deplete potassium ion concentration in the blood, may cause hypokalaemia.
All corticosteroids antagonise the effects of neuromuscular blocking agents, such as vecuronium.
Oral contraceptives have been shown to prolong the half-life of hydrocortisone and thus potentiate its anti-inflammatory effects.

4.6 Fertility, Pregnancy and Lactation

Effects on fertility.

4.7 Effects on Ability to Drive and Use Machines

The effects of this medicine on a person's ability to drive and use machines were not assessed as part of its registration.

4.8 Adverse Effects (Undesirable Effects)

An itching or burning sensation may be experienced when using this medication.
Topical corticosteroids may cause adverse dermatological effects. Adverse dermatological effects are most likely to occur in intertriginous and facial areas. Local adverse corticosteroid effects occur most frequently with occlusive dressings, especially with prolonged therapy, and may require discontinuation of the dressings. Atrophy of the epidermis, subcutaneous tissue and dermal collagen; drying and cracking or tightening of the skin may occur. Epidermal thinning, telangiectasia, increased fragility of cutaneous blood vessels, purpura and atrophic striae are also reported.
Other adverse dermatologic effects of topical corticosteroids include acneiform eruption, vesiculation, irritation, pruritus, hypertrichosis, rosacea-like eruptions on the face, erythema, hyperesthesia, perioral dermatitis, burning or stinging sensation, folliculitis, and hypopigmentation.
Adverse dermatological effects usually improve when the drug is discontinued but may persist for long periods; atrophic striae may be permanent. In addition to the other adverse dermatological effects of topical corticosteroid therapy, maceration of the skin and miliaria may occur, especially when occlusive dressings are used. Topically applied steroids are generally nonsensitising, but allergic contact dermatitis may occur rarely.
Topical corticosteroids should be used with caution in the management of psoriasis (see Section 4.4 Special Warnings and Precautions for Use).
Topical corticosteroids should also be used with caution in patients with impaired T cell function or in those patients receiving other immunosuppressive therapy. The result of this impairment may be the activation of latent infection or exacerbation of intercurrent infections (see Section 4.4 Special Warnings and Precautions for Use).
Any cardiovascular adverse events are unlikely with topical hydrocortisone therapy, however, prolonged prolific use may result in a transient hypertension as a result of fluid retention.
Long term corticosteroid use has resulted in Benign lntracranial Hypertension, with most reports occurring in children.
Corticosteroids have documented effects on serum lipids, including increased total cholesterol, increased low density lipoproteins and increased triglyceride levels.
Topical and systemic corticosteroid therapy has been implicated in posterior subcapsular cataract formation, elevated intraocular pressure, optic nerve damage and papilloedema.
Cataracts, although primarily reported with systemic corticosteroid use, have been reported with use of topical preparations.
Hydrocortisone has least potential for causing glaucoma, but reports have demonstrated this complication in patients using topical preparations on the face.
In long-term treatment of extensive skin areas with occlusive dressings, one should bear in mind the possibility of inhibition of adrenal function. Therefore, adrenal function should be monitored under these circumstances.

Post marketing.

Eye disorders.

Reporting suspected adverse effects.

4.9 Overdose

Acute ingestion or accidental poisoning, even in massive doses, is rarely a clinical problem. Treatment should be symptomatic and supportive. Excessive chronic exposure results in adverse systemic effects. In such cases the use of topical corticosteroid should be discontinued, with the consideration to tapering the dose. Emesis or activated charcoal is not usually indicated unless multiple ingestion is suspected. Support the patient as necessary and treat symptomatically.
For information on the management of overdose, contact the Poison Information Centre on 131126 (Australia).

5 Pharmacological Properties

5.1 Pharmacodynamic Properties

Mechanism of action.

Clinical trials.

5.2 Pharmacokinetic Properties

The rate and extent of hydrocortisone absorption through the skin varies among individual patients. Following topical application of a corticosteroid to most areas of normal skin, only minimal amounts of the lipophilic drug partitions into the predominantly aqueous dermo-epidermal layer (viable epidermis + dermis) and subsequently the systemic circulation.

Absorption.

Distribution.

Metabolism.

Excretion.

5.3 Preclinical Safety Data

Genotoxicity.

Carcinogenicity.

6 Pharmaceutical Particulars

6.1 List of Excipients

The inactive ingredients are: soft white paraffin, liquid paraffin, cetomacrogol 1000, cetostearyl alcohol, chlorocresol, citric acid, sodium citrate dihydrate and purified water.

6.2 Incompatibilities

Incompatibilities were either not assessed or not identified as part of the registration of this medicine.

6.3 Shelf Life

In Australia, information on the shelf-life can be found on the public summary of the Australian Register of Therapeutic Goods (ARTG). The expiry date can be found on the packaging.

6.4 Special Precautions for Storage

Store below 25°C.

6.5 Nature and Contents of Container

Epoxy-coated Al tube contains 30 g of hydrocortisone acetate 10 mg/g cream.

6.6 Special Precautions for Disposal

In Australia, any unused medicine or waste material should be disposed of by taking to your local pharmacy.

6.7 Physicochemical Properties

Hydrocortisone is a corticosteroid and chemically described as 17-hydroxycorticosterone or 11,17,21-Trihydroxypregn-4-ene-3,20-dione. Hydrocortisone acetate is chemically described as hydrocortisone 21-acetate.
The molecular formula of hydrocortisone acetate is C₂₃H₃₂O₆.
The molecular weight of hydrocortisone acetate is 404.5.

Chemical structure.

CAS number.

7 Medicine Schedule (Poisons Standard)

Pharmacist Only Medicine (S3).

Summary Table of Changes