DESCRIPTION:

Contains lidocaine HCl 3% and hydrocortisone acetate 0.5% microdispersed in an AcidMantle vehicle. Lidocaine is chemically designated as acetamide, 2-(diethylamino)-N-(2,6-dimethylphenyl), and has the following structure:

Hydrocortisone acetate has a chemical name pregn-4-ene-3, 20-dione, 21-(acetyloxy)-11,17-dihydroxy-(11β). It has the following structure formula:

Each gram of LIDAMANTLE HC® Cream contains Lidocaine HCl 30 mg, Hydrocortisone Acetate 5 mg, Aluminum Sulfate, Calcium Acetate, Cetyl Alcohol, Glycerin, Hydrochloric Acid, Light Mineral Oil, Methylparaben, Petrolatum, Polysorbate 60, Propylene Glycol, Propylparaben, Purified Water, Stearyl Alcohol, Sodium Hydroxide, Sorbitan Stearate and Stearic Acid.

Each gram of LIDAMANTLE HC® Lotion contains Lidocaine HCl 30 mg, Hydrocortisone Acetate 5 mg, Aluminum Sulfate, Calcium Acetate, Cetyl Alcohol, Glycerin, Hydrochloric Acid, Light Mineral Oil, Methylparaben, Petrolatum, Polysorbate 60, Propylene Glycol, Propylparaben, Purified Water, Stearyl Alcohol, Sodium Hydroxide, Sorbitan Stearate and Stearic Acid.

CLINICAL PHARMACOLOGY:

MECHANISM OF ACTION: LIDAMANTLE HC® Cream and LIDAMANTLE HC® Lotion release lidocaine from an AcidMantle vehicle to stabilize the neuronal membrane by inhibiting the ionic fluxes required for initiation and conduction of impulses, thereby effecting local anesthetic action. AcidMantle vehicle lowers pH to increase protection against alkaline irritants and to provide a favorable environment for healing. Hydrocortisone acetate provides relief of inflammatory and pruritic manifestations of corticosteroid responsive dermatoses.

PHARMACOKINETICS:

Lidocaine may be absorbed following topical administration to mucous membranes, its rate and extent of absorption depending upon the specific site of application, duration of exposure, concentration, and total dosage. In general, the rate of absorption of local anesthetic agents following topical application occurs most rapidly after intratracheal administration. Lidocaine is also well-absorbed from the gastrointestinal tract, but little intact drug appears in the circulation because of biotransformation in the liver.

Lidocaine is metabolized rapidly by the liver, and metabolites and unchanged drug are excreted by the kidneys. Biotransformation includes oxidative N-dealkylation, ring hydroxylation, cleavage of the arride linkage, and conjugation. N-dealkylation, a major pathway of biotransformation, yields the metabolites monoethylglycinexylidide and glycinexylidide. The pharmacological/toxicological actions of these metabolites are similar to, but less potent than, those of lidocaine. approximately 90% of lidocaine administered is excreted in the form of various metabolites, and less than 10% is excreted unchanged. The primary metabolite in urine is a conjugate of 4-hydroxy-2, 6-dimethylaniline.

The plasma binding of lidocaine is dependent on drug concentration, and the fraction bound decreases with increasing concentration. At concentrations of 1 to 4 g of free base per mL, 60 to 80 percent of lidocaine is protein bound. Binding is also dependent on the plasma concentration of the alpha-1-acid glycoprotein.

Lidocaine crosses the blood-brain and placental barriers, presumably by passive diffusion.

Studies of lidocaine metabolism following intravenous bolus injections have shown that the elimination half-life of this agent is typically 1.5 to 2 hours. Because of the rapid rate at which lidocaine is metabolized, any condition that affects liver function may alter lidocaine kinetics. The half-life may be prolonged two-fold or more in patients with liver dysfunction. Renal dysfunction does not affect lidocaine kinetics but may increase the accumulation of metabolites.

Factors such as acidosis and the use of CNS stimulants and depressants affect the CNS levels of lidocaine required to produce overt systemic effects. Objective adverse manifestations become increasingly apparent with increasing venous plasma levels above 6 g free base per mL. In the rhesus monkey arterial blood levels of 18-21 g/mL have been shown to be threshold for convulsive activity.

The extent of percutaneous absorption of topical corticosteroids is determined by many factors including the vehicle, the integrity of the epidermal barrier, and the use of occlusive dressings.

Topical corticosteroids can be absorbed from normal intact skin. Inflammation and/or other disease processes in the skin increase percutaneous absorption. Occlusive dressings substantially increase the percutaneous absorption of topical corticosteroids. Thus, occlusive dressings may be a valuable therapeutic adjunct for treatment of resistant dermatoses.

Once absorbed through the skin, topical corticosteroids are handled through pharmacokinetic pathways similar to systemically administered corticosteroids. Corticosteroids are bound to plasma protein in varying degrees. Corticosteroids are metabolized primarily in the liver and are then excreted by the kidneys. Some of the topical corticosteroids and their metabolites are also excreted into the bile.

INDICATIONS:

Anti-inflammatory anesthetic for relief of pruritus, pruritic eczemas, abrasions, minor burns, insect bites, pain, soreness and discomfort due to pruritus ani, pruritus vulvae, hemorrhoids, anal fissures, and similar conditions of the skin and mucous membranes.

CONTRAINDICATIONS:

Tuberculous or fungal lesions of skin vaccinia, varicella and acute herpes simplex and in persons who have shown hypersensitivity to any of its components. Lidocaine is contraindicated in patients with a known history of hypersensitivity to local anesthetics of the amide type. Topical corticosteroids are contraindicated in those patients with a history of hypersensitivity to any of the components of the preparation.

WARNINGS:

For external use only. Not for ophthalmic use.

PRECAUTIONS:

If irritation or sensitivity occurs or infection appears, discontinue use and institute appropriate therapy. If extensive areas are treated, the possibility of systemic absorption exists. Systemic absorption of topical steroids has produced reversible hypothalamicpituitary-adrenal (HPA) axis suppression, manifestations of Cushing’s syndrome, hyperglycemia, and glycosuria in some patients. Conditions which augment systemic absorption include the application of the more potent steroids, use over large surface areas, prolonged use, and the addition of occlusive dressings. Therefore, patients receiving a large dose of potent topical steroids applied to a large surface area, or under an occlusive dressing, should be evaluated periodically for evidence of HPA axis suppression. If noted, an attempt should be made to withdraw the drug, to reduce the frequency of application, or to substitute a less potent steroid. Recovery of the HPA axis function is generally prompt and complete upon discontinuation of the drug. Infrequently, signs and symptoms of steroid withdrawal may occur, requiring supplemental systemic corticosteroids. Children may absorb proportionately larger amounts of topical corticosteroids and thus be more susceptible to systemic toxicity. If irritation develops, topical steroids should be discontinued and appropriate therapy instituted. In the presence of dermatological infections, the use of an appropriate antifungal or antibacterial agent should be instituted. If a favorable response does not occur promptly, the corticosteroid should be discontinued until the infection has been adequately controlled.

DOSAGE AND ADMINISTRATION:

Apply a thin film to the affected area two or three times daily or as directed by a physician.

HOW SUPPLIED:

LIDAMANTLE HC® Cream:
3 oz (85 g) tube NDC 10337-710-19
LIDAMANTLE HC® Lotion:
177 mL bottle NDC 10337-715-10

KEEP THIS AND ALL MEDICATIONS OUT OF THE REACH OF CHILDREN.

Store at controlled room temperature 15°-30° C (59°-86° F).Protect from freezing.

Mtd. for:
DOAK DERMATOLOGICS
A SUBSIDIARY OF BRADLEY PHARMACEUTICALS, INC.
383 Route 46 West
Fairfield, NJ 07004-2402 USA
www.doakderm.com

Mfd. by: Groupe PARIMA, Inc.
Montreal, QC H4S 1X6 CANADA

IL137-R5
REV 0305

PACKAGE LABEL – PRINCIPAL DISPLAY PANEL – 3 oz LABEL

NDC 10337-710-19

Net Wt. 3 oz. (85 g)

Rx Only

LIDAMANTLE® HC Cream
(Lidocaine HCl 3% - Hydrocortisone Acetate 0.5%)

PACKAGE LABEL – PRINCIPAL DISPLAY PANEL – 3 oz CARTON

Rx Only

NDC 10337-710-19

LIDAMANTLE® HC Cream
(Lidocaine HCl 3% - Hydrocortisone Acetate 0.5%)

Net Wt. 3 oz. (85 g)