SOLARAZE (diclofenac sodium) topical gel

SOLARAZE (diclofenac sodium) topical gel

SOLARAZE (diclofenac sodium) topical gel

Solaraze® (diclofenac sodium) topical gel, 3%, intended for dermatologic use, contains the active ingredient, diclofenac sodium, in a clear, transparent, colorless to slightly yellow gel base. Diclofenac sodium is a white to slightly yellow crystalline powder. It is freely soluble in methanol, soluble in ethanol, sparingly soluble in water, slightly soluble in acetone, and partially insoluble in ether. The chemical name for diclofenac sodium is:

Sodium [o-(2,6-dichloranilino) phenyl] acetate

Diclofenac sodium has a molecular weight of 318.13.

The CAS number is CAS-15307-79-6.

Solaraze also contains benzyl alcohol, hyaluronate sodium, polyethylene glycol monomethyl ether, and purified water.

1 g of Solaraze® (diclofenac sodium) topical gel contains 30 mg of the active substance, diclofenac sodium.

INDICATIONS AND USAGE

Solaraze® is indicated for the topical treatment of actinic keratoses (AK).

Mechanism of Action

The mechanism of action of diclofenac sodium in the treatment of actinic keratoses (AK) is unknown.

DOSAGE AND ADMINISTRATION

Use the lowest effective dosage for the shortest duration consistent with individual patient treatment goals

Apply Solaraze gently to lesion areas twice daily.

To adequately cover each lesion. Use 0.5 g of gel (pea size) on each 5cm x 5 cm lesion site. The recommended duration of therapy is from 60 days to 90 days. Complete healing of the lesion(s) or optimal therapeutic effect may not be evident for up to 30 days following cessation of therapy. Lesions that do not respond to therapy should be re-evaluated and management reconsidered.

Avoid contact of Solaraze with eyes and mucous membranes.

CONTRAINDICATIONS

Solaraze is contraindicated in the following patients:

  • With known hypersensitivity (e.g., anaphylactic reactions and serious skin reactions) to diclofenac or any components of the drug product
  • With the history of asthma, urticaria, or other allergic type reactions after taking aspirin or other NSAIDs. Severe, sometimes fatal, anaphylactic reactions to NSAIDs have been reported in such patients  
  • Application on damaged skin resulting from any etiology, including exudative dermatitis, eczema, infected lesions, burns or wounds
  • In the setting of coronary bypass graft (CABG) surgery

WARNINGS AND PRECAUTIONS

Anaphylactic Reactions: Diclofenac has been associated with anaphylactic reactions in patients with and without known hypersensitivity to

diclofenac and in patients with aspirin-sensitive asthma . Seek emergency help if an anaphylactic reaction occurs.

Exacerbation of Asthma Related to Aspirin Sensitivity: A subpopulation of patients with asthma may have aspirin-sensitive asthma which may include chronic rhinosinusitiscomplicated by nasal polyps; severe, potentially fatal bronchospasm; and/or intolerance to aspirin and other NSAIDs.

Because cross-reactivity between aspirin and other NSAIDs has been reported in such aspirin-sensitive patients, Solaraze is contraindicated in patients with this form of aspirin sensitivity. When Solaraze is used in patients with preexisting asthma (without known aspirin sensitivity), monitor patients for changes in the signs and symptoms of asthma.

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Serious Skin Reactions: NSAIDs, including diclofenac, can cause serious skin adverse reactions such as exfoliative dermatitis, Stevens-JohnsonSyndrome (SJS), and toxic epidermal necrolysis (TEN), which can be fatal. These serious events may occur without warning. Inform patients about the signs and symptoms of serious skin reactions, and to discontinue the use of Solaraze at the first appearance of skin rash or any other sign of hypersensitivity. Solaraze is contraindicated in patients with previous serious skin reactions to NSAIDs. Do not apply Solaraze to open skin wounds, infections, or exfoliative dermatitis, as it may affect absorption and tolerability of the drug.

Cardiovascular Thrombotic Events: Clinical trials of several COX-2 selective and nonselective NSAIDs of up to three years duration have shown an increasedrisk of serious cardiovascular (CV) thrombotic events, including myocardial infarction (MI) and stroke, which can befatal. Based on available data, it is unclear that the risk for CV thrombotic events is similar for all NSAIDs. The relativeincrease in serious CV thrombotic events over baseline conferred by NSAID use appears to be similar in those with and without known CV disease or risk factors for CV disease. However, patients with known CV disease or risk factors had a higher absolute incidence of excess serious CV thrombotic events, due to their increased baseline rate. Some observational studies found that this increased risk of serious CV thrombotic events began as early as the first weeks of treatment. The increase in CV thrombotic risk has been observed most consistently at higher doses.

Gastrointestinal Bleeding, Ulceration, and Perforation: NSAIDs, including diclofenac, cause serious GI adverse events including inflammation, bleeding, ulceration, andperforation of the esophagus, stomach, small intestine, or large intestine, which can be fatal. These serious adverse eventscan occur at any time, with or without warning symptoms, in patients treated with NSAIDs.

Hepatotoxicity: Physicians should measure transaminases at baseline and periodically in patients receiving long-term therapy with diclofenac, because severe hepatotoxicity may develop without a prodrome of distinguishing symptoms. The optimum times for making the first and subsequent transaminase measurements are not known. Based on clinical trial data and postmarketing experiences, transaminases should be monitored within 4 to 8 weeks after initiating treatment with diclofenac. However, severe hepatic reactions can occur at any time during treatment with diclofenac.

If abnormal liver tests persist or worsen, if clinical signs and/or symptoms consistent with liver disease develop, or if systemic manifestations occur (e.g., eosinophilia, rash, abdominal pain, diarrhea, dark urine, etc.), Solaraze should be discontinued immediately.

Hypertension: NSAIDs, including Solaraze, can lead to new onset of hypertension or worsening of pre-existing hypertension, either ofwhich may contribute to the increased incidence of CV events. Patients taking angiotensin converting enzyme (ACE)inhibitors, thiazide diuretics, or loop diuretics may have impaired response to these therapies when taking NSAIDs.

Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS): Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS) has been reported in patients taking NSAIDs such asSolaraze. Some of these events have been fatal or life-threatening. DRESS typically, although not exclusively, presents with fever, rash, lymphadenopathy, and/or facial swelling. Other clinical manifestations may include hepatitis, nephritis, hematological abnormalities, myocarditis, or myositis. Sometimes symptoms of DRESS may resemble an acute viral infection. Eosinophilia is often present. Because this disorder is variable in its presentation, other organ systems not noted here may be involved. It is important to note that early manifestations of hypersensitivity, such as fever or lymphadenopathy, may be present even though rash is not evident. If such signs or symptoms are present, discontinue Solaraze and evaluate the patient immediately.

Premature Closure of Fetal Ductus Arteriosus: Avoid use of NSAIDs, including Solaraze, in pregnant women at about 30 weeks gestation and later. NSAIDs, including Solaraze, increase the risk of premature closure of the fetal ductus arteriosus at approximately this gestational age.

Oligohydramnios/Neonatal Renal Impairment: Use of NSAIDs, including diclofenac, at about 20 weeks gestation or later in pregnancy may cause fetal renal dysfunctionleading to oligohydramnios and, in some cases, neonatal renal impairment. These adverse outcomes are seen, on average,after days to weeks of treatment, although oligohydramnios has been infrequently reported as soon as 48 hours afterNSAID initiation. Oligohydramnios is often, but not always, reversible with treatment discontinuation. Complications ofprolonged oligohydramnios may, for example, include limb contractures and delayed lung maturation.

Hematologic Toxicity: Anemia has occurred in NSAID-treated patients. This may be due to occult or gross blood loss, fluid retention, or an incompletely described effect on erythropoiesis. If a patient treated with Solaraze has any signs or symptoms of anemia, monitor hemoglobin or hematocrit.

Masking of Inflammation and Fever: The pharmacological activity of Solaraze in reducing inflammation, and possibly fever, may diminish the utility ofdiagnostic signs in detecting infections.

Laboratory Monitoring: Because serious GI bleeding, hepatotoxicity, and renal injury can occur without warning symptoms or signs, considermonitoring patients on long-term NSAID treatment with a CBC and a chemistry profile periodically

Photosensitivity: Patients should minimize or avoid exposure to natural or artificial sunlight (tanning beds or UVA/B treatment) whileusing Solaraze. If patients need to be outdoors while using Solaraze, they should wear loose-fitting clothes that protectskin from sun exposure and discuss other sun protection measures with their physician. Advise patients to discontinuetreatment with Solaraze at the first evidence of sunburn.

Exposure to Eyes and Mucosal Membranes: Avoid contact of Solaraze with eyes and mucosa. Advise patients that if contact in the eye, or mucosal membranes occurs,immediately wash out the eye or mucosal membranes with water or saline and consult a physician if irritation persists formore than an hour.

Oral Nonsteroidal Anti-inflammatory Drugs: Concomitant use of oral and topical NSAIDs may result in a higher rate of hemorrhage, more frequent abnormalcreatinine, urea and hemoglobin. Do not use Solaraze in combination with an oral NSAID unless the benefit outweighsthe risk and periodic laboratory evaluations are conducted.

DRUG INTERACTIONS

Drugs That Interfere with Hemostasis: Diclofenac and anticoagulants such as warfarin have a synergistic effect on bleeding. The concomitant use of diclofenac and anticoagulants have an increased risk of serious bleeding compared to the use of either drug alone.

Monitor patients with concomitant use of Solaraze with anticoagulants (e.g., warfarin), antiplatelet agents (e.g., aspirin), selective serotonin reuptake inhibitors (SSRIs), and serotonin norepinephrine reuptake inhibitors (SNRIs) for signs of bleeding.

Aspirin: In a clinical study, the concomitant use of an NSAID and aspirin was associated with a significantly increased incidence of GI adverse reactions as compared to use of the NSAID alone.

ACE Inhibitors, Angiotensin Receptor Blockers, and Beta-Blockers: NSAIDs may diminish the antihypertensive effect of angiotensin converting enzyme (ACE)inhibitors, angiotensin receptor blockers (ARBs), or beta-blockers (including propranolol).

Diuretics: Clinical studies, as well as post-marketing observations, showed that NSAIDs reduced the natriuretic effect of loop diuretics (e.g., furosemide) and thiazide diuretics in some patients. This effect has been attributed to the NSAID inhibition of renal prostaglandin synthesis.

Digoxin: The concomitant use of diclofenac with digoxin has been reported to increase the serumconcentration and prolong the half-life of digoxin.

Lithium: NSAIDs have produced elevations in plasma lithium levels and reductions in renal lithiumclearance. The mean minimum lithium concentration increased 15%, and the renal clearancedecreased by approximately 20%. This effect has been attributed to NSAID inhibition of renalprostaglandin synthesis.

Methotrexate: Concomitant use of NSAIDs and methotrexate may increase the risk for methotrexate toxicity(e.g., neutropenia, thrombocytopenia, renal dysfunction).

Cyclosporine: Concomitant use of Solaraze and cyclosporine may increase cyclosporine’s nephrotoxicity.

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NSAIDs and Salicylates: Concomitant use of Solaraze with other NSAIDs or salicylates (e.g., diflunisal, salsalate)increases the risk of GI toxicity.

USE IN SPECIFIC POPULATIONS

Pregnancy: Use of NSAIDs, including Solaraze, can cause premature closure of the fetal ductus arteriosus and fetal renal dysfunctionleading to oligohydramnios and, in some cases, neonatal renal impairment. Because of these risks, limit dose and durationof Solaraze use between about 20 and 30 weeks of gestation and avoid Solaraze use at about 30 weeks of gestation andlater in pregnancy.

Lactation: Data from published literature cases with oral preparations of diclofenac indicate the presence of small amounts ofdiclofenac in human milk. There are no data on the effects on the breastfed infant, or the effects on milk production. Thedevelopmental and health benefits of breastfeeding should be considered along with the mother’s clinical need forSolaraze and any potential adverse effects on the breastfed infant from the Solaraze or from the underlying maternalcondition.

Females and Males of Reproductive Potential

Female Infertility: Based on the mechanism of action, the use of prostaglandin mediated NSAIDs, including Solaraze, may delay or prevent rupture of ovarian follicles, which has been associated with reversible infertility in some women.

Pediatric Use: Actinic keratoses is not a condition seen within the pediatric population. Solaraze should not be used by children.

OVERDOSAGE

Symptoms following acute NSAID overdosages have been typically limited to lethargy, drowsiness, nausea, vomiting, and epigastric pain, which have been generally reversible with supportive care. Gastrointestinal bleeding, hypertension, acute renal failure, respiratory depression, and coma have been reported.

Manage patients with symptomatic and supportive care following an NSAID overdosage. There are no specific antidotes.

Forced diuresis, alkalinization of urine, hemodialysis, or hemoperfusion may not be useful due to high protein binding.

In the event of oral ingestion, resulting in significant systemic side effects, it is recommended that the stomach be emptied by vomiting or lavage. In addition to supportive measures, the use of oral activated charcoal may help to reduce the absorption of diclofenac.

For additional information about overdosage treatment, call a poison control center (1-800-222-1222).

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