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Plaquenil
Generic Name: Hydroxychloroquine Sulfate
Drug Category: Antimalaria
Litigation Alert Level: Medium
This drug has been approved for use by males and females over the age of 6 years old for a maximum duration of 5 years.
| Approved Uses |
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Indicated for: Malaria: PLAQUENIL is indicated in adult and pediatric patients for the:
Rheumatoid Arthritis: • Treatment of acute and chronic rheumatoid arthritis in adults. Systemic Lupus Erythematosus: • Treatment of systemic lupus erythematosus in adults. Chronic Discoid Lupus Erythematosus: • Treatment of chronic discoid lupus erythematosus in adults. PLAQUENIL is not recommended for:
Prior to prescribing PLAQUENIL for the treatment or prophylaxis of malaria, consult the Centers for Disease Control and Prevention (CDC) Malaria website. Treatment must start 2 weeks before travel to an endemic area. Advise the patient to take the prophylaxis dosage once a week, starting 2 weeks prior to travel to the endemic area, on the same day every week, continuing the same weekly dose while in the endemic area, and for 4 weeks after leaving the endemic area. Safety and efficacy have not been established in the chronic use of PLAQUENIL for systemic lupus erythematosus and juvenile idiopathic arthritis in children. PLAQUENIL is not recommended in pediatric patients less than 31 kg because the lowest available strength (200 mg) exceeds the recommended dose for these patients and it cannot be divided. For radical cure of P. vivax and P. ovale infections, concomitant therapy with an 8 aminoquinoline drug is necessary. Corticosteroids, salicylates, and other antirheumatic agents may be used concomitantly with PLAQUENIL. PLAQUENIL is contraindicated in patients with known hypersensitivity to 4-aminoquinoline compounds. In general, dose selection in geriatric patients should start with the lowest recommended dose, taking into consideration the greater frequency of decreased hepatic, renal or cardiac function, and of concomitant disease or other drug therapy. A reduction in the dosage of PLAQUENIL may be necessary in patients with hepatic or renal disease. Irreversible retinal damage was observed in some patients treated with hydroxychloroquine sulfate and it is related to cumulative dosage and treatment duration. In patients of Asian descent, retinal toxicity may first be noticed outside the macula. Risk factors for retinal damage include daily hydroxychloroquine sulfate dosages ≥5 mg/kg of actual body weight, durations of use greater than five years, renal impairment, use of concomitant drug products such as tamoxifen citrate, and concurrent macular disease. Within the first year of starting PLAQUENIL, a baseline ocular examination is recommended including best corrected distance visual acuity (BCVA), an automated threshold visual field (VF) of the central 10 degrees (with retesting if an abnormality is noted), and spectral domain ocular coherence tomography (SD-OCT). For patients at higher risk of retinal damage, monitoring should include annual examinations which include BCVA, VF and SD-OCT. For patients without significant risk factors, annual retinal exams can usually be deferred until five years of treatment. In patients of Asian descent, it is recommended that visual field testing be performed in the central 24 degrees instead of the central 10 degrees. Administration of PLAQUENIL in patients with psoriasis may precipitate a severe flare-up of psoriasis. Administration of PLAQUENIL in patients with porphyria may exacerbate porphyria. Avoid PLAQUENIL in patients with psoriasis or porphyria, unless the benefit to the patient outweighs the possible risk. Skeletal muscle myopathy or neuropathy leading to progressive weakness and atrophy of proximal muscle groups, depressed tendon reflexes, and abnormal nerve conduction, have been reported. Suicidal behavior has been reported in patients treated with PLAQUENIL. Alert patients to contact their healthcare provider if they experience new or worsening depression, suicidal thoughts or behavior, or mood changes. PLAQUENIL can cause severe and potentially life-threatening hypoglycemia, in the presence or absence of antidiabetic agents. Antimalarial compounds should be used with caution in patients with hepatic disease or alcoholism or in conjunction with known hepatotoxic drugs. A reduction in dosage may be necessary in patients with hepatic or renal disease, as well as in those taking medicines known to affect these organs. PLAQUENIL may cause myelosuppression including aplastic anemia, agranulocytosis, leukopenia, or thrombocytopenia. Monitor blood cell counts periodically in patients on prolonged PLAQUENIL therapy. Hemolysis has been reported in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency. Monitor for hemolytic anemia as this can occur, particularly in association with other drugs that cause hemolysis. Skeletal muscle myopathy or neuropathy leading to progressive weakness and atrophy of proximal muscle groups, depressed tendon reflexes, and abnormal nerve conduction, have been reported. Serious adverse reactions have been reported with the use of PLAQUENIL including Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), drug reaction with eosinophilia and systemic symptoms (DRESS syndrome), acute generalized exanthematous pustulosis (AGEP). Fatal and life-threatening cases of cardiotoxicity, including cardiomyopathy, have been reported in patients treated with PLAQUENIL. Signs and symptoms of cardiac compromise have occurred during acute and chronic PLAQUENIL treatment. Patients may present with ventricular hypertrophy, pulmonary hypertension and conduction disorders including sick sinus syndrome. ECG findings include atrioventricular, right or left bundle branch block. PLAQUENIL has a potential to prolong the QT interval. Ventricular arrhythmias (including torsades de pointes) have been reported in PLAQUENIL-treated patients. The magnitude of QT prolongation may increase with increasing concentrations of the drug. Therefore, the recommended dose should not be exceeded. Avoid PLAQUENIL administration in patients with congenital or documented acquired QT prolongation and/or known risk factors for prolongation of the QT interval such as:
Therefore, PLAQUENIL is not recommended in patients taking other drugs that have the potential to prolong the QT interval. Monitor cardiac function as clinically indicated during PLAQUENIL therapy. Correct electrolyte imbalances prior to use. Discontinue PLAQUENIL if cardiotoxicity is suspected. PLAQUENIL can lower the seizure threshold. Co-administration of PLAQUENIL with other antimalarials known to lower the seizure threshold (e.g., mefloquine) may increase the risk of seizures. PLAQUENIL may enhance the effects of insulin and antidiabetic drugs, and consequently increase the hypoglycemic risk. Therefore, a decrease in dosage of insulin and other antidiabetic drugs may be necessary. The activity of antiepileptic drugs might be impaired if co-administered with PLAQUENIL. Concomitant PLAQUENIL and digoxin therapy may result in increased serum digoxin levels: serum digoxin levels should be closely monitored in patients receiving combined therapy. Concomitant use of PLAQUENIL and methotrexate may increase the incidence of adverse reactions. An increased plasma cyclosporin level was reported when cyclosporin and PLAQUENIL were co-administered. Chloroquine has been reported to reduce the bioavailability of praziquantel. Interaction of praziquantel with hydroxychloroquine cannot be ruled out. Antacids and kaolin can reduce absorption of chloroquine; an interval of at least 4 hours between intake of these agents and chloroquine should be observed. Interaction of antacids and kaolin with hydroxychloroquine cannot be ruled out. Lack of efficacy of hydroxychloroquine was reported when rifampicin was concomitantly administered. Avoid concomitant use of rifampicin. Concomitant use of cimetidine resulted in a 2-fold increase of exposure of chloroquine, which is structurally related to hydroxychloroquine. Interaction of cimetidine with hydroxychloroquine cannot be ruled out. Avoid concomitant use of cimetidine. In a study of healthy volunteers, chloroquine significantly reduced the bioavailability of ampicillin. Long-term studies in animals have not been conducted to evaluate the carcinogenic potential of PLAQUENIL. The mutagenic potential of hydroxychloroquine was not evaluated. However, chloroquine has been shown to be a catalytic inhibitor of DNA repair enzymes (topoisomerase II) and to produce weak genotoxic effects through this mode of action. Data from published epidemiologic and clinical studies have not established an association with PLAQUENIL use during pregnancy and major birth defects, miscarriage, or adverse maternal or fetal outcomes. Hydroxychloroquine readily crosses the placenta with cord blood levels corresponding to maternal plasma levels. Published lactation data report that hydroxychloroquine is present in human milk at low levels. |
| Off-label Uses |
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• Chronic use of hydroxychloroquine sulfate for systemic lupus erythematosus and juvenile idiopathic arthritis in children. GoToSource • Primary sjögren syndrome. GoToSource • Dermatomyositis. GoToSource • Adjunctive therapy for schizophrenia. GoToSource • Adjunctive therapy for dyslipidemia. GoToSource • Erosive osteoarthritis. GoToSource • Perniosis. GoToSource • Slowing the progression of HIV. GoToSource • Chronic Q fever. GoToSource • Antiplatelet agent. GoToSource • Porphyria cutanea tarda. GoToSource • Idiopathic follicular mucinosis. GoToSource • Interstitial lung disease. GoToSource • Non-small-cell lung cancer. GoToSource • Adjunctive therapy for advanced solid tumors and melanoma. GoToSource • Lipoatrophic panniculitis. GoToSource • Annular elastolytic giant cell granuloma. GoToSource • Prophylaxis of pulmonary embolism. GoToSource • Adjuvant therapy in preeclampsia. GoToSource • Kikuchi-fujimoto disease. GoToSource • Recurrent thrombosis. GoToSource • Chronic lymphocytic leukemia. GoToSource • COVID-19 infection. GoToSource |
| Adverse Events |
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⚠️ Increased risk of hemolytic anemia in patients with G6PD gene variation. Cardiotoxicity, prolonged QT interval, congestive heart failure, death, retinopathy (damage to the retina of the eyes), neuromyotoxicity (damage to the nervous system) including bilateral progressive proximal weakness of the lower extremities with variable polyneuropathy. GoToSource Hyperpigmentation (dark spots on the skin). GoToSource Acute generalized exanthematous pustulosis (skin eruption). GoToSource Urinary incontinence (loss of bladder control). GoToSource Depression, anxiety and suicidal ideation. GoToSource Acute toxic hepatitis (inflammation of the liver). GoToSource Severe myopathy (disorder of the skeletal muscles). GoToSource Acquired lysosomal storage disorder (lack of specific enzymes that break down certain lipids (fats) or carbohydrates (sugars) in the body). GoToSource Toxic epidermal necrolysis (potentially life-threatening skin reaction). GoToSource Seizures. GoToSource Induction, exacerbation or relapse of psoriasis. GoToSource Hypoglycemia (low blood sugar). GoToSource Hearing loss. GoToSource Phospholipidosis (excess accumulation of phospholipids, a class of lipids, in tissues). GoToSource |
| Litigation |
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Lawsuits filed for stevens-johnson syndrome and toxic epidermal necrolysis. |
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