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Acitretin
Overview
What is Acitretin?
Acitretin, a retinoid, is available in 10 mg, 17.5 mg, 22.5 mg, and 25 mg gelatin capsules for oral administration. Chemically, acitretin is all-trans-9-(4-methoxy-2,3,6-trimethylphenyl)-3,7-dimethyl-2,4,6,8-nonatetraenoic acid. It is a metabolite of etretinate and is related to both retinoic acid and retinol (vitamin A). It is a yellow to greenish-yellow powder with a molecular weight of 326.44. The structural formula is:
Each capsule contains acitretin, microcrystalline cellulose, maltodextrin, sodium ascorbate, gelatin, black imprinting ink (the solid components are shellac glaze, propylene glycol and iron oxide black).
Gelatin capsule shells contain gelatin, red ferric oxide (10 mg, 22.5 mg and 25 mg only), yellow ferric oxide (17.5 mg and 25 mg only), sodium lauryl sulfate, and titanium dioxide (10 mg, 17.5 mg and 25 mg only).
What does Acitretin look like?
What are the available doses of Acitretin?
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What should I talk to my health care provider before I take Acitretin?
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How should I use Acitretin?
Acitretin capsules USP are indicated for the treatment of severe psoriasis in adults. Because of significant adverse effects associated with its use, acitretin capsules USP should be prescribed only by those knowledgeable in the systemic use of retinoids. In females of reproductive potential, acitretin capsules USP should be reserved for non-pregnant patients who are unresponsive to other therapies or whose clinical condition contraindicates the use of other treatments (see boxed — acitretin capsules USP can cause severe birth defects).
Most patients experience relapse of psoriasis after discontinuing therapy. Subsequent courses, when clinically indicated, have produced efficacy results similar to the initial course of therapy.
There is intersubject variation in the pharmacokinetics, clinical efficacy, and incidence of side effects with acitretin. A number of the more common side effects are dose-related. Individualization of dosage is required to achieve sufficient therapeutic response while minimizing side effects. Therapy with acitretin should be initiated at 25 to 50 mg per day, given as a single dose with the main meal. Maintenance doses of 25 to 50 mg per day may be given dependent upon an individual patient’s response to initial treatment. Relapses may be treated as outlined for initial therapy.
When acitretin is used with phototherapy, the prescriber should decrease the phototherapy dose, dependent on the patient’s individual response (see ).
Females who have taken TEGISON
(etretinate) must continue to follow the contraceptive recommendations for TEGISON
. TEGISON
is no longer marketed in the US; for information, call Watson Laboratories, Inc. at 1-800-272-5525.
Information for Pharmacists:
Acitretin must only be dispensed in no more than a monthly supply. An Acitretin Medication Guide must be given to the patient each time acitretin is dispensed, as required by law.
What interacts with Acitretin?
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What are the warnings of Acitretin?
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What are the precautions of Acitretin?
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What are the side effects of Acitretin?
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What should I look out for while using Acitretin?
Pregnancy Category X:
(See boxed .)
Acitretin is contraindicated in patients with severely impaired liver or kidney function and in patients with chronic abnormally elevated blood lipid values (see boxed , and ).
An increased risk of hepatitis has been reported to result from combined use of methotrexate and etretinate. Consequently, the combination of methotrexate with acitretin is also contraindicated (see ).
Since both acitretin and tetracyclines can cause increased intracranial pressure, their combined use is contraindicated (see ).
Acitretin
is contraindicated in cases of hypersensitivity (e.g., angioedema, urticaria) to the preparation (acitretin or excipients) or to other retinoids.
(See also boxed .)
Skeletal Abnormalities:
In adults receiving long-term treatment with acitretin, appropriate examinations should be periodically performed in view of possible ossification abnormalities (see ADVERSE REACTIONS). Because the frequency and severity of iatrogenic bony abnormality in adults is low, periodic radiography is only warranted in the presence of symptoms or long-term use of acitretin. If such disorders arise, the continuation of therapy should be discussed with the patient on the basis of a careful risk/benefit analysis. In clinical trials with acitretin, subjects were prospectively evaluated for evidence of development or change in bony abnormalities of the vertebral column, knees, and ankles.
Of 380 subjects treated with acitretin, 15% had preexisting abnormalities of the spine which showed new changes or progression of preexisting findings. Changes included degenerative spurs, anterior bridging of spinal vertebrae, diffuse idiopathic skeletal hyperostosis, ligament calcification, and narrowing and destruction of a cervical disc space. De novo changes (formation of small spurs) were seen in 3 subjects after 1½ to 2½ years.
Six of 128 subjects treated with acitretin showed abnormalities in the knees and ankles before treatment that progressed during treatment. In 5, these changes involved the formation of additional spurs or enlargement of existing spurs. The sixth subject had degenerative joint disease which worsened. No subjects developed spurs de novo. Clinical complaints did not predict radiographic changes.
Lipids and Possible Cardiovascular Effects:
Blood lipid determinations should be performed before acitretin is administered and again at intervals of 1 to 2 weeks until the lipid response to the drug is established, usually within 4 to 8 weeks. In subjects receiving acitretin during clinical trials, 66% and 33% experienced elevation in triglycerides and cholesterol, respectively. Decreased high density lipoproteins (HDL) occurred in 40% of subjects. These effects of acitretin were generally reversible upon cessation of therapy.
Subjects with an increased tendency to develop hypertriglyceridemia included those with disturbances of lipid metabolism, diabetes mellitus, obesity, increased alcohol intake, or a familial history of these conditions. Because of the risk of hypertriglyceridemia, serum lipids must be more closely monitored in high-risk patients and during long-term treatment.
Hypertriglyceridemia and lowered HDL may increase a patient’s cardiovascular risk status. Although no causal relationship has been established, there have been postmarketing reports of acute myocardial infarction or thromboembolic events in patients on therapy with acitretin. In addition, elevation of serum triglycerides to greater than 800 mg per dL has been associated with fatal fulminant pancreatitis. Therefore, dietary modifications, reduction in dose of acitretin, or drug therapy should be employed to control significant elevations of triglycerides. If, despite these measures, hypertriglyceridemia and low HDL levels persist, the discontinuation of acitretin should be considered.
Ophthalmologic Effects:
The eyes and vision of 329 subjects treated with acitretin were examined by ophthalmologists. The findings included dry eyes (23%), irritation of eyes (9%), and brow and lash loss (5%). The following were reported in less than 5% of subjects: Bell’s palsy, blepharitis and/or crusting of lids, blurred vision, conjunctivitis, corneal epithelial abnormality, cortical cataract, decreased night vision, diplopia, itchy eyes or eyelids, nuclear cataract, pannus, papilledema, photophobia, posterior subcapsular cataract, recurrent sties, and subepithelial corneal lesions.
Any patient treated with acitretin who is experiencing visual difficulties should discontinue the drug and undergo ophthalmologic evaluation.
Pancreatitis:
Lipid elevations occur in 25% to 50% of subjects treated with acitretin. Triglyceride increases sufficient to be associated with pancreatitis are much less common, although fatal fulminant pancreatitis has been reported. There have been rare reports of pancreatitis during therapy with acitretin in the absence of hypertriglyceridemia.
Pseudotumor Cerebri:
Acitretin and other retinoids administered orally have been associated with cases of pseudotumor cerebri (benign intracranial hypertension). Some of these events involved concomitant use of isotretinoin and tetracyclines. However, the event seen in a single patient receiving acitretin was not associated with tetracycline use. Early signs and symptoms include papilledema, headache, nausea and vomiting, and visual disturbances. Patients with these signs and symptoms should be examined for papilledema and, if present, should discontinue acitretin immediately and be referred for neurological evaluation and care. Since both acitretin and tetracyclines can cause increased intracranial pressure, their combined use is contraindicated (see ).
Capillary leak syndrome, a potential manifestation of retinoic acid syndrome, has been reported in patients receiving acitretin. Features of this syndrome may include localized or generalized edema with secondary weight gain, fever, and hypotension. Rhabdomyolysis and myalgias have been reported in association with capillary leak syndrome, and laboratory tests may reveal neutrophilia, hypoalbuminemia, and an elevated hematocrit. Discontinue acitretin if capillary leak syndrome develops during therapy.
Exfoliative dermatitis/erythroderma has been reported in patients receiving acitretin.Discontinue acitretin if exfoliative dermatitis/erythroderma occurs during therapy.
What might happen if I take too much Acitretin?
In the event of acute overdosage, acitretin must be withdrawn at once. Symptoms of overdose are identical to acute hypervitaminosis A (e.g., headache and vertigo). The acute oral toxicity (LD) of acitretin in both mice and rats was greater than 4,000 mg per kg.
In one reported case of overdose, a 32-year-old male with Darier’s disease took 21 x 25 mg capsules (525 mg single dose). He vomited several hours later but experienced no other ill effects.
All female patients of childbearing potential
1) Have a pregnancy test at the time of overdose; 2) Be counseled as per the boxed and sections regarding birth defects and contraceptive use for at least 3 years’ duration after the overdose.
How should I store and handle Acitretin?
Store at 20°C to 25°C (68°F to 77°F). Excursion permitted between 15°C to 30°C (59°F to 86°F). See USP controlled room temperature.Discard any unused EMFLAZA Oral Suspension remaining after 1 month of first opening the bottle. Store at 20°C to 25°C (68°F to 77°F). Excursion permitted between 15°C to 30°C (59°F to 86°F). See USP controlled room temperature.Discard any unused EMFLAZA Oral Suspension remaining after 1 month of first opening the bottle. White to off-white body and a brown cap, 10 mg, imprinted in black “WPI” on the capsule cap and “2263” on the capsule body; bottles of 30 (NDC 0591-2263-30). Yellow to light yellow body and cap, 17.5 mg, imprinted in black “WPI” on the capsule cap and “2264” on the capsule body; bottles of 30 (NDC 0591-2264-30).Brown body and cap, 22.5 mg, imprinted in black with “WPI” on the capsule cap and “2265” on the capsule body; bottles of 30 (NDC 0591-2265-30). Yellow to light yellow body and a brown cap, 25 mg, imprinted in black “WPI” on the capsule cap and “2266” on the capsule body; bottles of 30 (NDC 0591-2266-30). Store at 20° to 25°C (68° to 77°F) [See USP Controlled Room Temperature]. Protect from light. Avoid exposure to high temperatures and humidity after the bottle is opened. White to off-white body and a brown cap, 10 mg, imprinted in black “WPI” on the capsule cap and “2263” on the capsule body; bottles of 30 (NDC 0591-2263-30). Yellow to light yellow body and cap, 17.5 mg, imprinted in black “WPI” on the capsule cap and “2264” on the capsule body; bottles of 30 (NDC 0591-2264-30).Brown body and cap, 22.5 mg, imprinted in black with “WPI” on the capsule cap and “2265” on the capsule body; bottles of 30 (NDC 0591-2265-30). Yellow to light yellow body and a brown cap, 25 mg, imprinted in black “WPI” on the capsule cap and “2266” on the capsule body; bottles of 30 (NDC 0591-2266-30). Store at 20° to 25°C (68° to 77°F) [See USP Controlled Room Temperature]. Protect from light. Avoid exposure to high temperatures and humidity after the bottle is opened. White to off-white body and a brown cap, 10 mg, imprinted in black “WPI” on the capsule cap and “2263” on the capsule body; bottles of 30 (NDC 0591-2263-30). Yellow to light yellow body and cap, 17.5 mg, imprinted in black “WPI” on the capsule cap and “2264” on the capsule body; bottles of 30 (NDC 0591-2264-30).Brown body and cap, 22.5 mg, imprinted in black with “WPI” on the capsule cap and “2265” on the capsule body; bottles of 30 (NDC 0591-2265-30). Yellow to light yellow body and a brown cap, 25 mg, imprinted in black “WPI” on the capsule cap and “2266” on the capsule body; bottles of 30 (NDC 0591-2266-30). Store at 20° to 25°C (68° to 77°F) [See USP Controlled Room Temperature]. Protect from light. Avoid exposure to high temperatures and humidity after the bottle is opened. White to off-white body and a brown cap, 10 mg, imprinted in black “WPI” on the capsule cap and “2263” on the capsule body; bottles of 30 (NDC 0591-2263-30). Yellow to light yellow body and cap, 17.5 mg, imprinted in black “WPI” on the capsule cap and “2264” on the capsule body; bottles of 30 (NDC 0591-2264-30).Brown body and cap, 22.5 mg, imprinted in black with “WPI” on the capsule cap and “2265” on the capsule body; bottles of 30 (NDC 0591-2265-30). Yellow to light yellow body and a brown cap, 25 mg, imprinted in black “WPI” on the capsule cap and “2266” on the capsule body; bottles of 30 (NDC 0591-2266-30). Store at 20° to 25°C (68° to 77°F) [See USP Controlled Room Temperature]. Protect from light. Avoid exposure to high temperatures and humidity after the bottle is opened. White to off-white body and a brown cap, 10 mg, imprinted in black “WPI” on the capsule cap and “2263” on the capsule body; bottles of 30 (NDC 0591-2263-30). Yellow to light yellow body and cap, 17.5 mg, imprinted in black “WPI” on the capsule cap and “2264” on the capsule body; bottles of 30 (NDC 0591-2264-30).Brown body and cap, 22.5 mg, imprinted in black with “WPI” on the capsule cap and “2265” on the capsule body; bottles of 30 (NDC 0591-2265-30). Yellow to light yellow body and a brown cap, 25 mg, imprinted in black “WPI” on the capsule cap and “2266” on the capsule body; bottles of 30 (NDC 0591-2266-30). Store at 20° to 25°C (68° to 77°F) [See USP Controlled Room Temperature]. Protect from light. Avoid exposure to high temperatures and humidity after the bottle is opened.
Clinical Information
Chemical Structure
No Image foundClinical Pharmacology
Absorption:
Oral absorption of acitretin is optimal when given with food. For this reason, acitretin was given with food in all of the following trials. After administration of a single 50 mg oral dose of acitretin to 18 healthy subjects, maximum plasma concentrations ranged from 196 to 728 ng per mL (mean: 416 ng per mL) and were achieved in 2 to 5 hours (mean: 2.7 hours). The oral absorption of acitretin is linear and proportional with increasing doses from 25 to 100 mg. Approximately 72% (range: 47% to 109%) of the administered dose was absorbed after a single 50 mg dose of acitretin was given to 12 healthy subjects.
Distribution:
Metabolism:
: Ethanol.
Following oral absorption, acitretin undergoes extensive metabolism and interconversion by simple isomerization to its 13-cis form (cis-acitretin). The formation of cis-acitretin relative to parent compound is not altered by dose or fed/fast conditions of oral administration of acitretin. Both parent compound and isomer are further metabolized into chain-shortened breakdown products and conjugates, which are excreted. Following multiple-dose administration of acitretin, steady-state concentrations of acitretin and cis-acitretin in plasma are achieved within approximately 3 weeks.
Elimination:
Non-Clinical Toxicology
Pregnancy Category X:(See boxed .)
Acitretin is contraindicated in patients with severely impaired liver or kidney function and in patients with chronic abnormally elevated blood lipid values (see boxed , and ).
An increased risk of hepatitis has been reported to result from combined use of methotrexate and etretinate. Consequently, the combination of methotrexate with acitretin is also contraindicated (see ).
Since both acitretin and tetracyclines can cause increased intracranial pressure, their combined use is contraindicated (see ).
Acitretin
is contraindicated in cases of hypersensitivity (e.g., angioedema, urticaria) to the preparation (acitretin or excipients) or to other retinoids.
(See also boxed .)
Skeletal Abnormalities:
In adults receiving long-term treatment with acitretin, appropriate examinations should be periodically performed in view of possible ossification abnormalities (see ADVERSE REACTIONS). Because the frequency and severity of iatrogenic bony abnormality in adults is low, periodic radiography is only warranted in the presence of symptoms or long-term use of acitretin. If such disorders arise, the continuation of therapy should be discussed with the patient on the basis of a careful risk/benefit analysis. In clinical trials with acitretin, subjects were prospectively evaluated for evidence of development or change in bony abnormalities of the vertebral column, knees, and ankles.
Of 380 subjects treated with acitretin, 15% had preexisting abnormalities of the spine which showed new changes or progression of preexisting findings. Changes included degenerative spurs, anterior bridging of spinal vertebrae, diffuse idiopathic skeletal hyperostosis, ligament calcification, and narrowing and destruction of a cervical disc space. De novo changes (formation of small spurs) were seen in 3 subjects after 1½ to 2½ years.
Six of 128 subjects treated with acitretin showed abnormalities in the knees and ankles before treatment that progressed during treatment. In 5, these changes involved the formation of additional spurs or enlargement of existing spurs. The sixth subject had degenerative joint disease which worsened. No subjects developed spurs de novo. Clinical complaints did not predict radiographic changes.
Lipids and Possible Cardiovascular Effects:
Blood lipid determinations should be performed before acitretin is administered and again at intervals of 1 to 2 weeks until the lipid response to the drug is established, usually within 4 to 8 weeks. In subjects receiving acitretin during clinical trials, 66% and 33% experienced elevation in triglycerides and cholesterol, respectively. Decreased high density lipoproteins (HDL) occurred in 40% of subjects. These effects of acitretin were generally reversible upon cessation of therapy.
Subjects with an increased tendency to develop hypertriglyceridemia included those with disturbances of lipid metabolism, diabetes mellitus, obesity, increased alcohol intake, or a familial history of these conditions. Because of the risk of hypertriglyceridemia, serum lipids must be more closely monitored in high-risk patients and during long-term treatment.
Hypertriglyceridemia and lowered HDL may increase a patient’s cardiovascular risk status. Although no causal relationship has been established, there have been postmarketing reports of acute myocardial infarction or thromboembolic events in patients on therapy with acitretin. In addition, elevation of serum triglycerides to greater than 800 mg per dL has been associated with fatal fulminant pancreatitis. Therefore, dietary modifications, reduction in dose of acitretin, or drug therapy should be employed to control significant elevations of triglycerides. If, despite these measures, hypertriglyceridemia and low HDL levels persist, the discontinuation of acitretin should be considered.
Ophthalmologic Effects:
The eyes and vision of 329 subjects treated with acitretin were examined by ophthalmologists. The findings included dry eyes (23%), irritation of eyes (9%), and brow and lash loss (5%). The following were reported in less than 5% of subjects: Bell’s palsy, blepharitis and/or crusting of lids, blurred vision, conjunctivitis, corneal epithelial abnormality, cortical cataract, decreased night vision, diplopia, itchy eyes or eyelids, nuclear cataract, pannus, papilledema, photophobia, posterior subcapsular cataract, recurrent sties, and subepithelial corneal lesions.
Any patient treated with acitretin who is experiencing visual difficulties should discontinue the drug and undergo ophthalmologic evaluation.
Pancreatitis:
Lipid elevations occur in 25% to 50% of subjects treated with acitretin. Triglyceride increases sufficient to be associated with pancreatitis are much less common, although fatal fulminant pancreatitis has been reported. There have been rare reports of pancreatitis during therapy with acitretin in the absence of hypertriglyceridemia.
Pseudotumor Cerebri:
Acitretin and other retinoids administered orally have been associated with cases of pseudotumor cerebri (benign intracranial hypertension). Some of these events involved concomitant use of isotretinoin and tetracyclines. However, the event seen in a single patient receiving acitretin was not associated with tetracycline use. Early signs and symptoms include papilledema, headache, nausea and vomiting, and visual disturbances. Patients with these signs and symptoms should be examined for papilledema and, if present, should discontinue acitretin immediately and be referred for neurological evaluation and care. Since both acitretin and tetracyclines can cause increased intracranial pressure, their combined use is contraindicated (see ).
Capillary leak syndrome, a potential manifestation of retinoic acid syndrome, has been reported in patients receiving acitretin. Features of this syndrome may include localized or generalized edema with secondary weight gain, fever, and hypotension. Rhabdomyolysis and myalgias have been reported in association with capillary leak syndrome, and laboratory tests may reveal neutrophilia, hypoalbuminemia, and an elevated hematocrit. Discontinue acitretin if capillary leak syndrome develops during therapy.
Exfoliative dermatitis/erythroderma has been reported in patients receiving acitretin.Discontinue acitretin if exfoliative dermatitis/erythroderma occurs during therapy.
Ethanol:
Clinical evidence has shown that etretinate can be formed with concurrent ingestion of acitretin and ethanol (see boxed AND and ).
Glyburide:
In a trial of 7 healthy male volunteers, acitretin treatment potentiated the blood glucose-lowering effect of glyburide (a sulfonylurea similar to chlorpropamide) in 3 of the 7 subjects. Repeating the trial with 6 healthy male volunteers in the absence of glyburide did not detect an effect of acitretin on glucose tolerance. Careful supervision of diabetic patients under treatment with acitretin is recommended (see and ).
Hormonal Contraceptives:
It has not been established if there is a pharmacokinetic interaction between acitretin and combined oral contraceptives. However, it has been established that acitretin interferes with the contraceptive effect of microdosed progestin “minipill” preparations. Microdosed “minipill” progestin preparations are not recommended for use with acitretin (see ).
Methotrexate:
An increased risk of hepatitis has been reported to result from combined use of methotrexate and etretinate. Consequently, the combination of methotrexate with acitretin is also contraindicated (see ).
Phenytoin:
Tetracyclines:
Since both acitretin and tetracyclines can cause increased intracranial pressure, their combined use is contraindicated (see and ).
Vitamin A and Oral Retinoids:
Concomitant administration of vitamin A and/or other oral retinoids with acitretin must be avoided because of the risk of hypervitaminosis A.
Other:
There appears to be no pharmacokinetic interaction between acitretin and cimetidine, digoxin, or glyburide. Investigations into the effect of acitretin on the protein binding of anticoagulants of the coumarin type (warfarin) revealed no interaction.
A description of the materials is provided below. The main goals of the materials are to explain the program requirements, to reinforce the educational messages, and to assess program effectiveness.
The includes:
The also includes a voluntary patient survey for women of childbearing potential to assess the effectiveness of the
Education and Pregnancy Prevention for Acitretin (EPPA) Program
www.acitretinEPPA.com
Hypervitaminosis A produces a wide spectrum of signs and symptoms primarily of the mucocutaneous, musculoskeletal, hepatic, neuropsychiatric, and central nervous systems. Many of the clinical adverse reactions reported to date with administration of acitretin resemble those of the hypervitaminosis A syndrome.
Adverse Events/Postmarketing Reports:
In to the events listed in the tables for the clinical trials, the following adverse events have been identified during postapproval use of acitretin. Because these events are reported voluntarily from a population of uncertain size, it is not always possible to reliably estimate their frequency or establish a causal relationship to drug exposure.
Cardiovascular:
Acute myocardial infarction, thromboembolism (see ), stroke.
Immune System Disorders:
Hypersensitivity, including angioedema and urticaria (see ).
Nervous System:
Myopathy with peripheral neuropathy has been reported during therapy with acitretin. Both conditions improved with discontinuation of the drug.
Psychiatric:
Aggressive feelings and/or suicidal thoughts have been reported. These events, including self-injurious behavior, have been reported in patients taking other systemically administered retinoids, as well as in patients taking acitretin. Since other factors may have contributed to these events, it is not known if they are related to acitretin (see ).
Reproductive:
Vulvo-vaginitis due to .
Skin and Appendages:
Thinning of the skin, skin fragility, and scaling may occur all over the body, particularly on the palms and soles; nail fragility is frequently observed. Madarosis and exfoliative dermatitis/erythroderma have been reported (see ).
Vascular Disorders:
Clinical Trials:
During clinical trials with acitretin, 513 of 525 (98%) subjects reported a total of 3,545 adverse events. One-hundred sixteen subjects (22%) left trials prematurely, primarily because of adverse experiences involving the mucous membranes and skin. Three subjects died. Two of the deaths were not drug-related (pancreatic adenocarcinoma and lung cancer); the other subject died of an acute myocardial infarction, considered remotely related to drug therapy.
The tables below list by body system and frequency the adverse events reported during clinical trials of 525 subjects with psoriasis.
Table 3. Adverse Events Frequently Reported during Clinical Trials
Percent of Subjects Reporting (N = 525)
Table 4. Adverse Events Less Frequently Reported during Clinical Trials (Some of Which
May Bear No Relationship to Therapy)
Percent of Subjects Reporting (N = 525)
Laboratory:
Therapy with acitretin induces changes in liver function tests in a significant number of patients. Elevations of AST (SGOT), ALT (SGPT) or LDH were experienced by approximately 1 in 3 subjects treated with acitretin. In most subjects, elevations were slight to moderate and returned to normal either during continuation of therapy or after cessation of treatment. In subjects receiving acitretin during clinical trials, 66% and 33% experienced elevation in triglycerides and cholesterol, respectively. Decreased high density lipoproteins (HDL) occurred in 40% (see ). Transient, usually reversible elevations of alkaline phosphatase have been observed.
Table 5 lists the laboratory abnormalities reported during clinical trials.
Table 5. Abnormal Laboratory Test Results Reported during Clinical Trials
Percent of Subjects Reporting
To report SUSPECTED ADVERSE EVENTS, contact at or FDA at 1-800-FDA-1088 or
for voluntary reporting of adverse reactions.
Reference
This information is obtained from the National Institute of Health's Standard Packaging Label drug database.
"https://dailymed.nlm.nih.gov/dailymed/"
While we update our database periodically, we cannot guarantee it is always updated to the latest version.
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