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mycophenolate 250 mg capsule (generic cellcept)

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Uses

Mycophenolate mofetil (CellCept) is used for the prevention of rejection of kidney, heart, or liver allografts. The manufacturer recommends that mycophenolate mofetil be used in conjunction with cyclosporine and corticosteroid therapy. Mycophenolate mofetil also has been used in the management of Crohn's disease.

Mycophenolate sodium (Myfortic) is used in conjunction with cyclosporine and corticosteroid therapy for the prevention of rejection of kidney allografts.

Renal Allotransplantation

Adult Patients

Mycophenolate mofetil is used for the prevention of rejection of renal allografts in adults and pediatric patients 3 months to 18 years of age. In clinical trials in renal transplant patients, a regimen consisting of mycophenolate mofetil, cyclosporine, and corticosteroids was more effective than regimens consisting of either azathioprine or placebo in combination with cyclosporine and corticosteroids in preventing acute rejection, graft loss, or death at 6 months following transplantation.

Efficacy and safety of mycophenolate mofetil has been evaluated in 3 randomized, double-blind, multicenter trials in adults undergoing cadaveric renal transplantation. In each trial, mycophenolate mofetil was given in 2 different dosages (1 or 1.5 g twice daily) in immunosuppressive regimens that included cyclosporine, corticosteroids, and (in one study) antithymocyte globulin. Mycophenolate mofetil was compared with azathioprine (1-2 mg/kg daily or 100-150 mg daily) in 2 studies and with placebo in a third study; patients receiving azathioprine or placebo in these studies also received cyclosporine and corticosteroids. In these trials, the primary efficacy end point was the rate of treatment failure, defined as the first occurrence of an acute episode of biopsy-proven acute rejection, death, graft loss, or early termination of the study for any reason without a prior biopsy-proven acute rejection episode, in the first 6 months after transplantation. Results of these studies indicate that mycophenolate mofetil was more effective than azathioprine or placebo in reducing the incidence of treatment failure at 6 months following transplantation. When mycophenolate mofetil was compared with azathioprine, the treatment failure rates at 6 months for mycophenolate mofetil 2 g, mycophenolate mofetil 3 g, azathioprine (1-2 mg/kg daily), and azathioprine (100-150 mg daily) were 31.1-38.2, 31.3-34.8, 47.6, and 50%, respectively.When mycophenolate mofetil was compared with placebo, treatment failure rates at 6 months for mycophenolate mofetil 2 g, mycophenolate mofetil 3 g, and placebo were 30.3, 38.8, and 56%, respectively. The cumulative incidence of combined 1-year graft loss or patient death for mycophenolate mofetil 2 g, mycophenolate mofetil 3 g, and control (placebo or azathioprine), were 8.5-11.7%, 10-11.5, and 11.5-13.6%, respectively.

Mycophenolate sodium is used for the prevention of rejection of renal allographs in adults and pediatric patients 5-16 years of age. In clinical trials in de novo or stable renal transplant patients, a regimen consisting of mycophenolate sodium, cyclosporine, and/or corticosteroids was as effective as a regimen consisting of mycophenolate mofetil, cyclosporine, and corticosteroids in preventing acute rejection, graft loss, or death.

Mycophenolate mofetil therapy has been associated with a high incidence of adverse GI effects and a high proportion of patients receiving the drug required dosage reductions, interruptions in therapy, or discontinuance of the immunosuppressant due to adverse effects. Such changes in drug therapy have a negative impact on transplant outcomes (higher incidence of acute rejection, decreased graft survival). Mycophenolate sodium delayed-release tablets were designed to improve GI tolerance by delaying release of mycophenolic acid until the drug reaches the small intestine. However, results of comparative clinical studies have shown that incidence of adverse GI effects reported in patients receiving mycophenolate sodium have been similar to those in patients receiving mycophenolate mofetil.

Safety and efficacy of mycophenolate sodium delayed-release tablets have been evaluated in 2 multicenter, randomized, double-blind, comparative trials. In one 12-month study, 423 de novo renal transplant patients (18-75 years of age) who were receiving their first cadaveric (84%), living- unrelated, or human leukocyte antigen (HLA)-mismatched living-related donor kidney transplant, were randomized to receive (within 24-48 hours of transplantation) mycophenolate sodium (mycophenolic acid 720 mg twice daily) or mycophenolate mofetil (1 g twice daily) in conjunction with cyclosporine and corticosteroids. Patients undergoing transplantation at centers that routinely used induction therapy with antithymocyte or antilymphocyte antibody preparations (about 41%) were allowed to receive such therapy. The primary efficacy end point was the rate of treatment failure, defined as the first occurrence of acute rejection episode (biopsy-proven), graft loss, death, or loss to follow-up, in the first 6 months after transplantation. Mycophenolate sodium was as effective as mycophenolate mofetil in reducing the incidence of treatment failure rates at 6 and 12 months following transplantation. The treatment failure rates at 6 months for mycophenolate sodium and mycophenolate mofetil in this study were 25.8 and 26.2%, respectively, while at 12 months, treatment failure rates were 28.6 and 28.1%, respectively.

In the other 12-month study, maintenance therapy with mycophenolate sodium delayed-release tablets has been evaluated in 322 renal transplant patients (18-75 years of age) who had undergone primary or secondary cadaveric or living donor kidney transplantation, were at least 6 months posttransplant, and were receiving immunosuppressive regimens that included mycophenolate mofetil and cyclosporine, with or without corticosteroids, for at least 2 weeks before study entry. Patients were randomized to continue mycophenolate mofetil (1 g twice daily) or to switch to mycophenolate sodium (mycophenolic acid 720 mg twice daily). The incidence of treatment failure (defined as the first occurrence of acute rejection episode [biopsy-proven], graft loss, death, or loss to follow-up) at 6 and 12 months in patients receiving mycophenolate sodium was similar to that in patients receiving mycophenolate mofetil. The treatment failure rates at 6 months for mycophenolate sodium and mycophenolate mofetil in this study were 4.4 and 6.7%, respectively, while at 12 months, treatment failure rates were 7.5 and 12.3%, respectively. Results of this and other studies indicate that mycophenolate sodium can be substituted for mycophenolate mofetil without loss of efficacy.

Pediatric Patients

In an open-label multicenter study in pediatric patients 3 months to 18 years of age who underwent cadaveric renal transplantation, mycophenolate mofetil was administered by oral suspension in a dosage of 600 mg/m twice daily (maximum daily dosage 1 g twice daily) in conjunction with cyclosporine and corticosteroids. In this study, the overall biopsy-proven rejection rate at 6 months was comparable to that reported in adults. In addition, the rate of biopsy-proven rejection was similar across the various age groups (i.e., 3 months to younger than 6 years of age, 6 years to younger than 12 years of age; 12-18 years of age). At 12 months, the combined incidence of graft loss (5%) and patient death (2%) in children was similar to that observed in adults.

Safety and efficacy of mycophenolate sodium have been established in stable renal transplant pediatric patients 5-16 years of age. Use of mycophenolate sodium in this age group is supported by evidence from adequate and well controlled studies in stable adult renal transplant patients (who received mycophenolate sodium therapy) and limited pharmacokinetic data in stable renal transplant pediatric patients 5-16 years of age. Safety and efficacy of mycophenolate sodium in pediatric de novo renal transplant patients have not been established .

Cardiac Allotransplantation

Mycophenolate mofetil is used in adults for the prevention of rejection of cardiac allografts. This indication for mycophenolate mofetil is based on the results of one double-blind, randomized, multicenter active-controlled trial that enrolled 650 adults (578 of whom received at least one dose of either study drug) undergoing their first cardiac transplantation. Patients were randomized to receive oral mycophenolate mofetil (1.5 g twice daily) or oral azathioprine (1.5-3 mg/kg daily) in immunosuppressive regimens that included cyclosporine and corticosteroids. In this study, there were 2 primary efficacy end points; the first one was defined as the proportion of patients who had at least one endomyocardial biopsy-proven rejection with hemodynamic compromise after transplantation, underwent retransplantation, or died within the first 6 months, while the second primary efficacy end point was defined as the proportion of patients who died or underwent retransplantation during the first 12 months after the original transplantation. At 6 months, the incidence of biopsy-proven rejection accompanied by hemodynamic compromise in patients receiving mycophenolate mofetil (35%) was similar to that seen in patients receiving azathioprine (32%). At 12 months, mycophenolate mofetil was at least as effective as azathioprine in preventing death or retransplantation (6.2 vs 11.4%, respectively).

Use of an immunosuppressive regimen consisting of mycophenolate mofetil in conjunction with sirolimus and a corticosteroid following 12 weeks of therapy with a regimen consisting of mycophenolate mofetil, cyclosporine or tacrolimus, and a corticosteroid was investigated in the Heart Spare the Nephron (HSN) clinical trial in patients undergoing cardiac transplantation. The trial was designed to investigate whether switching from cyclosporine or tacrolimus to sirolimus at 12 weeks after transplantation would be associated with beneficial effects on renal function. The study was terminated early due to a higher than expected incidence of acute rejection in patients switched to sirolimus.

Hepatic Allotransplantation

Mycophenolate mofetil is used in adults for the prevention of rejection of liver allografts. This indication for mycophenolate mofetil is based on the results of one double-blind, randomized, active-controlled, multicenter trial that enrolled 565 adults undergoing primary hepatic allotransplantation. Patients were randomized to receive mycophenolate mofetil (1 g IV twice daily for up to 14 days, followed by 1.5 g given orally twice daily) or azathioprine (1-2 mg/kg IV daily followed by the same dosage orally) in immunosuppressive regimens that included cyclosporine and corticosteroids. In this study, there were 2 primary efficacy end points; the first was defined as the proportion of patients who had one or more biopsy-proven and treated rejection, who underwent retransplantation, or who died, while the second primary efficacy point was defined as the proportion of patients who experienced graft loss (by death or undergoing retransplantation) during the first 12 months after the primary transplantation. At 6 months, the incidence of one or more episodes of biopsy-proven and treated rejection, retransplantation, or death was 38.5 or 47.7% in those receiving mycophenolate mofetil or azathioprine, respectively. At 12 months, mycophenolate mofetil and azathioprine were similarly effective in preventing retransplantation or death.

Crohn's Disease

Mycophenolate mofetil has been used in the management of Crohn's disease. The comparative efficacy of mycophenolate mofetil versus azathioprine has been investigated in several studies. In a randomized, comparative, prospective trial that included 70 patients with moderately to severely active Crohn's disease, efficacy of mycophenolate mofetil was evaluated in the management of corticosteroid-dependent chronically active Crohn's disease. In this study, the Crohn's Disease Activity Index (CDAI) was used for clinical assessment. The CDAI score is based on subjective observations by the patient (e.g., the daily number of liquid or very soft stools, severity of abdominal pain, general well-being) and objective evidence (e.g., number of extraintestinal manifestations, presence of an abdominal mass, use or nonuse of antidiarrheal drugs, the hematocrit, body weight). Patients with a CDAI score of 150 to greater than 300 were randomized to receive prednisolone (50 mg daily initially and tapered to a maintenance dosage of 5 mg daily) concomitantly with mycophenolate mofetil (15 mg/kg daily; approximately 1.5 g daily) or azathioprine (2.5 mg/kg daily). One month after randomization, efficacy of mycophenolate mofetil was similar to that of azathioprine (median reduction of 120 points for mycophenolate mofetil versus 97 points for azathioprine) in patients with moderately active disease (CDAI of 150-300), while in patients with severely active disease (CDAI exceeding 300), use of mycophenolate mofetil was associated with substantially greater reduction in CDAI scores than azathioprine (median reduction of 265 points for mycophenolate mofetil versus 117 points for azathioprine). During 2-6 months of therapy, CDAI scores remained stable and at comparable levels in mycophenolate-treated patients with moderately and severely active disease. However, after 6 months of therapy, there was a clear trend for a continuous decrease in CDAI scores in patients with severely active disease who were receiving azathioprine.

Efficacy of mycophenolate mofetil also has been evaluated in several small uncontrolled trials in patients with refractory Crohn's disease.While results of some clinical studies have indicated that mycophenolate mofetil may be beneficial in some patients with chronically active disease (including those with fistulizing disease) who did not respond or were intolerant of other immunosuppressants, results of other clinical trials in patients with chronically active disease refractory to corticosteroids, mercaptopurine, or azathioprine have not demonstrated such benefit. Although mycophenolate has been well tolerated in many of these studies, it should be considered that the drug has been associated rarely with an increased incidence of adverse GI effects (e.g., ulceration, hemorrhage, perforation) and mycophenolate should be used with caution in patients with active serious GI disease. In general, mycophenolate mofetil should be reserved for patients with Crohn's disease who are refractory to or intolerant of azathioprine, mercaptopurine, methotrexate, or infliximab. Additional well-controlled studies are needed to define the role, if any, of mycophenolate mofetil in the management of refractory Crohn's disease.

For further information on the management of Crohn's disease,

Dosage and Administration

Reconstitution and Administration

Mycophenolate mofetil and mycophenolate sodium are administered orally; mycophenolate mofetil hydrochloride is administered by IV infusion. When mycophenolate is used for the prevention of rejection of organ allographs, the drug is used concomitantly with an immunosuppressive regimen that includes cyclosporine and corticosteroids; other immunosuppressive agents including antithymocyte globulin, antilymphocyte globulin, muromonab-CD3, basiliximab, or daclizumab (no longer commercially available in the US), also have been used.

The US Food and Drug Administration (FDA) currently requires that the manufacturer's patient information (medication guide) for mycophenolate mofetil or mycophenolate sodium be distributed to every patient each time the drug is dispensed. Because of the teratogenic potential of the drug, mycophenolate oral and parenteral preparations should be handled and prepared with care. Mycophenolate mofetil tablets should not be crushed and capsules should not be opened or crushed. Mycophenolate sodium delayed-release tablets should not be crushed, chewed, or cut. Inhalation of mycophenolate mofetil powder contained in the oral capsules or in the oral suspension (before and after reconstitution) and contact with the skin or mucous membranes should be avoided. In addition, contact with mycophenolate mofetil hydrochloride IV solution should be avoided. In case of accidental skin or mucous membrane contact, the affected area should be washed thoroughly with soap and water. If contact with the eyes occurs, they should be washed with water. The manufacturer recommends wiping up any spilled drug with a wet paper towel.

IV mycophenolate mofetil hydrochloride, which should be initiated within 24 hours following transplantation, generally is reserved for patients who cannot tolerate or are unable to take an oral dosage form. The drug can be administered IV for up to 14 days. Oral therapy should replace parenteral therapy as soon as possible.

Mycophenolate mofetil hydrochloride powder for injection is reconstituted by adding 14 mL of 5% dextrose injection to a vial labeled as containing 500 mg of mycophenolate mofetil; the vial should be gently shaken. The reconstituted solution is slightly yellow. For a 1-g infusion dose, the contents of 2 such reconstituted vials are added to 140 mL of 5% dextrose injection while for a 1.5-g infusion dose, the contents of 3 such reconstituted vials are added to 210 mL of 5% dextrose injection; the concentration of mycophenolate mofetil in the resulting solutions is 6 mg/mL. IV administration of mycophenolate mofetil hydrochloride should be started within 4 hours of reconstitution and dilution of the drug; solutions should be stored at 25°C with excursions of 15-30°C permitted. Strict aseptic technique must be observed since the drug contains no preservative. Mycophenolate mofetil hydrochloride should not be admixed with other drugs nor should other drugs be infused simultaneously through the same IV line. Prior to administration, reconstituted and diluted solutions of mycophenolate mofetil hydrochloride should be inspected visually for particulate matter and discoloration; if particulate matter or discoloration is evident, the solution should be discarded.

Mycophenolate mofetil hydrochloride should be infused IV over at least 2 hours by either a peripheral or central vein; the drug should not be administered by rapid IV (''bolus'') injection or rapid IV infusion.

Oral mycophenolate mofetil should be administered as soon as possible following renal, cardiac, or hepatic transplantation.

Administration of mycophenolate mofetil with food does not affect the area under the plasma concentration-time curve (AUC) of mycophenolic acid; however, decreases (by about 40%) of peak plasma concentrations of mycophenolic acid have been observed. Therefore, the manufacturer recommends that mycophenolate mofetil tablets, capsules, and oral suspension be administered on an empty stomach (e.g., 1 hour before or 2 hours after a meal); however, in stable renal transplant recipients, the drug may be given with food, if necessary. If a dose is missed, the dose should be taken as soon as it is remembered unless it is time for the next dose; a double dose should not be taken to make up for a missed dose.

Mycophenolate sodium may be administered as soon as possible following renal transplantation in adults.

Mycophenolate sodium delayed-release tablets are administered on an empty stomach, 1 hour before or 2 hours after food. If a dose is missed, the dose should be taken as soon as it is remembered unless it is time for the next dose; a double dose should not be taken to make up for a missed dose. Administration of mycophenolate sodium with food does not affect the AUC of mycophenolic acid; however, decreases in peak plasma concentration (by about 33%) and delay in time to peak plasma concentrations (from 1.5-2.75 hours to 5 hours) have been observed. To reduce variability in mycophenolic acid absorption between doses, mycophenolate sodium should be taken on an empty stomach.

It is recommended that mycophenolate mofetil powder for oral suspension be reconstituted at the time of dispensing by adding 94 mL of water (about 47 mL initially followed by another 47 mL after vigorous shaking for 1 minute) to provide a suspension containing 200 mg/mL. The bottle should be shaken well again for 1 minute to suspend the powder. Mycophenolate mofetil oral suspension also can be administered by a nasogastric tube (minimum 1.7 mm in interior diameter; minimum French size number 8).

General Dosage

Dosage of mycophenolate mofetil and mycophenolate mofetil hydrochloride are both expressed in terms of mycophenolate mofetil. Dosage of mycophenolate sodium is expressed in terms of mycophenolic acid.

Commercially available mycophenolate mofetil tablets, capsules, and oral suspension reportedly are bioequivalent. Mycophenolate sodium delayed-release tablets should not be used interchangeably with mycophenolate mofetil tablets, capsules, or oral suspension without supervision of a clinician, because absorption of the drug from these preparations is not equivalent. In a study in stable renal transplant recipients, administration of single oral doses of mycophenolate sodium delayed-release tablets (mycophenolic acid 720 mg) or mycophenolate mofetil 1-g oral preparations resulted in bioequivalent mycophenolic acid exposure.

Adults

Renal Allotransplantation

For the prevention of renal allograft rejection in adults, the usual dosage of mycophenolate mofetil is 1 g administered IV or orally twice daily. Although 2- and 3-g daily dosages of mycophenolate mofetil have been used in clinical trials, no efficacy advantage could be shown for the higher dosage in the overall renal transplant patient population. In addition, 2-g daily dosages of mycophenolate mofetil were associated with a superior safety profile when compared with the 3-g daily dosage.

When mycophenolate sodium delayed-release tablets are used for the prevention of renal allograft rejection in adults, the usual dosage is 720 mg of mycophenolic acid twice daily.

Cardiac Allotransplantation

For the prevention of cardiac allograft rejection in adults, the usual dosage of mycophenolate mofetil is 1.5 g administered IV or orally twice daily (3 g total daily dosage).

Hepatic Allotransplantation

For the prevention of hepatic allograft rejection in adults, the usual dosage of mycophenolate mofetil hydrochloride is 1 g administered IV twice daily or 1.5 g administered orally twice daily.

Crohn's Disease

For the management of Crohn's disease in adults who do not respond to or were intolerant of other immunosuppressants (e.g., azathioprine, mercaptopurine), mycophenolate mofetil dosages of 1-2 g daily have been used.

Pediatric Patients

Renal Allotransplantation

For the prevention of renal allograft rejection in pediatric patients 3 months to 18 years of age, the usual dosage of mycophenolate mofetil (as the oral suspension) is 600 mg/m administered orally twice daily, up to a maximum dosage of 1 g twice daily. Children with a body surface area of 1.25-1.5 m can receive 750 mg (as capsules) twice daily for a total daily mycophenolate mofetil dosage of 1.5 g, while children with a body surface area greater than 1.5 m can receive a dosage of 1 g (as capsules or tablets) twice daily for a total daily mycophenolate mofetil dosage of 2 g.

Mycophenolate sodium should be administered as maintenance therapy only in stable pediatric renal transplant recipients; safety and efficacy of the drug in de novo pediatric renal transplant recipients have not been established.

For the prevention of renal allograft rejection in pediatric patients 5-16 years of age, the usual dosage of mycophenolic acid (administered as mycophenolate sodium delayed-release tablets) is 400 mg/m twice daily (up to a maximum of 720 mg twice daily). Pediatric patients with a body surface area of 1.19-1.58m may receive a daily dosage of 1080 mg (administered as three 180-mg tablets or one 180-mg tablet and one 360-mg tablet twice daily). Pediatric patients with a body surface area greater than 1.58m may receive a daily dosage of 1440 mg (administered as four 180-mg tablets or two 360-mg tablets twice daily). A mycophenolate sodium dosage form suitable for providing an appropriate dosage for pediatric patients with a body surface area less than 1.19 m is not commercially available in the US.

Special Populations

Dosage adjustment of mycophenolate mofetil preparations or mycophenolic acid (administered as mycophenolate sodium delayed-release tablets) is not necessary in renal transplant recipients experiencing postoperative delayed graft function. No dosage adjustment is necessary in renal transplant recipients with severe hepatic parenchymal disease; however, it is not known whether dosage adjustment is needed in hepatic impairment of other etiologies.

Mycophenolate mofetil dosages exceeding 1 g twice daily should be avoided in renal transplant recipients with severe chronic renal impairment (GFR less than 25 mL/minute per 1.73 m) beyond the immediate posttransplant period.

If neutropenia (absolute neutrophil count [ANC] of less than 1300/mm) develops, mycophenolate therapy should be temporarily discontinued or the dosage reduced, suitable diagnostic tests be performed, and appropriate patient management be instituted.

Mycophenolate mofetil dosage adjustment based solely on age is not necessary in geriatric patients 65 years of age or older.

When mycophenolate sodium is used in geriatric adults, the maximum recommended dosage is mycophenolic acid 720 mg twice daily.

Cautions

Contraindications

Known hypersensitivity to mycophenolate mofetil, mycophenolate sodium, mycophenolic acid, or any ingredient in the formulation. Mycophenolate mofetil hydrochloride for IV injection contains polysorbate (Tween) 80 and should not be used in patients with known severe hypersensitivity to the surfactant.

Warnings/Precautions

Warnings

Mycophenolate shares the toxic potentials of currently available immunosuppressive agents. Immunosuppression with the drug may result in increased susceptibility to infection (e.g., infectious complications) and the possible development of lymphoma. Such risk appears to be related to the intensity and duration of immunosuppression rather than to the use of any specific immunosuppressive agent. Mycophenolate mofetil and mycophenolate sodium should be used by clinicians experienced in immunosuppressive therapy and the management of patients receiving these drugs. Patients receiving the drug should be managed in facilities equipped with adequate laboratory and supportive medical resources, and the clinician responsible for maintenance therapy should have complete information requisite for follow-up of the patients. Patients should be advised to read the medication guide for mycophenolate mofetil or mycophenolate sodium that is provided each time the drug is dispensed.

Carcinogenicity

Potential for the development of lymphoma and other malignancies, particularly of the skin, which may result from immunosuppression. Because of the increased risk for skin cancer, patients should be advised to limit their exposure to sunlight or other UV light by wearing protective clothing and using sunscreen with a high protection factor.

Lymphoproliferative disease or lymphoma occurred in 0.4-1.3% of allograft recipients receiving mycophenolate in conjunction with other immunosuppressive agents in clinical studies. Non-melanoma skin carcinoma was reported in 0.9-4.2% of patients while other types of malignancy were reported in 0.5-2.1% of patients.

Fetal/Neonatal Morbidity and Mortality

Mycophenolate may cause fetal toxicity when administered to pregnant women. Use of mycophenolate mofetil has been associated with increased risk of first-trimester pregnancy loss and serious congenital malformations. Information on pregnancy outcome in transplant recipients has been compiled by the National Transplantation Pregnancy Registry (NTPR). Information on 33 pregnancies in transplant recipients who received mycophenolate mofetil during pregnancy has been reported to the registry; there were 15 spontaneous abortions (45%) and 18 live-born infants; 4 of these infants had structural abnormalities (22%). NTPR data indicate that congenital abnormalities have occurred in 4-5% of neonates born to transplant recipients receiving other immunosuppressive agents. Postmarketing data are available on 77 women exposed to mycophenolate mofetil during pregnancy; 25 had a spontaneous abortion and 14 had a malformed infant or fetus. Fetal anomalies reported include ear abnormalities (43%, from postmarketing data), other orofacial deformities (e.g., cleft lip, cleft palate), and malformations of the limbs, heart, esophagus, and kidneys.

Teratogenic and embryocidal effects have been observed in animals receiving mycophenolate at doses 0.02-0.9 times the recommended human dose. Fetal anomalies have included anophthalmia, agnathia, and hydrocephaly in rats, and ectopia cordis, ectopic kidneys, diaphragmatic hernia, and umbilical hernia in rabbits.

Mycophenolate should be used during pregnancy only when the potential benefits justify the possible risks to the fetus. Women of childbearing potential should be informed of the potential risks of fetal toxicity prior to the initiation of therapy. A reliable blood or urine pregnancy test (i.e., having a sensitivity of at least 25 mIU/mL for human chorionic gonadotropin [HCG]) should be performed within 1 week prior to beginning mycophenolate therapy, and therapy with the drug should not be initiated until a report of the pregnancy test is available indicating that results are negative. Women of childbearing potential should use 2 reliable forms of contraception for at least 4 weeks prior to, throughout, and for at least 6 weeks after discontinuance of mycophenolate, unless the patient commits to continuous abstinence from heterosexual contact. Concomitant use of mycophenolate and certain oral hormonal contraceptives may result in decreased concentrations of the oral hormonal contraceptive.(See Drug Interactions: Oral Contraceptives.)

If mycophenolate is administered during pregnancy or if a patient becomes pregnant while receiving the drug, the patient should be informed of the potential hazard to the fetus. In certain situations, maternal benefits may outweigh the risks to the fetus. Women exposed to mycophenolate during pregnancy should be encouraged to enroll in the NTPR.

Infectious Complications

Use of immunosuppressive agents, including mycophenolate, may result in increased susceptibility to infection (i.e., opportunistic infections, sepsis, life-threatening/fatal infections). In clinical studies, serious infections (e.g., sepsis, fatal infections) occurred in 2% of renal and cardiac allograft recipients and in 5% of hepatic allograft recipients receiving mycophenolate mofetil. In one clinical study, the overall incidence of opportunistic infections in cardiac allograft recipients receiving mycophenolate mofetil was about 10% higher than in those receiving azathioprine; however, such difference was not associated with excess mortality associated with the infection or sepsis in patients receiving mycophenolate mofetil. Viral infections (e.g., cytomegalovirus [CMV] infections, herpes simplex, herpes zoster) have been reported more frequently in cardiac transplant recipients receiving mycophenolate mofetil than in those receiving azathioprine. Meningitis, infectious endocarditis, tuberculosis, and atypical mycobacterial infections have been reported during postmarketing surveillance of the drug.

Latent Viral Infections

Immunosuppressed patients are at an increased risk for opportunistic infections, including reactivation of latent viral infections. These include BK virus-associated nephropathy (BKVN), which has been reported in patients receiving immunosuppressants, including mycophenolate mofetil, cyclosporine, sirolimus, and tacrolimus. Primary infection with polyoma BK virus typically occurs in childhood; following initial infection, the virus remains latent, but reactivation may occur in immunocompromised patients. BKVN has principally been observed in renal transplant patients (usually within the first year posttransplantation), and may result in serious outcomes, including deterioration of kidney function and renal allograft loss. Risk of BK virus reactivation appears to be related to the degree of overall immunosuppression rather than use of any specific immunosuppressive agent; patients receiving a maintenance immunosuppressive regimen of at least 3 drugs appear to be at highest risk. Patients should be monitored for possible signs of BKVN, including deterioration in renal function, during therapy with mycophenolate mofetil or mycophenolate sodium; screening assays for polyomavirus replication also have been recommended by some clinicians. Early intervention in patients who develop BKVN is critical; a reduction in immunosuppressive therapy should initially be considered in such patients. Although a variety of other treatment approaches have been used anecdotally in patients with BKVN, including antiviral therapy (e.g., cidofovir), leflunomide, IV immunoglobulins, and fluoroquinolone antibiotics, additional experience and well-controlled studies are necessary to more clearly establish the optimal treatment of such patients.

Progressive multifocal leukoencephalopathy (PML), an opportunistic viral infection of the brain, has been reported during postmarketing experience with mycophenolate mofetil (CellCept). PML is caused by the JC virus and typically occurs in immunocompromised patients. At least 17 cases (10 confirmed, 7 possible) of PML have been reported in patients receiving mycophenolate mofetil; death occurred in at least 7 patients. Most reported cases of PML have occurred in patients who were receiving mycophenolate mofetil for the prevention of rejection of a solid organ transplant or for the management of systemic lupus erythematosus (SLE). These patients also were receiving other immunosuppressants (i.e., corticosteroids, cyclosporine, tacrolimus, and azathioprine in transplant recipients; corticosteroids, cyclophosphamide, and cyclosporine in SLE patients) or had compromised immune function. Hemiparesis, apathy, confusion, cognitive impairment, and ataxia were the most common manifestations of PML observed in these patients.

To date, no cases of PML have been reported in patients receiving mycophenolate sodium (Myfortic). Because mycophenolate sodium is converted to the same active metabolite (mycophenolic acid) as mycophenolate mofetil, use of mycophenolate sodium is expected to be associated with the same risk of PML as use of mycophenolate mofetil.

The possible diagnosis of PML should be considered in immunocompromised patients receiving mycophenolate who experience neurologic manifestations. Consultation with a neurologist is advised as clinically indicated. Decreasing total immunosuppression may improve the outcome of PML, but also may increase the risk of graft rejection in transplant recipients. Clinicians should consider the potential risks versus benefits of reduced immunosuppression.

Hematologic Effects

Severe neutropenia (i.e., absolute neutrophil counts [ANC] of less than 500/mm) has been reported in up to 2, 2.8, or 3.6% of renal, cardiac, or hepatic allograft recipients, respectively, receiving 3-g daily dosages of mycophenolate mofetil.

Neutropenia has been observed most frequently between 31-180 days posttransplant in patients receiving immunosuppressive therapy for the prevention of rejection of kidney, heart, or liver allograft. Neutropenia may be related to mycophenolate, concomitant therapies, viral infection, or a combination of these causes.

Complete blood cell counts (CBCs) should be performed weekly during the first month of therapy, twice monthly during the second and third month, and then monthly thereafter, during the first year. If neutropenia (ANC of less than 1300/mm) develops, mycophenolate therapy be temporarily discontinued or the dosage reduced, suitable diagnostic tests be performed, and appropriate patient management be instituted.

Pure red cell aplasia (PRCA), a condition in which red blood cell precursors in the bone marrow are absent or nearly absent, has been reported in patients receiving immunosuppressive regimens containing mycophenolate mofetil. At least 41 cases of PRCA have been reported in patients receiving mycophenolate mofetil. Some of these patients also were receiving other immunosuppressants, including alemtuzumab, azathioprine, and tacrolimus. Because these patients were receiving multiple immunosuppressive agents, the relative contribution of mycophenolate mofetil and other immunosuppressants to the development of PRCA is not known. Risk of PRCA also should be considered in patients receiving mycophenolate sodium, because this drug is converted to the same active metabolite (mycophenolic acid) as mycophenolate mofetil. PRCA can produce varying degrees of anemia from subclinical to severe; manifestations may include fatigue, lethargy, pallor, weakness, tachycardia, and/or dyspnea. Although the mechanism for mycophenolate-induced PRCA has not been determined, immunosuppression may play a role. In some cases, PRCA was found to be reversible with dosage reduction or discontinuance of mycophenolate mofetil. However, clinicians should consider the possibility of graft rejection if immunosuppression is reduced in transplant patients; any changes in immunosuppressive therapy should be implemented under appropriate medical supervision.

Major Toxicities

GI Effects

Severe GI bleeding (requiring hospitalization) has occurred in 3, 1.7, or 5.4% of renal, cardiac, or hepatic transplant recipients, respectively, receiving 3-g daily dosages of mycophenolate mofetil in clinical studies. In studies evaluating safety of mycophenolate sodium, severe GI bleeding was reported in 1% of de novo renal transplant patients and 1.3% of those receiving maintenance therapy. Mycophenolate mofetil therapy is associated with a high incidence of adverse GI effects; mycophenolate sodium delayed-release tablets were developed to improve GI tolerance. However, adverse GI effects in patients receiving mycophenolate sodium in comparative clinical studies have been similar to those in patients receiving mycophenolate mofetil. Because mycophenolate mofetil and mycophenolate sodium have been associated with adverse GI effects and rarely with serious GI effects (ulceration, hemorrhage, or perforation), the drugs should be administered with caution in patients with active serious GI disease.

General Precautions

Hypoxanthine Phosphoribosyltransferase Deficiency

Because mycophenolic acid inhibits inosine monophosphate dehydrogenase, mycophenolate mofetil and mycophenolate sodium should be avoided, on theoretical grounds, in patients with rare hereditary deficiency of hypoxanthine-guanine phosphoribosyltransferase (HGPRT), including Kelley-Seegmiller or Lesch-Nyhan syndrome.

Phenylketonuria

Individuals with phenylketonuria and those who must restrict their intake of phenylalanine should be warned that mycophenolate mofetil oral suspension contains aspartame (NutraSweet), which is metabolized in the GI tract to provide about 0.56 mg of phenylalanine per 5 mL of the suspension.

Specific Populations

Pregnancy

Category D., and see Fetal/Neonatal Morbidity and Mortality under Warnings/Precautions: Warnings, in Cautions.

Lactation

Mycophenolic acid is distributed into milk in rats; not known whether this drug is distributed into milk in humans. Discontinue nursing or the drug, taking into account the importance of the drug to the woman. Women should not breast-feed for at least 6 weeks after discontinuance of mycophenolate sodium therapy.

Pediatric Use

Safety of mycophenolate mofetil for the prevention of rejection of renal allografts in children 3 months to 18 years of age is based on data from a pediatric pharmacokinetic and safety study. The manufacturer states that safety and efficacy of mycophenolate mofetil in pediatric patients younger than 3 months of age receiving renal allografts have not been established. In addition, safety and efficacy have not been established in pediatric patients younger than 18 years of age receiving allogenic cardiac or hepatic transplants.

Limited data are available concerning use of mycophenolate mofetil in pediatric patients. In one study in children 1-18 years of age receiving mycophenolate mofetil 600 mg/m (oral suspension) twice daily following renal transplantation, pharmacokinetic parameters, including the AUC were similar to those reported in adult renal transplant recipients receiving mycophenolate mofetil 1 g twice daily. Results of several pediatric studies and analysis of an open-label study in children 3 months to 18 years of age undergoing renal transplantation suggest that the safety profile in children generally is similar to that in adults, although a difference in the incidence of certain adverse effects (e.g. abdominal pain, fever, infection, pain, sepsis, diarrhea, vomiting, pharyngitis, respiratory tract infection, hypertension, and anemia) has been higher in pediatric patients than in adults. In clinical studies in pediatric patients, lymphoproliferative malignancies have been reported rarely (about 1.4%), while other types of malignancies were not observed in children in these studies. Severe GI bleeding (requiring hospitalization) has been reported in 3.4% of pediatric patients undergoing renal transplantation.

Safety and efficacy of mycophenolate sodium in stable renal transplant pediatric patients 5-16 years of age is based on evidence from adequate and well controlled studies in stable adult renal transplant patients receiving mycophenolate sodium and limited pharmacokinetic data in stable renal transplant pediatric patients 5-16 years of age. Safety and efficacy of mycophenolate sodium have not been established in pediatric de novo renal transplant patients.

Limited data are available concerning use of mycophenolate sodium in pediatric patients. Following administration of a single dose of mycophenolate sodium (mycophenolic acid 450 mg/m) in stable pediatric renal transplant patients 5-16 years of age, peak plasma concentrations and area under the plasma concentration-time curve (AUC) of mycophenolic acid were 33 and 18% higher, respectively, than those reported in adults receiving the same dose based on body surface area (720 mg). The clinical importance of these findings remains to be determined. Pharmacokinetic data is not available in pediatric patients younger than 5 years of age.

Geriatric Use

Clinical studies of mycophenolate did not include sufficient numbers of patients 65 years of age or older to determine whether they respond differently than younger adults. While other clinical experience has not revealed differences in response, drug dosages should be selected cautiously in geriatric patients. The greater frequency of decreased hepatic, renal, and/or cardiac function and of concomitant diseases and drug therapy observed in the elderly also should be considered. Geriatric patients may be at increased risk of developing GI hemorrhage, pulmonary edema, or certain infections (e.g., invasive CMV infection) than younger patients.

Hepatic Impairment

No dosage adjustment for mycophenolate preparations is necessary for renal transplant recipients with severe hepatic parenchymal disease; not known whether dosage adjustment is needed for other hepatic diseases. No data are available for cardiac transplant recipients with severe hepatic parenchymal disease.

Renal Impairment

Administration of a single dose of mycophenolate mofetil in individuals with severe long-term renal impairment (glomerular filtration rate less than 25 mL/minute per 1.73 m) has resulted in higher AUC values for mycophenolic acid and the phenolic glucuronide of mycophenolic acid than values in individuals with less severe impairment or no impairment.

Patients receiving mycophenolate mofetil who experience posttransplant delay in graft function generally have AUC values for mycophenolic acid that are similar to those not experiencing graft function delay; however, the AUC for the phenolic glucuronide of mycophenolic acid is increased twofold to threefold in patients experiencing delayed graft function compared with those not experiencing delayed function. Dosage adjustment does not appear to be necessary in these patients; however, patients should be carefully observed.

No data are available on the use of mycophenolate mofetil in cardiac or hepatic transplant recipients with severe chronic renal impairment; mycophenolate mofetil may be used in these patients if the potential benefits outweigh the potential risks.

Studies evaluating the pharmacokinetics of mycophenolate sodium have not been conducted in patients with renal impairment. AUC values for mycophenolic acid in patients with renal impairment receiving mycophenolate sodium are not expected to increase appreciably relative to values in patients with normal renal function; however, AUC values for the phenolic glucuronide metabolite of mycophenolic acid are expected to increase substantially with decreased renal function. Plasma concentrations of mycophenolic acid and the phenolic glucuronide of mycophenolic acid may be increased in patients with severe renal impairment (glomerular filtration rate less than 25 mL/minute per 1.73 m) compared with plasma concentrations of healthy individuals and those with mild to moderate renal impairment. Patients with severe renal impairment should be carefully observed for possible adverse effects associated with increased plasma concentrations of free (unbound) mycophenolic acid and the phenolic glucuronide of mycophenolic acid. Safety of long-term exposure to increased concentrations of the phenolic glucuronide of mycophenolic acid remains to be determined.

Common Adverse Effects

The most frequently reported adverse effects associated with mycophenolate mofetil therapy are diarrhea, leukopenia, sepsis, vomiting, higher frequency of infections, including opportunistic infections (e.g., CMV infections, herpes zoster, herpes simplex, candidal infections, aspergillosis, and Pneumocystis carinii pneumonia). Adverse reactions occurring in 20% or more of patients receiving mycophenolate mofetil include pain (e.g., abdominal, chest, back), fever, headache, anemia (e.g., hypochromic), thrombocytopenia, leukocytosis, urinary tract infection, abnormal renal function, hypertension, hypotension, cardiovascular disorder, tachycardia, edema (e.g., peripheral) hypercholesteremia, hypokalemia, hyperkalemia, hyperglycemia, increases in blood urea nitrogen (BUN) and serum creatinine concentration, increased lactic dehydrogenase, hypomagnesemia, hypocalcemia, constipation, dyspepsia, nausea, vomiting, anorexia, abnormal liver function test results, cough, dyspnea, lung disorder, sinusitis, pleural effusion, rash, tremor, insomnia, dizziness, anxiety, and paresthesia.

The adverse effect profile in patients receiving IV mycophenolate mofetil hydrochloride is similar to that in patients receiving oral mycophenolate mofetil; phlebitis and thrombosis have been reported in 4% of patients receiving IV infusion of the drug.

In controlled studies in patients undergoing renal transplantation, the overall safety profile in those receiving mycophenolate mofetil 2 g daily was better than in those receiving 3 g daily. The types of adverse effects reported in renal, cardiac, or hepatic transplant studies generally are similar (except for those unique to the specific organ involved).

The most frequent adverse effects reported in patients receiving mycophenolate sodium include constipation, nausea, diarrhea, urinary tract infection, and nasopharyngitis. Adverse reactions occurring in 20% or more of patients receiving mycophenolate sodium include leukopenia, vomiting, dyspepsia, CMV infections, insomnia, and postoperative pain. In controlled studies in patients undergoing renal transplantation, the incidence of adverse effects reported in patients receiving mycophenolate sodium was similar to that reported in patients receiving mycophenolate mofetil.

Drug Interactions

Immunosuppressants

In clinical trials in patients undergoing transplant procedures, mycophenolate mofetil has been administered concurrently with cyclosporine, antithymocyte globulin (equine), muromonab-CD3, and/or corticosteroids; the manufacturer states that safety and efficacy of mycophenolate mofetil in combination with immunosuppressive agents other than these agents have not been determined.

In clinical trials in patients undergoing renal transplantation, mycophenolate sodium has been administered concurrently with cyclosporine, antithymocyte globulin, antilymphocyte globulin, muromonab-CD3, basiliximab, daclizumab (no longer commercially available in the US), and/or corticosteroids; the manufacturer states that safety and efficacy of mycophenolate sodium in combination with immunosuppressive agents other than these agents have not been determined.

Potential pharmacodynamic interaction (bone marrow suppression) with azathioprine. Concomitant use not recommended.

Concomitant use of mycophenolate mofetil with mycophenolate sodium is not recommended. Potential pharmacodynamic interaction (bone marrow suppression).

Concomitant use of mycophenolate mofetil without cyclosporine results in increased systemic exposure to mycophenolic acid compared with use of mycophenolate mofetil with cyclosporine. The lower systemic exposure to mycophenolic acid when mycophenolate mofetil is used with cyclosporine has been attributed to cyclosporine-induced inhibition of multidrug-resistance-associated protein 2 transporter in the biliary tract; inhibition of this transporter prevents excretion of the phenolic glucuronide of mycophenolic acid into bile (the phenolic glucuronide of mycophenolic acid is converted to mycophenolic acid via enterohepatic recirculation). Use of mycophenolate mofetil or mycophenolate sodium with or without cyclosporine does not affect plasma cyclosporine concentrations.

Anti-infective Agents

Pharmacokinetic interaction with co-trimoxazole unlikely.

Potential pharmacokinetic interaction with concomitant use of rifampin with mycophenolate mofetil (decreased systemic exposure to mycophenolic acid). Concomitant use of mycophenolate mofetil and rifampin not recommended unless benefit outweighs risk.

Concomitant use of mycophenolate mofetil and the anti-infective combination of norfloxacin and metronidazole not recommended due to potential pharmacokinetic interaction (decreased systemic exposure to mycophenolic acid); however, no substantial effect on systemic exposure to mycophenolic acid was observed when mycophenolate mofetil was administered with norfloxacin or metronidazole.

Concomitant administration of mycophenolate mofetil and oral ciprofloxacin or amoxicillin plus clavulanic acid decreased median trough concentrations of mycophenolic acid (active metabolite of mycophenolate mofetil) by approximately 50% in 3 days following initiation of antibiotic therapy in one study in renal transplant recipients. The potential mechanism for this drug interaction may be an antibiotic-induced reduction in glucuronidase-possessing enteric bacteria resulting in decreased enterohepatic recirculation of mycophenolic acid. Because changes in mycophenolic acid concentrations did not necessarily correlate with overall drug exposure, the clinical importance of these findings is not clear.

Antiviral Agents

Potential pharmacokinetic interaction with concomitant use of acyclovir with mycophenolate mofetil (increased plasma concentrations of acyclovir and the phenolic glucuronide of mycophenolic acid). Potential pharmacokinetic interaction with ganciclovir and valganciclovir in patients with renal impairment (increased plasma concentrations of the metabolites of the drugs). If acyclovir or ganciclovir is used in patients receiving mycophenolate sodium, blood cell counts should be monitored during treatment with the antiviral agent.

Antacids

Potential pharmacokinetic interaction (decreased plasma concentrations of mycophenolic acid) with antacids containing aluminum and magnesium hydroxides. Mycophenolate mofetil or mycophenolate sodium may be used in patients receiving these antacids; however, the immunosuppressant should not be administered simultaneously with the antacids.

Salicylates

Potential pharmacokinetic interaction based on in vitro data (increased free fraction of mycophenolic acid).

Cholestyramine

Potential pharmacokinetic interaction (decreased plasma concentrations of mycophenolic acid). Administration of mycophenolate mofetil or mycophenolate sodium with cholestyramine or other agents that interfere with enterohepatic recirculation of the drug is not recommended.

Oral Contraceptives

Potential pharmacokinetic interaction with concomitant use of levonorgestrel with mycophenolate mofetil (decreased plasma concentrations of levonorgestrel). Pharmacokinetic interaction unlikely with concomitant use of mycophenolate mofetil with ethinyl estradiol, desogestrel, or gestodene. Pharmacokinetic interaction unlikely with mycophenolate sodium. Oral contraceptives should be administered with caution in patients receiving mycophenolate and additional methods of birth control methods should be used.

Phosphate Binders

Potential pharmacokinetic interaction with concomitant administration of sevelamer and mycophenolate mofetil (decreased plasma concentrations of mycophenolic acid). The manufacturer recommends that sevelamer or other non-calcium-containing phosphate binders be given 2 hours after the administration of mycophenolate mofetil.

Probenecid and other Inhibitors of Tubular Secretion

Potential pharmacokinetic interaction based on animal data (increased plasma concentrations of mycophenolic acid and the phenolic glucuronide of mycophenolic acid).

Drugs that Alter Intestinal Flora

Drugs that alter intestinal flora may interfere with mycophenolate mofetil or mycophenolate sodium by disrupting enterohepatic recirculation; interference with the hydrolysis of the phenolic glucuronide metabolite of mycophenolic acid to mycophenolic acid may decrease the amount of mycophenolic acid available for absorption.

Vaccines

Potential interaction with live virus vaccine (decreased response to vaccination). Avoid use of live virus vaccine in patients receiving mycophenolate mofetil or mycophenolate sodium. Vaccination with influenza virus vaccine inactivated may be of value.

Pharmacokinetics

Absorption

Mycophenolate mofetil is rapidly absorbed following oral administration; bioavailability is 94%. Following oral and IV administration, mycophenolate mofetil undergoes rapid and complete metabolism to mycophenolic acid, the active metabolite. Mycophenolate mofetil tablets, capsules, and oral suspension are bioequivalent.

Following oral administration of the delayed-release tablets (mycophenolate sodium), mycophenolic acid is released in the small intestine; bioavailability is 72%.

Mycophenolate sodium delayed-release tablets cannot be used interchangeably with mycophenolate mofetil tablets, capsules, or oral suspension without clinician supervision. Single oral doses of mycophenolate sodium delayed-release tablets (mycophenolic acid 720 mg) and mycophenolate mofetil 1 g result in bioequivalent mycophenolic acid exposure.

Food decreases peak plasma concentrations of mycophenolic acid (by 33-40%); no effect on the mycophenolic acid AUC.

Plasma concentrations of free (unbound) mycophenolic acid and total mycophenolic acid glucuronide have increased in nontransplant individuals with severe chronic renal impairment (GFR <25 mL/minute per 1.73 m). Plasma mycophenolic acid concentrations in patients with delayed graft function similar to values in patients not experiencing delayed graft function.

Pharmacokinetic parameters, including AUC, in children 1-18 years of age receiving mycophenolate mofetil 600 mg/m (oral suspension) twice daily following renal transplantation, are similar to values in adult renal transplant recipients receiving 1 g twice daily. Peak plasma concentrations and AUC of mycophenolic acid in stable pediatric renal transplant patients 5-16 years of age receiving a single dose of mycophenolate sodium (mycophenolic acid 450 mg/m) increased (33 and 18%, respectively) relative to adults receiving the same dose based on body surface area. Clinical importance not determined.

Distribution

Mycophenolic acid is >=97-98% bound to plasma protein (mainly albumin).

Elimination

Mycophenolate mofetil undergoes complete metabolism to mycophenolic acid; metabolism occurs presystemically following oral administration. Mycophenolic acid is metabolized by glucuronyl transferase to the phenolic glucuronide of mycophenolic acid. The phenolic glucuronide is converted to mycophenolic acid via enterohepatic recirculation.

Mycophenolate mofetil is excreted in urine (93%) as the phenolic glucuronide of mycophenolic acid (87%) and in feces (6%). Mycophenolate sodium is excreted principally in urine as phenolic glucuronide of mycophenolic acid (>60%) and as unchanged mycophenolic acid (3%).

The half-life of mycophenolic acid is 8-17.9 hours.

Plasma concentrations of mycophenolic acid glucuronide are higher in nontransplant subjects with severe renal impairment than in those with mild impairment or normal renal function. Plasma concentrations of mycophenolic acid glucuronide are higher in transplant patients with delayed renal graft function than in patients not experiencing delayed graft function. Dialysis does not remove mycophenolic acid. Pharmacokinetic studies in patients with alcoholic cirrhosis indicate that hepatic mycophenolic acid glucuronidation is not affected by hepatic parenchymal disease; hepatic disease with other etiologies (e.g., biliary cirrhosis) may show a different effect.

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