Temixys (lamivudine/tenofovir disoproxil fumarate)
Last reviewed · Source: First Databank (FDB) drug data
Overview
Tenofovir disoproxil fumarate (tenofovir DF), an antiretroviral agent, is a human immunodeficiency virus (HIV) nucleotide reverse transcriptase inhibitor that is active against HIV and hepatitis B virus (HBV).
Lamivudine, an antiretroviral agent, is a human immunodeficiency virus (HIV) nucleoside reverse transcriptase inhibitor (NRTI) that is active against HIV and hepatitis B virus (HBV).
Tenofovir disoproxil fumarate (tenofovir DF), a synthetic antiretroviral agent, is a human immunodeficiency virus (HIV) nucleotide reverse transcriptase inhibitor. Tenofovir DF is a prodrug and is inactive until it undergoes diester hydrolysis in vivo to tenofovir and is subsequently metabolized to the active metabolite, tenofovir diphosphate. After conversion to the pharmacologically active metabolite, tenofovir inhibits replication of retroviruses, including HIV type 1 (HIV-1), by interfering with viral RNA-directed DNA polymerase (reverse transcriptase).
In vitro and in vivo studies indicate that tenofovir is active against HIV-1 and hepatitis B virus (HBV); the drug also has some activity against HIV-2.
Like HIV nucleoside reverse transcriptase inhibitors (NRTIs), the antiviral activity of tenofovir depends on intracellular conversion to an active metabolite; however, tenofovir is a nucleotide containing a phosphonate group and the steps and enzymes involved in enzymatic conversion to the active metabolite differ from those involved in the conversion of NRTIs. Tenofovir is phosphorylated by cellular nucleotide kinases to tenofovir diphosphate; tenofovir diphosphate is a structural analog of deoxyadenosine-5'-triphosphate, the usual substrate for viral RNA-directed DNA polymerase. Although other mechanisms may be involved in the antiretroviral activities of the drug, tenofovir diphosphate appears to compete with deoxyadenosine-5'-triphosphate for viral RNA-directed DNA polymerase and for incorporation into viral DNA.
Following incorporation of tenofovir diphosphate into the viral DNA chain, DNA synthesis is prematurely terminated because the absence of the 3'-hydroxy group on the drug prevents further 5' to 3' phosphodiester linkages.
Tenofovir diphosphate is a weak inhibitor of mammalian DNA alpha- and beta-polymerases and mitochondrial DNA gamma-polymerase. In vitro studies using human hepatoblastoma cells, skeletal muscle cells, or renal proximal tubule epithelial cells indicate that tenofovir has only a low potential to induce mitochondrial toxicity.
HIV-1 strains with reduced susceptibility to tenofovir DF can be produced in vitro and strains with reduced susceptibility to tenofovir have emerged during therapy with the drug. Resistant strains have contained a K65R substitution in reverse transcriptase. HIV-1 with a K70E substitution that results in low-level reduced susceptibility to tenofovir also have been selected in vitro and identified in clinical isolates.
Cross-resistance occurs between tenofovir and some NRTIs. The K65R and K70E substitutions selected by tenofovir also are selected in some patients treated with abacavir or didanosine; isolates with such substitutions may show reduced susceptibility to emtricitabine and lamivudine. Therefore, presence of the K65R or K70E substitution may result in cross-resistance between tenofovir and NRTIs.
In vitro studies indicate that HIV isolates with multiple substitutions associated with zidovudine resistance have reduced susceptibility to tenofovir. Cross-resistance between tenofovir and HIV protease inhibitors (PIs) or HIV nonnucleoside reverse transcriptase inhibitors (NNRTIs) is unlikely.
Tenofovir inhibits HBV replication through competitive inhibition of viral reverse transcriptase. Although treatment-emergent amino acid substitutions have been reported in patients with HBV infection who received at least 24 weeks of tenofovir DF monotherapy and remained viremic, no specific substitutions occurred at a sufficient frequency to be associated with tenofovir resistance (genotypic and phenotypic analysis). Tenofovir may be active against some HBV strains that are resistant to adefovir and/or lamivudine.
However, cross-resistance occurs among the HBV nucleoside/nucleotide reverse transcriptase inhibitors and some adefovir-, entecavir-, lamivudine-, or telbivudine-resistant HBV may have reduced susceptibility to tenofovir.
When a 300-mg tenofovir DF tablet is administered with a high-fat meal, plasma tenofovir concentrations and AUC are increased; pharmacokinetics are not appreciably affected by administration with a light meal.
The pharmacokinetics of tenofovir DF in healthy individuals is similar to that in individuals with HIV-1 infection. Following oral administration of tenofovir DF in fasting HIV-infected individuals, oral bioavailability of tenofovir is approximately 25% and peak plasma concentrations are attained in about 1 hour. Pharmacokinetics are dose proportional over a tenofovir DF dosage range of 75-600 mg and are not affected by repeated dosing.
In a single-dose study in nonfasting individuals, mean peak plasma concentrations of tenofovir were 26% lower when tenofovir DF was administered as an oral powder compared with administration as tablets; however, the mean AUC of tenofovir was similar with both preparations. Food delays the time to peak plasma concentrations by approximately 1 hour. Administration of 300 mg of tenofovir DF (as tablets) following a high-fat meal (approximately 700-1000 kcal containing 40-50% fat) increases oral bioavailability resulting in a 14% increase in peak plasma concentrations and 40% increase in AUC.
Administration of tenofovir DF with a light meal does not have a clinically important effect on the pharmacokinetics of tenofovir compared to administration in the fasting state.
In vitro, tenofovir is less than 0.7 or 7.2% bound to plasma or serum proteins, respectively, over the concentration range of 0.01-25 mcg/mL. Following oral administration of tenofovir DF, there is some evidence that tenofovir is distributed into semen and vaginal tissue and cervicovaginal fluid in low concentrations. Very low concentrations may be distributed into saliva.
Tenofovir DF requires initial diester hydrolysis for conversion to tenofovir and subsequent phosphorylation by cellular enzymes to form the active tenofovir diphosphate. Tenofovir and its prodrug are not substrates of cytochrome P-450 (CYP) isoenzymes. Tenofovir is eliminated principally by the kidneys via glomerular filtration and active tubular secretion.
Following multiple oral doses, approximately 32% of a dose is eliminated in urine over 24 hours. Tenofovir is removed by hemodialysis; following a 300-mg dose of tenofovir DF, a 4-hour hemodialysis session removes approximately 10% of the dose. Following a single oral dose, the terminal elimination half-life of tenofovir is approximately 17 hours.
Clinical studies did not include sufficient numbers from racial and ethnic groups other than white patients to adequately determine potential pharmacokinetic differences among these populations. Pharmacokinetics of tenofovir DF are similar in male and female patients.
Lamivudine, an antiretroviral agent, is a human immunodeficiency virus (HIV) nucleoside reverse transcriptase inhibitor (NRTI). Following conversion to a pharmacologically active metabolite, lamivudine apparently inhibits replication of human retroviruses by interfering with viral RNA-directed DNA polymerase (reverse transcriptase). Lamivudine, therefore, exerts a virustatic effect against retroviruses by acting as a reverse transcriptase inhibitor.
Like other HIV nucleoside reverse transcriptase agents and other nucleoside antiviral agents, the antiviral activity of lamivudine appears to depend on intracellular conversion of the drug to a 5'-triphosphate metabolite; thus, 2',3'-dideoxy,3'-thiacytidine-5'-triphosphate (3TC-TP) and not unchanged lamivudine appears to be the pharmacologically active form of the drug. 3TC-TP is a structural analog of deoxycytidine triphosphate (dC-TP), the natural substrate for reverse transcriptase (viral RNA-directed DNA polymerase). Although other mechanisms may be involved in the antiretroviral activity of the drug, 3TC-TP appears to compete with naturally occurring dC-TP for incorporation into viral DNA by reverse transcriptase.
Following incorporation of 3TC-TP into the viral DNA chain instead of dC-TP, viral DNA synthesis is terminated prematurely because the absence of a 3'-hydroxy group on the oxathiolane ring prevents further 5' to 3' phosphodiester linkages.
Lamivudine is rapidly absorbed from the GI tract in patients with HIV or hepatitis B virus (HBV) infection. In HIV-infected patients or healthy individuals, peak plasma concentrations are achieved within 0.5-2 hours after a single dose. The absolute bioavailability of lamivudine 150-mg scored tablets and oral solution in adults is similar (86 and 87%, respectively).
In a crossover study in healthy adults evaluating the steady-state pharmacokinetics of lamivudine administered in a once-daily regimen (300-mg tablet once daily) or twice-daily regimen (150-mg tablet twice daily), AUC was similar with both regimens; however, peak plasma concentrations were 66% higher and trough concentrations were 53% lower with the once-daily regimen compared with the twice-daily regimen.
The absolute bioavailability of lamivudine tablets and lamivudine oral solution is lower in children than in adults. In addition, the relative bioavailability of the oral solution is approximately 40% lower than that of the tablets in children, despite no difference between the preparations in adults. It has been suggested that lower lamivudine exposures reported in pediatric patients receiving lamivudine oral solution are likely due to an interaction between lamivudine and concomitant solutions containing sorbitol (e.g., abacavir oral solution).
Data from pharmacokinetic studies evaluating once- and twice-daily lamivudine regimens in HIV-1-infected pediatric patients 3 months through 12 years of age indicate that AUCs attained with once-daily regimens were similar to those attained with twice-daily regimens when comparing the dosage regimens within the same formulation (i.e., either tablets or the oral solution). However, mean peak plasma concentrations were approximately 80-90% higher with once-daily lamivudine regimens compared with twice-daily lamivudine regimens.
Pharmacokinetics of lamivudine in pregnant women are similar to those reported in nonpregnant adults and postpartum women. Food does not appear to affect the AUC of lamivudine. In a small study in HIV-infected patients, peak plasma concentrations of lamivudine were decreased 40% and the rate of absorption was reduced when lamivudine was administered with food, but clinically important decreases in systemic availability of the drug (AUC) were not observed.
Lamivudine is distributed into CSF. In HIV-infected children who received oral lamivudine in a dosage of 8 mg/kg daily, CSF concentrations ranged from 0.04-0.3 mcg/mL and were 5.6-30.9% of concurrent serum concentrations. Lamivudine crosses the placenta and is distributed into cord blood and amniotic fluid.
Lamivudine concentrations in amniotic fluid are typically twofold higher than maternal serum concentrations and have ranged from 1.2-2.5 mcg/mL or 2.1-5.2 mcg/mL when lamivudine dosage in the mother was 150 or 300 mg twice daily, respectively. Lamivudine is distributed into milk. Lamivudine is less than 36% bound to plasma proteins.
Intracellularly, lamivudine is phosphorylated and converted by cellular enzymes to the active 5'-triphosphate metabolite. Lamivudine is not substantially metabolized by cytochrome P-450 (CYP) isoenzymes. Metabolism is a minor route of elimination of lamivudine; the only known metabolite is the trans-sulfoxide metabolite.
The majority of a lamivudine dose is eliminated unchanged in urine by active organic cationic secretion. Within 12 hours after an oral dose, approximately 5% is excreted in urine as the trans-sulfoxide metabolite. In single-dose studies in healthy individuals or patients with HIV or HBV infection, the mean plasma half-life of lamivudine was 5-7 hours.
The plasma half-life in HIV-infected children 4 months to 14 years of age is 2 hours.
The pharmacokinetics of lamivudine are not altered in patients with hepatic impairment. In patients with impaired renal function, peak plasma concentrations, AUC, and plasma half-life of lamivudine are increased. Hemodialysis increases lamivudine clearance; however, the length of time of hemodialysis (4 hours) is insufficient to substantially alter mean lamivudine exposure after a single dose of the drug.
Continuous ambulatory peritoneal dialysis and automated peritoneal dialysis have negligible effects on lamivudine clearance. There are no significant or clinically relevant racial or gender differences in lamivudine pharmacokinetics.
USES: This combination product is used with other HIV medications to help control HIV infection. It helps to decrease the amount of HIV in your body so your immune system can work better. This lowers your chance of getting HIV complications (such as new infections, cancer) and improves your quality of life.
This product is a combination of 2 different drugs: lamivudine and tenofovir. Lamivudine is called a nucleoside reverse transcriptase inhibitor and tenofovir is called a nucleotide reverse transcriptase inhibitor. Lamivudine and tenofovir are often called NRTIs.
Lamivudine/tenofovir is not a cure for HIV infection. To decrease your risk of spreading HIV disease to others, continue to take all HIV medications exactly as prescribed by your doctor. Use an effective barrier method (latex or polyurethane condoms/dental dams) during sexual activity as directed by your doctor.
Do not share personal items (such as needles/syringes, toothbrushes, and razors) that may have contacted blood or other body fluids. Consult your doctor or pharmacist for more details.
Generic name: lamivudine/tenofovir disoproxil fumarate
Pronunciation: (la-MIV-ue-deen/ten-OF-oh-vir)
Reference product & biosimilars
No reference, biosimilar or interchangeable associated with this drug.
Today’s intelligence on Temixys
Indications
The following indications are listed for Temixys:
- Hiv Infection
Also known as: Human Immunodeficiency Virus Disease, Human Immunodeficiency Virus Infection.
Dosing
Although tenofovir DF is a prodrug that requires metabolism for activation, dosage of the drug is expressed in terms of the prodrug diester (i.e., tenofovir DF).
Dosage of tenofovir DF oral powder containing 40 mg/g is expressed as the number of scoops of powder.
Single-entity tenofovir DF is commercially available as tablets or oral powder.
Tenofovir DF tablet is administered orally once daily without regard to meals.
Tenofovir DF oral powder is administered once daily. Measure the appropriate dosage of the oral powder using only the scoop provided by the manufacturer. One level scoop delivers 1 g of powder, which contains 40 mg of tenofovir DF. Mix the required number of scoops of the powder with 2-4 ounces of soft food that can be swallowed without chewing (e.g., applesauce, baby food, yogurt), and ingest the entire mixture immediately to avoid a bitter taste. Do not administer the oral powder in a liquid since the powder may float to the top of the liquid, even after stirring.
Store tenofovir DF oral power and tablets at 25oC (excursions permitted to 15-30oC). Dispense in the original container, and keep the container tightly closed.
Lamivudine is administered orally once or twice daily without regard to meals.
For the treatment of HIV-1 infection, lamivudine is commercially available as an oral solution containing 10 mg/mL or tablets containing 150 or 300 mg of the drug (Epivir(R), generic). The 150-mg scored tablets are the preferred preparation in pediatric patients who weigh 14 kg or more and can swallow tablets. The oral solution should be used in those unable to safely and reliably swallow tablets. Lamivudine is used in conjunction with other antiretrovirals for the treatment of HIV-1 infection.
For the treatment of chronic HBV infection, lamivudine is commercially available as an oral solution containing 5 mg/mL or film-coated tablets containing 100 mg of the drug (Epivir-HBV(R), generic). The 5-mg/mL oral solution should be used in patients requiring a dosage less than 100 mg and in children unable to reliably swallow tablets.
Lamivudine preparations labeled by FDA for treatment of chronic HBV infection should not be used in HIV-infected patients because they contain a lower dosage of the drug than that required for treatment of HIV-1 infection. If such preparations are used for the management of chronic HBV infection in a patient with unrecognized or untreated HIV infection, rapid emergence of HIV resistance is likely to result because of the subtherapeutic dose and the inappropriateness of monotherapy for HIV-infected individuals.
Store lamivudine 100-mg, 150-mg, and 300-mg tablets at 25degreesC (excursions permitted between 15-30degreesC). Store lamivudine 5-mg/mL oral solution at 20-25degreesC and store lamivudine 10-mg/mL oral solution at 25degreesC.
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No dosing information is available for this tab.
Drug interactions
Tenofovir disoproxil fumarate (tenofovir DF) is a substrate of the P-glycoprotein (P-gp) transport system and breast cancer resistance protein (BCRP). Tenofovir and its prodrug (tenofovir DF) are not substrates of cytochrome P-450 (CYP) isoenzymes; in vitro studies indicate tenofovir does not inhibit CYP isoenzymes 3A4, 2D6, 2C9, or 2E1, but may have a slight inhibitory effect on CYP1A.
The following drug interactions are based on studies using tenofovir DF; refer to the full prescribing information for further details. Additional drug interactions may exist for fixed-combinations containing emtricitabine and tenofovir DF (Truvada(R)); doravirine, lamivudine, and tenofovir DF (Delstrigo(R)); efavirenz, emtricitabine, and tenofovir DF (Atripla(R)); emtricitabine, rilpivirine, and tenofovir DF (Complera(R)); elvitegravir, cobicistat, emtricitabine, and tenofovir DF (Stribild(R)); and efavirenz, lamivudine, and tenofovir (Symfi(R) and Symfi Lo(R)). When a fixed combination is used, interactions associated with each drug in the fixed combination should be considered. See the full prescribing information for drug interactions of each combination product.
The following drug interactions are based on studies using lamivudine. Additional drug interactions may exist for fixed-dose combination products containing lamivudine/zidovudine (Combivir(R), generic) , abacavir/lamivudine (Epzicom(R), generic) , abacavir/lamivudine/zidovudine (Trizivir(R), generic) , lamivudine/tenofovir disoproxil fumarate (Cimduo(R)) , doravirine/lamivudine/tenofovir disoproxil fumarate (Delstrigo(R)) , dolutegravir/lamivudine (Dovato(R)) , efavirenz/lamivudine/tenofovir disoproxil fumarate (Symfi(R); Symfi(R) Lo) , and abacavir/dolutegravir/lamivudine (Triumeq(R); Triumeq PD(R)). See the full prescribing information for information on each of these combination products.
There are no contraindication interactions for this drug.
There are no severe interactions for this drug.
There are no moderate interactions for this drug.
Contraindications
*None.
*Previous hypersensitivity to lamivudine.
There are no contraindication contraindications for this drug.
There are no severe contraindications for this drug.
There are no moderate contraindications for this drug.
Adverse reactions
The most common adverse effects (incidence >=10%; grades 2-4) in HIV-infected patients receiving tenofovir DF are rash, diarrhea, headache, pain, depression, asthenia, and nausea.
The most common adverse effect (all grades) in HBV-infected patients with compensated liver disease was nausea (9%).
The most common adverse effects (incidence >=10%; all grades) in HBV-infected patients with decompensated liver disease were abdominal pain, nausea, vomiting, pruritus, insomnia, dizziness, and pyrexia.
Adverse reactions in pediatric patients were consistent with those observed in adults.
In the treatment of HIV infection in adults, the most common reported adverse reactions (incidence >=15%) were headache, nausea, malaise and fatigue, nasal signs and symptoms, diarrhea, and cough. In the treatment of HIV infection in pediatric patients, the most common reported adverse reactions (incidence >=15%) were fever and cough.
In the treatment of HBV infection, the most common reported adverse reactions (incidence >=10% and reported at a rate greater than placebo) were ear, nose, and throat infections; sore throat; and diarrhea.
There are no severe adverse reactions for this drug.
There are no less severe adverse reactions for this drug.
Precautions
No enhanced messaging available.
Safety and efficacy of tenofovir DF for treatment of HIV-1 infection in pediatric patients 2 to <18 years of age are supported by data from 2 randomized controlled trials. Peak plasma concentrations and AUC of tenofovir in HIV-1-infected pediatric patients 2 to <18 years of age receiving 8 mg/kg of tenofovir DF (up to 300 mg) once daily as oral powder or receiving 300 mg once daily as tablets were similar to peak plasma concentrations and AUC reported in adults receiving 300 mg once daily. Safety and efficacy of tenofovir DF for treatment of HIV-1 infection have not been established in children <2 years of age weighing <10 kg.
In HBV-infected pediatric patients 12 to <18 years of age receiving tenofovir DF 300 mg once daily as tablets, and pediatric patients 2 to <12 years of age receiving 8 mg/kg of tenofovir DF (up to 300 mg) once daily as tablets or oral powder, tenofovir exposures were similar to those reported in HIV-1-infected adults receiving identical doses.
Safety and efficacy of tenofovir DF for treatment of chronic HBV infection have not been established in children <2 years of age weighing <10 kg.
The safety and efficacy of lamivudine for the treatment of HIV-1 (Epivir(R)) have been established in pediatric patients 3 months of age and older. The scored tablet is the preferred formulation for HIV-1-infected pediatric patients weighing at least 14 kg for whom a solid dosage form is appropriate; in the ARROW trial, pediatric patients who received the oral solution had lower rates of virologic suppression, lower plasma lamivudine exposure, and developed viral resistance more frequently.
The safety and efficacy of lamivudine for the treatment of chronic HBV (Epivir-HBV(R)) in pediatric patients younger than 2 years of age have not been established.
The Antiretroviral Pregnancy Registry (APR) monitors pregnancy outcomes in women exposed to tenofovir DF during pregnancy. Clinicians are encouraged to register patients in the APR by calling 1-800-258-4263 or visiting https://www.apregistry.com/.
Based on prospective data from the APR, the prevalence of birth defects in live births was 2.3% and 2.1% following first and second/third trimester exposure, respectively, to tenofovir DF-containing regimens. The overall risk of birth defects with first-trimester exposure for tenofovir DF was not markedly different compared to the background rate for major birth defects of 2.7% in the United States reference population of the Metropolitan Atlanta Congenital Defects Program (MACDP). Limitations of using an external comparator (the MACDP) include differences in populations and methodology, and confounding due to the underlying disease. The rate of miscarriage is not reported in the APR. Tenofovir crosses the human placenta.
In published studies that included HBV-infected pregnant women treated with tenofovir DF, an increased risk of adverse pregnancy-related outcomes was not observed with use of tenofovir DF during the third trimester. Two stillbirths were identified, and there was 1 major birth defect (talipes) and 1 occurrence of multiple congenital abnormalities (not further specified) in infants exposed to tenofovir DF. No clinically relevant drug-related safety findings were found in infants exposed to tenofovir DF during late gestation.
Animal reproduction studies did not find any adverse developmental effects when tenofovir DF was administered at doses >=14 (tenofovir DF) and exposures 2.7 (tenofovir) times the recommended daily dose of tenofovir DF in humans.
Lamivudine crosses the placenta and is distributed into cord blood in concentrations similar to maternal serum concentrations.
To monitor maternal-fetal outcomes of pregnant women exposed to antiretroviral agents, including lamivudine, the Antiretroviral Pregnancy Registry was established. Clinicians are encouraged to contact the registry at 800-258-4263 or https://www.apregistry.com/ to report cases of prenatal exposure to antiretroviral agents.
Data from the Antiretroviral Pregnancy Registry show no difference in the risk of overall major birth defects for lamivudine compared with the background rate for major birth defects in the US reference population of the Metropolitan Atlanta Congenital Defects Program (MACDP). Reproduction studies in rats or rabbits using oral lamivudine dosages that resulted in plasma concentrations up to approximately 35 times higher than plasma concentrations attained with the recommended human dosage used for the treatment of HIV infection in adults have not revealed evidence of teratogenicity. Although there was evidence of early embryolethality in rabbits at exposure levels similar to those observed in humans, this effect was not seen in rats at exposure levels up to 35 times higher than those in humans.
Tenofovir is distributed into human milk in low concentrations. In a study of breast-feeding women (not infected with HIV) who were on a tenofovir-containing regimen started between 1-24 weeks postpartum, tenofovir was undetectable in the plasma of most infants after 7 days of treatment in mothers. No serious adverse events were reported in mothers or infants.
It is not known whether tenofovir DF affects human milk production or has effects on the breast-fed infant.
The HHS perinatal HIV transmission guideline provides updated recommendations on infant feeding. The guideline states that patients with HIV should receive evidence-based, patient-centered counseling to support shared decision making about infant feeding. During counseling, patients should be informed that feeding with appropriate formula or pasteurized donor human milk from a milk bank eliminates the risk of postnatal HIV transmission to the infant. Additionally, achieving and maintaining viral suppression with antiretroviral therapy during pregnancy and postpartum reduces the risk of breastfeeding HIV transmission to <1%, but does not completely eliminate the risk. Replacement feeding with formula or banked pasteurized donor milk is recommended when patients with HIV are not on antiretroviral therapy and/or do not have a suppressed viral load during pregnancy (at a minimum throughout the third trimester), as well as at delivery.
If using tenofovir DF for the treatment of HBV infection, consider the developmental and health benefits of breast-feeding and the importance of tenofovir DF to the mother along with the potential adverse effects on the breast-fed infant from the drug or from the underlying maternal condition.
Lamivudine is distributed into milk in humans. It is not known whether the drug affects human milk production or affects the breast-fed infant.
The HHS perinatal HIV transmission guideline provides updated recommendations on infant feeding. The guideline states that patients with HIV should receive evidence-based, patient-centered counseling to support shared decision making about infant feeding. During counseling, patients should be informed that feeding with appropriate formula or pasteurized donor human milk from a milk bank eliminates the risk of postnatal HIV transmission to the infant. Additionally, achieving and maintaining viral suppression with antiretroviral therapy during pregnancy and postpartum reduces the risk of breastfeeding HIV transmission to <1%, but does not completely eliminate the risk. Replacement feeding with formula or banked pasteurized donor milk is recommended when patients with HIV are not on antiretroviral therapy and/or do not have a suppressed viral load during pregnancy (at a minimum throughout the third trimester), as well as at delivery.
If lamivudine is being used for treatment of chronic HBV infection, the benefits of breast-feeding and the importance of lamivudine to the woman should be considered along with the potential adverse effects on the breast-fed infant from the drug or from the underlying maternal condition.
The manufacturer makes no specific dosage recommendations for geriatric patients. Select dosage with caution because of age-related decreases in hepatic, renal, and/or cardiac function and concomitant disease and drug therapy.
Use with caution in geriatric patients because of age-related decreases in hepatic, renal, and/or cardiac function and concomitant disease and drug therapy.
Clinical studies did not include sufficient numbers of patients >=65 years of age to determine whether they respond differently to tenofovir DF than younger adults. Select dosage in geriatric patients with caution because of the greater frequency of decreased hepatic, renal, and/or cardiac function and of concomitant disease or drug therapy. Pharmacokinetic studies have not been conducted in patients >=65 years of age.
Clinical trials of lamivudine (Epivir(R) and Epivir-HBV(R)) did not include sufficient numbers of patients 65 years of age or older to determine whether they respond differently from younger subjects. Use caution when administering lamivudine to geriatric patients, reflecting the greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy.
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Last reviewed · Source: First Databank (FDB) drug data
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