Aciclovir

Offer surplus and non-recyclable solutions to a licensed disposal company. Contact a licensed professional waste disposal service to dispose of this material. Dissolve or mix the material with a combustible solvent and burn in a chemical incinerator equipped with an afterburner and scrubber.

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational exposure or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal, aquatic, and plant life; and conformance with environmental and public health regulations.

SRP: The scientific literature for the use of contact lenses by industrial workers is inconsistent. The benefits or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.

Acyclovir has been used concomitantly with zidovudine ... without evidence of increased toxicity; however, neurotoxicity (profound drowsiness and lethargy), which recurred on rechallenge, has been reported in at least one patient with acquired immunodeficiency syndrome (AIDS) during concomitant therapy with the drugs. Neurotoxicity was evident within 30-60 days after initiation of IV acyclovir therapy, persisted with some improvement when acyclovir was administered orally, and resolved following discontinuance of acyclovir in this patient.

This study reports the effects of a combination of azidothymidine plus acyclovir on both pluripotent (spleen colony forming units) and committed (granulocyte-macrophage colony forming units; erythroid burst forming units) murine hemopoietic progenitors. Administration of azidothymidine alone was associated with severe hematotoxicity, as shown by the marked decrease of all the hemopoietic progenitor populations tested, that is, spleen colony forming units, granulocyte-macrophage colony forming units, and erythroid burst forming units. This, however, was followed by a prompt recovery of hemopoiesis. Administration of acyclovir alone did not modify the hematological parameters studied, whereas the combined administration of azidothymidine and acyclovir led to changes in peripheral blood cells and bone marrow hemopoietic progenitors that were, on the whole, not significantly different from those observed with azidothymidine alone. Only the decrease in spleen colony forming units was significantly more severe, but their recovery was as rapid as that of the committed progenitors. Thus, in this experimental setting, the addition of acyclovir to azidothymidine does not appear to increase the hematotoxicity of the latter.

The combined effect of acyclovir and chlorhexidine on the replication and DNA synthesis of herpes simplex virus was studied. Acyclovir and chlorhexidine showed synergism in the inhibition of the viral replication by enhancing in part the reduction of viral DNA synthesis. These data indicate that combined therapy with acyclovir and chlorhexidine might be beneficial for the control of intraoral herpetic infections.

Acyclovir may decrease the renal clearance of other drugs eliminated by active renal secretion, such as methotrexate.

For more Interactions (Complete) data for ACYCLOVIR (6 total), please visit the HSDB record page.

Despite widespread use, there is little evidence that acyclovir when given orally causes significant liver injury. Serum enzyme levels generally do not change during oral acyclovir therapy. High dose intravenous administration of acyclovir is associated with renal dysfunction and thrombocytopenia, and occasionally with transient mild-to-moderate elevations in serum ALT levels, which have been asymptomatic and self-limited. There have rare instances of acute, clinically apparent liver injury reported that were attributed to acyclovir or valacyclovir (a prodrug of acyclovir with better oral absorption), but these have not been particularly convincing. Some degree of liver injury and even jaundice can occur during the course of herpes simplex or varicella zoster infection, and these complications could be mistaken for drug induced liver injury. Furthermore, in the reported cases, patients were receiving other medications and had other unlying comorbidities that may have been responsible for the liver injury.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 10(SRC), determined from a structure estimation method(2), indicates that acyclovir is expected to have very high mobility in soil(SRC). Volatilization of acyclovir from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 3.2X10-22 atm-cu m/mole(SRC), using a fragment constant estimation method(3). Acyclovir is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 5.4X10-15 mm Hg at 25 °C(SRC), determined from a fragment constant method(4). A biodegradation half-life of 5.3 hours using activated sludge(5) suggests that biodegradation may be an important environmental fate process in soil(SRC).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 10(SRC), determined from a structure estimation method(2), indicates that acyclovir is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 3.2X10-22 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). According to a classification scheme(5), an estimated BCF of 3(SRC), from its log Kow of -1.56(6) and a regression-derived equation(2), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Hydrolysis is not expected to be an important environmental fate process since this compound lacks groups that hydrolyze under environmental conditions(3). A biodegradationhalf-life of 5.3 hours using activated sludge(7) suggests that biodegradation may be an important environmental fate process in water(SRC).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), acyclovir, which has an estimated vapor pressure of 5.4X10-15 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase acyclovir may be removed from the air by wet or dry deposition(SRC). Acyclovir contains chromophores that absorb at wavelengths >290 nm(3) and, therefore, may be susceptible to direct photolysis by sunlight(SRC).

Acute kidney injury (AKI) is the most significant adverse effects of parenteral acyclovir administration. The incidence of AKI is comparable to other nephrotoxic medications such as aminoglycosides. Patients with CKD are at higher risk. Dose adjustment of acyclovir for ideal body weight and baseline renal function is imperative. A study regarding the pharmacokinetics of acyclovir demonstrated that a patient's glomerular filtration and tubular secretion contribute to its renal excretion.

Using a structure estimation method based on molecular connectivity indices(1), the Koc of acyclovir can be estimated to be 10(SRC). According to a classification scheme(2), this estimated Koc value suggests that acyclovir is expected to have very high mobility in soil.

/HUMAN EXPOSURE STUDIES/ In a controlled study in men receiving chronic oral acyclovir (400 mg or 1 g daily) therapy, there was no evidence of clinically important effects on sperm count, motility, or morphology during 6 months of therapy and 3 months of post-treatment follow-up.

/HUMAN EXPOSURE STUDIES/ Acyclovir is used to treat herpes infections in preterm and term infants; however, the influence of maturation on drug disposition and dosing requirements is poorly characterized in this population. /The authors/ administered intravenous acyclovir to preterm and term infants <31 days postnatal age and collected plasma samples. /Researchers/ performed a population pharmacokinetic analysis. The primary pharmacodynamic target was acyclovir concentration >/= 3 mg/L for >/=50% of the dosing interval. The final model was simulated using infant data from a clinical database. The analysis included 28 infants (median 30 weeks gestation). Acyclovir pharmacokinetics was described by a 1-compartment model: clearance (L/hr/kg) = 0.305 x (postmenstrual age (PMA)/31.3 weeks). This equation predicts a 4.5-fold increase in clearance from 25 to 41 weeks PMA. With proposed dosing, the pharmacodynamic target was achieved in 91% of infants: 20 mg/kg every 12 hr in infants <30 weeks PMA; 20 mg/kg every 8 hours in infants 30 to <36 weeks PMA; 20 mg/kg every 6 hr in infants 36-41 weeks PMA. Acyclovir clearance increased with infant maturation. A dosing strategy based on PMA accounted for developmental changes in acyclovir disposition to achieve the surrogate pharmacodynamic target in the majority of infants.

/SIGNS AND SYMPTOMS/ Overdoses involving ingestions of up to 100 capsules (20 g) have been reported. Adverse events that have been reported in association with overdosage include agitation, coma, seizures, and lethargy. Precipitation of acyclovir in renal tubules may occur when the solubility (2.5 mg/mL) is exceeded in the intratubular fluid. Overdosage has been reported following bolus injections or inappropriately high doses, and in patients whose fluid and electrolyte balance were not properly monitored. This has resulted in elevated BUN and serum creatinine, and subsequent renal failure. In the event of acute renal failure and anuria, the patient may benefit from hemodialysis until renal function is restored.

/SIGNS AND SYMPTOMS/ Aciclovir, like other anti-HIV nucleoside analogues, has been associated with a rare (1 in 10(+5) to 1 in 10(+6) patients) idiosyncratic syndrome of a progressive increase in the activity of liver enzymes in serum, fulminating hepatic steatosis and lactic acidosis. Failure to discontinue the drug can lead to death.

For more Human Toxicity Excerpts (Complete) data for ACYCLOVIR (16 total), please visit the HSDB record page.

The Approved Drug Products with Therapeutic Equivalence Evaluations identifies currently marketed prescription drug products, including acyclovir, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act.

The Approved Drug Products with Therapeutic Equivalence Evaluations identifies currently marketed prescription drug products, including acyclovir sodium, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act. /Acyclovir sodium/

Aciclovir is used intravenously in the treatment of severe initial and recurrent mucocutaneous infections caused by HSV-1, HSV-2 and varicella-zoster virus (chickenpox virus) in adults and children. It is also the drug of choice for treatment of herpes simplex encephalitis.

THERAPEUTIC CATEGORY (VETERINARY): Antiviral

MEDICATION

Antiviral Agents

Use (kg) in Switzerland (2009): >250

Guanine is alkylated with 2-(chloromethoxy)ethylbenzoate and the resulting ester hydrolyzed to the product.

Reaction of 2,6-dichloro-9-(2-benzoyloxyethoxymethyl) purine with methanolic ammonia, followed by treatment with nitrous acid and then with methanolic ammonia yields acyclovir.

Topical: Ointment: 5%, Zovirax (Biovail)

Oral: Capsules: 200 mg Zovirax (with parabens), (GlaxoSmithKline); Suspension: 200 mg/5mL Acyclovir Suspension (with parabens), (Alpharma), Zovirax (with glycerin parabens and sorbitol), (GlaxoSmithKline); Tablets: 400 mg Zovirax (with povidone), GlaxoSmithKline, 800 mg Zovirax (with povidone), GlaxoSmithKline.

Acyclovir sodium: Parenteral: For injection, concentrate, for IV infusion only: 25 mg (of acyclovir) per mL (500 mg, 1 g) Acyclovir Sodium Injection (Mayne), 50 mg (of acyclovir) per mL (500 mg, 1 g) Acyclovir Sodium Injection (American Pharmaceutical Partners), For Injection, for IV infusion only: 500 mg (of acyclovir) Acyclovir Sodium for Injection (Abbott, American Pharmaceutical Partners, Bedford), Zovirax (GlaxoSmithKline), 1 g (of acyclovir) Acyclovir Sodium for Injection (Abbott, Bedford), Zovirax (GlaxoSmithKline).