CMV retinitis may be associated with CMV disease elsewhere in the body. The Vitrasert Implant provides localized therapy limited to the implanted eye. The Vitrasert Implant does not provide treatment for systemic CMV disease. Patients should be monitored for extraocular CMV disease.

As with any surgical procedure, there is risk involved. Potential complications accompanying intraocular surgery to place the Vitrasert Implant into the vitreous cavity may include, but are not limited to, the following: vitreous loss, vitreous hemorrhage, cataract formation, retinal detachment, uveitis, endophthalmitis, and decrease in visual acuity.

Following implantation of the Vitrasert Implant, nearly all patients will experience an immediate and temporary decrease in visual acuity in the implanted eye which lasts for approximately two to four weeks post-operatively. This decrease in visual acuity is likely a result of the surgical implant procedure.

As with all intraocular surgery, sterility of the surgical field and the Vitrasert Implant should be rigorously maintained. The Vitrasert Implant should be handled only by the suture tab in order to avoid damaging the polymer coatings since this could affect release rate of ganciclovir inside the eye. The Vitrasert Implant should not be resterilized by any method.

A high level of surgical skill is required for implantation of the Vitrasert Implant. A surgeon should have observed or assisted in surgical implantation of the Vitrasert Implant prior to attempting the procedure.

Information for Patients

The Vitrasert Implant is not a cure for CMV retinitis, and some immunocompromised patients may continue to experience progression of retinitis with the Vitrasert Implant. Patients should be advised to have ophthalmologic follow-up examinations of both eyes at appropriate intervals following implantation of the Vitrasert Implant.

As with any surgical procedure, there is risk involved. Potential complications accompanying intraocular surgery to place the Vitrasert Implant into the vitreous cavity may include, but are not limited to, the following: intraocular infection or inflammation, detachment of the retina, and formation of cataract in the natural crystalline lens.

Following implantation of the Vitrasert Implant, nearly all patients will experience an immediate and temporary decrease in visual acuity in the implanted eye which lasts for approximately two to four weeks post-operatively. This decrease in visual acuity is likely a result of the surgical implant procedure.

The Vitrasert Implant only treats eyes in which it has been implanted. Additionally, because CMV is a systemic disease, patients should be monitored for extraocular CMV infections (e.g., pneumonitis, colitis) in the body.

Patients should be advised that ganciclovir has caused decreased sperm production in animals and may cause infertility in humans. Women of childbearing potential should be advised that ganciclovir causes birth defects in animals and should not be used during pregnancy.

Patients should be advised that ganciclovir has caused tumors in animals. Although there is no information from human studies, ganciclovir should be considered a potential carcinogen.

Drug Interactions

No drug interactions have been observed with the Vitrasert Implant. There is limited experience with use of retinal tamponades in conjunction with the Vitrasert Implant.

Carcinogenesis, Mutagenesis

Ganciclovir was carcinogenic in the mouse at oral doses of 20 and 1000 mg/kg/day. At the dose of 1000 mg/kg/day there was a significant increase in the incidence of tumors of the preputial gland in males, forestomach (nonglandular mucosa) in males and females, and reproductive tissues (ovaries, uterus, mammary gland, clitoral gland, and vagina) and liver in females. At the dose of 20 mg/kg/day, a slightly increased incidence of tumors was noted in the preputial and harderian glands in males, forestomach in males and females, and liver in females. Except for histiocytic sarcoma of the liver, ganciclovir-induced tumors were generally of epithelial or vascular origin. Although the preputial and clitoral glands, forestomach, and harderian glands of mice do not have human counterparts, ganciclovir should be considered a potential carcinogen in humans.

Ganciclovir increased mutations in mouse lymphoma cells and DNA damage in human lymphocytes in vitro at concentrations between 50-500 and 250-2000 µg/mL, respectively. In the mouse micronucleus assay, ganciclovir was clastogenic at doses of 150 and 500 mg/kg (IV) (2.8 - 10x human exposure based on AUC) but not 50 mg/kg (exposure approximately comparable to the human based on AUC). Ganciclovir was not mutagenic in the Ames Salmonella assay at concentrations of 500-5000 µg/mL.

Impairment of Fertility

Ganciclovir caused decreased mating behavior, decreased fertility, and an increased incidence of embryolethality in female mice following intravenous doses of 90 mg/kg/day. Ganciclovir caused decreased fertility in male mice and hypospermatogenesis in mice and dogs following daily oral or intravenous administration of doses ranging from 0.2-10 mg/kg.

Pregnancy: Teratogenic Effects: Pregnancy Category C

Ganciclovir has been shown to be embryotoxic in rabbits and mice following intravenous administration and teratogenic in rabbits. Fetal resorptions were present in at least 85% of rabbits and mice administered 60 mg/kg/day and 108 mg/kg/day, respectively. Effects observed in rabbits included: fetal growth retardation, embryolethality, teratogenicity, and/or maternal toxicity. Teratogenic changes included cleft palate, anophthalmia/microphthalmia, aplastic organs (kidney and pancreas), hydrocephaly, and brachygnathia. In mice, effects observed were maternal/fetal toxicity and embryolethality.

Daily intravenous doses of 90 mg/kg administered to female mice prior to mating, during gestation, and during lactation caused hypoplasia of the testes and seminal vesicles in the month-old male offspring, as well as pathologic changes in the nonglandular region of the stomach (see Carcinogenesis, Mutagenesis subsection).

Although each Vitrasert Implant contains from 4.5 to 6.4 mg of ganciclovir, which is released locally in the vitreous, there are no adequate and well-controlled studies in pregnant women on the effects of the Vitrasert Implant. Therefore, the Vitrasert Implant should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.

Nursing Mothers

It is not known whether ganciclovir from the Vitrasert Implant is excreted in human milk. Daily intravenous doses of 90 mg/kg administered to female mice prior to mating, during gestation, and during lactation caused hypoplasia of the testes and seminal vesicles in the month-old male offspring, as well as pathologic changes in the non-glandular region of the stomach. Because many drugs are excreted in human milk and, because carcinogenicity and teratogenicity effects occurred in animals treated with ganciclovir, mothers should be instructed to discontinue nursing if they have a Vitrasert Implant.

Pediatric Use

Safety and effectiveness in pediatric patients below 9 years of age have not been established.

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