Quick Guide to AIDS-Related CMV
Treatment for CMV Retinitis
(Systemic)
Resistance/Intolerance to
Treatment
Treatment for CMV
Gastrointestinal Disease
Treatment for General CMV
Disease in Children
Treatment for CMV
Neurologic Disease
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Pathogen:
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Sites of Infection:
Most frequently the retina, colon and esophagus in AIDS patients; also the lungs, brain, heart, thymus, pancreas, larynx, thyroid, kidneys, gallbladder, liver, and adrenal glands.
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Symptoms:
CMV Encephalitis:
While CMV is not considered a neutropenic disease, cases of CMV
encephalitis
have been reported.Symptoms include headache, confusion, and
fever.
CMV Esophagitis:
Most commonly includes painful
swallowing or
the sense of food sticking in the throat. May also include chest pain
or hiccups.
CMV Colitis:
May include intermittent or persistent diarrhea with cramping,
abdominal pain,
involuntary rectal spasms, weight loss and general status
deterioration.
CMV Gastritis:
May be asymptomatic but often results in
severe
continuous upper abdominal pain fever, hemorrhage or obstruction.
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Diagnosis:
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Treatment for CMV Retinitis (Systemic):
Foscarnet appears equivalent to ganciclovir in limiting the spread of CMV retinitis; however, it may confer a survival benefit over ganciclovir in patients with advanced HIV, presumably because of its intrinsic anti-HIV activity. The NEI/ACTG study for ocular complications of AIDS (Meinert et al.) randomized 234 patients with CMV retinitis to receive ganciclovir (107 patients) or foscarnet (127 patients). The trial was suspended after 19 months when a significant mortality benefit associated with foscarnet was observed. Although both drugs were equally effective in halting progression of CMV retinitis, the median survival was 12.6 months in the foscarnet group and 8.5 months in the ganciclovir group. This survival benefit could not be attributed to differences in antiretroviral therapy between the two groups. However, foscarnet was associated with substantial toxicity: 22/39 treatment switches from foscarnet to ganciclovir were attributed to foscarnet toxicity, while only 1/14 switches from ganciclovir to foscarnet was attributed to ganciclovir toxicity.
Ganciclovir has been demonstrated to delay progression of peripheral CMV retinitis in AIDS patients (Peripheral CMV retinitis is not immediately sight threatening). Spector et al. randomized 22 patients to deferred treatment and 13 to immediate treatment with ganciclovir (5 mg/kg bid for 14 days followed by 5 mg/kg qd for 14 weeks). Patients in the deferred group were offered ganciclovir if retinitis progressed, 10/13 in the immediate group, and 20/22 in the deferred group had progressive CMV retinitis. The median time to progression was 13.5 days for the deferred group versus 49.5 days for the immediate treatment group (P = 0.001).
The results of a clinical trial in patients who required retreatment of CMV after maintenance therapy has failed were recently reported (Jabs et al.). The study (ACTG 228) compared ganciclovir to foscarnet to a foscarnet/ganciclovir combination in recently treated patients who reported CMV disease progression. A total of 271 patients were randomized to one of three arms; foscarnet (90 mg/kg q 12h x 14 days with 120 mg/kg qd maintenance), ganciclovir (5.0 to 7.5 mg/kg q 12h x 14 days with 10 mg/kg qd maintenance), or a combination of foscarnet (90 mg/kg q 12h x 14 days with 90 mg/kg qd maintenance) and ganciclovir (5 mg/kg qd x 14 days with 5 mg/kg qd maintenance therapy). CMV retinitis progression was reported at 4.8 months in the combination group, 2.1 months in those who received ganciclovir alone, and 1.6 months in those who received foscarnet alone (P = 0.00002). 'Those who reported disease progression in the monotherapy groups were switched to the alternate monotherapy treatment; those who progressed in the combination group received higher doses of both drugs. For patients originally receiving either ganciclovir or foscarnet monotherapy, a median of 1.6 relapses were reported. There was no significant difference between switching to the alternate treatment and remaining on the initial regimen. However rates of visual field loss were significantly lower in the combination group (16- degrees/month compared to 18- and 31- degrees/month) (P = 0.003). Quality of life scores reported were significantly better in the ganciclovir monotherapy group.
MSL-109, a human anti-CMV monoclonal antibody, is being studied in combination with either foscarnet or ganciclovir for the treatment of retinitis (ACTG 266). This phase II double-blind, placebo-controlled trial will randomize patients to one of two doses of MSL-109 or placebo to be administered concomitantly with standard induction therapy. A second study is being conducted by the Studies of the Ocular Complications of AIDS (SOCA) of the National Eye Institute (NEI) with the ACTG (ACTG 294). This trial compares MSL-109 (60 mg IV once every two weeks) to placebo in 167 patients receiving standard therapy for either newly diagnosed or relapsed CMV retinitis.
An intraocular ganciclovir implant has been reported to delay progression of peripheral CMV retinitis. A New Drug Application (NDA) has been submitted to the Food and Drug Administration and has been reviewed by an advisory committee to the FDA, which has recommended approval.
The Chiron Ganciclovir Implant Study Group (Kupperman et al.) has reported the results from a randomized trial examining two release rates of an intraocular ganciclovir implant (1µg/h and 2 µg/h) versus standard dose intravenous ganciclovir. A total of 188 patients with symptomatic CMV retinitis were evenly divided to receive either of the two intraocular ganciclovir doses or IV ganciclovir. While no significant differences in disease progression were reported between the two intraocular dose groups, significant delays in disease progression were reported after 182 days in the 2 µg/h ganciclovir implant group and 72 days in the ganciclovir group (P = 0.000 1). The rate of other eye involvement was 40% in the implant group and 16% in the IV group (NS). Extraocular disease occurred in 15% of the patients in the implant groups combined. There was a slight decrease in visual acuity in the immediate post-operative period for implant patients, although visual acuity returned to preoperative levels within 24 weeks. No statistical differences in survival were reported. Incidences of endophthalmitis, retinal detachment, and vitreous hemorrhage were higher in the implant groups. However, due to the use of G-CSF required by neutropenic patients receiving ganciclovir infusions, the incidences of catheter related sepsis and severe nausea was higher in the IV group.
Martin et al. randomized twenty six patients (30 eyes) to either immediate treatment with a 1 µg/h intraocular ganciclovir implant or deferreded treatment None of the patients enrolled had received prior treatment for CMV retinitis. The median time to progression of retinitis was 15 days in the deferred group (n = 16) versus 226 days in the immediate treatment group (n = 14)(P < .00001). In the entire study population, biopsy- proven visceral CMV disease developed in 8/26 (31%) patients and 67% of the 26 patients developed retinitis in the fellow eye. Seven patients (18%) suffered a treatment-induced retinal detachment, with five occurring between days 30 and 64. There were 2 cases of persistent hypotony reported.
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Resistance/Intolerance to Treatment:
The manufacturer of HPMPC (cidofovir), a cytosine-derived nucleotide analogue with a long intracellular half-life, has submitted a New Drug Application (NDA) to the Food and Drug Administration seeking approval of intravenous cidofovir for patients intolerant or failing ganciclovir or foscarnet. HPMPC must be administered with probenecid to protect against renal toxicities.
Lalezari et al. recently presented data from a study comparing two maintenance doses of HPMPC (3 mg/kg vs. 5 mg/kg every other week) in 60 patients who failed induction therapy with either ganciclovir or foscarnet. AR patients received weekly HPMPC (5 mg/kg) for two weeks as induction therapy. No statistically significant difference was seen between the two maintenance doses; a median of 115 days to progression was reported in the 5 mg/kg group and a median of 49 days to progression in the 3 mg/kg group. Adverse reactions due to concomitant of probenecid were reported in 29/60 (48%) patients enrolled.
Lalezari et al. have reported results from a phase II/III immediate versus deferred trial of intravenous HPMPC. In this study, 40 patients were randomized to receive either immediate treatment with HPMPC (5 mg/kg every week for two weeks) or placebo until disease progressed. Time to progression in the immediate treatment group was 120 days, whereas time to progression in the deferred treatment arm was 22 days. Eleven patients (27%) reported renal toxicities. Toxicities attributed to concomitant probenecid use were reported in 38% of patients enrolled.
Phase I/II dose-escalating studies of intravenous HPMPC have been reported in subjects with CMV viruria. Polis et al. administered HPMPC 0.5, 1.5 or 5 mg/kg weekly or twice weekly, with or without probenecid, to 20 patients. CMV urine cultures became negative in 4/6 evaluable patients receiving the highest doses of HPMPC. The maximum tolerated dose was determined to be about 5 mg/kg weekly, with proteinuria, glycosuria, and creatinine elevations being the dose limiting toxicities. Concomitant probenecid administration appeared to protect against renal toxicity.
Two recently reported small case studies (Kirsch et al.) of intravitreal HPMPC (cidofovir) suggest that prolonged control of CMV retinitis may be achieved with a single injection. In the first study, patients who had failed or were non- compliant with standard therapy received one 10, 20, 40 or 100 µg injection with concomitant oral probenecid. Patients were assigned to doses in a non- randomized fashion. The median progression time reported in those patients who received a single 20 µg injection was 64 days; data from other diseases were invaluable. No cases of endophthalmitis were reported. In the second case study, 17 patients (24 eyes) received a single dose of intravitreal HPMPC (20 µg) with oral probenecid. The median time to progression after the initial injection was 55 days. Disease progression was reported in 8/24 eyes treated. These eyes were retreated; median time to progression in retreated eyes was 64 days.
ISIS 2922, an antisense compound for the intravitreal treatment of CMV retinitis in patients who have failed standard therapy, is currently under investigation. In May 1995, the manufacturer suspended patient recruitment because of safety concerns, including the development of decreased peripheral vision with retinal pigment epithelial cell stippling in 20% of patients receiving intravitreal injections at the highest dose. Two phase III trials are currently enrolling. For patients With CMV intolerant or failing standard therapy who do not qualify for the two trials, a compassionate use program is available.
A phase I/II dose-ranging study of ISIS 2922 has been reported. The manufacturer reports that 10 patients with CMV retinitis were treated intravitreally with ISIS 2922 once a week for 4 weeks and every two weeks thereafter. Two patients received 75 µg (low-dose), 3 received 150 µg (middle- dose) and 5 received 300 µg (high-dose). Responses were observed in 0/2, 2/3, and 5/5 in the low, middle, and high dose groups, respectively. Side effects observed were vitreal inflammation, temporary loss of color vision and ocular discomfort.
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Treatment for CMV Gastrointestinal
Disease:
A randomized controlled study compared ganciclovir with foscarnet for induction therapy in patients with CMV gastrointestinal disease (Blanshard et al.). Nineteen patients were randomized to receive ganciclovir and 25 patients to foscarnet. Mean duration of treatment was 15 days. Endoscopic improvement was observed in 84% and 81% of ganciclovir and foscarnet subjects, respectively. Adverse drug effects occurred with equal frequency in both groups.
Dietrich et al. treated 10 patients, 5 with upper GI CMV disease and 5 with lower GI disease with foscarnet (90 mg/kg IV q12h). Mild edema was noted in 2/10 patients (20%) but resolved. 8/10 patients (80%) required 6 weeks of treatment for complete response. 9/10 (90%) responded histopathologically (P =.0067) and 9/10 responded endoscopically (P =.0004).
A phase III randomized, open-label trial of foscarnet for the treatment of CMV colitis is currently underway.
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Treatment for General CMV Disease in
Children:
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Treatment for CMV Neurologic Disease:
A pilot study is being developed by the AIDS Clinical Trials Group (ACTG 305) of cerebrospinal fluid penetration and response to ganciclovir and foscarnet in presumed CMV neurologic disease.
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Maintenance Treatment :
Drew et al. compared oral and intravenous ganciclovir in 123 patients with newly diagnosed CMV retinitis. 123 patients received induction therapy with IV ganciclovir for three weeks. 117 patients had stable CMV after induction therapy and were entered in the maintenance phase of the study. 57 were randomized to receive induction and maintenance therapy with intravenous ganciclovir (5 mg/kg/day) and 60 were randomized to oral ganciclovir 1,000 mg tid for 20 weeks. When photographic exams were compared on a blinded basis, there was no statistical difference in the mean time to progression (62 days in the IV group vs. 57 days in the oral group. However, median time to progression was 49 days for the IV group and 29 days for the oral group. When progression was monitored by unmasked fundoscopic exam, the mean time to progression was 98 days in the IV group vs. 68 days in the oral group (P = 0.027). No statistically significant difference in visual acuity was observed between groups. Twenty (34%) patients in the IV group compared to 12 (19%) in the oral group developed neutropenia (NS); 13 patients (22%) in the IV group developed sepsis compared to 3 (S%) in the oral group (P < 0.05).
A European study by Volker et al. enrolled 159 patients with newly diagnosed CMV retinitis to compare oral ganciclovir to IV ganciclovir for the maintenance of CMV retinitis. After induction therapy with IV ganciclovir, patients were randomized to receive in a 2:1 ratio oral ganciclovir (500 mg PO 6 x d) or IV ganciclovir (5 mg/kg IV qd) for 20 weeks. When photographic exams were compared on a blinded basis, there was no statistical difference in the mean time to progression (62 days in the IV group vs. 51 days in the oral group). When progression was monitored by unmasked fundoscopic exam, the mean time to progression was 109 days in the IV group vs. 86 days in the oral group (P = 0.02). GI disturbances were more frequent in the oral treatment group, and neutropenia and leukopenia occurred more frequently in the IV group.
In a study by Squires et al., 220 patients with stable CMV retinitis who were receiving intravenous ganciclovir for <4 months were randomized to receive IV ganciclovir 5 mg/kg/d (n = 70), oral ganciclovir 500 mg six times daily (n = 74) oral ganciclovir 1,000 mg three times daily (n = 76) for 20 weeks. When photographic exams were compared on a blinded basis, the mean time to progression was 66, 53, and 54 days in the IV, 500 mg PO, and 1,000 mg PO groups, respectively (difference not significant). When progression was monitored by unmasked fundoscopic exam, the mean time to progression was 99 days in the IV group vs. 75 days in the 500 mg oral group (P = 0.023) vs. 77 days for the 1,000 mg oral groups (P = 0.082). No statistically significant differences in mortality, treatment failure, ophthalmic change, or neutropenia were observed among groups. Sepsis occurred more frequently in the IV group.
Jacobson et al. (1992) treated 30 patients with CMV retinitis who completed a two-week induction course with ganciclovir with either combined or alternating ganciclovir and foscarnet. Patients were randomized to either ganciclovir (3.75 mg/kg/d) plus foscarnet (60 mg/kg/d), or ganciclovir (6 mg/kg/d) alternating daily with foscarnet (120 mg/kg/d). 12/15 subjects in the combination group and 15/15 in the alternating group were evaluable. Median time to retinitis progression was >12 weeks for the combination group and >20 weeks for the alternating groups (difference not significant). Grade 4 neutropenia was seen in 6/12 patients on the combination and 4/15 on the alternating regimen.
In a randomized dose-comparison study of maintenance foscarnet (90 or 120 mg/kg/day), Jacobson et al. (1993) demonstrated that survival was significantly greater at the higher dose without statistically significant evidence of increased serious toxicity. However, there was significantly greater minor toxicity and a trend toward greater serious toxicity at the higher dose. 32 patients who completed a two-week induction treatment with foscarnet (60 mg/kg three times daily) were randomized; 15 patients received foscarnet 90 mg/kg/day and 17 received 120 mg/kg/day. Median survival ft-from the time of study entry was 157 days and 336 days for subjects in the 90 and 120 mg/kg/day groups, respectively (P <0.001). Transient ionized hypocalcemia occurred significantly more often in the 120 mg/kg group.
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Prophylaxis:
Spector et al. randomized 725 patients with CD4+ counts < 50 cells/mm3 or CD4+ counts < 100 cells/mm3 and a history of an AIDS-related opportunistic infection to receive oral ganciclovir 1,000 mg q8h or placebo. After 20 months, the Data Safety Monitoring Board (DSMB) halted the trial due to significant differences between the two arms and all participants were offered open-label ganciclovir. The mean CD4+ count at the time of entry was 26 cells/mm3; median CD4+ count at baseline was 21 cells/mm3. All patients enrolled were followed by an ophthalmologist and had a Careful eye exam every three months regardless of symptoms. At the time of analysis, CMV disease occurred in 76/239 (30%) patients in the placebo group and 76/486 (16%) patients in the ganciclovir group (P =.0001). Death occurred in 66/239(29%) patients in the placebo group and 109/486 (22%) patients in the ganciclovir group (P =.08). Drew et al. have recently reported that the prevalence of ganciclovir resistance was low (< 1%) after a mean of 8.3 months of prophylaxis.
Brosgart et al. recently reported the results of a randomized, placebo-controlled trial of the safety and efficacy of oral ganciclovir for prophylaxis of CMV disease (CPCRA 023). 954 patients with fewer than100 CD4+ cells/mm3 were randomized to either 1,000 mg q8h oral ganciclovir (n = 622) or placebo (n = 332). The mean CD4+ count upon entry was 44 cells/mm3; median CD4+ count at baseline was 34 cells/mm3. All patients were followed by a primary care physician and referred to an ophthalmologist if symptoms were reported by the patient. No statistical difference was reported between the two groups in terms of CMV disease development or survival. 99/622 (15.9%) in the ganciclovir group and 55/332 (16.7%) in the placebo group developed CMV disease. Reported deaths were 221/622 (35.5%) and 132/332 (37.7%), respectively. The development of CMV retinitis was reported in 74/622 (11.9%) patients receiving ganciclovir and 44/332 (13.3%) patients receiving placebo. CMV colitis rates were 21/622 (3.4%) and 12/332 (3.6%), respectively.
Valacyclovir has been found to be moderately effective in preventing CMV disease in HIV-positive people (Feinberg et al). ACTG 204 was a phase III randomized, placebo-controlled study of valacyclovir versus two doses of acyclovir for the prevention of CMV disease. While the trial was prematurely closed due to higher monthly rates in the valacyclovir group, the differences were not statistically significant. This study treated 1227 patients with CD4+ cell counts under 100 cells/mm3 with either valacyclovir (2 g qid or acyclovir (800 mg qid or 400 mg bid). The diagnosis of CMV retinitis was based on clinical examination by an ophthalmologist every 6 months. Confirmed CMV endpoints were reached in 51/523 (11.7%) in the valacyclovir group and 123/174 (17.5%) in the acyclovir groups combined (P = 0.03).
Oral acyclovir is not effective in preventing CMV disease in HIV infected people. Drew et al. randomized 93 HIV-positive symptomatic patients to receive AZT 600 mg daily with acyclovir 4,800 mg PO /d (n = 52) or with placebo (n = 41) to determine if high-dose ACV suppresses CMV viruria. Urine was obtained at 3 month intervals for at least 6 months. The addition of acyclovir did not suppress CMV excretion in the urine in these patients.
Youle et al. enrolled 302 CMV-seropositive subjects with CD4 count
<150/mm3 in a double-blind placebo-controlled trial
study in oral
high-dose acyclovir (800 mg PO four times daily for 48 weeks) in
combination
with anti-retroviral treatment for the prevention of CMV disease. All
patients
received AZT, ddl or AZT/ddC; in addition half received acyclovir and
half
received placebo. After more than one year follow-up 16/153
acyclovir-
recipients and 9/149 placebo recipients developed confirmed CMV
disease
(difference not significant).
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REFERENCES:
Boivin G et al. Evaluation of the cytomegalovirus DNA load and
polymorphonuclear leukocytes (PMNL) of HIV-infected patients
using
quantitative PCR (Q-PCR). Abstract #11, 3rd Conf on Human Retro
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Cinque P et al. Ganciclovir therapy for cytomegalovirus infection of
the central
nervous system in AIDS patients: Monitoring by CMV-DNA detection
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Cochereau-Massin I et al. Intravitreal ganciclovir: a 3-year
experience.
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Cribbin K et al. Intravitreal ganciclovir in patients resistant to
ganciclovir and
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Crumpacker C et al. Oral vs. intravenous ganciclovir (GCV) as
maintenance
treatment of newly diagnosed cytomegalovirus retinitis (CMVR) in
AIDS. 1st Nat
Conf Hum Retrov, Abstract 538: 154, 1993.
Dieterich D et al. Ganciclovir treatment of cytomegalovirus colitis in
AIDS: A
randomized, double-blind, placebo-controlled multicenter study. JID
167: 278-
282, 1993.
Dietrich D et al. Treatment of gastrointestinal cytomegalovirus
infection using
twice daily administration of foscarnet in AIDS patients. 1st Nat Conf
Hum
Retrov Abstract 5l3: 146, 1993.
Drew WL et al. Oral ganciclovir as maintenance treatment for
cytomegalovirus
retinitis in patients with AIDS. NEJM 333: 615-20, 1995.
Drew WL et al. Failure of acyclovir to suppress excretion in
symptomatic HIV
antibody-positive patients. Abstract 1115, 32nd ICAAC, Anaheim,
1992.
Drew WL et al. Prevalence of ganciclovir resistant cytomegalovirus
during oral
ganciclovir prophylaxis. Abstract #LB 16, 3rd Conf on Human Retro
and Opport
lnfect, Washington DC, 1996.
Feinburg J et al. Phase III study of valacyclovir for cytomegalovirus
prophylaxis
in patients with advanced HIV disease. 35th ICAAC, Abstract #1214,
San
Francisco, 1995.
Jabs D et al. Combination therapy for retinitis: Results of ACTG 228.
20th ACTG,
Washington DC, 1995.
Jacobson MA et al. Phase II dose-ranging trial of foscarnet salvage
therapy for
cytomegalovirus retinitis in AIDS patients intolerant of or resistant to
ganciclovir (ACTG protocol 093). AIDS 8: 451-459, 1994.
Jacobson MA et al. A dose-ranging study of daily maintenance
intravenous
foscarnet therapy for cytomegalovirus retinitis in AIDS. JID 168: 444
448,
1993.
Jacobson MA et al. Randomized phase I study of combined vs.
alternating
foscarnet (PFA)/ganciclovir (GCV) maintenance therapy (Rx) for CMV
retinitis.
32nd ICAAC, Abstract #1223, 1992.
Kirsch LS et al. Phase I/II study of intravitreal cidofovir for the
treatment of
cytomegalovirus retinitis in patients with the acquired
immunodeficiency
syndrome. Am J Ophthalmol 119:466-76, 1995.
Kirsch LS et al. Intravitreal cidofovir treatment of cytomegalovirus
retinitis in
patients with acquired immune deficiency syndrome. Ophthalmology
102: 533-
42, 1995.
Kupperman B et al. A randomized controlled multicenter trial of
sustained-
release intraocular ganciclovir implant in AIDS patients with CMV
retinitis. 35th
ICAAC, Abstract #1215, San Francisco, 1995.
Lalezari J et al. A randomized controlled study of cidofovir for
relapsing
cytomegalovirus retinitis in patients with AIDS. 35th ICAAC, Abstract
#LB-9,
San Francisco, 1995.
Martin EF et al. Treatment of cytomegalovirus retinitis with an
intraocular
sustained -released ganciclovir implant. A randomized controlled
clinical trial.
Arch Ophthalmol 112: 1521-1539, 1994.
Meinert CL et al. Studies of the Ocular Complications of AIDS
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AIDS Clinical Trials Group. Mortality in patients with the acquired
immunodeficiency syndrome treated with either foscarnet or
ganciclovir for
cytomegalovirus retinitis. NEJM 326(4): 213-220, 1992.
Nightingale SD et al. An intraocular slow-releasing ganciclovir drug
delivery
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Polis M et al. A phase I/II dose escalation trial of (s)-1-[3-hydroxy-
2-
(Phosphonymethoxy)propylcytosine (HPMPC) in HIV-infected
persons with
CMV viruria. 33rd ICAAC Abstract #98, 1993.
Salzberger B el al. Foscarnet and ganciclovir combination therapy
for severe
CMV-disease in HIV-infected patients. Abstract PO-BO8-1233, IX Intl
Conf
AIDS, Berlin, 1993.
Spector S et al. Pharmacokinetics, safety, and antiviral profiles of oral
ganciclovir in persons infected with human immunodeficiency virus:
a phase
I/II study. JID 171:1431-7, 1995.
Spector S et al. A randomized, controlled study of intravenous
ganciclovir
therapy for cytomegalovirus peripheral retinitis in patients with
AIDS. JID 168:
557-563, 1993.
Squires K et al. Oral ganciclovir (POG) versus intravenous ganciclovir
(IVG)
maintenance therapy for cytomegalovirus (CMV) retinitis in patients
with AIDS:
preliminary results of a phase III study. 1st Nat Conf Hm Retrov,
Abstract 540:
154, 1993.
Verdejo J et al. Intravenous ganciclovir for cytomegalovirus
treatment (CMV)
retinitis. Abstract PoB 3175, VIII Intl Conf AIDS, Amsterdam 1992.
Volker K et al. Intravenous versus oral ganciclovir.
European/Austrailian
comparative study of efficacy and safety in the prevention of
cytomegalovirus
retinitis recurrence in patients with AIDS. AIDS 9: 471-477, 1995.
Youle M et al. Effects of high-dose acyclovir on herpesvirus disease
and survival
in patients with advanced HIV disease: a double-blind, placebo-
controlled study,
AIDS 8: 641-649, 1994.
Lalezari JP et al. The safety, pharmacokinetics, and anti-CMV activity
of weekly
HPMPC in HIV-positive patients excreting CMV. 1st Nat Conf Hum
Retrov,
Abstract 541: 154, 1993.
Leach CT et al. A longitudinal study of cytomegalovirus infection in
human
immunodeficiency virus type 1-seropositive homosexual men:
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Medina DJ et al. Ganciclovir antagonizes the anti-human
immunodeficiency
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Nelson M et al. Foscarnet in the treatment of cytomegalovirus
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Plotkin SA et al. Vaccines for varicella-zoster virus and
cytomegalovirus: recent progress. Science 265: 1393-1395, 1994.
Blanshard C et al. Treatment of AIDS-associated gastrointestinal
cytomegalovirus
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JID 172:622-8, 1995.
OTHER REPORTS:
Balfour H et al. A Randomized, placebo-controlled trial of oral
acyclovir for the
prevention of cytomegalovirus disease in recipients of renal
allografts. NEJM
320(21): 1381-7, 1990.
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