Iritis Associated with Intravenous Cidofovir

Iritis Associated with Intravenous Cidofovir Alice L Tseng, Clive B Mortimer, and Irving E Salit

OBJECTIVE:

To report two patients with AIDS and cytomegalovirus retinitis who developed iritis after receiving intravenous cidofovir. Both experienced recurrent symptoms upon rechallenge. CASE SUMMARIES: Two HIV-positive patients with cytomegalovirus retinitis infections previously controlled with intravenous ganciclovir or foscarnet were treated with intravenous cidofovir. Symptoms of iritis developed after the second or third dose of cidofovir. One patient experienced symptoms unilaterally, while the other patient had bilateral symptoms. In both patients, the iritis resolved with topical ophthalmic therapy, but recurred following subsequent infusions of cidofovir. Therapy with cidofovir was discontinued, and no further recurrences of iritis were noted. One patient had post-inflammatory fixed dilated pupils. CONCLUSIONS: Iritis can uncommonly occur in patients receiving intravenous cidofovir and oral probenecid. With prompt drug discontinuation and administration of topical corticosteroids and/or mydriatic agents, symptoms are usually reversible. KEY WORDS: cytomegalovirus, retinitis, iritis, cidofovir. Ann Pharmacother 1999;33:167-71.

C

idofovir (1-[(S)-3-hydroxy-2-(phosphonomethoxy) propyl]cytosine dihydrate) is a cytosine nucleotide analog with potent in vitro and in vivo activity against a variety of laboratory and clinical isolates of herpesviruses, including cytomegalovirus (CMV).1-4 Cidofovir diphosphate, the active intracellular metabolite, suppresses viral DNA synthesis by selectively inhibiting CMV DNA polymerase. Unlike acyclovir or ganciclovir, which require intracellular activation by virally encoded enzymes such as thymidine kinase, phosphorylation of cidofovir to its active form occurs via cellular enzymes, and is thus independent of virus infection. Cidofovir diphosphate has a long intracellular half-life (17–30 h), which allows for infrequent dosing. An injectable formulation (Vistide, Gilead Sciences, Inc.) for intravenous infusion has recently been approved in the US for the treatment of CMV retinitis in patients with AIDS.5

Alice L Tseng PharmD, HIV Pharmacotherapy Specialist, The Toronto Hospital; Lecturer, Faculty of Pharmacy, University of Toronto, Toronto, Ontario, Canada Clive B Mortimer MD, Staff Ophthalmologist, Department of Medicine, The Toronto Hospital Irving E Salit MD, Director, Immunodeficiency Clinic, Department of Medicine, The Toronto Hospital; Associate Professor, Faculty of Medicine, University of Toronto Reprints: Alice L Tseng PharmD, Immunodeficiency Clinic, CW-G315, The Toronto Hospital, 101 College St., Toronto M5G 2C4, Ontario, Canada, FAX 416/3404890, E-mail [email protected]

In Phase II/III trials, the major dose-limiting toxicity noted with intravenous cidofovir was dose-dependent nephrotoxicity, including proteinuria, azotemia, elevations in serum creatinine, and rarely, metabolic acidosis and Fanconi’s syndrome.5,6 Other major adverse reactions include neutropenia, ocular hypotony, fever, bacterial infection, dyspnea, nausea/vomiting, diarrhea, and asthenia.5,6 Oral probenecid is routinely recommended with cidofovir in order to decrease the risk of nephrotoxicity and ocular toxicity.5 Probenecid also decreases the uptake of cidofovir into the ciliary body epithelium, thus reducing the potential for adverse ocular effects, including ocular hypotony and iritis. While adverse ocular effects, primarily iritis, have been frequently reported in conjunction with intravitreal cidofovir administration,7-9 such events have not been observed commonly with treatment involving the intravenous formulation of cidofovir. We report two patients with AIDS who developed recurrent iritis while receiving intravenous cidofovir for the management of CMV retinitis. CASE REPORTS

CASE 1 The patient was a 33-year-old HIV-positive white man with hepatic lymphoma in remission since 1993 and bilateral CMV retinitis since November 1993. At that time the CD4+ count was 28 cells/mm3. The CMV retinitis was treated initially with intravenous foscarnet, then ganciclovir. The retinitis was stable until July 1995 when he received intraocular foscarnet because of advancing retinitis. The retinitis came under control again until March 1996 when the patient again required treatment with intraocular foscarnet. Combination intravenous therapy with ganciclovir and foscarnet was used and the retinitis went into remission again. For convenience, he opted to switch his therapy to cidofovir plus probenecid. At this time, the visual acuity was 6/6 in both eyes. He received the first intravenous dose in July 1996 and a second dose one week later (Table 1). Two weeks after the second cidofovir dose, the patient developed symptoms of ocular pain and inflammation, and ocular examination findings later supported the diagnosis of iritis. At that time, the retinitis was completely inactive. He was treated with topical prednisolone and homatropine, which resulted in improvement of the iritis. In September 1996 he received the third cidofovir treatment and two days later had a reactivation of iritis. The patient was retreated with topical ophthalmic therapy. One week later, the iritis was improving, but he noted an influenza-like illness with fatigue and headaches. In addition, the patient’s renal function had declined significantly (creatinine clearance decreased from 87 mL/min at baseline to 31 mL/min 10 days after the third cidofovir infusion). At the end of September, he received a transfusion and the fourth and final infusion of cidofovir, which was followed by se-

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vere worsening of the iritis two days later with sudden decline in vision and severe ocular pain. Ten days later, the iritis had become very severe, and the patient was legally blind. At this time, his renal function declined again. In addition to topical therapy, the patient required subconjunctival injections of a mydriatic, but the pupil remained fixed. Visual acuity worsened and was only 6/12 in both eyes. Intensive topical and subconjunctival therapy was continued and six weeks later the iritis had almost completely resolved. The pupil remained fixed and the visual acuity in the right eye was 6/12 and in the left eye was 6/9. Concomitant medications at the time of the cidofovir therapy included ritonavir, trimethoprim/sulfamethoxazole, didanosine, acyclovir, and later, zidovudine and lamivudine. After discontinuing the cidofovir, the patient was switched back to combination therapy using ganciclovir plus foscarnet. His renal function returned to normal (serum creatinine 1.12 mg/dL) one month after the last cidofovir dose. CASE 2 A 30-year-old white man, HIV-positive since 1985, was diagnosed with CMV retinitis in his right eye in May 1995. He was initially treated with intravenous foscarnet, and the retinitis was stable until February 1996, when he was again treated with foscarnet due to disease progression. Intravenous ganciclovir was subsequently added for synergistic antiviral effect and the retini-

tis stabilized. Ten months later, foscarnet was discontinued, and he continued with intravenous ganciclovir. In February 1997, ganciclovir was discontinued, and intravenous cidofovir was started (Table 2). He received cidofovir 5 mg/kg with probenecid as per the manufacturer’s protocol. At this time, the patient had no vision with his right eye; left eye visual acuity was 6/6. He received a second dose one week later and a third dose two weeks after that. Six days after his third cidofovir infusion, the patient complained of a red, painful right eye. Upon examination, the patient had diffuse conjunctival injection and a reactive pupil, with no hemorrhage seen. He was prescribed topical ophthalmic therapy with perilimbal injection, and the symptoms resolved one week later. Because of the severity of the ocular symptoms, both the physician and the ophthalmologist advised against continuing cidofovir and suggested resuming ganciclovir therapy. However, the patient refused and insisted on continuing with cidofovir. The patient received two additional doses of cidofovir two weeks apart. In May 1997, he experienced a decline in his renal function (increased serum creatinine to 2.49 mg/dL) as well as recurrent bilateral iritis. The cidofovir was discontinued and intravenous ganciclovir was restarted. At the four months followup, the patient’s renal function had returned to normal. His ocular symptoms gradually resolved over a period of six months, with no further episodes of iritis. Concomitant medications at the time of cidofovir use included ethambutol, clarithromycin, trimetho-

Table 1. Cidofovir-Associated Uveitis: Time Course and Ocular Findings in Patient 1 CDV Dose Number (1996)

Time Since Last CDV Injection (d)

Baseline 1; July 29 2; August 6

15 17 37

3; September 18

4; September 30

Ocular Findings/ Visual Acuity

Symptoms none

OD 6/6 OS 6/6

PERL, no RAPD, stable CMV retinitis

vision subjectively unchanged ocular pain, redness

OD 6/7 OS 6/6

eyes stable; no new activity

OD 6/15 OS 6/9

increased inflammation bilaterally; 1–2+ cells, 1+ flare, iris red and dilated

iritis improved

OD 6/12 (PH) keratitic precipitates in both eyes OS 6/9 –2 (PH)

3 7

reactivation of iritis iritis resolved

8

influenza-like illness; declining renal function severe worsening of iritis; sudden decline in vision

3 11

slight improvement in iritis uveitis between 1+ 2+

30

vision improving

no new visual symptoms

12 wk 16 wk

OD 6/12 OS 6/9 OD 6/7; 3.1 OS 6/9; 3.1

OD CF3 OS CF3 (legally blind)

12 23

8 wk

Ocular Examination

no ocular complaints

OD 6/12 OS 6/12 OD 6/9; 3.2 OS 6/15; 3.3 OD 6/12; 3.2 OS 6/9; 3.3 OD 6/9 +2 OS 6/12 OD 6/9; 3.1 OS 6/12; 3.1

Intervention

homatropine bid, voltaren tid add Pred Forte

Pred Forte for 5 d, then discontinued

eyes stable CMV stable in both eyes

severe anterior and posterior uveitis; no reactivation of CMV pupils partially dilated pupil still bound down uveitis: much less flare, no cells; pupils fixed from iritis; CMV stable OD: no flare or cells; OS: minimal flare and cells; red, dilated, fixed pupils OD: minimal flare, no cells; OS: mild flare, occasional cell both eyes stable

Pred Forte hourly while awake, atropine 1% tid continue atropine repeat subconjunctival injections of mydriatic in each eye taper local treatments

uveitis resolving

uveitis resolving

CDV = cidofovir; CF = counts fingers; CMV = cytomegalovirus; OD = right eye; OS = left eye; PERL = pupils equal, reactive to light; PH = pinhole; RAPD = relative afferent pupillary defect.

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prim/sulfamethoxazole, fluconazole, sertraline, methylphenidate, flurazepam, and morphine.

Discussion Uveitis is a general term used to describe inflammation of the eye involving the iris, ciliary body, and/or choroid. Although most commonly idiopathic or autoimmune in origin, uveitis is occasionally associated with systemic diseases, including rheumatoid arthritis, sarcoidosis, syphilis, and Lyme disease.10-12 In patients infected with HIV, uveitis has been reported most commonly with infectious organisms, including bacterial, fungal, viral, and protozoal pathogens.13-20 Although HIV can be recovered from most ocular tissues, the ability of the virus itself to cause clinically apparent ocular disease in patients is unclear, and primary HIV-induced uveitis is rare.21-24 Uveitis is occasionally drug-related,25-32 and has been observed with the use of rifabutin in patients with HIV.33 If left untreated, uveitis may become chronic and eventually lead to decreased visual acuity secondary to cataract formation, cystoid macular edema, or secondary glaucoma. Treatment strategies usually include discontinuation of the suspected drug and administration of cycloplegic drops and topical or systemic glucocorticoids.12 Generally, symptoms are reversible within a few weeks with prompt management. In preliminary trials,7-9 administration of intravitreal cidofovir was noted to be associated with a 14–20% risk of

mild to moderate iritis. Iritis usually occurred anterior to the lens–iris diaphragm, and was associated with nongranulomatous keratitic precipitates and, occasionally, posterior synechiae. Symptoms included mild pain, photophobia, and visual blurring within the first two weeks after a cidofovir injection. All cases of iritis resolved within two weeks with administration of topical steroids and cycloplegia. No long-term adverse visual effects were noted.7-9 The risk of iritis was significantly higher in patients whose injection was not preceded by oral probenecid, compared with patients who had received such prophylaxis. In one study,7 iritis occurred after four of seven injections or 57% in patients who did not receive oral probenecid, versus 14 of 101 injections or 14% in those who did receive oral probenecid (p = 0.003). In another case series9 involving 130 injections of cidofovir 20 µg in 69 eyes, concomitant probenecid was found to decrease the frequency of iritis from 71% to 18% (p = 0.0089). Oral probenecid is routinely recommended with cidofovir in order to decrease the risk of nephrotoxicity and ocular toxicity.5 Probenecid antagonizes the active tubular secretion of cidofovir by competing for uptake at the proximal tubule site. Probenecid also decreases the uptake of cidofovir into the ciliary body epithelium, thus reducing the potential for adverse ocular effects, including ocular hypotony and iritis. According to data collected from Phase II/III clinical trials and postmarketing safety reports,6 iritis and uveitis

Table 2. Cidofovir-Associated Uveitis: Time Course and Ocular Findings in Patient 2 CDV Dose Number (1997)

Time Since Last CDV Injection (d)

Symptoms

1; February 26

Ocular Findings/ Visual Acuity OD HM; no J OS 6/6–3; J1 OD HM OS 6/6; J1

2; March 5

Ocular Examination

Intervention

no evidence of CMV in unaffected eye

3; March 19 7 15

painful eye OD; photosensitivity severe uveitis in OD

OD HM 1 OS 6/6

2+ cells, 2+ flare in anterior chamber OD: 3+ flare, 3+ cells, bound down pupil

perilimbal injection, DF qid add atropine 1% tid and increase steroid to 6 times/d

4; April 3 14

OD HM1; no J OS 6/6; J1

OD: cataract, anterior uveitis

OD HM OS 6/7; J1 OD unable to finger count; sees shadows OS 20/20 OD HM 3 OS 20/20

OD: flare ++, cells ++, cataract

5; April 18 11 18 35

worsening renal function bilateral ocular pain severe uveitis in OD

4 mo

no new ocular complaints

5 mo

no new ocular complaints

7 mo

OD HM 3 OS 20/20

OD: cataract, fixed dilated pupil, chronic uveitis, 2+ flare, 2+ cells

OD: advanced cataract, mid-dilated pupil, minimal uveitis, flare +/–, cells +/– OD: cataract, posterior synechiae, trace cells in anterior chamber

change to iv ganciclovir continue to treat OD symptomatically with steroid drops as above

continue drops in OD

CDV = cidofovir; CMV = cytomegalovirus; DF = detects fingers; HM = hand movement; J = Jager visual acuity chart; OD = right eye; OS = left eye.


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have been reported in approximately 2% of patients treated with intravenous cidofovir. The low frequency of adverse ocular events compared with those seen with intravitreal cidofovir is likely due to lower intraocular cidofovir concentrations achieved after intravenous drug administration. In reported cases, symptoms developed within two weeks to five months after initiating therapy, with similar distribution between unilateral and bilateral ocular involvement. In the majority of cases, ophthalmic steroids were prescribed, with beneficial effect. While concomitant drug information was not always available, there did not appear to be a relationship to other drugs with a potential to cause uveitis, including rifabutin.34 The patients we report had a clear association of newonset iritis three to four weeks after intravenous cidofovir administration, despite use of oral probenecid. Both patients were taking other medications, some of which have been associated with uveitis29,31; however, in both patients, the onset and resolution of uveitis was temporally related to the administration and discontinuation of cidofovir, and concomitant medications remained stable during this time. It is interesting to note that both patients also developed renal dysfunction while on intravenous cidofovir. Theoretically, declining renal function could lead to drug accumulation, with possible increased risk of ocular toxicity. However, both patients initially experienced episodes of uveitis in the absence of renal failure. In a published case series,35 renal dysfunction was not noted to be more common in patients experiencing cidofovir-related iritis versus controls. In both of our patients, iritis resolved with topical therapy, but recurred with subsequent cidofovir infusions. Following discontinuation of cidofovir, neither patient experienced any further active iritis, but one patient had fixed pupils from synechiae. Furthermore, although iritis can occur with CMV retinitis, neither patient had active retinitis at the time of the iritis.

While iritis has been reported to occur in up to 20% of patients receiving intravitreal injections of cidofovir, the incidence of iritis associated with intravenous administration is less commonly reported, perhaps in part due to lower achievable intraocular drug concentrations. Data from our patients as well as from the cases reported in clinical trials suggest that patients present clinically with unilateral or bilateral symptoms of acute onset of ocular pain, photophobia, and visual loss, from two weeks to up to five months following initiation of intravenous cidofovir. With prompt drug discontinuation and administration of topical corticosteroids and/or mydriatic agents, symptoms are generally reversible within a few weeks.

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EXTRACTO OBJETIVO:

Reportar dos casos de pacientes de sida con retinitis causados por CMV, los cuales desarrollaron iritis después de recibir cidofovir (CDV) por vía endovenosa. Ambos pacientes experimentaron síntomas recurrentes después de reiniciar el medicamento. RESUMEN: Dos pacientes con VIH positivo, previamente controlado con ganciclovir endovenoso o foscarnet, fueron tratados con CDV por vía endovenosa para tratar su retinitis. Los pacientes desarrollaron síntomas de iritis después de la segunda o tercera dosis de CDV. Un paciente experimentó síntomas unilaterales mientras que el otro paciente tenía síntomas bilaterales. En ambos pacientes la iritis se resolvió con terapia oftálmica tópica pero recurrió después de la subsiguiente infusión de CDV. La terapia con CDV fue descontinuada y no se observaron subsiguientes recurrencias de iritis. Un paciente tuvo pupilas dilatadas fijas post inflamatorias.

CONCLUSIONES:

Iritis puede no ocurrir comunmente en pacientes que reciben cidofovir endovenoso y probenecid oral. Los síntomas pueden usualmente revertirse al descontinuar prontamente el medicamento y con aplicaciones oftálmicas de corticosteroide tópico y/o agente midriático. WILMA M GUZMÁN

RÉSUMÉ OBJECTIF: Décrire deux cas de patients sidéens ayant une rétinite à cytomégalovirus (CMV) et qui ont développé une iritis suite à l’administration intraveineuse de cidofovir (CDV); les patients recevaient aussi du probénécide oral. Les deux patients ont présenté des symptômes récurrents lors d’une réexposition. RÉSUMÉ: Deux personnes infectées par le VIH ayant des rétinites à CMV, contrôlées antérieurement par du ganciclovir intraveineux ou du foscarnet, ont reçu du CDV intraveineux. Des symptômes d’iritis sont apparus dans un cas, après la deuxième dose de CDV, et dans l’autre cas après la troisième dose. Un patient a présenté des signes unilatéraux alors que chez l’autre, on notait la présence de signes bilatéraux. Chez les deux patients, un traitement ophtalmique topique a permis d’enrayer l’iritis, mais cette dernière est réapparue lors d’infusions subséquentes de CDV. La thérapie par le CDV a été cessée et aucun symptôme d’iritis n’a été noté par la suite. Un patient a présenté des pupilles postinflammatoires fixes et dilatées. CONCLUSIONS: Une iritis peut se développer, bien que rarement, chez des patients recevant du CDV intraveineux et du probénécide oral. Avec un arrêt rapide du médicament et l’administration topique de corticostéroïdes associés ou non à un agent mydriatique, les symptômes sont habituellement réversibles.


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