Clinical and Experimental Ophthalmology

(2002)

30

, 147–148

Case Report

_________________________________________

Case Report

Hypersensitivity reaction to intravitreal clindamycin therapy

Peter Kim

MBBS(Hons)

, Nancy Younan

MBBS MPH

and Minas T Coroneo

FRANZCO

Department of Ophthalmology, Prince of Wales Hospital, University of New South Wales, Sydney, New South Wales, Australia

A

BSTRACT

A Caucasian woman presenting with recurrence of intra-ocular toxoplasmosis was given intravitreal clindamycin. Shesubsequently developed a hypersensitivity reaction in theform of a generalized erythematous rash. To the authors’knowledge, hypersensitivity reactions to an antibiotic given bythe intravitreal route have not previously been reported.

Key words:

clindamycin, hypersensitivity reaction, intra-vitreal injection.

C

ASE

R

EPORT

A 57-year-old Caucasian woman with a history of oculartoxoplasmosis presented with a 5-day history of rightcentral scotoma. On examination she had a right visualacuity of 6/60 and a left visual acuity of 6/6. Examination ofthe right eye showed inferior keratic precipitates. She hadanterior chamber cells (10 per high power field) with 1+flare and moderate vitreous haze and cells. There was anactive area of chorioretinitis, superotemporal to the macula.The diagnosis was reactivation of right ocular toxoplasmo-sis. Examination of the left eye was normal.

She had past medical history of ulcerative colitis.She was admitted to hospital and commenced on clinda-

mycin (300 mg orally q.i.d.), trimethoprim with sulfa-methoxazole (double strength one tablet orally b.d.), guttaeprednisolone acetate 1% (6 times daily OD), guttae atro-pine (1% b.d. OD) and IV methylprednisolone (500 mgthree doses given over the following 6 days). Toxocara,CMV and HIV serology were negative.

The visual acuity improved to 6/36 and the anteriorchamber activity decreased. She was discharged on oraltrimethoprim with sulfamethoxazole and clindamycin aswell as guttae prednisolone acetate 1% OD and guttaeatropine OD and oral prednisone.

Three days later she presented with a generalized ery-thematous macular rash over the scalp, face, arms, thigh andtrunk. The ocular appearance was unchanged from that ondischarge. As she was unwell, she was admitted and treatedwith promethazine hydrochloride. The rash was thoughtto be due to an allergic reaction to trimethoprim with

sulfamethoxazole, which was consequently ceased. She wascontinued on clindamycin, oral prednisone, guttae pred-nisolone acetate 1% and atropine 1%. She improved clini-cally with resolution of her rash and she was discharged onthe above medications excluding trimethoprim with sulfam-ethoxazole.

However, she represented again 3 days later with vomitingand similar rash. This time the rash was thought to be due toclindamycin, which was subsequently ceased. She was treatedmedically as per the previous episode, and following recoveryand resolution of the rash, she was discharged on oral pred-nisone, guttae prednisolone acetate 1% and atropine 1%.

She was followed up as an outpatient. The keratic precip-itates and anterior chamber activity resolved. The chorioret-inal lesion became inactive. The oral prednisone as well asthe topical guttae prednisolone acetate 1% were graduallyweaned. The atropine was ceased. She achieved a visualacuity of 6/18.

Approximately 4 months after the initial presentation sheagain had a sudden reduction in right visual acuity associ-ated with a painful red eye. The right visual acuity haddecreased to 6/60. A fresh chorioretinal lesion close to themacula was seen. She was commenced on oral pyrimeth-amine 25 mg b.d. and folic acid 5 mg twice weekly. She hadalready been on oral prednisone due her ulcerative colitis,and this was continued. However, her visual acuity wors-ened to 1/60. She was then given intravitreal clindamycin(1 mg/0.1 mL) and dexamethasone (0.4 mg/0.1 mL). Unfor-tunately, 2 days later the rash redeveloped. The rash wasconsidered to be due to the intravitreal clindamycin.

Treatment continued on pyrimethamine and prednisone.The rash resolved and the patient felt well again. Over theensuing few weeks the active lesion healed, and the anteriorchamber activity resolved. During this time, her oral andtopical prednisone were weaned and the pyrimethamine wasceased. Her best corrected right visual acuity stabilized at3/60 due to macular scarring.

The left visual acuity remained at 6/4.

D

ISCUSSION

Ocular toxoplasmosis is a common and preventable cause ofsevere visual loss and blindness in immunocompromised as

�

Correspondence:

Dr Minas T Coroneo, Department of Ophthalmology, Prince of Wales Hospital, High Street, Randwick, NSW 2031, Australia.

Email: M.Coroneo@unsw.edu.au

148 Kim

et al

.

well as healthy individuals.

1

There are no antiparasiticagents able to eradicate

Toxoplasmosis gondii

from oculartissues. Thus the aim of therapeutic interventions is tocontrol proliferating parasites during the active phase ofinfection.

1

The optimal treatment for ocular toxoplasmosis is con-troversial.

2

A number of different antimicrobial/antiparasiticagents are used, as well as systemic corticosteroids. Themost commonly used regimens include pyrimethamine,sulfadiazine and corticosteroids as well as pyrimethamine,sulfadiazine, clindamycin and corticosteroids.

3

To the best of our knowledge, there are no studiescomparing the use of oral versus intravenous steroid in thetreatment of ocular toxoplasmosis. Intravenous steroids wereused in this case as they have a shorter onset of actioncompared with oral steroids. Also, the efficacy of high doseintravenous methylprednisolone therapy in patients with avariety of inflammatory eye diseases, including uveitis, hasbeen reported.

4

Sight-threatening toxoplasmic retinochoroiditis close tofixation is usually treated with a combination of antitoxo-plasmic medications and corticosteroids.

5

The antibioticcombination of trimethoprim with sulfamethoxazole andclindamycin has been effective for lesions involving or closeto the macula, with severe systemic complications beingrare.

5

Clindamycin, alone or in combination, has been an effec-tive agent in the treatment of ocular toxoplasmosis. Theability of clindamycin to penetrate and act upon theencysted form of the parasite and to accumulate in the uvealtissues of the eye makes it an effective drug.

2

This antibioticwas initiated in our patient.

We reviewed the literature and found that hypersensitiv-ity to oral or parenteral clindamycin therapy was rare withan approximate incidence of 0.4% or lower.

6

Intravitreal injections of clindamycin and dexamethasoneare well tolerated and may be an effective alternative tosystemic therapy for sight-threatening chorioretinitis dueto

T. gondii

.

7

Our literature search did not show any reportsof adverse reactions to intravitreal clindamycin therapy. Wechose to rechallenge the patient with intravitreal clinda-mycin because of the rarity of hypersensitivity reactions todrugs given intravitreally. This may be explained by thepresence of the blood ocular barrier.

Unfortunately, our patient developed a generalizedmacular rash whilst on clindamycin therapy.

We present the first known case of hypersensitivity reac-tion to intravitreal clindamycin in the form of a skin rash.

R

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