Vol. 108, No.6 Letters to the Journal 733

Exogenous Lactase in the Treatmentof Oral Acyclovir Intolerance

Richard 1. Manka, M.D.Department of Ophthalmology, University of Min­nesota.

Inquiries to Richard L. Manka, M.D., P.O. Box 130,Devils Lake, ND 58301.

In patients with herpes simplex encephalitis,acyclovir has been shown to decrease mortali­ty.' The ocular complications of herpes zosterophthalmicus have been reduced by the adrnin­istra tion of oral acyclovir. 2 Oral acyclovir alsohas been useful in the treatment of herpessimplex ocular infections.! Gastrointestinal up­set, including diarrhea, however, has been not­ed in some individuals who take oral acyclovir.We recently used oral lactase to treat a case ofintolerance to oral acyclovir in a lactose­intolerant individual.

A 24-year-old man with a 16-year history ofherpes simplex keratitis continued to have fre­quent recurrences with progressive cornealscarring while using numerous topical antiviralagents. The patient was given oral acyclovirwith good response, but was forced to discon­tinue the acyclovir because of chronic diarrhea,which recurred each time the acyclovir wastaken. Unfortunately, the keratitis recurredwhen the patient was not taking the acyclovir.The patient had a history of intolerance tomilk products, believed to be a lactose intoler­ance. We believed the intolerance to oral acy­clovir was because of the lactose in oral acyclo­vir tablets. The patient was then givenacyclovir (200 mg, five times daily) and orallactase in the form of one Lactaid caplet (3,000Food Chemicals Codex units of lactase activityper capsule) five times daily. The patient hashad no recurrence of the diarrhea since treat­ment began in July 1989.

Oral acyclovir tablets contain lactose. Lactoseintolerance is a common cause of intolerance tomilk and milk products. This intolerance isthought to be caused by a lack of the intestinalenzyme, lactase. Persistence of intestinal lac­tase after infancy is believed to be an autosomaldominant characteristic. In North Americanadults, lactose maldigestion is found in approx­imately 79% of native Americans, 75% ofblacks, 51% of Hispanics, and 21% of whites."With widespread use of oral acyclovir, thepotential for intolerance to the lactose is sig­nificant. The addition of exogenous lactase tomilk in adult lactase deficiency has been shown

to be a convenient and effective way to correctlactose malabsorption. 5 Thus, supplemental ex­ogenous lactase may be useful in patients withgastrointestinal intolerance to oral acyclovirbecause of lactose intolerance.

References

1. Whitley, R. J.: Herpes simplex virus infectionsof the central nervous system. A review. Am. J. Med.85:61, 1988.

2. Cobo, M.: Reduction of the ocular complicationsof herpes zoster ophthalmicus by oral acyclovir. Am.J. Med. 85:90, 1988.

3. Schwab, 1. R.: Oral acyclovir in the manage­ment of herpes simplex ocular infections. Ophthal­mology 95:423, 1988.

4. Scrimshaw, N. S., and Murray, E. B.: The ac­ceptability of milk and milk products in populationswith a high prevalence of lactose intolerance. Am. J.Clin. Nutr. 48:1079, 1988.

5. Larni, F., Callegari, c.. Tatali, M., Graziano, L.,Guidetti, C.; Miglioli, M., and Barbara, L.: Efficacy ofaddition of exogenous lactase to milk in adult lactasedeficiency. Am. J. Gastroenterol. 83:1145, 1988.

Multifocal Choroiditis UveitisOccurring After Herpes ZosterOphthalmicus

Steven M. Bloom, M.D.,and Lory Snady-McCoy, M.D.Department of Ophthalmology, Tufts-New EnglandMedical Center.

Inquiries to Lory Snady-McCoy, M.D., New EnglandMedical Center, Department of Ophthalmology, Box450,750 Washington St., Boston, MA 02111.

Ocular herpes zoster infection most com­monly causes anterior segment inflammation.Herpes zoster has been implicated as a cause ofthe acute retinal necrosis syndrome and hasbeen reported to occur after herpes zoster der­matitis.! Although granulomatous choroiditishas been noted histopathologically," in a re­view of the literature, we found no clinicaldescription or documentation of a multifocalchoroiditis uveitis occurring after herpes zosterophthalmicus. Our patient had herpes zosterdermatitis and ipsilateral scleritis, anterior uve­itis, vitritis, and a multifocal choroiditis thatclinically resembled birdshot chorioretinop-

734 AMERICAN JOURNAL OF OPHTHALMOLOGY December, 1989

athy. This case does not appear to represent avariant of the acute retinal necrosis syndromebecause the necrotizing retinitis and occlusiveretinal vasculitis so characteristic of this dis­ease:' were not present.

This 67-year-old man developed a herpeszoster infection of the ophthalmic first branchof the left trigeminal nerve. Initially treatedwith topical acyclovir ointment and oral pred­nisone, he developed an anterior uveitis thatwas unresponsive to fluorometholone drops.He was referred to our institution six weekslater because of persistent ocular inflammation,pain, decreased vision, and floaters in the lefteye.

Visual acuity was R.E.: 20/25 and L.E.: 20/70.The skin of his left upper face was scarred fromthe resolving rash. There was decreased skinand corneal sensation. The superotemporalsclera was thinned and injected (Fig. 1). Thecornea was without staining or infiltrates. A 2+aqueous cell and flare were present. The intra­ocular pressure was 17 mm Hg in each eye. Thefundus appeared grossly normal although onlya hazy view was obtained because of manynonpigmented vitreous cells. Fluorescein angi­ography showed several areas of macular andperipheral hyperfluorescence and good retinaland choroidal perfusion. No retinal vascularstaining or leakage was evident. Prednisoloneacetate 1% drops were instilled in the left eye fourtimes a day pending preliminary laboratoryresults. Laboratory results including completeblood cell count, erythrocyte sedimentationrate, serology, tuberculosis testing, urinalysis,and chest x-ray were normal. HLA testing was

Fig. 1 (Bloom and Snady-McCoy). Sector scleritisoccurring after herpes zoster ophthalmicus.

Fig. 2 (Bloom and Snady-McCoy). Unilateral, paleyellow areas at the level of the choroid and retinalpigment epithelium. These areas were hyperfluores­cent on fluorescein angiography.

negative for A29 and positive for A3, B7, andB18.

Ten days later vitreous cellular reaction hadimproved, which permitted visualization ofpale yellow areas in the superior macula. Visualacuity was unchanged. The patient was given aperiorbital injection of 40 mg of triamcinolone.One week later, visual acuity was L.E.: 20/40,and there was no anterior chamber reaction.Many nonpigmented cells were still present inthe vitreous cavity. The triamcinolone injectionwas repeated. Over the next several months,the vitreous opacities cleared, which permittedvisualization of multifocal, flat, round, paleyellow areas throughout the left fundus at thelevel of the choroid and retinal pigment epithe­lium (Fig. 2). There was hyperfluorescence onfluorescein angiography. The final visual acuitywas R.E.: 20/25 and L.E.: 20/30 nine monthsafter our initial examination.

Hedges and Albert" gave histopathologic evi­dence of a granulomatous choroiditis occurringafter ocular herpes zoster infection. Some oftheir patients also had granulomatous inflam­mation of the posterior ciliary arteries. Thus,multifocal choroiditis seen in our patient couldbe explained by either choroidal granuloma­tous inflammation, choroidal infarction causedby occlusion of the posterior ciliary arteries, orboth. Priem and Oosterhuis' noted that thedistribution of the lesions in birdshot chorioret-

Vol. 108, No.6 Letters to the Journal 735

inopathy follow the distribution of the majorchoroidal veins. This may explain the ophthal­moscopic similarities between birdshot chorio­retinopathy and the findings in our patient.

References

1. Yeo, J. H., Prepose, J.S., Stewart, J. A.,Sternberg, P., Jr., and Liss, R. A.: Acute retinalnecrosis syndrome following herpes zoster dermati­tis. Ophthalmology 93:1418, 1986.

2. Hedges, T. R., III, and Albert, D. M.: The pro­gression of the ocular abnormalities of herpes zoster.Histopathologic observations of nine cases. Oph­thalmology 89:165,1977.

3. Fisher, J. P., Lewis, M. 1., Blumenkranz, M.,Culbertson, W. W., Flynn, H. W., Clarkson, J. G.,Gass, J. D. M., and Norton, E. W D.: The acute reti­nal necrosis syndrome. Pt. 1. Clinical manifestations.Ophthalmology 89:1309, 1982.

4. Priem, H. A., and Oosterhuis, J. A.: Birdshotchorioretinopathy. Clinical characteristics and evolu­tion. Br. J. Ophthalmol. 72:646, 1988.

Bilateral Acute Retinal Necro.sisSyndrome

Theodore Rabinovitch, M.D.,Robert A. Nozik, M.D.,and Michael P. Varenhorst, M.D.Francis I. Proctor Foundation, University of Califor­nia (T.R., R.A.N.), and Vitreoretinal Consultantsand Surgeons (M.P.V.).

Inquiries to Robert A. Nozik, M.D., Francis I. ProctorFoundation, Room 5-315, University of California, SanFrancisco, CA 94143.

In 1969, a 38-year-old woman was examinedat the Proctor Uveitis Clinic. She complained offloaters and blurred vision in her left eye.Examination disclosed a severe inflammatoryreaction in the anterior chamber, mutton-fatkeratic precipitates, marked vitreous opacity,vasculitis, and disk edema. Ophthalmoscopyshowed a ring-like deposition of white exudatesurrounding the entire periphery with sharpgeographic margins posteriorly. The examiningphysicians were unable to reach an etiologicdiagnosis at that time. Systemic prednisonewas prescribed for the patient. The regimen,however, failed to halt progression of the dis-

Fig. 1 (Rabinovitch, Nozik, and Varenhorst). Righteye in April 1982. Focal patch of retinitis alonginferotemporal arcade.

ease. A dense cataract eventually formed with360-degree posterior synechiae. The patientlost light perception and the eye becamephthisic.

In 1982, she had an area of retinitis along theinferotemporal arcade of the right eye (Fig. 1).This improved after several weeks of oral corti­costeroids. She was seen again March 10, 1988,because of floaters and blurred vision in herright eye. A small patch of retinitis originatedin the area of the retina that had healed sixyears previously. A much larger area of retinitiswas also evident in the far temporal peripheryseparated from the smaller lesion by thehealthy retina (Fig. 2). Acute retinal necrosiswas diagnosed, and the patient was given in­travenous acyclovir and corticosteroids, fol­lowed by prophylactic laser photocoagulation.In August 1988 visual acuity was 20/400.

This case represents probable bilateral acuteretinal necrosis, during an interval of 19 years.A mild self-limited episode in the right eye hadapparently occurred in 1982, similar to therecent report by Matsuo and associates.' Theclear, concise description of the fundusfindings in the left eye in 1969 are identical tothe classic signs we now recognize as acuteretinal necrosis. That the fellow eye can beaffected long after the initial episode is notwidely recognized. Ludwig, Zegarra, and