Berninger, Thomas

Bogner, Johannes R.

Geier, Stephan A.

Goebel, Frank-Detlef

Held, Manfred

Klauß, Volker

Kronawitter, Ursula

English

Open Access LMU

University Eye Hospital MWlich. MWlich, Gemwoy SA Geier T&minger V KlauS! Mediziaiscbe Polildiaik, Ulliversity of MlHlich, "'~1 MHeld JRBognu U Kronawitter FDGoebel Conespoodell« 10: Dr Siephan A Geier, UpjYerSity Eyc Hospital Munjcb, MIottWdenstraSK 8, DW-8000 Munich 2, G,,,,,,,,, . Aa:q>Icd for publicaOOIl 26 JllIIuary ]993 Impairment of tritan colour vision after initiation of treatment with zidovudine in patients with HIV disease or AIDS Stephan A Geier, Manfred Held, Johannes R Bogner, Ursula Kronawitter, Thomas Berninger, Volker Klauss, Frank D Goebel Zidovudine (3' -azido-2' ,3' - dideoxythymidinc) is a drug with provcd antihuman immuno-deficicncy virus (HIV) reverse traßscriptase activity. It has bcen clearly demonstrated that thc bcnefits of zidovudinc outwcigb the risks of its usc. H Different adversc effeets have bcen reponed for zidovudine, including anacmia, neutropenia. nausea, vomiting, myalgias, abnor-malities of livcr funetion, bluish nail pigmenta-tion, headachcs, myositis, and trichiasis." Colom vision deficits have bcen reponed for patients with AIDS or HIV disease," and it has been shown that this defect is most prominent for tritan vision. ' The patbogencsis of eolour vision defieits in patients with HIV disease remains unclear. We wish to repon the occur-renee of a temporary decrease in tritan colour contrast sensitivity in two patients with HIV disease starting or restarting treaunent with zidovudine. Casereports OASE 1 A 31-year-old patient was referred to the university eye hospital for routine examination after diagnosis of HIV infection and Iympha-denopathy syndrome. Tbe patient had attended the medical outpatient clink because of a 1 month history of fever aeeompanicd by swcU-ing of lymph nodes. He tested HIV positive for the first time during this diagnostic examination whieh was 2 wecks before lhc first ophthalmie examination. Visual acuity was 20120 in both eyes with correction. Biomicroscopic examina-tion revealed normal findings except for a discrete sludging of the blood column in the conjunctival vessels. On indirect ophthalmo-scopy five cotton wool spots were seen in the right eye, and one in the left eye. Colour contrast scnsitivity was tested using a high sensitivity computer graphlcs system devcloped by Ardcn et al.'o Tbe thresholds for the three colour 3XCS were within normal limits: tritan right eye (RE) 4·7, and left eye (LE) 4·2; deutan RE 3·3, and LE 3·2; protan RE 3·0, and LE 3·1. Tbe age corrected normal mucs 3ft (mean (2 SE»): tritan 3·9 (2·2); deutan 4·3 (2·2); and protan 4·0 (1·9). Tbe absolute CD4+ Iymphocytc count was 219 x 10'11, and treatment with zidovudine (500 mg per day) was staned. Thls was the only drug administered to the patient. Seven days after initiation of treatment with zidovudine the patient attended hospital with a 3 day experienee of sligbtly blurred vision in both eycs. Ophthal-mie examination, and deutan and protan colour vision were unchanged, but tritan vision was impaired: tritan RE 7·4,and LE 7·S. Zidovudine treatment was continued. One weck later the subjective symptoms disappearcd. Tritan thres-holds were REj·4, and LE 4·6. On subS;CQuent foUow ups tritan vision improved to baseline levels, and was in a range betwecn 3·7 and 4· 3 in both eyes. OASE 2 Tbe second patient was a 26-year-old woman with a 9 month history of AIDS after one episode of Pnewnocystis carinii pneumonia. She was referred to the university eye hospital for ophthalmie examination because of diplopia. Treatment with zidovudine bad been dis-continued 2 months earlier because of neutm-penia, but the patient was still on Pneumocystis cannii prophylaxis with trimethoprim and sulphamethoxazole. Tbe absolute CD4+ Iymphocyte count was 70x 10"11. Visua1 acuity was 20120 in both eyes with correction. Ophthalmie examination revealed a sixth nerve palsy of the right eye. Otherwise ophthalmie examination was nonnal and colouf contrast sensitivity thresholds were within nonnallimits: tritan RE 3·g, and LE 3·9; deutan RE 3·6, and LE 3·6; protan RE 3·7. and LE 3·7. Cranial magnetic resonance imaging showed a lesion in the area of the right pons and a second lesion in the left anterior part of the corpus eallosum, both with surrounding oedema. Clear ring-like enhancement was seen after application of Gd-DTPA. The location of the lesion in the pons was in accordance with compressive damage to the intracerebral path of the sixth nervc. Thc diagnosis of cerebral toxoplasmosis was assumed, and treatment with pyrimetha-mine (50 mg per day), c1indamycin (2400 mg per day), and folinic acid (15 mg per day) was started. Ten days later diplopia disappeared. Treatment with zidovudine (500 mg per day) was re-establisbed 2 months later. Tritan COIOUf contrast sensitivity increased to RE 6·4, and LE 6·5 measured 3 days after the reJ.D.luauon of treatment with zidovudine, but otherwise ophthalmie findings were normal, especially the values for deutan and protan vision. Two weeks later tritan eolour contrast sensitivity was RE 3'5, and LE 3·8 and other findings were unehanged. Comment Alterations of eolour vision bave been reported for numerous drugs."" Aequired alterations of tritan vision are usually related to retinal damage." Tberefore, the dyschromatopsia in the (Wo reported cases is expected to be related to retinal damage. Recently, retinal damage bas been reported for ehildren treated with 2' ,3' - dideoxyinosine." The authors used electropbysiological methods to measure retinal funetion, but no testS for colour vision were perfonned. They suggest that 2' ,3'-dideoxyinosine, whieh is also a dideoxy-nucleoside like zidovudine, causes a diffuse dysfunction of the retinal pigment epithelium. The pathogenesis of eolour vision deficits in patients with symptomatic HIV infection or AIDS remains unclear. It was proposed that the HIV-related retinal mieroangiopathic syndrome plays an importaDt role in the pathogenesis of those colour vision deficits. Our observations suggest that a temporary shift in tritan colour vision is an adverse effect at the beginning of treatment with zidovudine. Tbis shift in tritan vision might be due to a temporary interference of zidovudine with the production of visual pigment, or a temporary alteration of the pig-ment epithelium. Nevertheless, other factors may underly the changes. It cannot be ruled out that long tenn application of zidovudine might contribute to the development of colour vision deficits described for patients with HIV disease. Health care professionals involved in the treat-ment of patients with HlV disease sbould be aware of any abnormal deug or disease related effects. Th.i5 study was supponro by Bundnmini"mum fllr Forschung und Technologie, and by lIundesministerium fUr Gcsundtw:it, Germany, gnIll FKZ BGA 1II-002·89IFVP. We wish 10 thank Mn eh Hönnann m.d Mn cand mcd H Sdunidt'Kittler for I.beir Mlp. 1 Co«)' L, Fleming TR. Treatm~nl nfHIV infectioo - progrns in penpectin. N E"IlJ Md 1992; 326; 484-6. 2 Fisch! MA, Richmann l)l), Hansen N, CoUkr AC, Cam JT, Pani MF, lIal. Tht safety and dlicac:y ofzidovudioe(AZT) in I.be treatmellt of 5Ubj«tS with miI<!1y sympiomatic human immuDOde6cieocy virus (ype 1 (HlV) infecUoo; • double· btind, pIacdlo contro!lcd triaI. AM J"mn Md 1990; IU: 727- 37. . 3 Volberdiq PA, Lapkos SW, Koch MA, Pettinelli C, M)'ttS MW, Boot.b DK,lIal. Zidovudioe in asyDlplom;otic human immunodeficiency vints infecUoo: a COIluolkd triaI in per300S with fewer thao SOO CD4-positivc aUs p" cubic millimeter. N Eftgll Md 1990; 322: 941- 9. 4 HamillOfI JD, Harupn PM, Simbt-nwff MS, Day PL, Diamood GR, DickiwotJ GM, ., DI. A C<,lIItrolied Irial of early v ..... us lal~ treatment with zidovudine in symplomatic human immUDOddiciency vints infection. N E..,I J Mt4 1992; 326: 437-43. S Gniwn NMH, üget L, Park LP, Vcrmund SH, IXtcls R, Rinaldo CR, ,I ~I. 1M dfects 0fI t urvjva/ of nrly untment of hWlWl immUDOddiciency vinls infectioo. N Eftgl] Md 1992; 326: 1037-42. 6 K1ulIDID NE, Hintbom DR. Excnsiv~ powth of eyeiashes in • patif:ot with AIDS brinllmlted wi!h zidovudine IUlluJ. N E,.,IJ Md 1991; 324: 1896. 7 YaKboan R, MiISU)'lI H, My ..... CE, Brod<:r S. Clinical phannaco!osy of 3' ·ozjOO.2 ' ,3' -dideoJ;ythymidine (zXIovudine) and ..,laled dideoxynudeosides. N Eftgl] Md 1989; 321: 726-38. 8 Quiccno JI, Cappardli E, Sadun M, Muoguia D, Grant I, UsthaUI A, ,I al. VisuaI dysfunction wilhoul ..,tinitis in patienlS with ac:quired immune dc6c;"ncy syndrome. A",] 0p4Wr111tt1l 1992; IU: 1-13. 9 Geier SA, BemlngerT, Kromwiner U, Bopter JR , Kbuss V, Goebcl F·D. Colour vision in AIDS ""lieDIS md HIV positives. Vllth International Coaferm« 0fI AIDS, FIon:nc:e, 16-21 June 1991. Abstractbook, Abstracl MB 2417, 1991: 286. 10 Ardcn G8, GUndiz K, Peny S. CnIour vision lesting with • compUter (I1Iphi<;:sS)'$tml . eli" V;'Sci 1988; 2: 303-20. 11 Lyle WM. Drugs and coruiitions which may affC'Cl coIoLU' vWolI. Part I: Drop and chcmia.l •. J A", Op/qMtrric Aß 1974;45:47. 12 Zr=ner E. Neurophysiological aspects of colour vision in ~Ies. In: Sr;wIin I1f Mom fvroctimt. Vol 9. New Ynrk· Hri<klberg: Sprutger, 1973. 13 Hart WM. Acquired dyschromaIOps.ias. S_ Op/u1uWrwl 1987;32: 10-31. 14 Whi1C\lp SM, Butler KM, Carv.so R, dc Smel MD, Rubin B, HIISSOII RN, " al. Retina! loIicily in human inunllllO-defic:M:ucy vintl-infC'Clro chiJdren IJaled wi!h 2',3'· dideoxyinos.int. A"'J OpIIlIuJImoII992; IU: 1- 7. 

Impeirment of tritan colour vision after initiations of treatment with zidovudine in patients with HIV disease or AIDS

Universität München: Elektronischen Publikationen

University Eye Hospital 
MWlich. MWlich, 
Gemwoy 
SA Geier 
T&minger 
V KlauS! 
Mediziaiscbe Polildiaik, 
Ulliversity of MlHlich, 
"'~1 
MHeld 
JRBognu 
U Kronawitter 
FDGoebel 
Conespoodell« 10: 
Dr Siephan A Geier, 
UpjYerSity Eyc Hospital 
Munjcb, MIottWdenstraSK 8, 
DW-8000 Munich 2, G,,,,,,,,, . 
Aa:q>Icd for publicaOOIl 
26 JllIIuary ]993 
Impairment of tritan colour vision after initiation of 
treatment with zidovudine in patients with HIV 
disease or AIDS 
Stephan A Geier, Manfred Held, Johannes R Bogner, Ursula Kronawitter, Thomas Berninger, 
Volker Klauss, Frank D Goebel 
Zidovudine (3' -azido-2' ,3' - dideoxythymidinc) 
is a drug with provcd antihuman immuno-
deficicncy virus (HIV) reverse traßscriptase 
activity. It has bcen clearly demonstrated that 
thc bcnefits of zidovudinc outwcigb the risks of 
its usc. H Different adversc effeets have bcen 
reponed for zidovudine, including anacmia, 
neutropenia. nausea, vomiting, myalgias, abnor-
malities of livcr funetion, bluish nail pigmenta-
tion, headachcs, myositis, and trichiasis." 
Colom vision deficits have bcen reponed for 
patients with AIDS or HIV disease," and it has 
been shown that this defect is most prominent 
for tritan vision. ' The patbogencsis of eolour 
vision defieits in patients with HIV disease 
remains unclear. We wish to repon the occur-
renee of a temporary decrease in tritan colour 
contrast sensitivity in two patients with HIV 
disease starting or restarting treaunent with 
zidovudine. 
Casereports 
OASE 1 
A 31-year-old patient was referred to the 
university eye hospital for routine examination 
after diagnosis of HIV infection and Iympha-
denopathy syndrome. Tbe patient had attended 
the medical outpatient clink because of a 
1 month history of fever aeeompanicd by swcU-
ing of lymph nodes. He tested HIV positive for 
the first time during this diagnostic examination 
whieh was 2 wecks before lhc first ophthalmie 
examination. Visual acuity was 20120 in both 
eyes with correction. Biomicroscopic examina-
tion revealed normal findings except for a 
discrete sludging of the blood column in the 
conjunctival vessels. On indirect ophthalmo-
scopy five cotton wool spots were seen in the 
right eye, and one in the left eye. Colour contrast 
scnsitivity was tested using a high sensitivity 
computer graphlcs system devcloped by Ardcn 
et al.'o Tbe thresholds for the three colour 3XCS 
were within normal limits: tritan right eye (RE) 
4·7, and left eye (LE) 4·2; deutan RE 3·3, and 
LE 3·2; protan RE 3·0, and LE 3·1. Tbe age 
corrected normal mucs 3ft (mean (2 SE»): tritan 
3·9 (2·2); deutan 4·3 (2·2); and protan 4·0 (1·9). 
Tbe absolute CD4+ Iymphocytc count was 
219 x 10'11, and treatment with zidovudine (500 
mg per day) was staned. Thls was the only drug 
administered to the patient. Seven days after 
initiation of treatment with zidovudine the 
patient attended hospital with a 3 day experienee 
of sligbtly blurred vision in both eycs. Ophthal-
mie examination, and deutan and protan colour 
vision were unchanged, but tritan vision was 
impaired: tritan RE 7·4,and LE 7·S. Zidovudine 
treatment was continued. One weck later the 
subjective symptoms disappearcd. Tritan thres-
holds were REj·4, and LE 4·6. On subS;CQuent 
foUow ups tritan vision improved to baseline 
levels, and was in a range betwecn 3·7 and 4· 3 in 
both eyes. 
OASE 2 
Tbe second patient was a 26-year-old woman 
with a 9 month history of AIDS after one episode 
of Pnewnocystis carinii pneumonia. She was 
referred to the university eye hospital for 
ophthalmie examination because of diplopia. 
Treatment with zidovudine bad been dis-
continued 2 months earlier because of neutm-
penia, but the patient was still on Pneumocystis 
cannii prophylaxis with trimethoprim and 
sulphamethoxazole. Tbe absolute CD4+ 
Iymphocyte count was 70x 10"11. Visua1 acuity 
was 20120 in both eyes with correction. 
Ophthalmie examination revealed a sixth nerve 
palsy of the right eye. Otherwise ophthalmie 
examination was nonnal and colouf contrast 
sensitivity thresholds were within nonnallimits: 
tritan RE 3·g, and LE 3·9; deutan RE 3·6, and 
LE 3·6; protan RE 3·7. and LE 3·7. 
Cranial magnetic resonance imaging showed a 
lesion in the area of the right pons and a second 
lesion in the left anterior part of the corpus 
eallosum, both with surrounding oedema. Clear 
ring-like enhancement was seen after application 
of Gd-DTPA. The location of the lesion in the 
pons was in accordance with compressive 
damage to the intracerebral path of the sixth 
nervc. Thc diagnosis of cerebral toxoplasmosis 
was assumed, and treatment with pyrimetha-
mine (50 mg per day), c1indamycin (2400 mg per 
day), and folinic acid (15 mg per day) was 
started. Ten days later diplopia disappeared. 
Treatment with zidovudine (500 mg per day) was 
re-establisbed 2 months later. Tritan COIOUf 
contrast sensitivity increased to RE 6·4, and LE 
6·5 measured 3 days after the reJ.D.luauon of 
treatment with zidovudine, but otherwise 
ophthalmie findings were normal, especially the 
values for deutan and protan vision. Two weeks 
later tritan eolour contrast sensitivity was 
RE 3'5, and LE 3·8 and other findings were 
unehanged. 
Comment 
Alterations of eolour vision bave been reported 
for numerous drugs."" Aequired alterations 
of tritan vision are usually related to retinal 
damage." Tberefore, the dyschromatopsia in the 
(Wo reported cases is expected to be related to 
retinal damage. 
Recently, retinal damage bas been reported 
for ehildren treated with 2' ,3' - dideoxyinosine." 
The authors used electropbysiological methods 
to measure retinal funetion, but no testS for 
colour vision were perfonned. They suggest that 
2' ,3'-dideoxyinosine, whieh is also a dideoxy-
nucleoside like zidovudine, causes a diffuse 
dysfunction of the retinal pigment epithelium. 
The pathogenesis of eolour vision deficits in 
patients with symptomatic HIV infection or 
AIDS remains unclear. It was proposed that the 
HIV-related retinal mieroangiopathic syndrome 
plays an importaDt role in the pathogenesis of 
those colour vision deficits. Our observations 
suggest that a temporary shift in tritan colour 
vision is an adverse effect at the beginning of 
treatment with zidovudine. Tbis shift in tritan 
vision might be due to a temporary interference 
of zidovudine with the production of visual 
pigment, or a temporary alteration of the pig-
ment epithelium. Nevertheless, other factors 
may underly the changes. It cannot be ruled out 
that long tenn application of zidovudine might 
contribute to the development of colour vision 
deficits described for patients with HIV disease. 
Health care professionals involved in the treat-
ment of patients with HlV disease sbould be 
aware of any abnormal deug or disease related 
effects. 
Th.i5 study was supponro by Bundnmini"mum fllr Forschung 
und Technologie, and by lIundesministerium fUr Gcsundtw:it, 
Germany, gnIll FKZ BGA 1II-002·89IFVP. 
We wish 10 thank Mn eh Hönnann m.d Mn cand mcd H 
Sdunidt'Kittler for I.beir Mlp. 
1 Co«)' L, Fleming TR. Treatm~nl nfHIV infectioo - progrns 
in penpectin. N E"IlJ Md 1992; 326; 484-6. 
2 Fisch! MA, Richmann l)l), Hansen N, CoUkr AC, Cam JT, 
Pani MF, lIal. Tht safety and dlicac:y ofzidovudioe(AZT) 
in I.be treatmellt of 5Ubj«tS with miI<!1y sympiomatic human 
immuDOde6cieocy virus (ype 1 (HlV) infecUoo; • double· 
btind, pIacdlo contro!lcd triaI. AM J"mn Md 1990; IU: 
727- 37. . 
3 Volberdiq PA, Lapkos SW, Koch MA, Pettinelli C, M)'ttS 
MW, Boot.b DK,lIal. Zidovudioe in asyDlplom;otic human 
immunodeficiency vints infecUoo: a COIluolkd triaI in 
per300S with fewer thao SOO CD4-positivc aUs p" cubic 
millimeter. N Eftgll Md 1990; 322: 941- 9. 
4 HamillOfI JD, Harupn PM, Simbt-nwff MS, Day PL, 
Diamood GR, DickiwotJ GM, ., DI. A C<,lIItrolied Irial of 
early v ..... us lal~ treatment with zidovudine in symplomatic 
human immUDOddiciency vints infection. N E..,I J Mt4 
1992; 326: 437-43. 
S Gniwn NMH, üget L, Park LP, Vcrmund SH, IXtcls R, 
Rinaldo CR, ,I ~I. 1M dfects 0fI t urvjva/ of nrly untment 
of hWlWl immUDOddiciency vinls infectioo. N Eftgl] Md 
1992; 326: 1037-42. 
6 K1ulIDID NE, Hintbom DR. Excnsiv~ powth of eyeiashes in 
• patif:ot with AIDS brinllmlted wi!h zidovudine IUlluJ. 
N E,.,IJ Md 1991; 324: 1896. 
7 YaKboan R, MiISU)'lI H, My ..... CE, Brod<:r S. Clinical 
phannaco!osy of 3' ·ozjOO.2 ' ,3' -dideoJ;ythymidine 
(zXIovudine) and ..,laled dideoxynudeosides. N Eftgl] Md 
1989; 321: 726-38. 
8 Quiccno JI, Cappardli E, Sadun M, Muoguia D, Grant I, 
UsthaUI A, ,I al. VisuaI dysfunction wilhoul ..,tinitis in 
patienlS with ac:quired immune dc6c;"ncy syndrome. A",] 
0p4Wr111tt1l 1992; IU: 1-13. 
9 Geier SA, BemlngerT, Kromwiner U, Bopter JR , Kbuss V, 
Goebcl F·D. Colour vision in AIDS ""lieDIS md HIV 
positives. Vllth International Coaferm« 0fI AIDS, 
FIon:nc:e, 16-21 June 1991. Abstractbook, Abstracl MB 
2417, 1991: 286. 
10 Ardcn G8, GUndiz K, Peny S. CnIour vision lesting with • 
compUter (I1Iphi<;:sS)'$tml . eli" V;'Sci 1988; 2: 303-20. 
11 Lyle WM. Drugs and coruiitions which may affC'Cl coIoLU' 
vWolI. Part I: Drop and chcmia.l •. J A", Op/qMtrric Aß 
1974;45:47. 
12 Zr=ner E. Neurophysiological aspects of colour vision in 
~Ies. In: Sr;wIin I1f Mom fvroctimt. Vol 9. New Ynrk· 
Hri<klberg: Sprutger, 1973. 
13 Hart WM. Acquired dyschromaIOps.ias. S_ Op/u1uWrwl 
1987;32: 10-31. 
14 Whi1C\lp SM, Butler KM, Carv.so R, dc Smel MD, Rubin B, 
HIISSOII RN, " al. Retina! loIicily in human inunllllO-
defic:M:ucy vintl-infC'Clro chiJdren IJaled wi!h 2',3'· 
dideoxyinos.int. A"'J OpIIlIuJImoII992; IU: 1- 7. 


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Impeirment of tritan colour vision after initiations of treatment with zidovudine in patients with HIV disease or AIDS

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