effects side ocular induced-Drug  • PART7  

b.Rashes

c.Vasculitis

3. Hyperpigmentation eyelids and conjunctiva

Probable

1. Cystoid macular edema

2. Color vision abnormalities

3. Visual hallucinations

Conditional/Unclassified

1. Diplopia (only with generalized myopathy)

2. Nystagmus (overdose)

Clinical significance

This drug is usually used in combination with many other drugs, so it is often difficult to put a direct cause-and-effect relationship between the drug and an ocular side effect. There have, however, been a number of reports of cystoid macular edema while on this agent that have resolved when the drug was discontinued. Lalonde et al (1991) support this with a case of positive dechallenge/rechallenge data. Geier et al (1993) ­reported cases of tritan color vision defects secondary to zidovudine. Clearly, hypertrichosis (Klutman and Hinthorn 1991 and National Registry cases) can occur as well as skin rashes secondary to zidovudine. Hyperpigmentation of the eyelids, conjunctiva, fingernails, etc., especially in heavily pigmented people, has been reported. Diplopia may occur secondary to a generalized myopathy. Nystagmus has only been reported in overdose situations.

References and Further Reading

Geier SA, Held M, Bogner J, et al. Impairment of tritan colour vision after initiation of treatment with zidovudine in patients with HIV disease or AIDS. Br J Ophthal 77: 315–316, 1993.

Klutman NE, Hinthorn DR. Excessive growth of eyelashes in a patient with AIDS being treated with zidovudine. N Engl J Med 324(26): 1896, 1991.

Lalonde RG, Deschênes JG, Seamone C. Zidovudine-induced macular edema. Ann Int Med 114(4): 297–298, 1991.

Luchi M, Warren KA, Saverhagen C, Hinthorn D. Transient visual loss due to severe anemia in a patient with AIDS. J La State Med Soc 151(2): 82-85, 1999.

Merenich JA, et al. Azidothymidine-induced hyperpigmentation mimicking primary adrenal insufficiency. Am J Med 86: 469–470, 1989.

Spear JB, Kessler HA, Nusinoff Lehrman S, de Miranda P. Zidovudine overdose. First report of ataxia and nystagmus: case report. Ann Int Med 109: 76–77, 1988.

Steinfeld SD, Demols P, Van Vooren JP, et al. Zidovudine in primary Sjogren’s syndrome. Rheumatol 38(9): 814–817, 1999.

Strominger MB, Sachs R, Engel HM. Macular edema from zidovudine? Ann Int Med 115(1): 67, 1991.

Wilde MI, Langtry HD. Zidovudine: an update of its pharmacodynamic and pharmacokinetic properties, and therapeutic efficacy. Drugs 46(3): 515–578, 1993.

Class: Amebicides

Generic names: 1. Broxyquinoline; 2. diiodohydroxyquinoline (iodoquinol).

Proprietary names: 1. Starogyn, 2. Sebaquin, Yodoxin.

Primary use

These amebicidal agents are effective against Entamoeba histolytica.

Ocular side effects

Systemic administration

Certain

1.Decreased vision

2.Optic atrophy

3.Optic neuritis – subacute myelo-optic neuropathy (SMON)

4.Nystagmus

5.Toxic amblyopia

6.Macular edema

7.Macular degeneration

8.Diplopia

9.Absence of foveal reflex

10. Problems with color vision

a.Color vision defect

b.Purple spots on white background

Clinical significance

Major toxic ocular effects may occur with long-term oral administration of these amebicidal agents, especially in children. Since they are given orally for Entamoeba histolytica, most reports are from the Far East. Data suggest that these amebicides may cause SMON. This neurologic disease has a 19% incidence of decreased vision and a 2.5% incidence of toxic amblyopia. It has been suggested that in patients being treated for acrodermatitis enteropathica, a disease of inherited zinc deficiency, optic atrophy may be secondary to zinc deficiency instead of diiodohydroxyquinoline. Since long-term quinolone exposure has been shown to result in accumulation of the drug in pigmented tissues, retinal degenerative changes may be observed. The best overall review of this subject is in Grant and Schuman (1993).

References and Further Reading

Baumgartner G, et al. Neurotoxicity of halogenated hydroxyquinolines: clinical analysis of cases reported outside Japan. J Neurol Neurosurg Psychiatry 42: 1073, 1979.

Committee on Drugs, 1989–1990. Clioquinol (iodochlorhydroxyquin, vioform) and iodquinol (diiodohydroxyquin): blindness and neuropathy. Pediatrics 86(5): 797–798, 1990.

Grant WM, Schuman JS. Toxicology of the Eye. 4th edn. Charles C Thomas,­ Springfield, IL, pp 282–283 and 842–843, 1993.

Guy-Grand B, Basdevant A, Soffer M. Oxyquinoline neurotoxicity. Lancet I 993, 1983.

Hanakago R, Uono M. Clioquinol intoxication occurring in the treatment of acrodermatitis enteropathica with reference to SMON outside of Japan. Clin Toxicol 18: 1427, 1981.

Hansson O, Herxheimer A. Neurotoxicity of oxyquinolines. Lancet 2: 1253, 1980.

Kauffman ER, et al. Clioquinol (iodochlorhydroxyquin, vioform) and iodoquinol (diiodohydroxyquin): blindness and neuropathy. Pediatrics 86: 978-979, 1990.

Kono R. Review of subacute myelo-optic neuropathy (SMON) and studies done by the SMON research commission. Jpn J Med Sci Biol 28(suppl): 121, 1975.

Oakley GP. The neurotoxicity of the halogenated hydroxyquinolines. JAMA 225: 395–397, 1973.

Ricoy JR, Ortega A, Cabello A. Subacute myelo-optic neuropathy (SMON). First Neuro-pathological report outside Japan. J Neurol Sci 53: 241, 1982.

Rose FC, Gawel M. Clioquinol neurotoxicity: an overview. Acta Neurol Scand 70(suppl 100): 137–145, 1984.

Shibasaki H, et al: Peripheral and central nerve conduction in subacute myelo-optic neuropathy. Neurology 32: 1186, 1982.

Shigematsu I. Subacute myelo-optic neuropathy (SMON) and clioquinol. Jpn J Med Sci Biol 28(suppl): 35–55, 1975.

Sturtevant FM. Zinc deficiency Acrodermatitis enteropathica, optic atrophy SMON, and 5,7-dihalo-8-quinolinols. Pediatrics 65: 610, 1980.