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 Table of Contents  
CASE REPORT
Year : 2022  |  Volume : 2  |  Issue : 3  |  Page : 655-656

Bilateral corneal drug deposits due to olanzapine


Guru Nanak Eye Centre, New Delhi, India

Date of Submission04-Jul-2021
Date of Acceptance16-Dec-2021
Date of Web Publication16-Jul-2022

Correspondence Address:
Dr. Nisha Bharti
302, Ambika Enclave, New Delhi - 110 078
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijo.IJO_1792_21

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  Abstract 


A 21-year-man male patient presented for a regular eye check-up. He was a known case of bipolar affective disorder and was on the antipsychotic drug, olanzapine, for 12 years. Slit-lamp examination showed peripheral anterior-mid stromal, bilateral, whitish, diffuse pigmentary deposition. Olanzapine is a second-generation atypical antipsychotic used in the treatment of schizophrenia and bipolar disorders. In this case report, we describe a case of corneal deposits related to another new generation atypical antipsychotic agent, olanzapine.

Keywords: Antipsychotics, cornea, pigmentary deposits


How to cite this article:
Jain P, Gupta I, Bharti N, Ghosh S. Bilateral corneal drug deposits due to olanzapine. Indian J Ophthalmol Case Rep 2022;2:655-6

How to cite this URL:
Jain P, Gupta I, Bharti N, Ghosh S. Bilateral corneal drug deposits due to olanzapine. Indian J Ophthalmol Case Rep [serial online] 2022 [cited 2022 Aug 13];2:655-6. Available from: https://www.ijoreports.in/text.asp?2022/2/3/655/351128



A 21-year-old male patient who was a known case of bipolar affective disorder and was on the antipsychotic drug, olanzapine, for 12 years presented for regular eye check up. Slit-lamp examination showed peripheral anterior-mid stromal, bilateral, whitish, diffuse pigmentary deposition. Olanzapine is a second-generation atypical antipsychotic used in the treatment of schizophrenia and bipolar disorders. In this case report, we describe a case of corneal deposits related to another new generation atypical antipsychotic agent, olanzapine


  Case Report Top


A 21-year-old male with bipolar affective disorder (BPD) presented to our outpatient department for a regular eye checkup. The best-corrected visual acuity was 6/9 OU. On slit-lamp examination, the central cornea was clear, but peripheral cornea showed bilateral diffuse pigmentary deposits up to the anterior mid stroma of the cornea [Figure 1]a and [Figure 1]b. The rest of the ocular examination, including fundus examination, was unremarkable. General inspection showed no cutaneous pigmentation. On enquiring about the medical history, the patient was a known case of BPD since the last 12 years and on treatment with T. sodium valproate 500 mg BD, T. olanzapine 5 mg BD, T. trihexyphenidyl 2 mg OD, and T. clonazepam 0.5 mg HS.
Figure 1: (a and b) Showing diffuse pigmentary corneal deposits in the periphery similar to arcus

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Anterior segment optical coherence tomography (ASOCT) showed a mild hyper-reflective area with anterior mid stromal involvement in the peripheral cornea in both eyes [Figure 2]a and [Figure 2]b. The clinical appearance of the corneal deposition was similar to the distinctive pattern of swirling lines in the epithelium classical of chlorpromazine-induced ocular toxicity, although the patient had never taken this drug in the past.[1] To rule out arcus juvenilis, a thorough blood investigation including complete blood count and lipid profile was ordered which came out to be normal. Ocular side effects of valproate include cataract, diplopia, nystagmus, oscillopsia, and visual hallucinations.[2] Clonazepam, an anticonvulsant and anxiolytic, has been linked to “white-dot-like” retinopathy that can be seen using ophthalmoscopy and confirmed with fundus autofluorescence.[3] Trihexyphenidyl is used to treat extrapyramidal symptoms and may cause mydriasis, which can lead to blurred vision and photophobia. Our patient did not have any subjective or objective findings to suspect the antiepileptic-related ocular side effects.
Figure 2: (a and b) Showing hyperreflective area in the corneal periphery with anterior mid stromal involvement

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Thus, the patient was diagnosed with presumed olanzapine-related ocular toxicity. He was given spectacle correction and lubricating eyedrops and advised 6-monthly follow-ups.


  Discussion Top


Antipsychotics have been known to cause ocular pigmentary depositions. Ocular structures that are most affected include the eyelids, conjunctiva, cornea, and crystalline lens. The most common prevalent ocular side effect of phenothiazines, especially chlorpromazine, is anterior capsular and subcapsular lens pigmentation followed by corneal endothelial pigmentary deposits. The effect is dose-dependent and is frequently seen with chronic usage. This effect was first reported in 1964, where 70 patients on chronic chlorpromazine therapy for at least 3–5 years were found to have pigment deposition in skin, cornea, and lens capsule.[4] Subsequently, there were several reports of chlorpromazine-related ocular pigmentary depositions, especially over the cornea and lens capsule.[5],[6],[7] Other antipsychotics that were attributed to causing ocular pigmentary deposits include levomepromazine, fluphenazine, trifluoperazine, and clozapine.[8],[9],[10] To the best of our knowledge, there has been only one case report of anterior segment pigmentary deposits associated with olanzapine use, 2 years after the cessation of chlorpromazine.[11] It is postulated that chlorpromazine binds to the serotonin and dopamine receptors in the cornea, resulting in corneal deposition. This is followed by photosensitization of tissue proteins after the accumulation of the drug in these tissues. Olanzapine is a second-generation atypical antipsychotic agent with a high affinity for serotonin and dopamine receptors; thus, it can cause ocular depositions similar to phenothiazines.[11] Its adverse effects on glucose and lipid metabolism are of serious concern and can affect ocular structures more often than we anticipate.[12] However, further studies are needed to validate these hypotheses. In our patient, olanzapine may have produced side effects similar to phenothiazines as it also acts on dopamine receptors. These changes should be considered as possible side effects of olanzapine. Although the corneal deposits did not cause any diminution of vision in our patient, such a possibility cannot be ruled out.


  Conclusion Top


With newer atypical antipsychotics being increasingly used for their therapeutic superiority and fewer adverse effects in psychiatric disorders, we must carefully examine such patients. Patients on long-term olanzapine therapy should be considered for regular ophthalmological review.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Johnson AW, Buffaloe WJ. Chlorpromazine epithelial keratopathy. Arch Ophthalmol 1966;76:664-7.  Back to cited text no. 1
    
2.
Shinhora T, Periyasamy P, Bidasee K, Ayaki M, Rajan E. Epilepsy cataract: Valproic acid suppresses the Nrf2 dependent stress/antioxidant protection. Invest Ophthalmol Vis Sci 2013;54:5948.  Back to cited text no. 2
    
3.
Mateo J. Value of fundus autofluorescence imaging in a rare case of clonazepam associated retinopathy. Acta Ophthalmol 2012;90. doi: 10.1111/j. 1755-3768.2012.S076.x.  Back to cited text no. 3
    
4.
Greiner AC, Berry K. Skin pigmentation and corneal and lens opacities with prolonged chlorpromazine therapy. Can Med Assoc J 1964;90:663–5.  Back to cited text no. 4
    
5.
Webber SK, Domniz Y, Sutton GL, Rogers CM, Lawless MA. Corneal deposition after high-dose chlorpromazine hydrochloride therapy. Cornea 2001;20:217–9.  Back to cited text no. 5
    
6.
Koh V, Khor WB, Lim L. Chlorpromazine-induced corneal toxicity. Arch Ophthalmol 2012;130:1409.  Back to cited text no. 6
    
7.
Huff LS, Prado R, Pederson JF, Dunnick CA, Lucas LM. Chlorpromazine-induced skin pigmentation with corneal and lens opacities. Cutis 2014;93:247-50.  Back to cited text no. 7
    
8.
Kassman T, Wetterberg L. Lens opacities and porphobilinogen-like substance in urine associated with levomepromazine. Acta Psychiatr Scand 1967;43:163–8.  Back to cited text no. 8
    
9.
Ceylan E, Ozer MD, Yilmaz YC, Kartal B, Yildiz Ekinci D, Çinici E, et al. The ocular surface side effects of an anti-psychotic drug, clozapine. Cutan Ocul Toxicol 2016;35:62–6.  Back to cited text no. 9
    
10.
Borovik AM, Bosch MM, Watson SL. Ocular pigmentation associated with clozapine. Med J Aust 2009;190:210–1.  Back to cited text no. 10
    
11.
Choy BN, Ng AL, Shum JWH, Fan MCY, Lai JSM. A case report- Anti-psychotic agents related ocular toxicity. Medicine (Baltimore) 2016;95:e3360.  Back to cited text no. 11
    
12.
De Hert M, Detraux J, van Winkel R, Yu W, Correll CU. Metabolic and cardiovascular adverse effects associated with antipsychotic drugs. Nat Rev Endocrinol 2011;8:114-26.  Back to cited text no. 12
    


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