|Year : 2019 | Volume
| Issue : 6 | Page : 423-430
|Ocular side effects of systemic drugs used in dermatology
Bhanu Prakash1, H Mohan Kumar2, Saranya Palaniswami1, Borra Harish Lakshman2
1 Department of Dermatology, Vydehi Hospital, VIMS and RC, Bengaluru, Karnataka, India
2 Department of Ophthalmology, Sri Devaraj Urs Medical College and Research Centre, Kolar, Karnataka, India
|Date of Web Publication||7-Nov-2019|
Professor, Department of Dermatology, Vydehi Hospital, VIMS and RC, Bengaluru, Karnataka
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Some systemically used drugs in managing dermatologic disorders have associated severe side effects, of which eye involvement is very significant. There are various mechanisms for these drugs to cause damage to the eye. The damage to the eye can be acute as in Stevens–Johnson syndrome or chronic as with chloroquine and hydroxychloroquine toxicity. Knowledge about these drugs and information about the mechanisms and types of damage to the eye are essential. It is also important to understand the monitoring mechanisms to diagnose early and limit the damage. Newer investigative tools, especially the imaging techniques help us to diagnose the adverse effects at an early stage. All these issues are discussed in brief here.
Keywords: Adverse effects, dermatology, eye, systemic drugs
|How to cite this article:|
Prakash B, Kumar H M, Palaniswami S, Lakshman BH. Ocular side effects of systemic drugs used in dermatology. Indian J Dermatol 2019;64:423-30
|How to cite this URL:|
Prakash B, Kumar H M, Palaniswami S, Lakshman BH. Ocular side effects of systemic drugs used in dermatology. Indian J Dermatol [serial online] 2019 [cited 2020 Jan 19];64:423-30. Available from: http://www.e-ijd.org/text.asp?2019/64/6/423/270546
| Introduction|| |
There is a significant association between the skin and the eyes. There are some diseases which manifest jointly with the involvement of the skin and the eyes, called oculocutaneous diseases. There is another group where some drugs used commonly in managing skin diseases have a high incidence of eye side effects leading rarely to even blindness.
The eye is the second most common site to manifest drug toxicity, after the liver [Level II-1]. It is essential for a dermatologist to be aware of the potential complications before starting a systemic drug to limit eye damage [Level II-2].
| Level of Evidence|| |
- Level I: Evidence obtained from at least one properly designed randomized controlled trial
- Level II-1: Evidence obtained from well-designed controlled trials without randomization
- Level II-2: Evidence obtained from well-designed cohort or case-control analytic studies, preferably from more than one center or research group
- Level II-3: Evidence obtained from multiple time series with or without the intervention. Dramatic results in uncontrolled trials might also be regarded as this type of evidence
- Level III: Opinions of respected authorities, based on clinical experience, descriptive studies, or reports of the expert committee.
| Etiopathogenesis|| |
The drug reaches the eye via systemic circulation and through choroidal and retinal circulation. At times, the drug sensitizes the immune system to develop antibodies against ocular tissue or forms immune complex deposit and targets the eye. The drugs find difficulty in entering the eye because of its avascular structures such as cornea and vitreous. There are three major hindrances which impede drugs from causing toxicity in the eye: blood–brain barrier, blood-aqueous barrier, and blood-retinal barrier. In states of inflammation, the blood-aqueous and blood-retinal barriers leak and the drug finds its way into the eye.
Some of the predisposing factors for eye damage are listed in [Table 1].
The following hypothetical factors have been postulated to cause adverse effects in the eye:
- Specific biochemical reaction
- Altered metabolism of the drug
- A drug enters the systemic circulation and then the eye through retinal or uveal circulation. The normal anatomy further facilitates the drug to enter into structures such as lens, cornea
- The drug or its metabolite can accumulate in certain sites such as lens and cornea causing toxicity
- Drugs such as chloroquine and chlorpromazine have a high affinity to melanin and damage ocular tissues [Level II-3]
- Underlying liver or renal damage. Altered pharmacology such as decreased excretion, prolonged half-life, or metabolite formation leads to more drug concentration in the eye causing damage to ocular tissue [Level II-1]
- Lens filters ultraviolet (UV) rays in a normal eye. However, photosensitizers such as allopurinol, phenothiazine, and chloroquine. can cause changes in the lens, enhance the penetration of UV rays leading to eye changes such as cataract formation.
The drugs used commonly in dermatology causing definite ocular side effects are listed in [Table 2] and are discussed briefly here.
|Table 2: Systemic drugs commonly used in dermatology that can lead to eye damage|
Click here to view
| Antibiotics|| |
Massive doses can cause retinal hemorrhages, retinal edema, cotton-wool spots, arteriolar narrowing, venous beading, rubeosis iridis, neovascular granuloma, pigmentary retinopathy and optic atrophy. Preservatives (methylparaben, propylparaben, and edetate disodium) may play an additive role in the toxicity [Level II-2].
A study found a 4.5-fold increase in the risk of retinal detachment in patients using oral fluoroquinolones, observed within 5 days of starting the medication. The authors hypothesized that fluoroquinolones might alter the vitreous of the eye leading to the detachment, possibly in a similar way that fluoroquinolone use has been associated with an increased risk of Achilles tendon rupture [Level II-1].
Linezolid, an oxazolidinone antibiotic, can contribute to optic nerve damage when treated beyond 28 days [Level III].
Nalidixic acid causes increased fluid pressure, leading to headache, vision disturbance, color vision defect and swollen optic nerve, leading to papilledema, and reversible sixth nerve palsy.
Synthetic penicillins (amoxicillin and ampicillin) can cause mild redness of the eyes, itching, and dry eyes. They are commonly associated with causing Steven–Johnson syndrome (SJS) and toxic epidermal necrolysis.
Sulfonamides both topically and systemically administered cause the conjunctival and corneal scarring in SJS [Level I].
Tetracycline has similar side effects as synthetic penicillins. In addition, it causes light sensitivity, blurred vision, diplopia, and rarely papilledema. Long-term use has been associated with idiopathic intracranial hypertension sometimes leading to permanent vision loss. Pigmentation of various body sites including the skin, nails, bone, mouth, and eyes secondary to minocycline therapy is well-known. Although skin and mucosal pigmentation is reversible, eye pigmentation is usually irreversible. Scleral pigmentation consists of a blue-gray 3–5 mm band starting at the limbus. If pregnant women take tetracycline antibiotics, it may cause cataract in the developing fetus [Level III].
Phenytoin causes nystagmus, diplopia, frequent weakness of accommodation, and convergence.,
Chloroquine and hydroxychloroquine (HCQ) are used in treating various autoimmune diseases. Reported incidence of toxicity ranges from 1% to 25%. Studies have shown that the incidence of retinopathy is 10% and 4% in unmonitored patients taking 250 mg/d of chloroquine and 400 mg/d of HCQ [Level II-3]. The pattern of retinopathy caused by both HCQ and chloroquine is similar, but it is much less common with HCQ. They bind to melanin and gets concentrated in the iris, ciliary body, and retinal pigment epithelium (RPE), altering normal physiologic function. This leads to degenerative changes of the RPE. Early changes are characterized by the asymptomatic blunting of the foveal reflex and RPE granular pigmentary changes. Later with the progression of the disease, it manifests as blurred vision, scotomas, and photopsias. Bull's-eye maculopathy (BEM) and arterial attenuation occur in the later stages of the disease, [Level II-2]. Corneal deposits are frequently bilateral. Macular degeneration is reversible initially, but when the total dose is >100 g irreversible changes occur [Level II-2].
Chloroquine retinopathy progresses from near normal prematurity through the various stages of maculopathy and finally to end-stage maculopathy characterized by paracentral and eventually central scotoma with a characteristic BEM, a clear zone of depigmentation around the fovea.
Reported risk factors for ocular toxicity of the drug include age >60-year-old, high-fat level, daily dose >400 mg, or >6.5 mg/kg body weight for short individuals, cumulative dose >1000 g, duration of use >5 years, renal or hepatic dysfunction, obesity, and preexisting retinal disease or maculopathy [Level II-3].
Damage to the eyes can happen even after stopping the drug because of its long half-life (50 days). In fact, the drug may be detected in the blood and urine of the patients 5 years after stopping therapy. Damage has been reported to continue for up to 7 years after cessation of therapy [Level III].
There is no general consensus on the definition of true hydroxychloroquine retinopathy. Bernstein required the development of persistent paracentral or central visual field scotomas, >9 months treatment, a bull's eye lesion. Easterbrook suggested bilateral, reproducible, and positive field defects shown by two different visual field tests, namely, Amsler grid test and an automated 10° visual field test as definitive evidence of retinal toxicity.
The Royal College of Ophthalmologists and the American Academy of Ophthalmology (AAO) have published guidelines for baseline, and periodic tests to be done while on therapy with chloroquine and HCQ. They recommend baseline fundus examination and no examinations for 5 years. After 5 years, high-risk patients should be followed yearly and nonhigh risk patients should be followed at every 3 years [Level II-3].
Diagnosis of early antimalarial toxicity: Methods recommended include ophthalmological examination, visual field testing, color vision testing, fluorescein angiography, and electrophysiological tests. Central field testing comprising the Amsler grid and Humphrey field test are the two most commonly used visual field testing methods.,
Male patients should have a baseline color vision test performed to exclude any underlying congenital color deficiency that may otherwise be confused with toxicity. [Level II-3].
Using tools such as spectral-domain ocular coherence tomography multifocal electroretinogram (mf-ERG), or fundus autofluorescence will help detect retinopathy at an early stage [Level II-3].
There is currently no gold standard for identifying ocular toxicity before its development, which has led to controversy regarding recommendations for screening patients taking HCQ. Some authors, suggest that routine screening for ocular toxicity be abandoned when recommended dosages are prescribed. Canadian Rheumatology Association, Spalton and Block suggest screening once in 12–18 months, 3 years, and 5 years, respectively.
After examining the available evidence, the AAO recently recommended different screening approaches, according to the risk status [Level II-2].
In spite of differing recommendations, studies have confirmed the doctor's willingness to continue screening for eye toxicity due to factors such as legal liability and patient safety.,
| Antitubercular Drugs|| |
Rifabutin has been associated with a characteristic hypopyon, anterior uveitis, intermediate uveitis, panuveitis, and retinal vasculitis. Dosage, duration, and co-administration of drugs such as clarithromycin and ritonavir are significant risk factors through the inhibition of hepatic cytochrome P450 enzymes [Level-III].
Rifampin is intensely red and causes tears to become orange-red. Tears may permanently stain soft-contact lenses.
Ethambutol: Optic neuritis is the most important potential side effect of ethambutol hydrochloride. Retrobulbar neuritis is most common, with the involvement of either axial fibers or less commonly, periaxial fibers. It is an optic nerve toxin causing dose-dependent damage slowly and bilaterally, and irreversible changes. The incidence of nerve damage after 2 months of therapy is 18%, 6%, and 1% in participants receiving 35, 25, and 15 mg/kg/day of ethambutol, respectively [Level II-2]. There are two types of visual defects in ethambutol-induced damage. In the central type, there is central or centrocecal scotomas and impairment of blue-yellow color vision. Peripheral type causes red-green dyschromatopsia. The mean interval between the onset of therapy and toxic effects ranges from 3 to 5 months.
Regular eye examination aids in the early diagnosis. Visual field typically shows a cecocentral or bitemporal defect. Dyschromatopsia may be the earliest sign of toxicity, and blue-yellow color changes are the most common color defect.
Isoniazid rarely causes toxic optic neuropathy and optic atrophy, particularly when given in combination with ethambutol.
Some authors recommend stopping both isoniazid and ethambutol in severe ocular toxicity. In less severe cases, isoniazid should also be stopped if no vision improvement occurs 6 weeks after stopping ethambutol.,
| Nonsteroidal Anti-Inflammatory Drugs|| |
Ibuprofen causes disturbance of color vision, xerosis, diplopia, blurring of vision and optic neuritis, and permanent visual deformities in prolonged usage. Indomethacin causes whorl-like stromal opacities in 11%–16% of patients. Corneal deposit, diplopia, mydriasis, and possible retinal damage are also reported. These usually improve with discontinuation of the drug. Phenylbutazone, sulfa derivatives of nonsteroidal anti-inflammatory drugs, and acetaminophen are associated with Stevens Johnson syndrome [Level-III].
Because botulinum toxin diffuses into levator muscles, it may cause eyelid ptosis and double vision.
It is used in postmenopausal women or as an adjunct to systemic steroids therapy to prevent the bone calcium loss. It can cause reversible orbital inflammation, uveitis, and scleritis.,
Cyclosporine and tacrolimus
They cause reversible posterior encephalopathy syndrome. These patients will present with bilateral vision loss. Magnetic resonance imaging usually confirms the diagnosis and the source of the lesion.
Griseofulvin causes macular degeneration, macular edema, papilledema, pseudotumor cerebri, and photosensitivity.
Intravenous Cidofovir causes anterior uveitis in 26%–44% of patients. Patients are usually asymptomatic. All patients receiving cidofovir should be followed by careful eye examination. If anterior uveitis develops, withdrawal of cidofovir and treatment with topical steroids help to resolve the symptoms. Oral probenecid along with IV cidofovir delays the onset of uveitis [Level II-3].
Clofazimine is a red phenazine dye used mainly in leprosy and some other dermatological disorders. Clofazimine crystal deposition occurs in cornea leading to irreversible BEM and retinopathy, especially with dosages of 300 mg/day.
Steroids are commonly used for a wide range of dermatological conditions - allergies, inflammatory conditions, postherpetic neuralgia, autoimmune conditions, vesiculobullous disorders, etc. Any route of administration - topical, oral, intramuscular, intravenous, etc., can damage the eye. The two major complications of steroid use in the eye are cataract and glaucoma.
Cataract is often the posterior subcapsular type. Later, the anterior subcapsular can be affected. It develops rapidly and becomes symptomatic in weeks to months. In general, patients on <10 mg prednisolone/day, treated for <4 years do not develop cataract. Children are more susceptible and a genetic relation is also postulated to susceptibility. Once the cataract is formed, the course of the disease is not predictable. Some might resolve, whereas others may continue to progress.
Screening for cataracts may be performed by the slit-lamp examinations conducted three or four times a year for patients on long-term therapy and twice a year for patients taking intermittent topical ocular or systemic steroids [Level II-2].
Glaucoma usually manifests when steroids are used for at least 2 weeks. They are usually asymptomatic and reversible on discontinuation. Interestingly, glaucoma is more common in patients who are steroid responders. Glaucoma is more often associated with topical ocular or periocular steroids than with systemic steroids. A person with glaucoma planned for steroids therapy should consult an ophthalmologist for monitoring of eye pressure. Recommended screening includes a baseline intraocular pressure measurement, then routine pressure measurements obtained for every few weeks initially, and then every few months.
Interferon-α is a recombinant DNA-based protein. Toxicity is due to the deposition of immune complexes in the vessels and activated complement C5a with infiltration of leukocytes. Interferon causes the retinal damage anywhere from 2 weeks to 3 months after starting. Changes include cotton-wool spots, intra-retinal, preretinal hemorrhage, and macular edema finally leading to retinopathy. Other manifestations include central retinal artery and vein occlusion, cystoid macular edema, and optic disc edema leading to irreversible vision loss. They are more common in patients with diabetes and hypertension. The damage is asymptomatic, dose-independent and self-limiting with cessation of the drug.,
It is known to cause dryness of mucous membranes including the eye. Other ocular side effects include meibomian gland dysfunction, blepharoconjunctivitis, corneal opacities, decreased dark adaptation, keratitis, photophobia, teratogenic ocular abnormalities, and disturbances in the night vision. The dryness and irritation can cause difficulty in wearing the contact lenses. Visual disturbances may also occur as a part of pseudotumor cerebri.
Dermatologists should always ask patients about any vision symptoms before and during isotretinoin therapy and refer to ophthalmologist, if any complain. Another warning to be given is that it precludes them from having refracti meta-analytic study of reported adverse events due to isotretinoin grouped the adverse ocular events to isotretinoin into three as follows:
- “Certain” includes abnormal meibomian gland secretion, blepharoconjunctivitis, corneal opacities, decreased dark adaptation, decreased tolerance to contact lens, decreased vision, increased tear osmolarity, keratitis, meibomian gland atrophy, myopia, ocular discomfort, ocular sicca, photophobia, and teratogenic ocular abnormalities
- “Probable/Likely” are decreased color vision and permanent loss of dark adaptation and
- “Possible” association includes permanent keratoconjunctivitis sicca.
Guidelines for ocular examination for patients on isotretinoin are available [Level-I].
They decrease tears, leading to dry eye problem, pupillary dilatation, a decrease in focusing ability (accommodation), and worsen acute closed-angle glaucoma. Gonioscopy examination helps in the early diagnosis.,,
Antihitamines in people with narrow-angle glaucoma result in blurred vision, redness, halos around light objects, and pain.
Other ocular side effects include mydriasis (pupil dilation), dry eye, keratitis sicca, contact lens intolerance, decreased accommodation (focusing ability), etc. Antihistamines have weak atropine-like action, can cause mydriasis, anisocoria, decreased accommodation, and blurred vision.
Birth control pill
Birth control pills can lead to dry eye syndrome, photosensitivity, and rarely cataracts, macular degeneration, and retinal vascular problems.
Phosphodiesterase type 5 inhibitors
Phosphodiesterase type 5 inhibitors include sildenafil, vardenafil, and tadalafil. They inhibit cyclic guanosine monophosphate (cGMP)–phosphodiesterase type 5 (PDE 5), increasing the effect of nitric oxide which is responsible for the degradation of cGMP in the corpus cavernosum. Increased levels of cGMP result in smooth muscle relaxation and inflow of blood. These drugs have an affinity for PDE 6 enzyme found in the retina. Ocular side effects occur in 3%, 10%, and 50% of individuals taking 50 mg, 100 mg, and 200 mg doses, respectively [Level II-2]. The side effect starts 15–30 min after ingestion of the drug and peaks in 60 min. They include pupillary dilation, redness, dryness, blurred vision, and a temporary bluish discoloration to the vision. Caution is required in individuals with retinitis pigmentosa, macular degeneration, and diabetic retinopathy [Level-III].
Some patients, who have genetic disorders of retinal PDE, have been associated with nonarteritic ischemic optic neuropathy, leading to permanent vision loss. All patients had a low cup-to-disk ratio. “Disks at risk” are full disks with little to no cupping. The Federal Aviation Administration has recommended that pilots not to fly within 6 h of taking the drug.
Psoralens and psoralen-ultraviolet A (PUVA) are used in a wide range of dermatologic disorders commonly vitiligo and psoriasis. Adequate eye protection from sun is always advised to prevent the eye damage. Dermatologists who employ PUVA treatment should be concerned about photo keratoconjunctivitis and the dry eye syndrome. Guidelines should be strictly adhered to [Level-III].
Biologics are a new class of drugs with target specific action used as an alternative to conventional immunosuppressives and immunomodulators. They are used commonly in conditions such as psoriasis, pemphigus and related disorders, collagen vascular disorders, and extensive alopecia areata. Common drugs are alefacept, adalimumab, etanercept, infliximab, etc. Limited use of these drugs still has limited the expression of many side effects.
Optic neuritis, which is an inflammatory demyelination of the optic nerve, has been observed in patients on etanercept, infliximab, and adalimumab. Dermatologists should monitor for the early symptoms which include periocular pain and unilateral loss of visual acuity.
Etanercept is reported to cause orbital myositis, rituximab causing optic neuritis and uveitis, and secukinumab causing conjunctivitis are reported.
Role of dermatologist to limit eye side effects
Dermatologists need to be aware of ocular side effects potentially posed by certain common medications. Before starting on high-risk medications, they should ask about a history of glaucoma, cataract, or any other issues. While starting medications patients should be encouraged to report, if they notice any of the complaints as given in [Table 3]. Also they need to be cautious about the various factors that determine the damage to the eye [Table 4]. Correct diagnosis, using principles of rational prescription for a dermatologist goes a long way in minimizing the damage to the eye and thus saving the patient of a potential critical toxicity – blindness. Furthermore, prompt reporting of new adverse drug reactions will enhance our knowledge and effectively treat the patient.
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Conflicts of interest
There are no conflicts of interest.
| References|| |
Li J, Tripathi RC, Tripathi BJ. Drug-induced ocular disorders. Drug Saf 2008;31:127-41.
Daniel BS, Orchard D. Ocular side-effects of topical corticosteroids: What a dermatologist needs to know. Australas J Dermatol 2015;56:164-9.
Koneru PB, Lien EJ, Koda RT. Oculotoxicities of systemically administered drugs. J Ocul Pharmacol 1986;2:385-404.
Valerie Q, Wren OD. Ocular & visual side effects of systemic drugs clinically relevant toxicology and patient management. J Behav Optom 2000;11:149-57.
Gokulgandhi MR, Vadlapudi AD, Mitra AK. Ocular toxicity from systemically administered xenobiotics. Expert Opin Drug Metab Toxicol 2012;8:1277-91.
Mycek MJ, Harvey RA, Champe PC. Lippincott's Illustrated Reviews: Pharmacology. 2nd
ed. Philadelphia: Lippincott-Raven; 1997.
Jaanus SD, Bartlett JD, Hiett JA. Ocular effects of systemic drugs. In: Bartlett JD, Jaanus SD, editors. Clinical Ocular Pharmacology. 3rd
ed. Boston: Butterworth-Heinemann; 1995. p. 9571006.Hancock HA, Guidry C, Read RW, Ready EL, Kraft TW. Acute aminoglycoside retinal toxicityin vivo
and in vitro
. Invest Ophthalmol Vis Sci 2005;46:4804-8.
Etminan M, Forooghian F, Brophy JM, Bird ST, Maberley D. Oral fluoroquinolones and the risk of retinal detachment. JAMA 2012;307:1414-9.
Karuppannasamy D, Raghuram A, Sundar D. Linezolid-induced optic neuropathy. Indian J Ophthalmol 2014;62:497-500.
] [Full text]
Sethuraman G, Sharma VK, Pahwa P, Khetan P. Causative drugs and clinical outcome in Stevens Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), and SJS-TEN overlap in children. Indian J Dermatol 2012;57:199-200.
] [Full text]
Woodard DR, Woodard RB. Drugs in Primary Eye Care. 2nd
ed. Connecticut: Appleton and Lange; 1997.
Haskes C, Shea M, Imondi D. Minocycline-induced scleral and dermal hyperpigmentation. Optom Vis Sci 2017;94:436-42.
Santaella RM, Fraunfelder FW. Ocular adverse effects associated with systemic medications: Recognition and management. Drugs 2007;67:75-93.
Thakral A, Shenoy R, Deleu D. Acute visual dysfunction following phenytoin-induced toxicity. Acta Neurol Belg 2003;103:218-20.
Hilton EJ, Hosking SL, Betts T. The effect of antiepileptic drugs on visual performance. Seizure 2004;13:113-28.
Marmor MF, Carr RE, Easterbrook M, Farjo AA, Mieler WF; American Academy of Ophthalmology.
Recommendations on screening for chloroquine and hydroxychloroquine retinopathy: A report by the American Academy of Ophthalmology. Ophthalmology 2002;109:1377-81.
Pandya HK, Robinson M, Mandal N, Shah VA. Hydroxychloroquine retinopathy: A review of imaging. Indian J Ophthalmol 2015;63:570-4.
] [Full text]
Rosenthal AR, Kolb H, Bergsma D, Huxsoll D, Hopkins JL. Chloroquine retinopathy in the rhesus monkey. Invest Ophthalmol Vis Sci 1978;17:1158-75.
Spalton DJ. Retinopathy and antimalarial drugs – The British experience. Lupus 1996;5 Suppl 1:S70-2.
Ding HJ, Denniston AK, Rao VK, Gordon C. Hydroxychloroquine -related retinal toxicity. Rheumatology (Oxford) 2016; 55:957-67.
Anderson C, Blaha GR, Marx JL. Humphrey visual field findings in hydroxychloroquine toxicity. Eye (Lond) 2011;25:1535-45.
Tett SE, Cutler DJ, Day RO, Brown KF. Bioavailability of hydroxychloroquine tablets in healthy volunteers. Br J Clin Pharmacol 1989;27:771-9.
Vavvas D, Huynh N, Pasquale L, Berson EL. Progressive hydroxychloroquine toxicity mimicking low-tension glaucoma after discontinuation of the drug. Acta Ophthalmol 2010;88:156-7.
Bernstein HN. Ocular safety of hydroxychloroquine. Ann Ophthalmol 1991;23:292-6.
Easterbrook M. The ocular safety of hydroxychloroquine. Semin Arthritis Rheum 1993;23:62-7.
Bourke B, Jones S, Rajammal AK, Silman A, Smith R. Hydroxychloroquine and ocular toxicity recommendations on screening. The Royal College of Ophthalmologists in Association with the British Society for Rheumatology and the British Association of Dermatologists; 2009.
Marmor MF, Kellner U, Lai TY, Lyons JS, Mieler WF; American Academy of Ophthalmology, et al.
Revised recommendations on screening for chloroquine and hydroxychloroquine retinopathy. Ophthalmology 2011;118:415-22.
Easterbrook M. Detection and prevention of maculopathy associated with antimalarial agents. Int Ophthalmol Clin 1999;39:49-57.
Blyth C, Lane C. Hydroxychloroquine retinopathy: Is screening necessary? BMJ 1998;316:716-7.
Marmor MF, Carr RE, Easterbrook M, Farjo AA, Mieler WF; American Academy of Ophthalmology, et al.
Recommendations on screening for chloroquine and hydroxychloroquine retinopathy: A report by the American Academy of Ophthalmology. Ophthalmology 2002;109:1377-82.
Morsman CD, Livesey SJ, Richards IM, Jessop JD, Mills PV. Screening for hydroxychloroquine retinal toxicity: Is it necessary? Eye (Lond) 1990;4(Pt 4):572-6.
Silman A, Shipley M. Ophthalmological monitoring for hydroxychloroquine toxicity: A scientific review of available data. Br J Rheumatol 1997;36:599-601.
Canadian Rheumatology Association. Canadian consensus conference on hydroxychloroquine. J Rheumatol 2000;27:2919-21.
Block JA. Hydroxychloroquine and retinal safety. Lancet 1998;351:771.
Cox NH, Paterson WD. Ocular toxicity of antimalarials in dermatology: A survey of current practice. Br J Dermatol 1994;131:878-82.
Fraenkel L, Felson DT. Rheumatologists' attitudes toward routine screening for hydroxychloroquine retinopathy. J Rheumatol 2001;28:1218-21.
Shafran SD, Deschênes J, Miller M, Phillips P, Toma E. Uveitis and pseudojaundice during a regimen of clarithromycin, rifabutin, and ethambutol. MAC study group of the Canadian HIV trials network. N
Engl J Med 1994;330:438-9.
Chan RY, Kwok AK. Ocular toxicity of ethambutol. Hong Kong Med J 2006;12:56-60.
Huang SP, Chien JY, Tsai RK. Ethambutol induces impaired autophagic flux and apoptosis in the rat retina. Dis Model Mech 2015;8:977-87.
Kumar A, Sandramouli S, Verma L, Tewari HK, Khosla PK. Ocular ethambutol toxicity: Is it reversible? J Clin Neuroophthalmol 1993;13:15-7.
Melamud A, Kosmorsky GS, Lee MS. Ocular ethambutol toxicity. Mayo Clin Proc 2003;78:1409-11.
Rao LV, Bhandary SV, Devi AR, Ninan A, Jain V, Veluri H. Ocular toxicity of anti-tuberculous treatment. Kerala J Ophthalmol 2006;17:198-200.
Sivakumaran P, Harrison AC, Marschner J, Martin P. Ocular toxicity from ethambutol: A review of four cases and recommended precautions. N
Z Med J 1998;111:428-30.
Kokkada SB, Barthakur R, Natarajan M, Palaian S, Chhetri AK, Mishra P, et al.
Ocular side effects of antitubercular drugs – A focus on prevention, early detection and management. Kathmandu Univ Med J (KUMJ) 2005;3:438-41.
Muchnick BG. The ocular manifestations of systemic drugs. Today Optom 1998;75:44-52.
Kim SJ, Flach AJ, Jampol LM. Nonsteroidal anti-inflammatory drugs in ophthalmology. Surv Ophthalmol 2010;55:108-33.
Ricci LH, Navajas SV, Carneiro PR, Söderberg SA, Ferraz CA. Ocular adverse effects after facial cosmetic procedures: A review of case reports. J Cosmet Dermatol 2015;14:145-51.
McKague M, Jorgenson D, Buxton KA. Ocular side effects of bisphosphonates: A case report and literature review. Can Fam Physician 2010;56:1015-7.
Fraunfelder FW, Fraunfelder FT. Adverse ocular drug reactions recently identified by the national registry of drug-induced ocular side effects. Ophthalmology 2004;111:1275-9.
Kapoor KG, Mirza SN, Gonzales JA, Gibran SK. Visual loss associated with tacrolimus: Case report and review of the literature. Cutan Ocul Toxicol 2010;29:137-9.
Scott RA, Pavesio C. Ocular side-effects from systemic HPMPC (Cidofovir) for a non-ocular cytomegalovirus infection. Am J Ophthalmol 2000;130:126-7.
Yawalkar SJ, Vischer W. Lamprene (clofazimine) in leprosy. Basic information. Lepr Rev 1979;50:135-44.
Craythorn JM, Swartz M, Creel DJ. Clofazimine-induced bull's-eye retinopathy. Retina 1986;6:50-2.
Renfro L, Snow JS. Ocular effects of topical and systemic steroids. Dermatol Clin 1992;10:505-12.
Phulke S, Kaushik S, Kaur S, Pandav SS. Steroid-induced glaucoma: An avoidable irreversible blindness. J Curr Glaucoma Pract 2017;11:67-72.
David DS, Berkowitz JS. Ocular effects of topical and systemic corticosteroids. Lancet 1969;2:149-51.
Crochet M, Ingster-Moati I, Even G, Dupuy P. Retinopathy caused by interferon alpha associated with ribavirin therapy and the importance of the electro-oculogram: A case report. J Fr Ophtalmol 2004;27:257-62.
Medhat E, Esmat G, Hamza E, Abdel Aziz A, Fouad Fathalah W, Darweesh SK, et al.
Ophthalmological side effects of interferon therapy of chronic hepatitis C. Hepatobiliary Surg Nutr 2016;5:209-16.
Nishiwaki H, Ogura Y, Miyamoto K, Matsuda N, Honda Y. Interferon alfa induces leukocyte capillary trapping in rat retinal microcirculation. Arch Ophthalmol 1996;114:726-30.
Fraunfelder FT, Fraunfelder FW, Edwards R. Ocular side effects possibly associated with isotretinoin usage. Am J Ophthalmol 2001;132:299-305.
Richa S, Yazbek JC. Ocular adverse effects of common psychotropic agents: A review. CNS Drugs 2010;24:501-26.
Goethe JW, Woolley SB, Cardoni AA, Woznicki BA, Piez DA. Selective serotonin reuptake inhibitor discontinuation: Side effects and other factors that influence medication adherence. J Clin Psychopharmacol 2007;27:451-8.
Koçer E, Koçer A, Özsütçü M, Dursun AE, Krpnar İ. Dry eye related to commonly used new antidepressants. J Clin Psychopharmacol 2015;35:411-3.
Moschos MM, Nitoda E. The impact of combined oral contraceptives on ocular tissues: A review of ocular effects. Int J Ophthalmol 2017;10:1604-10.
Azzouni F, Abu Samra K. Are phosphodiesterase type 5 inhibitors associated with vision-threatening adverse events? A critical analysis and review of the literature. J Sex Med 2011;8:2894-903.
Pomeranz HD, Bhavsar AR. Nonarteritic ischemic optic neuropathy developing soon after use of sildenafil (viagra): A report of seven new cases. J Neuroophthalmol 2005;25:9-13.
Marmor MF, Kessler R. Sildenafil (Viagra) and ophthalmology. Surv Ophthalmol 1999;44:153-62.
Calzavara-Pinton PG, Carlino A, Manfredi E, Semeraro F, Zane C, De Panfilis G, et al.
Ocular side effects of PUVA-treated patients refusing eye sun protection. Acta Derm Venereol Suppl (Stockh) 1994;186:164-5.
Backman HA. The effects of PUVA on the eye. Am J Optom Physiol Opt 1982;59:86-9.
Shenoi SD, Prabhu S; Indian Association of Dermatologists, Venereologists and Leprologists. Photochemotherapy (PUVA) in psoriasis and vitiligo. Indian J Dermatol Venereol Leprol 2014;80:497-504.
] [Full text]
Lin EJ, Reddy S, Shah VV, Wu JJ. A review of neurologic complications of biologic therapy in plaque psoriasis. Cutis 2018;101:57-60.
Dogra S, Daroach M. Handbook of Biologics & Biosimilars in Dermatology. 1st
ed. New Delhi: Jaypee Brothers Medical Press; 2018. p. 206-18.
Prakash B, Nadig P, Nayak A. Rational prescription for a dermatologist. Indian J Dermatol 2016;61:32-8.
] [Full text]
Prakash B, Singh G. Pharmacovigilance: Scope for a dermatologist. Indian J Dermatol 2011;56:490-3.
] [Full text]
[Table 1], [Table 2], [Table 3], [Table 4]
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