CE Credit - Case Report

Atypical -Associated Band Keratopathy

Sara Moses, OD; Lisa Schifanella, OD, MS; Ellen Prewitt, OD, FAAO

Abstract enzyme (ACE), lysozyme and uric acid. A chest x-ray was also Band keratopathy is a chronic condition that involves the ordered to rule out . The results, summarized in deposition of crystals in the anterior layers of the . There Table 1, revealed no significant abnormalities, particularly no are many etiologies, both ocular and systemic, that can result elevation of uric acid levels. Consequently, the band keratopathy in the formation of these crystals. These conditions include was presumed idiopathic and treated with artificial tears three chronic ocular inflammation, hypercalcemia, and gout. Herein times per day in each eye. The patient was also sent for we report a case of band keratopathy due to gout and discuss surgery in order to improve visual function. the possible systemic etiologies and management of band keratopathy.. Initial best corrected visual acuities following cataract surgery were 20/20 in each eye. However, over the course of a year, Case Report vision was reduced to the 20/25 level OD and 20/40 level OS, A 55-year-old retired African American male presented with dry with no improvement by pinhole testing. examination eye complaints and mild blurry vision. He reported that comfort revealed progression of band keratopathy in each eye and was was improved with the use of artificial tears, but that his vision now within the visual axis of the left eye (Figures 1&2). remained blurry. Over the prior two years he had been followed for a slowly progressing peripheral band keratopathy OU. His Due to the advancement of band keratopathy, blood work medical history was significant for type 2 diabetes, hypertension, was repeated for magnesium, phosphorous, and uric acid sleep apnea, alcohol dependence, and chronic . levels. Results of lab testing revealed elevated uric acid levels (Table 2), which suggested a possible diagnosis of gout. Best corrected visual acuities measured 20/40-2 OD and The patient was referred to his primary care physician who 20/30- OS and showed no improvement with pinhole testing. confirmed the diagnosis and began treatment with 100 mg of Extraocular muscle and functions were normal in each allopurinol daily. Subsequent eye examinations have revealed eye. Intraocular pressures were 16 mmHg OD and 14 mmHg OS. no progression of band keratopathy in either eye since initiation of treatment for gout. The patient was referred to a corneal Slit lamp examination revealed normal lids and adnexa. The specialist for evaluation due to the reduction in , band keratopathy had progressed across the inferior cornea and the determination was made to continue with artificial tear OU but was not yet within the visual axis of either eye. Dilated therapy and monitoring for the time being. fundus examination revealed significant and an unremarkable posterior segment in each eye.

Due to the progressive nature of the presumed calcific band Table 1. keratopathy, labs were ordered including complete blood count Lab Test Result Reference Range (CBC), basic metabolic panel (Chem-8), angiotensin-converting BUN 11 7-18 mg/dL CO2 31 18.4-27.4 mEq/L Creatinine 1.11 0.7-1.4 mg/dL Glucose 109 70-105 mg/dL Sara Moses, OD- Charlie Norwood Veterans Affairs Medical Center Chloride 103 98-107 mmol/dL Lisa Schifanella, OD, MS - Tuscaloosa Veterans Affairs Medical Center Potassium 4.3 3.5-5.1 mmol/L Ellen Prewitt, OD, FAAO - Tuscaloosa Veterans Affairs Medical Center Correspondence to: Sara Moses OD Sodium 143 136-146 mmol/L Charlie Norwood Veterans Affairs Medical Center Uric acid 6.9 2.6-7.2 mg/dL 950 15th Street, Augusta, GA 30904 E-mail: [email protected] ACE 38 9-67 U/L The authors have no financial or proprietary interest in any material or method Calcium 9.5 8.9-10.4 mg/dL mentioned in this article. This article has been peer reviewed.

Atypical Gout-Associated Band Keratopathy 375 Figure 1. Figure 2.

Discussion Band keratopathy is an opacification of the cornea due to Table 2. deposition of crystals in Bowman’s layer. Typically, the band begins in the corneal periphery, slowly progressing centrally Lab Test Result Reference Range and toward the visual axis. Eventually, the deposits coalesce Magnesium 2.3 1.6-3 mg/dL in a horizontal band-like plaque from limbus to limbus. The Phosphorus 2.9 2.3-4.3 mg/dL deposits are most frequently composed of calcium, although other particles, such as cystine or uric acid, can also have a Uric acid 8.7 2.6-7.2 mg/dL similar presentation.

The appearance of the plaques can range from flat and increase with chronic ocular inflammation, such as in visually insignificant gray-white opacities to bulky flakes and with corneal endothelial compromise. with devastating visual consequences.18 The plaques characteristically have a “cheesy” appearance with clear holes Ocular Associations in the opacified band which aids in the differentiation between A strong association exists between band keratopathy and band keratopathy and other corneal dystrophies or opacities. chronic ocular inflammation from sarcoidosis, Vogt Koyanagi These holes occur where corneal nerves pass through Harada syndrome, and HLA B-27-related disorders such as Bowman’s membrane and inhibit the deposition of crystals.5,18 juvenile idiopathic arthritis and ankylosing spondylitis. In Visual acuity and ocular discomfort depend on the severity the case of sarcoidosis, the link is theorized to be related to and location of the disease. As the deposits collect within the elevated serum calcium and vitamin D levels.9,16 Although cornea, the epithelium can become rough and irregular. If the ocular involvement with sarcoidosis commonly presents as corneal epithelium degrades, recurrent corneal erosions may uveitis, granulomas, or periphlebitis, band keratopathy occur. occurs in 4-5% of ocular sarcoidosis cases. For patients with HLA-B27 associated uveitis, Verhagen et.al showed that band The development of the plaques in band keratopathy is thought keratopathy tends to develop in eyes with reduced vision, and to be a result of a chemical imbalance between the cornea and that the band keratopathy itself is rarely the cause of acuity the tear film.21 Precipitation of the plaques into the cornea occur loss.20 with an increase in calcium levels in the tear film or when the pH of the ocular surface becomes basic; occasionally both Ocular surgeries and injections are also known to be associated occur simultaneously.13 Broadly speaking, the levels of tear film with band keratopathy. The long-term presence of silicone oil calcium increase with elevated serum calcium levels as well in the eye after repair has been shown to as with significant evaporation of the tears. These conditions increase the risk of band keratopathy. This is especially true arise in sicca and a variety of systemic conditions that when the silicone oil enters the anterior chamber and contacts produce hypercalcemia such as end-stage renal disease and the corneal endothelium. Doostdar et.al proposed that because hyperparathyroidism. Ocular surface pH has been shown to silicone is known to promote calcium absorption in bones, it

376 Clinical & Refractive Optometry 32.3, 2021 Table 3. Band keratopathy associated Systemic Associations conditions2,16,17,18,21 Band keratopathy is associated with a variety of ocular and systemic conditions (Table 3). These conditions primarily revolve Ocular Idiopathic End-stage Chronic corneal edema Ophthalmic drops around two factors: ocular inflammation and hypercalcemia. - Endothelial - With phosphates When there is no evidence of an ocular inflammatory condition compromise - Phosphate-based present in the setting of band keratopathy, it becomes necessary Chronic uveitis irrigation after alkali to assess for systemic cause. Lab testing is extremely useful - Herpes simplex burn in detecting the systemic conditions associated with band - Herpes zoster - Acute retinal necrosis with silicone oil keratopathy. A typical panel of labs for band keratopathy Corneal dystrophies Intraocular injection will include CBC, Chem-8, uric acid, ACE, and lysozyme. The Neurotrophic keratitis - Tissue plasminogen Chem-8 will provide information relating to kidney function and Keratitis sicca activator (tPA) electrolyte levels, including serum calcium levels. The CBC, ACE, and lysozyme assist in assessing for chronic systemic Systemic Hypercalcemia: Gout inflammation. ACE and lysozyme, particularly when combined - End stage renal Cystinosis with a chest x-ray, are useful in detecting sarcoidosis, while uric disease Chemical exposure acid evaluates for gout. - Hyperparathyroidism - Mercury fumes - Sarcoidosis - Calcium bichromate - Milk-alkali syndrome Lithium Hypercalcemia is the primary etiology for band keratopathy - Paget disease Familial band keratopathy due to a systemic condition. The list of possible disease entities - Discoid lupus Vogt Koyanagi Harada that can result in hypercalcemia is extensive and includes end erythematosus syndrome stage renal disease, hyperparathyroidism, sarcoidosis, milk-alkali - Malignancy Juvenile Idiopathic - Tuberous sclerosis arthritis syndrome, Paget disease of bone, discoid lupus, erythematosus, - Excessive vitamin D Denosumab malignancy, tuberous sclerosis, and excessive vitamin D.9 As - Excessive calcium serum calcium levels rise, the concentration of calcium in the intake tears also elevates. Under alkaline or evaporative conditions, the calcium can precipitate and deposit within the anterior layers of the cornea resulting in the development of band keratopathy. may also promote a local increase of calcium and subsequent deposition resulting in band keratopathy.5,13 There are also The association between end stage renal disease (ESRD) case reports describing development of band keratopathy and band keratopathy has long been discussed. As kidney after the use of tissue plasminogen activator (tPA) in post function deteriorates, it is common to also develop renal cataract inflammation; possibly due to the phosphate buffer in hyperparathyroidism resulting in elevated serum calcium the tPA preparation or as a result of endothelial compromise. and phosphate levels. In 2016, Weng et al investigated the Endothelial dysfunction during periods of inflammation may risk of band keratopathy development in ESRD. Compared to allow excess phosphate and calcium to diffuse from the controls, there was shown to be a 12.21 times higher risk of aqueous into the stroma. When conditions normalize and developing band keratopathy in ESRD patients.21 It has even the endothelium resumes extracting water from the cornea, been suggested that band keratopathy may be one of the most the elevated concentrations of phosphate and calcium in the frequent ocular complications relating to ESRD. Although most stroma allow precipitation in the anterior layers of the cornea patients with ESRD will be aware of their kidney failure, it is where the alkaline pH is more favorable to deposition.14 important to assess kidney function when the etiology of band keratopathy is unknown. There has been one reported case of band keratopathy associated with iridocorneal endothelial syndrome (ICE).22 Systemic medications and supplements must also be In ICE syndrome, the corneal endothelial cells are replaced considered when determining the etiology of band keratopathy. by migrating epithelial-like cells resulting in endothelial Medications such as lithium and denosumab have been dysfunction, corneal edema, and stromal changes. In 2018 associated with elevated serum calcium and the development Zygoura et.al published a case of recurrent band keratopathy of band keratopathy. Lithium use has been associated with associated with ICE. The case reported a recurrence of band hypercalcemia and parathyroid gland enlargement. Denosumab keratopathy following chelation treatment with ethylene- is commonly used for postmenopausal osteoporosis as it diamine-tetra-acetic acid (EDTA), but resolution after a inhibits RANKL, a nuclear factor kappa-B ligand that regulates combined approach of chelation followed by Descemet osteoclastic bone resorption. In 2019 Nguyen et.al reported membrane endothelial keratoplasty (DMEK). During a DMEK a case of band keratopathy development after initiation of procedure, the dysfunctional endothelium is removed and denosumab therapy. It was suggested that the denosumab replaced by healthy endothelium from donor tissue. Two therapy caused an imbalance in calcium and phosphate levels years after the procedure the band keratopathy had not resulting in the corneal calcific deposits.17 In addition, Calcium returned, suggesting that the dysfunctional endothelium was supplements are often emphasized as therapy for treatment contributing to the development of the calcific plaques.22 and prevention of osteoporosis. However, elevated calcium

Atypical Gout-Associated Band Keratopathy 377 intake combined with absorbable alkali can result in a triad of The ocular manifestations are dependent on the location of the hypercalcemia, acute kidney injury, and metabolic alkalosis tophi within the ocular structures. These uric acid deposits have known as milk-alkali syndrome.19 Band keratopathy can also been found in the , bulbar , cornea, trabecular present in this condition. Milk-alkali syndrome was initially meshwork, and even the .8 The resulting ocular conditions common due to over-treatment of peptic ulcer disease but has can include retinal vein occlusions, iridocyclitis, ocular recently increased due to the emphasis on calcium in treatment hypertension, dry , and band keratopathy.1,10,12 for osteoporosis. Interestingly, band keratopathy resulting from gout is unique in that the deposits are made of uric acid crystals instead of Band keratopathy is also a frequent complication of cystinosis, a calcium crystals. rare autosomal recessive storage disorder. This disease results in cystine crystals accumulating in cells throughout the body The initial management of gout is focused on risk reduction due to a defect in a membrane protein carrier.15 The systemic including reducing consumption of alcohol and sugar, weight effects include endocrine dysfunction, neurologic deterioration, loss, and managing comorbidities. When gout flares inevitably myopathy, and blindness. The condition usually results in the arise, they are managed with systemic steroids or NSAIDs to need for a kidney transplant. The ocular complications leading control inflammation. These can be taken orally or injected to vision loss include , glaucoma and corneal into the specific gouty flare. When these two management disease. As the crystals deposit throughout the body, they can strategies are insufficient or when the disease is causing also deposit within the cornea, trabecular meshwork, iris, and damage to organs, reduction of systemic uric acid levels is retina. Corneal deposits typically present within the first year of attempted. Typically, patients with this level of gout are given life and do not always present as band keratopathy. medications such as allopurinol or losartan which promote the excretion of uric acid. As urate levels fall, the tophi Familial band keratopathy is a very rare cause of band depositions throughout the body are occasionally reabsorbed. keratopathy and there have only been a few cases reported. Although reabsorption of the tophi can be beneficial, the main A complete systemic and ocular workup must be completed goal of therapy is to reduce gout flares and prevent disease before determining the cause to be familial. Although no progression. specific gene has been identified for familial band keratopathy, mutations in the human NBC1 gene have been associated Management with renal tubular acidosis, band keratopathy, and cataracts.3 Due to the varied presentations of band keratopathy, Unfortunately, cases of familial band keratopathy appear management is dependent on each individual patient. Corneal to have higher rates of recurrence after treatment as the topography will give a sense of the extent of focal irregularities underlying condition cannot be resolved. and their potential effect on vision. In all cases, the underlying etiology must be investigated and managed in attempt to Gout prevent progression of the ocular and potential systemic One of the less common etiologies of band keratopathy is gout, disease. Treatment of an underlying condition such as uveitis also known as monosodium urate crystal deposition disease. or hypercalcemia may allow the band keratopathy to resolve Uric acid is a product of purine metabolism that is primarily without aggressive treatment.6,9 Patients with mild symptoms excreted through the kidneys. Although its exact biological of discomfort or decreased vision are treated with artificial function is unknown, it has shown some antioxidant activity and tears, gels, and/or ointments. These ocular lubricants promote may be useful as an indicator of cell death.11 Over the course of a healthy tear film and can discourage the deposition of crystals this disease, uric acid levels in the blood stream rise and begin into the cornea. For more moderate to severe cases of band to deposit in various locations throughout the body. These uric keratopathy with corneal erosions, bandage soft or scleral gas acid depositions, called tophi, have a predilection for joints, permeable contact lenses can be used to improve both comfort particularly in the lower extremities, and result in inflammatory and vision. outbreaks. Although many patients with elevated uric acid may remain asymptomatic for years, the overall course tends to be Surgical intervention is frequently utilized for visually significant one of exacerbations and remissions. or painful band keratopathy cases. The most common surgical procedure for band keratopathy involves chelation with The classic presentation for a patient with gout is a 30 to ethylene-diamine-tetra-acetic acid (EDTA).7 In order to reach the 60-year-old male with obesity, hypertension, and alcohol underlying keratopathy, the epithelium needs to be removed. dependence. There is a 3% prevalence of gout among American This removal can be accomplished under topical anesthetic adults. The primary risk factors for gout include obesity, either mechanically, or with alcohol. When used, alcohol cardiovascular disease, diabetes, chronic kidney disease, allows the epithelium to be elevated, removed, preserved and alcohol consumption, and age. Systemic manifestations then replaced after completion of the procedure. In theory, include gout flare of a single joint, polyarticular gout flare of this improves comfort after the procedure. After epithelial multiple joints, tendons, or bursas, and tophaceous gout in debridement, the calcium plaques are exposed and can be soft tissue. Depending on the location and size of the tophi, the removed either mechanically or with EDTA. When EDTA is discomfort can range from mild irritation to debilitating pain. used, it is applied to the plaques, either in a well, sponge, or

378 Clinical & Refractive Optometry 32.3, 2021 pledget. As a chelator, EDTA binds to the calcium in the lesion of gout: a case report and review of the literature. BMC resulting in the dissolution of the plaques on the cornea.2 This . 18:11. doi: 10.1186/s12886-018-0669-6 often takes several minutes and multiple applications of EDTA 9. Johnston, R. L., Stanford, M. R., Verma, S., Green, W. T., Graham, Once the plaques have been removed, the corneal surface is E. M. (1995). Resolution of calcific band keratopathy after often still irregular. Many surgeons elect to smooth the surface lowering elevated serum calcium in a patient with sarcoidosis. with a diamond burr or phototherapeutic keratectomy (PTK).4 British Journal of Ophthalmology, 79(11), 1050–1050. doi: After the procedure, the resulting corneal abrasion is often 10.1136/bjo.79.11.1050 treated with a bandage contact with or without an amniotic 10. Lee, C.-Y., Chen, H.-C., Sun, C.-C., Lin, H.-Y., Lu, K.-H., Huang, membrane transplant (AMT). Small studies have shown that a J.-Y., … Yang, S.-F. (2019). Gout as a Risk Factor for Dry Eye combination method involving EDTA, PTK, and AMT can reduce Disease: A Population-Based Cohort Study. Journal of Clinical healing time and reduce recurrence.2,7 Medicine, 8(1), 62. doi: 10.3390/jcm8010062 11. Liu, D., Yun,Y., Yang, D., Hu, X., Dong, X., Zhang, N., Zhang, L., Conclusion Yin, H., Duan, W. (2019). What Is the Biological Function of Uric Determining the underlying etiology of band keratopathy, Acid? An Antioxidant Neural Protection or a Biomarker for Cell whether ocular or systemic, is critical in the management of Death. Disease Markers. doi: 10.1155/2019/4081962 patients presenting with this condition. When ocular etiologies 12. Lo, W. R., Broocker, G., Grossniklaus, H. E. (2005). are absent, lab testing can often provide the information we Histopathologic Examination of Conjunctival Tophi in Gouty need to give the patient an appropriate referral for systemic Arthritis. American Journal of Ophthalmology, 140(6), 1152– diagnosis. As systemic conditions are not static, lab tests 1154. doi: 10.1016/j.ajo.2005.07.023 may return normal in early stages and should be reordered 13. Mansour, A. M., Haddad, R. (2016). Optical coherence if progression is noted. For many of these patients with tomography of band keratopathy. BMJ Case Reports. doi: conditions such as sarcoid, end-stage renal disease, and gout, 10.1136/bcr-2016-218216 co-management with other medical professionals is essential 14. Moisseiev, E., Gal, A., Addadi, L., Caspi, D., Shemesh, G., for comprehensive care. Michaeli, A. (2013). Acute calcific band keratopathy: Case report and literature review. Journal of Cataract and Refractive Bibliography Surgery. 39(2): 292-294. doi: 10.1016/j.jcrs.2012.12.020 1. Ao, J, Goldblatt, Jf. Casson, R. (2017). Review of the ophthalmic 15. Mungan, N. (2000). Ultrasound Biomicroscopy of the Eye in manifestations of gout and uric acid crystal deposition. Clinical Cystinosis. Archives of Ophthalmology, 118(10), 1329. doi: and Experimental Ophthalmology. 45: 73-80. Doi: 10.1111/ 10.1001/archopht.118.10.1329 ceo.12749 16. Nascimento, H., Yasuta, M. K., Marquezan, M. C., Salomão, G. 2. Al-Hity, A., Ramaesh, K., Lockington, D. (2017). EDTA chelation H. A., González, D., Francesconi, C., … Belfort, R. (2015). Uveitic for symptomatic band keratopathy: results and recurrence. band keratopathy: child and adult. Journal of Ophthalmic Eye, 32(1), 26–31. doi: 10.1038/eye.2017.264 Inflammation and Infection, 5(1). doi: 10.1186/s12348-015- 3. Arora, R., Shroff, D., Kapoor, S., Nigam, S., Narula, R., Chauhan, 0062-z D., Jain, P. (2007). 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Atypical Gout-Associated Band Keratopathy 379 INSTRUCTIONS FOR 1 HOUR OF COPE CE CREDIT

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Atypical Gout-Associated Band Keratopathy

1. Which of the following is NOT a condition that can cause band keratopathy? Gout Hypercalcemia Hyperkalemia Chronic ocular inflammation

2. Band keratopathy is an opacification of the cornea due to deposition of crystals in which corneal layer? Bowman’s layer Descemet’s membrane Corneal stroma Corneal endothelium

3. Which of the following is NOT a crystal composition seen in band keratopathy? Calcium Potassium Uric Acid Cystine

4. Which of the following conditions DOES NOT have a strong association with band keratopathy? COPE ACCREDITED POST-COURSE TEST POST-COURSE ACCREDITED COPE Sarcoidosis Prostatic hyperplasia Vogt Koyanagi Harada syndrome Juvenile arthritis

380 Clinical & Refractive Optometry 32.3, 2021 5. Known ocular associations with band keratopathy include all of the following except: Silicon oil in retinal detachment repair Ocular injections Macula degeneration Tissue plasminogen activator (tPA) in post cataract inflammation

6. Gout is a unique associated system condition due to the crystal formation in band keratopathy consisting of what composition? Calcium Uric Acid Potassium Cysteine

7. Which of the following systemic medications have been associated with elevated serum calcium and the development of band keratopathy? Lithium Denosumab Alendronate Both A and B

8. In all cases, what is the essential management for patients who present with band keratopathy? Monitor Artificial tears, gels and/or ointments Treatment of underlying condition Surgical intervention

9. What is the most common surgical procedure for band keratopathy? Chelation with ethylene-diamine-tetra-acetic acid (EDTA) Phototherapeutic keratectomy Amniotic membrane transplant Corneal transplant

10. Small studies have shown which of the following surgical treatments can reduce healing time and reduce reoccurrence? EDTA PTK AMT A combination method of EDTA, PTK and AMT COPE ACCREDITED POST-COURSE TEST POST-COURSE ACCREDITED COPE

Atypical Gout-Associated Band Keratopathy 381