Sarcoid-Induced Uveitis: A Tattooed Journey

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doi:10.62055/heegzzgxcpyu

ABSTRACT

BACKGROUND

When obtaining a patient’s social history, “Do you have a tattoo?” is not a commonly asked question. However, what if this information may become a critical part of their diagnosis? When a patient presents with an anterior uveitis that is suspicious for a systemic etiology, it is important to explore all areas of clinical care to determine the cause. Traditionally, the initial approach is to perform an appropriate lab work-up. Beyond this, areas of specialty that are typically considered include rheumatology, radiology, and infectious disease. However, this case report will present a patient that required intervention from dermatology to confirm the source of ocular inflammation.

CASE REPORT

A 66-year-old African American man presented to the eye clinic with a visual complaint of blur in his right eye for about a month. The patient’s social history was positive for multiple arm tattoos. Anterior segment examination revealed a diagnosis of granulomatous anterior uveitis OD. The patient was treated with a topical steroid and seen over an extended time period for multiple follow-up visits, during which he eventually developed anterior uveitis in his left eye as well. The patient’s blood work and chest and joint X-ray imaging were negative for sarcoidosis. However, the patient did notice concurrent inflammation of his arm tattoos. Tattoo biopsy conducted by dermatology revealed extensive noncaseating granulomas with foreign giant cells. These findings were consistent with a diagnosis of sarcoidosis. The patient was treated with oral pentoxifylline by his dermatologist to treat the sarcoidosis. Following systemic treatment, the patient returned multiple times to the eye clinic for treatment of granulomatous anterior uveitis with a topical steroid.

CONCLUSION

Knowing that tattoos can play a significant role in inflammation – both ocular and systemic – is very important in the management of ocular and systemic disease. If a patient presents with granulomatous anterior uveitis, even as an initial finding, further lab studies and testing should be conducted to rule out underlying systemic disease, such as sarcoidosis. In addition, patients who present with corresponding systemic signs and/or symptoms should certainly be evaluated for concurrent systemic disease. As the patient in this case demonstrated, normal ACE levels may not always indicate a negative sarcoid diagnosis. Although a patient may present with negative lab testing, if he or she has other clinical signs that raise suspicion for a particular diagnosis, it is essential for both the provider and the patient that further investigation be pursued. Thus, arriving at a proper and accurate diagnosis will yield the best visual outcome for the patient because that means receiving the appropriate treatment they need to manage their ocular inflammation.

Keywords: sarcoidosis, granulomatous, anterior uveitis, inflammation, tattoo

INTRODUCTION

Sarcoidosis is a granulomatous inflammatory disease that can affect many organs, including the eyes. Ocular sarcoidosis most commonly presents as bilateral anterior granulomatous uveitis, although it initially may be unilateral, with anterior or posterior synechiae and keratic precipitates (KPs) on the inferior cornea in 60 to 80 percent of cases.¹ KPs are described as large, mutton fat or “greasy” appearing. Two types of iris nodules may also present: Koeppe and Busacca. Koeppe nodules appear on the pupillary margin, while Busacca nodules appear on the iris stroma.² Common symptoms of anterior uveitis are blur, redness, pain, and photophobia.³

CASE REPORT

A 66-year-old African American man presented to the eye clinic for a six-month hypertensive retinopathy follow-up. At this visit, the patient mentioned having blur in his right eye for about a month. The patient’s ocular history was positive for mild hypertensive retinopathy in both eyes, nuclear sclerosis OU, ocular trauma secondary to a rake handle in the left eye more than 30 years ago with no ocular complications and an open-angle glaucoma suspect OU.  He had no prior history of ocular surgery. Ocular medications included naphazoline as needed OU. The patient’s medical history was positive for gout, hypertension and moderate chronic obstructive pulmonary disease. His systemic medications included naproxen sodium, amlodipine besylate, hydrochlorothiazide, lisinopril, albuterol, and budesonide. Family ocular and medical histories were unremarkable. He had no known drug allergies. His social history was positive for smoking, alcohol, marijuana use and multiple arm tattoos, with the most recent being 10 years ago and oldest 25 years ago. The patient was oriented to time, place, and person.

Entrance tests found best corrected visual acuities of 20/20 OD and OS. Pupils were equal, round and reactive to light with minimal reaction OD and no afferent pupillary defect OU. Ocular motility was full and smooth. Confrontation fields were full to finger count OD and OS.

Anterior segment slit-lamp examination of the right eye revealed significant corneal endothelial pigment with fine KPs, grade 1+ inferior superficial punctate keratitis (SPK), grade 3+ cells in the anterior chamber (based on the Standardization of Uveitis Nomenclature or SUN Working Group),⁴ a Busacca nodule at six o’clock, posterior synechiae clockwise from five to three o’clock with pockets of incomplete adherence, and pigment on the anterior lens capsule. The left eye had a clear cornea, quiet anterior chamber, and a flat iris.  The lids and lashes were clear, the bulbar conjunctivae had trace injection, the tear film was adequate, the angles were open and the lens was a grade 2+ nuclear sclerosis in both eyes. The intraocular pressure (IOP) was measured as 12 mmHg OD and 16 mmHg OS using Goldmann applanation tonometry (GAT).  The patient was dilated with 1% tropicamide and 2.5% phenylephrine OU. A second round of the same drops were instilled after due to poor initial dilation. Posterior segment evaluation of both eyes revealed vitreous syneresis, attenuation and mild crossing changes of the retinal blood vessels, flat and clear maculae, and a clear posterior pole. The optic nerves had flat, distinct margins with a cup-to-disc ratio of 0.55 and 0.65 in the right and left eye, respectively. On peripheral examination, the right eye was unremarkable and the left eye revealed a few blot hemorrhages in the temporal retina.

The exam was most consistent with  granulomatous anterior uveitis in the right eyewhich presents with anterior segment findings such as keratic precipitates, Busacca and/or Koeppe nodules, cells and/or flare in the anterior chamber and a low IOP.⁵ It is interesting to note that this patient did not present with the classic symptoms of anterior uveitis (e.g., pain and photophobia); his only ocular complaint was blur. The patient was educated on the findings and instructed to start topical prednisolone acetate 1% every three hours in the right eye while awake. Although this was an initial, unilateral presentation of anterior uveitis which would usually be presumed to be idiopathic, given the patient’s granulomatous anterior segment finding of a Bussaca nodule, a consult with the rheumatology department was ordered to rule out possible systemic etiologies, including sarcoidosis. Table 1 lists the labwork that was completed prior to his visit with rheumatology.

Table 1. Lab Testing

Rheumatology obtained X-ray imaging of the patient’s chest and joints where he was experiencing pain, including bilateral elbows and shoulders. The chest X-ray was ordered to rule out pulmonary involvement of sarcoidosis or tuberculosis. The X-ray of the joints was ordered to rule out erosive joint disease.

As for the retinal hemorrhages in the left eye, the patient had a previous blood work-up, along with a carotid doppler that came back negative. The retinal hemmorrhages were suspected to be an atypical complication of hypertension and were to be monitored at the next dilated exam. Patient was scheduled to return for a follow-up in four days.

Follow-up #1: 4 days later

Four days after initial presentation and with the use of prednisolone acetate 1% TID, he noted mild improvement in visual blur and denied symptoms of photophobia or pain in the right eye. Corrected distance visual acuities measured 20/20 OD, OS. Slit-lamp examination of the anterior segment in the right eye revealed all the same findings as the initial exam, but now with mild improvement of the anterior chamber reaction with grade 2+ cells. IOP was measured as 14 mmHg OD, OS. A drop of cyclopentolate hydrochloride ophthalmic solution 1% was instilled in the right eye to attempt to break the synechiae but was unsuccessful. The patient was educated on the findings and instructed to continue using prednisolone acetate 1% every three hours in the right eye while awake. Patient was scheduled to return for follow-up in three days.

Follow-up #2: 3 days later

At this follow-up visit, he noted that his vision in the right eye was improving. BCVA were 20/20-2 OD and 20/20 OS. Slit-lamp examination now revealed grade 1+ cells in the anterior chamber. The posterior synechiae was mildly improved compared to the earlier visits. IOP was measured as 11 mmHg OD, OS. One drop of tropicamide 1% and phenylephrine 10% were instilled in the right eye in an attempt to break the remaining synechiae. The drops only broke the synechiae superiorly. Dilated posterior segment exam in the right eye was unremarkable with no signs of inflammation. The patient was educated on the findings and instructed to decrease use of prednisolone acetate 1% to every four hours in the right eye while awake. Patient was scheduled for a follow-up in one week.

Follow-up #3: 1.5 weeks later

At this visit, he noted stable vision since the last exam. BCVA were 20/20 OD, OS. Slit-lamp examination of the anterior segment OD revealed similar corneal findings to previous visits, but now with only trace cell in the anterior chamber. There was still some posterior synechiae nasally, temporally and inferiorly. All other findings were the same. Slit-lamp examination of the anterior segment OS revealed new trace cell in the anterior chamber. IOP was measured as 12 mmHg OD, OS. The patient was diagnosed with anterior uveitis OU. He was instructed to reduce prednisolone acetate 1% to TID OD and to start prednisolone acetate 1% TID OS. Patient was scheduled to follow-up in one week.

Follow-up #4: 1 week later

At this visit, the patient’s symptoms had resolved. BCVA were 20/20 OD, OS. Slit lamp examination of the anterior chamber revealed trace cells in both eyes. All other findings remained the same. IOP measured 14 mmHg OD, OS. The patient was educated on findings and instructed to increase prednisolone acetate 1% use to QID OU due to the persistent inflammation. He was scheduled for a follow-up in one week.

Follow-up #5: 1.5 weeks later

The patient reported no ocular complaints on this follow up visit. BCVA were 20/20 OD, OS. Slit-lamp examination of the anterior segment in both eyes revealed a quiet anterior chamber. All other findings remained the same. GAT revealed an IOP of 15 mmHg OD and 16 mmHg OS. The patient was educated on the findings and instructed to slowly taper the prednisolone acetate 1% to TID OU for one week, BID OU for two weeks and QD OU for two weeks and then discontinue. The patient was scheduled to return in six weeks for follow-up and dilation.

The patient was also scheduled to see rheumatology in two months following this visit to follow-up with his test results. Table 2 lists the lab results from the rheumatology appointment.

Table 2. Patient’s lab results from Rheumatology.

Lab results were significant for positive HLA-B27 and a high ESR and CRP. Per rheumatology notes, the patient’s joint pain did not appear inflammatory in nature, which decreased the suspicion for HLA-B27 etiology. Although the patient had normal ranges of ACE, he admitted he noticed concomitant pain and swelling of all his arm tattoos with the onset of his uveitis. Because of this, rheumatology referred the patient to dermatology for biopsy of his tattoos to rule out sarcoidosis.

Figure 1. Inflammation of the patient’s tattoos on his right arm.

Follow-up #6: 6 weeks later

The patient returned for his follow-up with no ocular complaints. BCVA were 20/20 OD, OS. Slit-lamp examination of the anterior segment revealed no keratic precipitates of the cornea and trace cells in the anterior chamber of both eyes. GAT revealed an IOP of 17 mmHg OD and 18 mmHg OS. Posterior segment findings were unremarkable OU with no signs of inflammation or other retinopathy. Patient was educated on the findings and instructed to return at the same time as his dermatology appointment for follow-up. No topical steroid treatment was issued at this visit due to the strong likelihood of systemic etiology, which would warrant systemic treatment (pending confirmation from dermatology).

Follow-up #7:  4 weeks later

Prior to this visit, the patients’ tattoos biopsy results revealed extensive noncaseating granulomatous inflammation with foreign giant cells. Per dermatology, these findings were consistent with a diagnosis of sarcoidosis.

The patient returned for his uveitis follow-up, reporting intermittent “hazy” vision OU. BCVA were 20/25-2 OD and 20/25 OS. Slit-lamp examination of the anterior chamber revealed grade 1-2+ cells OD and quiet OS. GAT revealed an IOP of 08 mmHg OD and 09 mmHg OS. The right eye was dilated with tropicamide 1%. Posterior segment examination of the right eye revealed a cotton wool spot along the superior temporal arcade of the posterior pole. Views were limited due to a poorly dilated pupil. The patient was diagnosed with chronic granulomatous anterior uveitis OD secondary to sarcoidosis and other specified retinal disorder (cotton wool spot) OD likely due to chronic inflammation from sarcoid. The patient was educated on the findings and instructed to start cyclopentolate 1% TID OD for two weeks. Topical steroids were deferred at this time due to initiation of systemic oral medication pentoxifylline by dermatology for sarcoidosis, as the systemic medication may resolve the ocular inflammation once it takes effect. If there was no ocular improvement at the next follow-up, the plan was to restart a topical steroid.

The patient returned multiple times since the last follow-up and has been periodically treated for sarcoid-induced granulomatous anterior uveitis.

DISCUSSION

Sarcoidosis is a systemic inflammatory disease that creates noncaseating epithelioid granulomas in affected areas. Granulomas are formed as the body’s response to antigenic material and serve to block off outside pathogens, protecting adjacent tissue from harm. The exact etiology of this disease is unknown.⁶ One theory suggests that the disease develops in genetically susceptible individuals exposed to particular environmental triggers that incite an inflammatory immune response resulting in granulomas.⁷

The disease primarily targets the lungs and thoracic lymph nodes.⁶ The skin is the second most common organ affected in sarcoid.¹⁰ However, any part of the body can be involved. Because multiple organs can be involved, symptoms can be organ specific.⁷

Sarcoidosis more commonly affects African-Americans and women. Previous studies estimate the prevalence of the disease to be between 150,000 and 200,000 people in the United States.⁸

Sarcoidosis can manifest in many ways, including non-specific symptoms such as fever, fatigue, weight loss, and malaise. Symptoms are more common in African-Americans and Asian Indians; however there are 30 to 50 percent of patients who experience no symptoms and are diagnosed via routine chest imaging.⁷ It can present as an acute illness with sudden onset, known as Lofgren’s syndrome. This type of sarcoidosis is characterized by fever, painful skin lesions, ankle arthritis and/or bilateral hilar adenopathy on chest imaging. It can also present as a subacute disease with gradual onset.⁹ Chronic sarcoidosis can present subtly with symptoms related to the affected organ. Its course is usually long and involves relapses. This type of sarcoidosis affects 10 to 30 percent of patients.⁷

Ocular sarcoidosis can manifest in many different ways and any of the following ocular complications can occur: uveitis, episcleritis/scleritis, eyelid irregularities, conjunctival granuloma, optic neuropathy, lacrimal gland enlargement and/or orbital inflammation.¹¹

Sarcoid-induced uveitis can present as anterior, intermediate, posterior or panuveitis. Sarcoid is specifically known to cause granulomatous anterior uveitis, as in this patient’s presentation. Granulomatous anterior uveitis is classified as having one or more of the following presentations: large mutton fat KPs, iris or trabecular meshwork nodules and/or a choroidal granuloma.¹¹ The patient in this case initially presented with a Busacca nodule in the midperiphery of the iris in the right eye, a sign indicating granulomatous inflammation.

In general, episodes of anterior uveitis can be acute, chronic, or recurrent. It typically presents as unilateral inflammation with circumlimbal redness, occasionally fine or large KPs, and anterior chamber cells and flare. Common complications of anterior uveitis can present as decreased or increased IOP and posterior synechiae. Patients may experience symptoms of pain, photophobia, redness, blur and/or tearing.¹² Unusually, the patient in this case was only symptomatic for blur, despite having a significant anterior chamber reaction. He also presented with unilateral anterior chamber cells and flare, fine KPs, lower IOP in the affected eye and posterior synechiae. Further, per SUN classification, this patient had chronic anterior uveitis, given his relapse of inflammation less than 3 months after stopping treatment.⁴

Sarcoid uveitis can lead to blindness if not managed well. The main cause of vision loss is cystoid macular edema. A poor outcome in sarcoid uveitis is associated with the following risk factors: age, African-American race, female gender, chronic systemic disease, posterior segment involvement, peripheral punched out lesions in the retina, cystoid macular edema and glaucoma.¹³

The first line of management of anterior uveitis typically involves topical steroids. Commonly, prednisolone acetate 1% is used; dosing is dependent on the severity of the inflammation present. Cycloplegics may or may not be employed to help reduce any ocular pain and prevent posterior synechiae.¹⁴ Corticosteroid injections (subconjunctival, periocular or sub-tenon, or intravitreal) can be used in cases where there is posterior uveitis, poor response to topical treatment, or patient noncompliance. Intraocular biodegradable corticosteroid implants containing dexamethasone can also be used in cases of posterior uveitis.¹⁵ When topical or regional treatments are no longer effective at maintaining ocular inflammation or if the patient also has an underlying inflammatory disease, oral corticosteroids such as prednisone are considered. Complications to steroid treatments include increased IOP and cataract progression.¹¹

Systemic immunosuppressive agents are also considered in cases where there is an underlying systemic etiology. They can be indicated in patients who are corticosteroid reliant or intolerant. Another class of drugs known as biologic agents have been studied in the treatment of refractory noninfectious uveitis. In the context of sarcoid uveitis, these biologic agents are called tumor necrosis factor (TNF)-alpha inhibitors.¹¹ In sarcoidosis, the formation of granulomas is influenced by the release of TNF-alpha. Thus, by inhibiting TNF-alpha, the formation of these inflammatory cells is prevented.¹⁶

The patient in this case was initially treated with topical prednisolone acetate with good results. However, once a systemic etiology was identified as the cause of the uveitis, the patient was eventually put on systemic treatment with pentoxifylline, essentially a TNF-alpha inhibitor, to control his inflammation.¹⁶

In order to determine whether a patient needs systemic therapy, diagnostic laboratory testing is done to evaluate for an underlying etiology. This is typically done in bilateral, posterior, chronic or recurrent cases. It is also considered in cases where additional clinical findings are suggestive for further work-up (e.g. granulomatous signs).¹⁴ For patients who present with a single episode of unilateral anterior uveitis that resolves upon treatment and have no other findings that would warrant further testing, no other work-up is needed, as 48 to 70 percent of uveitis cases are idiopathic.^14,17

The patient in this case initially presented with a unilateral episode of anterior granulomatous uveitis. The granulomatous finding alone suggested further work-up. His unilateral anterior uveitis eventually became bilateral, which also would have warranted lab studies.

Basic lab studies for uveitis include complete blood count with differential, a basic metabolic panel, urinalysis and erythrocyte sedimentation rate. Testing for HLA-B27 spondyloarthropathies is also common, given pertinent systemic findings. If basic lab testing does not suggest a specific diagnosis, serologic testing for syphilis and chest radiography for sarcoid and tuberculosis are also considered.¹⁷

There is no gold standard test for the diagnosis of sarcoidosis. However, it has been associated with elevated levels of ACE. In patients with systemic disease, the sensitivity of elevated ACE levels ranges from 41 to 61 percent, and specificity ranges from 88 to 90 percent.¹⁸ ACE levels depict the amount of systemic granuloma present and tend to be elevated in patients with active disease affecting multiple organ systems. ACE levels vary depending on how the disease manifests in the body. Overall, ACE levels have been shown to be helpful in identifying those at a higher risk of having sarcoid and has a great negative predictive value. Thus, further testing is usually not necessary unless there is a high clinical suspicion of the disease. In such cases, a chest X-ray, chest computed tomography (CT) and/or biopsy are considered.¹⁸ The chest X-ray and chest CT would reveal bilateral hilar lymphadenopathy, while a biopsy would show sarcoid granulomas.^19,20

The patient in this case had basic lab testing done as well as extensive lab work for: HLA-B27 conditions, rheumatoid arthritis, general autoimmune disease, autoimmune vasculitis, sarcoid and tuberculosis. In addition, he had X-ray imaging of his chest and joints. Despite presenting with a normal ACE value and chest X-ray, there was still a high clinical suspicion of sarcoid. This was due to the patient’s complaint of having raised and inflamed skin surrounding his tattoos concurrently with his uveitis. Thus, the dermatology department was alerted and conducted a tissue biopsy of his tattooed skin, which revealed noncaseating granulomas, thus verifying a diagnosis of sarcoid induced uveitis.

The skin is the second most common organ affected by sarcoidosis. Cutaneous sarcoidosis has been reported in old scars, traumatized skin sites, and around embedded foreign bodies.²¹ When an individual gets a tattoo, they are exposing their dermis to exogenous pigments and dyes. These pigments and dyes may contain an antigen that induces a cell-mediated immune response such as granuloma formation, thereby making the tattoo the target of sarcoidosis.²¹ The exact pathophysiology is unclear. It is estimated that 1 to 2 per 10,000 tattooed persons in Western countries have sarcoidosis.²¹ In a recent comparative review by Kluger, a tattoo granulomatous reaction with sarcoidosis and uveitis can occur from 1 to 20 years after receiving the tattoo.²²

It is important to coordinate care with the appropriate providers for treatment and management. Depending on which organ systems are involved in sarcoidosis, there may be multiple specialists participating in the patient’s care. Because this patient had cutaneous and ocular sarcoid, he was managed by a rheumatologist, dermatologist, and an optometrist.

CONCLUSION

Knowing that tattoos can play a significant role in inflammation – both ocular and systemic – is very important in the management of ocular and systemic disease. If a patient presents with granulomatous anterior uveitis, even as an initial finding, further lab studies and testing should be conducted to rule out underlying systemic disease, such as sarcoidosis. In addition, patients who present with corresponding systemic signs and/or symptoms should certainly be evaluated for concurrent systemic disease. As the patient in this case demonstrated, normal ACE levels may not always indicate a negative sarcoid diagnosis. Although a patient may present with negative lab testing, if he or she has other clinical signs that raise suspicion for a particular diagnosis, it is essential for both the provider and the patient that further investigation be pursued. Thus, arriving at a proper and accurate diagnosis will yield the best visual outcome for the patient because that means receiving the appropriate treatment they need to manage their ocular inflammation.

REFERENCES

1. Allegri, P, et al. Sarcoid Uveitis: An Intriguing Challenger. Med. 2022 Jul 4;58(7):1-36.
2. Guney E, Tugal-Tutkun I. Symptoms and Signs of Anterior Uveitis. US Ophthalmic Rev. 2013;6(1):33-37.
3. Agrawal, RV, et al. Current Approach in Diagnosis and Management of Anterior Uveitis. Indian J. Ophthalmol. 2010 Jan-Feb;58(1):11-19.
4. Standardization of Uveitis Nomenclature (SUN) Working Group. Standardization of Uveitis Nomenclature for Reporting Clinical Data. Results of the First International Workshop. Am J Ophthalmol. 2005;140(3):509-516.
5. Bagheri N, Wajda BN, editors. Chapter 12: Uveitis. The Wills Eye Manual: Office and Emergency Room Diagnosis and Treatment of Eye Disease. 7th ed. Wolters Kluwer; 2017. p. 340–346.
6. Chen ES, Moller DR. Etiologies of Sarcoidosis. Clinic Rev Allerg Immunol. 2015 Mar 15;49(1):6–18.
7. Wu JJ, Rashcovsky KS. Sarcoidosis. Am Fam Physician. 2004 Jul 15;70(2):312-322.
8. Baughman RP, et al. Sarcoidosis in America. AnnalsATS. 2016 Aug 8;13(8):1244-1252.
9. Polverino F, et al. Clinical Presentations, Pathogenesis, and Therapy of Sarcoidosis: State of the Art. J Clin Med. 2020 Jul 24;9(8):2363.
10. Wanat, KA, Rosenbach M. Cutaneous Sarcoidosis. Clin Chest Med. 2015 Dec;36(4):685–702.
11. Pasadhika S, Rosenbaum JT. Ocular Sarcoidosis. Clin Chest Med. 2015 Dec 4;36(4):669-683.
12. Agrawal RV, et al. Current Approach in Diagnosis and Management of Anterior Uveitis. Indian J. Ophthalmol. 2010;58(1):11-19.
13. Jamilloux Y, et al. Sarcoidosis and Uveitis. Autoimmun Rev. 2014 Aug 1;13(8):840-849.
14. Harthan JS, et al. Diagnosis and Treatment of Anterior Uveitis: Optometric Management. Clin Optom. 2016 Mar 31;8:23-25.
15. Babu K, Padmamalini M. Medical Management of Uveitis – Current Trends. Indian J. Ophthalmol. 2013 Jun 6;61(6):277-283.
16. National Institutes of Health Clinical Center [Internet]. Treatment of Pulmonary Sarcoidosis With Pentoxifylline. c2008 – [cited 2008 Mar 4]. Available from: https://clinicaltrials.gov/ct2/show/study/NCT00001877.
17. Harman LE, et al. Uveitis: The Collaborative Diagnostic Evaluation. Am Fam Physician. 2014 Nov 15;90(10):711-716.
18. Niederer RL, et al. Serum Angiotensin-Converting Enzyme Has a High Negative Predictive Value in the Investigation for Systemic Sarcoidosis. Am J Ophthalmol. 2018;194:82-87.
19. Nunes H, et al. Imaging of Sarcoidosis of the Airways and Lung Parenchyma and Correlation with Lung Function. Eur Respir J. 2012;40:750-765.
20. Yanardag H, et al. Diagnosis of Cutaneous Sarcoidosis: Clinical and the Prognostic Significance of Skin Lesions. Multidiscip Respir Med. 2013 Mar 22;8(1):26.
21. Kluger N. Sarcoidosis on Tattoos: A Review of the Literature from 1939 to 2011. Sarcoidosis Vasc Diffuse Lung Dis. 2013 Aug 1;30(2):86–102.
22. Kluger N. Tattoo-Associated Uveitis with or without Systemic Sarcoidosis: A Comparative Review of the Literature. J Eur Acad Dermatol Venereol. 2018 Nov;32(11):1829-2042.

Simmy Panchal, OD, FAAO, Dipl. ABO

Salisbury VA Medical Center | Salisbury, NC

Dr. Panchal graduated from Pennsylvania College of Optometry in 2019 and completed an ocular disease, low vision and specialty contact lens residency at Ralph H. Johnson VAMC in Charleston, SC. She is currently a staff optometrist at Salisbury VAMC, where she largely precepts 4th year optometry externs, optometry residents and co-manages the specialty contact lens clinic.

Kelly Singleton, OD, MS

Ralph H. Johnson VA Medical Center | Charleston, SC

Dr. Singleton received her OD and MS degrees from the University of Alabama-Birmingham School of Optometry and completed her residency in Low Vision/Vision Rehabilitation at the University of Houston College of Optometry. She has enjoyed an extensive optometry career including owning her own practice with her husband and serving as the national physician liaison for an eyecare specific EHR company. She currently serves as the Residency Supervisor at the RHJ VA Medical Center in Charleston, SC and is an Assistant Professor at the Medical University of South Carolina. In her free time, she enjoys competitive dragon boating and traveling the world with her husband and four children.