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Article Date: 4/1/2014

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Systemic Disease-Induced DED

  systemic disease

Systemic Disease-Induced DED

Here’s how to improve patient care, increase retention, boost referrals and elevate the profession of optometry as a whole.


Treating dry eyes in patients with systemic disease offers many benefits to optometrists. First, when you are the doctor who recognizes the correlation between a systemic disease and dry eye and provides relief from patient symptoms, their appreciation for your clinical skills soars, thus increasing retention to your practice.

Second, educating the patient’s primary care provider of your diagnosis and treatment options strengthens your professional rapport: Managing these patients together creates networking opportunities, increases referrals and, ultimately, boosts your practice revenue.

A patient who has diabetic macular edema. A total of 20% to 53% of diabetic patients report significant dry eye.

Lastly, examining case history along with DED may lead you to be the first to discern a patient’s systemic etiology, thereby elevating our profession as a whole.

In some cases, conventional therapy for DED is effective in patients with systemic diseases. This involves (as specified by the American Optometric Association):

▸ Using artificial tears

▸ Conserving tears in the form of punctual occlusion

▸ Increasing tear production through cyclosporine (Restasis, Allergan) and/or omega-3 fatty acid nutritional supplements.

▸ Treating eyelid or ocular surface inflammation.

However, in other cases, this is not enough to relieve the patient’s symptoms. In addition, if a patient who has DED though no systemic disease diagnosis fails to respond to the aforementioned treatments, it’s crucial you refer them to their primary-care physician for a systemic disease assessment. In many of these cases, you’ll note ocular manifestations of a particular systemic disease, which aids the patient’s primary care physician in establishing a definitive diagnosis.

Here, I discuss the common systemic diseases associated with DED and additional treatment options.


A total of 20% to 53% of diabetic patients report significant dry eye. This correlation may be due, in part, to inflammation in these patients’ lacrimal gland.1

In addition, proliferative diabetic retinopathy patients exhibit significantly less tear film function, as measured by tear film break-up time, Schirmer I testing and rose bengal staining, than patients with non-proliferative diabetic retinopathy.2 This may be a direct result of the reduced corneal sensation that proliferative diabetic patients often report. Also, keep in mind that DED symptoms become more significant as the severity of diabetes worsens.

Hormone Replacement Therapy (HRT)

Although not a systemic disease, an apparent deleterious association between HRT and DED exists. HRT is used by an estimated 38% of postmenopausal women in the U.S., and its benefits include the decreasing of hot flashes, vaginal discomfort, night sweats and, less commonly, risk of osteoporosis.12

However, one study of 25,665 postmenopausal women found that each three-year increase in the duration of HRT-use was associated with a 15% elevation in the risk of clinically diagnosed DED or severe DED symptoms.13

Given the inflammatory process involved in diabetes-caused DED, prescribe antioxidants, such as nutritional supplements, and anti-inflammatory agents, including topical corticosteroids, to treat diabetic DED patients.


Rosacea-induced DED stems from meibomian gland dysfunction and the resulting evaporative tear loss. Tears of rosacea patients have increased interleukin-1 alpha concentrations, as well as a greater matrix metalloproteinase activity.3

Tetracycline often works well as a first line of defense here, as it has an inhibitory effect on both these factors.3 Also, experimental studies have provided evidence that dietary supplementation of omega-3 fatty acids is essential to modify inflammatory and immune reactions central to rosacea-induced DED. Their effects are brought about by modulation of the type and amount of eicosanoids and cytokines and by altering gene expression.4

In addition, educate ocular rosacea patients to avoid trigger foods (chocolate, tomatoes, citrus fruits, hot spices, alcohol and heated beverages), as well as to use sunscreen — direct exposure to these trigger foods and sunlight can trigger their DED symptoms.


As many as 20% of people with HIV/AIDS develop damaged lacrimal glands leading to ocular dryness.5 Though the entire pathogenesis of the aqueous tear deficiency in HIV-infected patients remains unclear, it may be associated with lymphocytic infiltration and destruction of the lacrimal gland acini and ducts.

Autoimmune diseases

The following autoimmune diseases are connected to DED:

Sjögren’s syndrome. DED in Sjögren’s syndrome is caused by decreased aqueous production — inflammatory changes in the lacrimal gland lead to reduced function. Most often seen in older women, Sjögren’s symptoms include dry eyes and dry mouth. Also, patients may report joint pain, corneal abrasions and/or fatigue.

Early diagnosis is crucial to preventing serious ocular events, such as corneal ulceration. Unfortunately, the pathogenesis for Sjögren’s syndrome is obscure, and a curative treatment is yet to be discovered.

Rheumatoid arthritis (RA). More than 90% of people who have RA also have DED, and 50% present with moderate to severe forms of the disease.6,7 Also, similar to diabetes, DED symptoms become more significant as the severity of RA worsens.8

Patients may present with ocular symptoms well before being diagnosed with RA. In these cases, refer the patient to a rheumatologist upon reports of joint discomfort — the hands are often affected early in the course of RA.

Use the previously mentioned conventional DED treatment with these patients.

Systemic Lupus Erythematosus (SLE). The most common ocular manifestation of SLE is keratoconjunctivitis sicca, with the majority of patients reporting at least one DED symptom.9 Also, SLE patients may develop Sjögren’s syndrome. Additionally, ocular symptoms, such as burning and gritty sandy sensation, may persist while the systemic disease is in remission.

Use the previously mentioned conventional DED treatment with these patients.

Thyroid eye disease. Long associated with DED, due to exophthalmos-related corneal exposure, thyroid disease also causes DED in the absence of exophthalmos, says recent research.10,11

Use the previously mentioned conventional DED treatment with these patients.

The road to recovery

Many systemic diseases can cause or exacerbate DED symptoms. Identifying and treating the underlying conditions enables you to achieve an optimal patient outcome. OM

1. Alves Mde C, Carvalheira JB, Modulo CM, Rocha EM. Tear film and ocular surface changes in diabetes mellitus. Arq Bras Oftalmol. 2008 Nov-Dec;71(6 Suppl):96-103.

2. Yu L, Chen X, Qin G, et al. Tear Film function in type 2 diabetic patients with retinopathy. Ophthalmologica. 2008;222(4):284-91.

3. Afonso AA, Sobrin L, Monroy DC, et al. Tear fluid gelatinase B activity correlates with IL-1 alpha concentration and fluorescein clearance in ocular rosacea. Invest Ophthalmol Vis Sci. 1999 Oct;40(11):2506-12.

4. Macsai MS. The role of omega-3 dietary supplementation in blepharitis and meibomian gland dysfunction (an AOS thesis). Trans Am Ophthalmol Soc. 2008;106:336-56.

5. Beyda N, Cluck D, Taba KE, Middlebrooks M. Ocular manifestations of systemic diseases. US Pharm. 2010;35(4):HS-2-HS-8.

6. Lemp MA. Dry eye (Keratoconjunctivitis Sicca), rheumatoid arthritis, and Sjogren’s syndrome. Am J Ophthalmol. 2005 Nov;140(5):898-9.

7. Fujita M, Igarashi T, Kurai T, et al. Correlation between dry eye and rheumatoid arthritis activity. Am J Ophthalmol. 2005 Nov;140(5):808-13.

8. Wolfe F, Michaud K. Prevalence, risk, and risk factors for oral and ocular dryness with particular emphasis on rheumatoid arthritis. J Rheumatol. 2008 Jun;35(6):1023-30.

9. Keating NL, Cleary PD, Rossi AS, et al. Use of hormone replacement therapy by postmenopausal women in the United States. Ann Intern Med. 1999 Apr 6;130(7):545-53.

10. Moss SE, Klein R, Klein BE. Long-term incidence of dry eye in an older population. Optom Vis Sci. 2008 Aug;85(8):668-74.

11. Bruscolini A, Abbouda A, Locuratolo N, et al. Dry Eye Syndrome in Non-Exophthalmic Graves’ Disease. Semin Ophthalmol. 2014 Jan 24.

12. Keating NL, Cleary PD, Rossi AS, et al. Use of hormone replacement therapy by postmenopausal women in the United States. Ann Intern Med. 1999 Apr 6;130(7):545-53.

13. Schaumberg DA, Buring JE, Sullivan DA, Dana MR. Hormone replacement therapy and dry eye syndrome. JAMA. 2001 Nov 7;286(17):2114–9.


JULY 2013
Anterior Segment in Review • page 14

Establish the Dry Eye Disease Visit • page 24

Discussing Dry Eye Disease • page 34

Dr. Ventocilla is the owner of Mark Ventocilla, OD, Inc., California Eye Wear and Elder Eye Care Group, PLC. He is a diplomat of the American Board of Optometry. E-mail him at, or send comments to

Optometric Management, Volume: 49 , Issue: April 2014, page(s): 23-25, 27-28

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