The annual ACR Review Course covered key topics on Saturday, including areas that should be more familiar to rheumatologists than they are.
“Virtually every rheumatic entity has an optic occurrence,” said James T. Rosenbaum, MD, Edward E. Rosenbaum Professor of Inflammatory Diseases and Chair of Arthritis and Rheumatic Diseases at the Oregon Health & Science University. “Too many rheumatologists are a bit intimidated by the eye.”
“RSVP” is a useful mnemonic, he said. R is for redness in one or both eyes, S is sensitivity to light, V is visual acuity changes, and P is for pain. If the patient is experiencing these symptoms, he said, consult ophthalmology.
Most rheumatoid arthritis patients have red eye, or conjunctivitis, usually caused by dry eye. Scleritis is uncommon but more clinically significant.
The ACR and EULAR issued new classification criteria for primary Sjögren’s syndrome in 2016. The new criteria include persistent dry eye, feelings of sand or gravel in the eyes, or use of tear substitutes more than three times a day.
Dry eye is a tear deficit, and tears are a combination of water from the lacrimal gland, mucins from Goblet cells, and oil from the Meibomian glands.
“To replace a tear, we need to replace all three elements, which no one has quite mastered,” Dr. Rosenbaum said.
Any autoimmune disease has some component of dry eye. The first step in treatment is to minimize the use of drying medications such as antidepressants or sleep medications. It can also help to humidify the sleeping room.
Reminding patients to blink frequently also helps. Blinking is the natural mechanism to refresh the tear film, but many people don’t blink when concentrating on visual tasks such as using a screen-based device or driving.
Tear replacements can help, but most contain preservatives, which with long-term use can irritate the cornea. Dr. Rosenbaum recommended preservative-free formulations or autologous serum.
Other treatments include topical cyclosporine or lifitegrast, punctal occlusion to inhibit tear film drainage, or scleral cataract lenses, which can be difficult for patients to tolerate.
Lupus patients with dry eye may have vision distortions. Fundus imaging may show spots that look like cotton wool, which indicate lupus-related retinopathy and CNS-related disease. Cotton wool spots are associated with elevated mortality in lupus.
Antimalarial medications can also cause retinopathy. Recommendations from the American Academy of Ophthalmology recommend limiting hydroxychloroquine to no more than 5 mg/kg of actual body weight. Patients on chloroquine should take no more than 2.3 mg/kg of actual body weight.
Axial spondyloarthritis (axial SpA) is a spectrum ranging from mild or early stage disease with no radiographic evidence of damage to radiographic sacroiliitis to ankylosing spondylitis. Mild and early stage disease often can be identified based on history, physical exam, and MRI of the sacroiliac joints.
“Inflammatory back pain is a hallmark of axial SpA,” said Lianne S. Gensler, MD, Associate Professor of Medicine and Director of the Ankylosing Spondylitis Clinic at the University of California, San Francisco. “All you need to image is the sacroiliac joints. Spinal MRI does not increase diagnostic yield in early disease, and radiographic imaging is unhelpful.”
Rheumatologists must also learn to read their own MRIs. Most radiologists are not trained to read inflammatory disease and are unfamiliar with spondyloarthropathies.
Two types of imaging are needed: STIR, which is fluid sensitive, and T1, which is fat sensitive. Inflammation is hyperintense on STIR and hypointense on T1, while fat metaplasia is the reverse. Sclerosis is hypointense on both, and erosions may not be evident on STIR and are hypointense on T1.
Both the ACR and EULAR have recent treatment guidelines that are helpful for most patients.
Dr. Gensler also advised a follow up with ophthalmology because uveitis is the most common extra-articular manifestation of axial SpA.
“Disease activity predicts progression in SpA,” she said. “When we control disease activity, we reduce radiographic progression.”
When a patient has elevated ANCA, think beyond vasculitis.
“The first thing you should think about is ANCA-associated vasculitis, which represents about 60 percent of cases,” said Sharon Chung, MD, MAS, Associate Professor of Medicine and Director of the Vasculitis Clinic at the University of California, San Francisco. “But there are other causes.”
Thyroid medications, particularly propylthiouracil, can elevate ANCA, sometimes years after treatment stops. Minocycline, penicillin-based antibiotics, and sulfa drugs can also elevate ANCA, as can allopurinol and anti-TNF agents.
“We see ANCA in almost all autoimmune diseases,” Dr. Chung said. “IBD has a high degree of ANCA, especially ulcerative colitis and Crohn’s. We also see ANCA in infective endocarditis, M. tuberculosis, and other infections, including helminth species. We do immunosuppression in our patients, which puts them at risk for some of these infections.”