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Figure. High-resolution 3-tesla MRIs of the brain following gadolinium contrast in a patient with vasculitis (left) and a patient with RCVS (right). Vessel wall enhancement and thickening (arrow) are present in the vasculitis patient, but minimal enhancement is present in the RCVS patient. Early recognition and diagnosis of RCVS can save patients the risks of unnecessary immunosuppression. One current project is the assessment of long-term outcomes of patients with RCVS. We are assessing this cohort of patients with validated instruments including the Headache Impact Test-6 (HIT-6), the Migraine Disability Assessment Test (MIDAS), the Barthel Index (BI), the Patient Health Questionnaire (PHQ-9) and the EQ-5D-5L. Data thus far indicate that the long-term outcome of patients with RCVS is favorable. Half of the patients continue to have headache, although it is decreased in severity and frequency. Despite a large percentage of initial ischemic stroke or hemorrhage in this surveyed cohort, all patients were living independently with little disability. However, pain and anxiety decreased quality of life among RCVS patients. Pursuing Radiologic and Basic Science Insights At the same time, we are partnering with our radiology colleagues to explore the utility of high-resolution 3-tesla MRI (HR-MRI) in distinguishing RCVS from CNS vasculitis. HR-MRI is a noninvasive method that has added value to vascular imaging by defining intracranial vessel wall characteristics (enhancement and thickening). To date, 26 patients (13 with RCVS and 13 with CNS vasculitis) have been included in our study. Interestingly, data have revealed that enhancement of the intracranial vessel wall by HR-MRI occurred mainly in the CNS vasculitis group as opposed to the RCVS group, where enhancement was minimal (see figure). HR-MRI appears to be a promising tool for differentiating RCVS from CNS vasculitis in the acute setting. We are also collaborating with scientists in Cleveland Clinic’s Lerner Research Institute to examine biomarkers in RCVS to better understand its pathophysiology and differentiate it from other cerebral arteriopathies. Dr. Hajj-Ali is a staff physician in the Center for Vasculitis Care and Research and the R.J. Fasenmyer Center for Clinical Immunology within the Department of Rheumatic and Immunologic Diseases. She can be reached at 216.444.9643 or hajjalr@ccf.org. Visit clevelandclinic.org/rheum Rheumatology Connections | Spring 2013 | Page 11
FRAX: Realizing Its Strengths Depends on Recognizing Its Limitations By Chad Deal, MD Case Presentation B.S. is a 65-year-old white woman who presented for osteoporosis evaluation. She had been treated with a bisphosphonate for three years immediately following menopause (ages 52 to 55). She had a lumbar spine T-score of –2.3 and a femoral neck T-score of –2.2. Her current bone density showed a significant decline of 8.6 percent in the spine and 7.0 percent in the hip when compared with her bone density three years earlier. Laboratory tests did not reveal a secondary cause for low bone mass and bone loss. She was taking adequate calcium and vitamin D and walked for exercise four times a week. Her 10-year absolute fracture risk based on the FRAX ® tool was 1.9 percent for hip fracture and 10.0 percent for major osteoporotic fractures. Current National Osteoporosis Foundation guidelines recommend treatment if the 10-year fracture risk is 3 percent or greater for the hip or 20 percent or greater for a major osteoporotic fracture (hip, spine, wrist or humerus). Even though B.S.’s fracture risk was below treatment thresholds, she was started on a bisphosphonate. FRAX Caveats: The Devil’s in the Details The appropriate use of FRAX as a tool for guiding treatment decisions is important in the clinic. With FRAX, as with all tools, understanding its strengths as well as its limitations is essential to making appropriate treatment decisions. The limitations are often called FRAX caveats. In the case of B.S., the most important limitation is that the FRAX model does not adjust for patients with rapid bone loss. Allowing this patient to continue losing bone at a rate of 7 to 8 percent every three years would result in increasing fracture risk over time. This is a case when treatment for prevention is appropriate in spite of her FRAX-generated 10-year fracture risk being below the National Osteoporosis Foundation treatment threshold. The sidebar (above right) lists clinical risk factors considered in FRAX. Many of these risk factors are dichotomous, involving a yes/no response (see screen shot on next page), yet in the real world these risk factors are more nuanced and complex. As a result, the dichotomous nature of some variables can result in either over- or underestimation of fracture risk. The risks for fracture in the FRAX model are averages in a large population of patients. Consider the following examples. Risk Factors Considered in FRAX — Not Always So Straightforward History of previous fracture Hip fracture in a parent Current smoking Glucocorticoid use (≥ 5 mg/d of prednisolone [or equivalent] for ≥ 3 months at any time) Secondary osteoporosis (used when risk is based on body mass index, not bone mass) Alcohol use ≥ 3 units a day Femoral neck bone mineral density in g/cm 2 Confirmed diagnosis of rheumatoid arthritis Race/ethnicity (used in U.S.) Age, height, weight Fracture history. A patient with one vertebral fracture has a fivefold increase in fracture risk, while a patient with two vertebral fractures has a twelvefold increase in risk. Despite this difference, FRAX allows previous fracture to be reported only as “yes” or “no” with no adjustment for multiple fractures or for fracture site. Smoking and alcohol use. FRAX assigns the same risk to a patient regardless of whether she smokes one pack a day or two packs a day or whether her alcohol use is three or six units daily. Moreover, “no” is the technically accurate entry for “current smoking” for a patient who quit a 40-year smoking habit six months ago, yet this leaves the skeletal effects of decades of smoking totally uncaptured. Glucocorticoid use. The same increase in fracture risk is assigned by FRAX for a patient on 60 mg of prednisone for temporal arteritis as for a patient who was on 5 mg of prednisone for three months five years ago. Rheumatoid arthritis. The severity of rheumatoid arthritis is likely to affect fracture risk (severe disease having a greater effect than mild disease), yet FRAX does not account for disease severity. Page 12 | Rheumatology Connections | Spring 2013 For referrals, call 800.223.2273, ext. 50096
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Rheumatology Connections - Cleveland Clinic

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