Treating an Elderly Patient With Osteoporosis, Sjogren's Syndrome, and Renal Insufficiency

Robert I. Fox, MD, PhD


April 16, 2008


What treatment modality should be used for an elderly woman (aged 65 years) with osteoporosis and Sjögren's syndrome with renal insufficiency who is on low-dose steroids? Is hydroxychloroquine a reasonable consideration?

Response From Expert


Robert I. Fox, MD, PhD
Professor and Member, Scripps Memorial Hospital and Research Foundation; Rheumatologist, Scripps Memorial Hospital, La Jolla, California

There are really 3 questions involved here. First, 65 years is hardly considered elderly as we want to consider the role of exercise and adequacy of vitamin D and calcium supplementation in any postmenopausal female with renal insufficiency. The patient needs to follow the usual recommendations regarding 1.5 g of calcium, as well as laboratory checks to make sure that adequate conversion of the recommended 800 units of vitamin D to 1,25 OH vitamin D has occurred.

The second question involves the role of steroids in osteoporosis, particularly when a patient has renal insufficiency, and nonsteroidal anti-inflammatory agents may exacerbate renal function. In general, the lower the steroid dose, the better in terms of osteoporosis, and low-dose steroids (less than 5 mg) may have minimal bone toxicity.

The third question involves the role of agents such as hydroxychloroquine in conditions such as Sjögren's syndrome or systemic lupus erythematosus. Antimalarial agents are a mainstay of therapy in both Sjögren's syndrome and systemic lupus erythematosus, where they are effective in controlling arthralgias, myalgias, and rash. More serious extraglandular manifestations or those resistant to antimalarials may require additional or different disease modifying agents.[1,2,3,4]


Glucocorticoid therapy is associated with an appreciable risk for bone loss, which is most pronounced in the first few months of use. In addition, glucocorticoids increase fracture risk, and fractures occur more at higher bone mineral density (BMD) values than in postmenopausal osteoporosis. Thus, glucocorticoid-induced bone loss should be treated aggressively in those already at high risk for fracture (ie, elderly patient, prior fragility fracture). Bone density measurements may help in assessing the need for agents including bisphosphonates.

Prevention and treatment strategies consist of attempts to reverse the glucocorticoid excess by decreasing the dose of exogenous glucocorticoid or treating the cause of endogenous cortisol overproduction; calcium and vitamin D supplementation; and, in some patients, pharmacologic therapy to minimize further bone loss or increase bone density. In addition, certain general principles should be followed in all patients receiving prolonged glucocorticoid therapy in an attempt to minimize bone loss. The glucocorticoid dose and the duration of therapy should be as low as possible, because even replacement doses can cause bone loss. Alternative therapy should be used whenever possible, including the use of hydroxychloroquine discussed above. There are substantial data supporting the use of antiresorptive agents, such as the bisphosphonates, for the prevention and treatment of glucocorticoid-induced bone loss. The therapeutic efficacy of bisphosphonates in patients with glucocorticoid-induced osteoporosis has been thought to be related to their ability to promote osteoclast apoptosis (programmed cell death). However, glucocorticoids may negate the proapoptotic effect of bisphosphonates, suggesting that these drugs may prevent glucocorticoid-induced bone loss by prolonging the lifespan of osteoblasts.

The American College of Rheumatology recommends the following for the prevention of bone loss and fractures in patients initiating prednisone in a dose of 5 mg/day or higher for more than 3 months, and for patients receiving long-term glucocorticoids in whom the BMD T-score (spine or hip) is below -1.0: calcium and vitamin D supplementation (1000 mg/day to 1500 mg/day and 800 IU/day, respectively). Bisphosphonate therapy -- using alendronate or risedronate at weekly intervals -- is generally the first drug of choice.

The bone loss induced by glucocorticoid therapy is related to the dose. Although low doses are therefore safer than high doses, there is controversy as to whether there is any safe dose of glucocorticoid, or if there is a dose at which there is no acceleration of bone loss. This issue is complicated by the observation that the disease for which the glucocorticoids are being given (eg, rheumatoid arthritis) may itself lead to loss of bone.

Buckley and colleagues[5] concluded from their study that low doses of glucocorticoids (5-9 mg daily of prednisone) may have an adverse effect on the skeleton, but that very low doses (1-4 mg daily) probably have little or no effect. The sparse data that have been published on alternate-day prednisone therapy suggests that this regimen is not protective of bone.[6]


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