Rob Volansky , 2025-05-09 09:30:00
DESTIN, Fla. — Rheumatologists are uniquely positioned to define and manage sarcopenia and frailty, according to a speaker at the Congress of Clinical Rheumatology East annual meeting.
“We as rheumatologists could have written the book on frailty before the geriatricians,” said Nancy E. Lane, MD, director of the Center for Musculoskeletal Health, and principal investigator of the NIH-funded Program on Sex Differences in Musculoskeletal Diseases Across the Lifespan, at the University of California Davis School of Medicine.
Although multiple tools can be used to assess and define frailty, Lane counseled that the Fried frailty phenotype is among the easiest to use.
“It includes weight loss, exhaustion, slow gait speed, weak grip strength and low energy,” she said. “We sure see all of it.”
Chronic inflammation and dysregulated immune cells working in the musculoskeletal, neurological and endocrine systems, among others, can lead directly to frailty, according to Lane. In addition, environmental factors like smoking, or reduced physical activity and the presence of M1 macrophages, can contribute to sarcopenia in patients with frailty resulting from a rheumatologic or autoimmune disease.
“Sarcopenia is one of the big physical signs of frailty,” she said.
Determining who is at risk for both sarcopenia and frailty is critical to managing these outcomes, according to Lane.
“As patients get older, you see the frailty index go up,” she said. “As patients are obese, you see the frailty index go up.”
Understanding how to assess frailty can have significant benefits for patients with rheumatic and autoimmune conditions like rheumatoid arthritis and osteoarthritis.
Muscle strength assessed using a hand gripper and the duration of a 6-meter walk can be important indicators of sarcopenia, according to Lane. Clinicians may also consider measuring appendicular skeletal muscle mass.
“There are very quantitative ways that we can make these diagnoses of frailty and sarcopenia,” Lane said. “If we are going to use them, we have to be correct in our diagnosis.”
A closer look at the biologic underpinnings of sarcopenia could also benefit rheumatologists. The proinflammatory cytokines commonly found in rheumatologic and autoimmune conditions — including TNF, interleukin (IL)-1, and IL-6 — increase proteolysis and decrease protein synthesis.
“It is no surprise that our patients’ muscles do not work very well,” Lane said.
This raises the question of whether medications that act on those cytokines could mitigate the onset of sarcopenia. According to Lane, few data are currently available to answer this question, but early indicators may suggest that while the action of these medications may be “a little bit peripheral to the muscle,” there could be benefit.
“There is a little bit of data that our biologic treatments may slow or reverse sarcopenia,” she said.
Although obesity can be a driver of both sarcopenia and frailty, Lane urged caution regarding quick fixes until further data emerge.
“GLP-1 and GIP agonists may improve body composition but may increase sarcopenia, or maybe not?” she said.
Similarly, metformin may have the capacity to reduce cell senescence, which can, in turn, mitigate frailty.
“Metformin is somewhat anti-inflammatory as it reduces insulin resistance,” she said. “However, there are lots of conflicting data — I do not know where to put it.”
Until data demonstrating these effects emerge, Lane counseled attendees to continue with the most obvious and tested approach any physician can recommend to mitigate both sarcopenia and frailty.
“It is very clear that exercise can improve mitochondrial function and improve muscle quality and function,” she said.
Sources/Disclosures
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Lane N. Sarcopenia and Frailty: When and How Should We Intervene As Rheumatologists? Presented at The Congress of Clinical Rheumatology East; May 1-4, 2025; Destin, Florida (hybrid meeting).
Disclosures:
Lane reports no relevant financial disclosures.
