PURPOSE OF REVIEW

Sarcopenia is a progressive, multifactorial geriatric syndrome linked to increased risk of falls, fractures, disability, frailty, and all-cause mortality. The pathophysiology of this complex syndrome remains unclear.

Emerging evidence suggests that chronically elevated parathyroid hormone (PTH) concentration may contribute to muscle decline, increasing the risk of sarcopenia. This review evaluates the most recent evidence on the role of PTH in sarcopenia.

RECENT FINDINGS

A recent meta-analysis of eleven observational studies involving 4759 participants supports an association between elevated PTH and a higher risk of sarcopenia.

Proposed mechanisms include PTH-mediated alterations in serum calcium levels and modulation of muscle protein metabolism by PTH and its N-terminal fragment. The metabolic effects of elevated PTH may also indirectly affect muscle mass by altering skeletal muscle energy metabolism.

SUMMARY

Elevated PTH concentration is increasingly linked to a higher risk of sarcopenia in older adults, although the biological mechanisms behind this remain only partially understood.

Most current evidence comes from observational studies and cannot establish causation. Future research should focus on mechanistic studies in humans and interventional trials to determine whether higher PTH concentrations directly cause muscle decline and whether correcting PTH concentrations can lead to significant improvements in muscle mass and function.