What is the primary cause of increased risk of hip fractures with long-term proton pump inhibitor use?

Long-term use of proton pump inhibitors (PPIs) is associated with an increased risk of hip fractures primarily due to altered calcium absorption. PPIs reduce gastric acid secretion, which is essential for the solubilization and absorption of calcium from the diet. When gastric acid is reduced, the availability of calcium in a bioavailable form diminishes, leading to decreased calcium absorption in the intestines. Over time, this deficiency can contribute to osteoporotic changes in bone density and consequently increase the risk of fractures, particularly in weight-bearing bones like the hip.

While all options pertain to aspects of bone health, increased bone mass is not accurate since the net effect of reduced calcium absorption is typically a decrease in bone density. Decreased vitamin D metabolism is unlikely to be directly related to PPI use, and enhanced bone repair is not associated as PPIs generally do not promote bone health. Therefore, the correct emphasis on altered calcium absorption captures the mechanism leading to increased fracture risk in those on long-term PPI therapy.