The findings of new research suggest that genetics may play a factor in who faces an increased risk of bone fractures from Fosamax and other similar bone-strengthening drugs.
In a study published in the November issue of the medical journal Calcified Tissue International, geneticists indicate that genetic variations affecting bone structure may explain why some long-term users of Fosamax suffer spontaneous fractures, which often occur following minimal or no trauma.
Fosamax (alendronate sodium) is a blockbuster medication introduced by Merck in 1995 for the treatment and prevention of osteoporosis. It belongs to a class of drugs known as bisphosponates, which fight against osteoporosis by slowing down bone remodeling enough to allow new bone growth to replace lost bone, reducing the risk of fractures associated with osteoporosis.
Although the drug is designed to strengthen bones, side effects of Fosamax have been linked to femur fractures among some users following long-term use, typically occurring during falls from standing height, while taking a step or other circumstances that would not normally result in a complete break of the thigh bone.
Researchers from the Texas Biomedical Research Institute conducted the study on baboons, leading to the conclusion that some women may genetically have slower remodeling already. When these users take Fosamax or other oral bisphosphonate medications, it could slow down bone remodeling even more and cause weaknesses that other people would not normally experience. This could explain the reports of atypical femur fractures from Fosamax and other similar medications following minimal trauma, the researchers suggest.
“This work is especially important in light of apparently rare but serious adverse conditions associated with potent remodeling suppression with some antiresorptive drugs. We and others have hypothesized that genetic variation may underlie heterogeneity in intracortical remodeling rates and outcomes, which may, in turn, provide a potential mechanism to explain variation in the efficacy of antiresorptive drugs as therapy for bone fragility,” the researchers concluded. “This supports the potential for a scenario in which certain individuals who are genetically predisposed to cortical microstructure that is less mechanically advantageous may experience disadvantageous responses to remodeling suppression such as being at higher risk for atypical femoral fractures. Further study will be necessary to specifically address this concept.”
Fosamax Fracture Lawsuits
The findings come as thousands of former users of the medication are currently pursuing Fosamax femur fracture lawsuits against Merck, alleging that the drug maker failed to adequately research the medication or warn about the risk of bone problems that may develop following long-term use.
Since May 2011, the federal Fosamax femure fracture litigation has been centralized in the U.S. District Court for the District of New Jersey for coordinated handling.
The first Fosamax trial over a femur fracture was held earlier this year, with a defense verdict returned. However, additional test cases are scheduled for trial in New Jersey State Court, where a group of 30 femur fracture cases have been prepared for early trial dates before Judge Carol Higbee in Atlantic County, with case-specific discovery complete.