Men's Osteoporosis Support GroupFracture risk and urinary pentosidine and plasma homocysteine levels J Bone Miner Metab. 2010 May 11. [Epub ahead of print]. Urinary pentosidine and plasma homocysteine levels at baseline predict future fractures in osteoporosis patients under bisphosphonate treatment. Shiraki M and others. PMID: 20458602. This Japanese study evaluated which risk factors predict incident fractures in patients treated with bisphosphonates. It included 251 people with osteoporosis, mean age 70.5 years, who were followed for 3.2 years. Multiple baseline data points were taken and evaluated over the entire study. Results showed 61 people had vertebral fractures during the study. The following factors were related to fracture risk: older individuals, lower lumbar bone mineral density (LBMD), higher prevalent (starting) number of fractures, and higher homocysteine and pentosidine levels than those who didn't fracture. These factors were not related to fracture risk: changes in LBMD, urinary N-terminal telopeptides of type I collagen (NTX), and bone-derived alkaline phosphatase showed no significant association with the occurrence of vertebral fractures. The authors concluded, "Higher baseline levels of pentosidine and homocysteine in osteoporosis patients are potential risk factors for incident vertebral fractures when these patients are treated with bisphosphonates." Editor's comments. This is the first time I recall reading about an association between increased vertebral fracture risk and increased levels of both urinary pentosidine and serum homocysteine. I don't have access to the full study where details might be helpful to explain these results. Not knowing exactly how much higher the fracture patients' pentosidine and homocysteine levels were than controls is important. At what level would we be concerned, for instance, if our test results were elevated? And what steps could we take to reduce them? Were their levels high due to disease conditions, such as diabetes, or due to what they were eating? I have done some reading regarding Advanced Glycation End products (AGEs) in the past. Since they are formed both externally and internally, their formation is complex, is related to diabetes, kidney, and many other diseases. Their levels are affected by what we eat. One item that I remember is that they can being greatly increased, for instance, in nuts and other foods by heating and browning them. So tasty, browned almonds,and other browned foods, might be delicious, but could increase fracture risk in some of us because the browning increases AGE levels in the nuts. More research is needed to verify if this is true, and how all the factors interrelate. You might want to discuss this study with your osteoporosis care provider to see if he/she feels your urinary pentosidine and serum homocysteine levels should be monitored along with the normal bone density testing that is done.
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