Michael Kleerekoper, MD, MACE, has joined the faculty at the University of Toledo Medical School where he is Professor in the Department of Internal Medicine and section chief of the Endocrinology Division. The author of numerous journal studies, Dr. Kleerekoper serves on the editorial boards for Endocrine Today, Endocrine Practice, Journal of Clinical Densitometry, Journal of Women's Health, Osteoporosis International and Calcified Tissue International. Dr. Kleerekoper is also a founding board member of the newly formed Academy of Women’s Health.

DXA under threat from many directions

If you are reading this blog, you must already be aware that in the United States, reimbursement for measurement of bone mineral density using DXA has been cut substantially over the last few years for all users except in hospital radiology suites. This has already led to a marked decrease in the number of private offices still offering DXA as an important diagnostic and monitoring tool.

As I have noted several times in the past, osteoporosis is still under-recognized and under-treated, so this decreasing availability and use of DXA is contrary to the important nationwide discussions about the needs to improve preventive care.

If that was not enough threat to those at risk of sustaining an osteoporosis-related fracture later in life (that includes every one of us unless we unfortunately die prematurely from something else), recent articles in the British Medical Journal1,2 have accepted that baseline DXA is important but have gone on to suggest that follow-up DXA to monitor progression or regression of disease is unnecessary. The current issue of the Journal of Bone and Mineral Research includes two point/counterpoint articles for and against serial measurement of DXA.3,4

What messages are being put forward in these four articles, and which are putting forward a sustainable opinion?

The articles in the BMJ, one a retrospective analysis of two articles published in 1996 and 1998 (what took you so long?) and the second an editorial, reasoned that the change in BMD was not the most reliable predictor of reduction in fracture occurrence and therefore serial BMD measurement was not helpful and should be discontinued.

The point/counterpoint articles in the JBMR provided very reasoned arguments for and against serial DXA. To get the full gist of their conflicting opinions, you will have to read the articles in full. In this blog, I want to emphasize just a couple of points.

To me, the take-home message was not whether serial DXA is a good or not good thing but that we have to be mindful whenever we translate data from randomized, double blind, placebo-controlled clinical trials into our clinical practice. Participants in these clinical trials are quite unlike the majority of patients you see day to day in your office, and this seems to hold true no matter what disease state or therapy is the subject of the trial.

In order to conduct and complete a randomized, controlled trial in the most cost-efficient, timely manner, the investigators are carefully selected and the trial participants even more so. Study subjects are carefully screened for potentially confounding health issues and for concomitant medication use. Investigators usually have to demonstrate that they can recruit study subjects in a timely manner, retain patients in the study and optimize adherence to study medication. Monitors not related to the drug company sponsoring the trial, or to the investigators conducting the trial, oversee every item documented about patient compliance to therapy, every reported adverse event, and make sure that every study outcome parameter has been obtained correctly.

In the field of osteoporosis, it has been reported from one such potential study center that fewer than 20% of patients referred to the practice for ongoing care were eligible for any one of the four randomized, controlled trials for which they were trying to enroll subjects.5

Randomized, controlled trials are critical for development of new therapies — try to imagine where we would be without them — but they are often not representative of the patient in your office right now. Case in point — the 66-year-old woman I saw recently who had sustained three fragility fractures during her three years of oral bisphosphonate therapy. I have good reason to believe that she was adherent to her medication as she claimed to be: She was certainly compulsive enough to hand me two double-spaced typed pages, the first one and a half pages listing her prescribed medications with the list of her concomitant diseases taking up the last half page. Assuming she did take her bisphosphonate on schedule on an empty stomach with a full glass of water, nothing else to eat or drink for 30 to 60 minutes all the while sitting or standing, who knows how any of the other medications may have affected the effectiveness of therapy or which of her diseases was overwhelming the effectiveness of therapy?

She was/is a candidate for osteoporosis therapy, but she is also, without question, a candidate for serial DXA — as often as once a year!

Not every patient will be like this, but at the same time, we cannot practice “cookie cutter� medicine. In some patients, particularly those who have not yet fractured, a baseline DXA with follow-up two or three years later may be appropriate. Interim measurement of a marker of bone resorption would also be appropriate during the first six months or so of therapy. Patients need early reinforcement that therapy is working as it should. In others the clinical situation will dictate more frequent BMD and biochemical monitoring.

I am confident that the authors of the articles arguing against serial DXA are aware of this, and many of them do monitor their patients on therapy. I am less confident that those insurance carriers who have to pay for the serial DXA will see it that way, or if they do, you will have to go through hoops to convince them one patient at a time. Time is of course something we all have aplenty of in day-to-day practice.

For more information:

1. Bell KJ. BMJ. 2009;338:b2266. PMID: 19549996.

2. Compston J. BMJ. 2009;338:b1276. PMID: 19549994.

3. Watts NB. J Bone Miner Res. 2009;24:1643-1646. PMID: 19712042.

4. Adler RA. J Bone Miner Res. 2009;24:1647-1648. PMID: 19702482.

5. Dowd R. Osteoporos Int. 2000;11:533-536. PMID: 10982170.