Bone densitometry as an adjunct to GnRH agonist therapy.

OBJECTIVE

To outline the optimal use of bone densitometry in women receiving gonadotropin releasing hormone (GnRH) agonist therapy.

STUDY DESIGN

The use of bone densitometry during clinical trials of the use of GnRH agonists in endometriosis has resulted in a number of publications with varying conclusions about the effects of these agents on the skeleton. A review of this literature, taking into account known concepts of bone physiology and the varying quantities measured by different bone densitometry devices, was done to place these results into a common framework. Within this context, a proposal is made for when and how to use various bone densitometry methods in individual patients and how to interpret the results properly.

RESULTS

Bone density in young women being treated for endometriosis is usually within the normal range, with even those 2 SD below normal not at significant risk of osteoporotic fracture. However, the clinical results show that most, if not all, women treated with GnRH agonists experience an increase in bone turnover due to estrogen deficiency during treatment, and this can result in a transient decrease in bone density. Even though the bone is regained after treatment is stopped, it may take years to recover fully. For those women who had low bone density to start, they may lose sufficient bone to increase their risk of osteoporotic fracture, and it is important to identify those individuals before treatment and to monitor them carefully. If the result of a peripheral bone density measurement (hand, forearm, heel) or central measurement (spine or hip) before treatment is higher than about 1 SD below a young normal mean, then even if a woman loses some bone, she will not have a significant increase in the risk of fracture. However, if a measurement is low (> 1 SD below the mean, putting her in the lower 15%), then it is advisable to have a spinal measurement by quantitative computed tomography or dual energy x-ray absorptiometry before and after therapy to determine what the bone changes are and to follow-up after the end of treatment. This is especially true if she decides to become pregnant, needs retreatment with a GnRH agonist or will be going through natural menopause in the near future; all can cause further bone loss.

CONCLUSION

Different bone density methods give different information and must be interpreted properly when used in evaluating patients on GnRH agonist therapy. Any bone measurement may be used to assess skeletal status before treatment, but if a peripheral bone measurement is low, it should be followed with a spinal measurement by quantitative computed tomography or dual energy x-ray absorptiometry so that the effect of the treatment can be monitored. Bone loss is transient with GnRH treatment, but only spinal measurements have sufficient sensitivity to follow patients and evaluate the skeletal changes in a meaningful way.