Abstract
Osteoporosis is a common, and potentially severe, complication seen in the heart transplant recipient. Frequently there is loss of bone mineral density prior to transplant that begins the downward spiral to fractures of the femoral neck and vertebrae. Multiple factors are responsible for the development of osteoporosis posttransplant. These factors include pretransplant bone mineral loss, use of corticosteroids and cyclosporine posttransplant, and development of persistent hypomagnesemia posttransplant. This article explores the relationship of serum magnesium levels to maintenance of bone mineral density.
OSTEOPOROSIS is the most common type of metabolic bone disease and is associated with a decrease in bone strength as well as a decrease in bone mineral density. 1 About 10 million people in the United States have osteoporosis today with another 34 million Americans at risk for low bone mass. 2 Individuals at risk for developing osteoporosis include those on corticosteroids, like most heart transplant recipients. 1,3 Although use of corticosteroids has decreased slightly, the most recently reported data by UNOS indicates that in the year 2000, 92.7% of heart transplant recipients were taking prednisone at time of discharge from the hospital. 4 While the role of calcium in the development of osteoporosis is well known, there is increasing evidence that alterations in magnesium also play an important role in the development of this devastating disease.
Osteoporosis is frequently asymptomatic until fractures occur. Patients may present with complaints of backache of variable intensity due to spontaneous vertebral fractures. 1,5 Worldwide, the incidence of vertebral fractures in heart transplant recipients is 1% to 44% while the incidence of necrosis of the femoral head is 1% to 9%. 5 Unfortunately, despite the frequency of osteoporosis, the mechanisms of bone loss after heart transplantation are still unclear. 6
The pathogenesis of osteoporosis in the transplant patient is multifactorial. Factors that contribute to its development prior to transplant include (1) a reduced exercise capacity due to underlying cardiac disease; (2) the presence of cardiac cachexia; (3) substance abuse, either smoking or alcohol abuse; (4) hypogonadism caused by the debilitating cardiac disease; (5) low calcium intake; and (6) the excessive use of loop diuretics. 5,7 While the patient awaiting heart transplantation does not usually have osteodystrophy (unlike prospective liver or renal transplant recipients), longitudinal studies have found that bone mineral density may be reduced by as much as 10% to 20% at the hip and spine prior to transplant. 8
After transplantation, there is an increase in bone metabolism leading to accelerated bone turnover with concomitant bone loss. 8,9 In the posttransplant period, the most rapid bone loss occurs during the first 3 months after transplant. During this period, the annualized rate of bone mineral loss in the lumbar spine and femoral neck approaches 20%. 10 This rapid loss of bone could not be entirely attributed to corticosteroid use alone, although that is most certainly a factor in this process. 3,9,11 Other factors that have been implicated include use of cyclosporine A and magnesium depletion. 9,10