Bone metabolism in patients more than five years after bone marrow transplantation

Abstract

Summary:We investigated the bone metabolism of 22 patients (median age 38 years) over 6 years after allogeneic bone marrow transplantation (BMT). Biplanar roentgenograms of the thoracic and lumbar spine were used to diagnose vertebral deformities caused by fractures. The actual bone mineral density (BMD) of the lumbar spine and the femoral neck were measured. Laboratory tests included calcium, phosphate, parathyroid hormone, a marker of bone resorption (beta-crosslaps, CTX), markers of bone formation (osteocalcin, bone-specific alkaline phosphatase), osteoprotegerin (OPG) -an antagonist of the osteoclast differentiation factor RANKL, and sex hormone status. One patient had a vertebral fracture. Seven patients (28%) had osteopenia in the lumbar spine while 12 patients (48%) had osteopenia in the femoral neck. Bone resorption was increased in nine patients (43%) and bone formation was increased in four patients (20%). BMT recipients had significantly increased serum levels of OPG (P ¼ 0.029). Three women (75%) and four men (25%) were hypogonadal. The data showed that BMD is reduced and bone metabolism is still disturbed more than 6 years after BMT. The RANKL/osteoprotegerin system appears to play an important role in the pathophysiology of late post transplantation osteoporosis.

Low bone mineral density is associated with insulin resistance in bone marrow transplant subjects

“…Despite the fact that the bone resorption stabilizes 1 year after BMT, many studies have reported high osteopenia prevalence: Kerschan-Schindl et al studied 22 individuals in Vienna, Austria, more than 5 years after BMT and they found a 28% prevalence of osteopenia in lumbar spine and a 48% prevalence of osteopenia in femoral neck. 3 Another study conducted in Geneva, Switzerland, enrolled 54 subjects 60.1±5.6 months after allogeneic BMT and also found a high osteopenia prevalence (43%). 1 So, the high prevalence of osteopenia (19.2%) and osteoporosis (17%) found in our study is not surprising.…”

“…However, as the post-transplant life expectation rises the post-transplant comorbidities also do. Osteopenia and osteoporosis have been reported after BMT in several studies [1][2][3][4] and the posttransplant subjects have a higher bone fracture risk when compared with a non-transplant population. 5 There is a decrease in bone formation with an increase in bone resorption in the immediate post-BMT period.…”

High prevalence of early-onset osteopenia/osteoporosis after allogeneic stem cell transplantation and improvement after bisphosphonate therapy

“…6 It has been described after hematopoietic stem cell transplantation (SCT) as well, with the majority of cases reported in alloSCT recipients. [7][8][9][11][12][13][14][15][16][17][18][19][20][21][22][24][25][26][27][28][29][30][31][32][33][34][35] AlloSCT-associated BMD loss is usually described in the first 6-12 months after the transplantation, but varies widely from 40 days 17 to 4-6 years after the transplantation, 30,31,34 and in some instances can persist for 10-12 years. 26,28 Baseline BMD pre-SCT is usually within the normal limits; [15][16][17]24,[27][28][29][30]33 the few exceptions noting high O/O prevalence pre-SCT are probably due to the underlying diseases or intensive chemotherapy prior to the transplantation.…”

What We Learn from Bone Complications in Congenital Diseases? Thalassemia, an Example

“…The amount of bone loss within 1 year after transplantation varied and was approximately 2% for the lumbar spine and 12% for the femoral neck. At 5 years after allogeneic BMT, the lumbar spine BMD was within normal limits, but the femoral neck BMD was decreased; osteopenia was present in 43% and osteoporosis in 7% of patients (Kerschan-Schindl et al, 2004). Schulte & Beelen, demonstrated data of rapid bone loss during the first 6 months after transplantation (5.7% at the lumbar spine and 6.9% to 8.7% at the femoral neck sites) with no further decline between months 6 and 12, and recovery of bone mass during further follow-up (Schulte & Beelen, 2004).…”

“…Kerschan-Schindl et al, conclude that BMT recipients may receive less pre-treatment impairing bone metabolism, experience fewer restrictions in mobility, and have a more normal nutritional status. Additionally, BMT recipients generally receive less subsequent immunosuppressive therapy which may induce osteopenia (Kerschan-Schindl et al, 2004). Thalassemic patients are in an increased risk of accelerated bone loss and thus osteoporosis, because BMT is a curative treatment for thalassemia, and many patients achieve a lifelong disease-free period after BMT.…”