Tartrate resistant acid phosphatase (TRAP) has been proposed as a new biochemical marker for bone resorption. We have compared this new marker, TRAP, with the classical biochemical markers of bone remodelling, serum alkaline phosphatase (sAP), serum osteocalcin (sBGP), and with the urinary hydroxyproline/creatinine ratio (uOHProl/creatinine), a routine marker of bone resorption. Serum TRAP was significantly higher in pagetic patients (n = 43) than in control subjects (n = 12) (13.02 +/- 4.7 vs 5.48 +/- 1.31 IU/L, P less than 0.001) and a significantly positive linear correlation was found between the sTRAP and uOHProl/creatinine ratio (y = 0.0051x - 0.0069, r = 0.82, P less than 0.001), between sTRAP and sAP (y = 19.3x - 85.0, r = 0.71, P less than 0.001) and also between sTRAP and sBGP (y = 0.02x + 2.23, r = 0.52, P less than 0.01). Serum TRAP levels were higher than the upper limit of normality in all our pagetic patients except for two, whose uOHProl/creatinine levels were in the normal range. We conclude that (1) sTRAP could be a parameter as sensitive as uOHProl/creatinine in the diagnosis of Paget's disease; (2) sTRAP and uOHProl/creatinine are both good markers of bone resorption; (3) the correlation found between sTRAP and formation markers (sAP and sBGP) makes sTRAP a marker of disease activity in Paget's disease of bone; (4) the assay of sTRAP is easier, faster, and of lower cost than the urinary hydroxyproline determination. We suggest that sTRAP determination could be used as a routine marker of bone resorption in Paget's disease of bone, as is the case with uOHProl determination.
Serum tartrate-resistant acid phosphatase (sTr-AcP) and bone mineral content (BMC) were measured in 29 women with postmenopausal osteoporosis and in 12 control women. Serum Tr-AcP was higher in osteoporotic patients than in controls and a negative linear correlation was found between sTr-AcP and BMC in osteoporotic women. These results suggest that sTr-AcP could be a useful marker for bone loss and consequently, for the measure of bone resorption rate in postmenopausal women.
To study the evolution of the bone mass by ultrasonic transmission after biliopancreatic diversion. Forty eight morbid obese patients were prospectively studied during 36 months following the Larrad biliopancreatic diversion. The bone metabolism was studied by PTHi and the urinary pirydinolines. The bone mass by echography and bone densitometry, which correlate to the levels of PTHi and pyridinolines. After 3 years the bone mass decreased from 50.15 +/- 7.31 kg/m(2), preoperatively, to 34.03 +/- 4.53 kg/m2 (p < 0.001). There was an increase of the PTHi value (from 71.4 +/- 79.6 to 91.65 +/- 43.06 pg/ml) (p = 0.01), and the urinary pirydinolines (from 7.93 +/- 4.06 an 11.4 +/- 10.12 nM/mM) (p < 0.05). The ultrasonic transmission speed increased (from 1,990.93 +/- 62.38 to 2,035.25 +/- 53.98 m/s). However, the bone mineral content (BMC) did not show changes (from 3,016.5 +/- 562.8 to 2,909.6 +/- 304.2 g), as well as the Bone Mineral Density (BMD) (of 1,174.2 +/- 98.8 g/cm2). Neither correlation was found between the BMD (r = 0.212; p = 0.6), the BMC (r =-0.125; p = 0.768), and the T-score (r = 0.592, p = 0.093). The study of the bone mass through ultrasonic transmission speed revealed low sensitivity during the assessment of the morbid obese patients. A percentage of cases of osteopenia were observed despite the fact that they are not reflected in the bone content or in the bone mass. Ultrasonic evaluation of bone mass has no value in the morbidly obese, by the clear negative correlation between ultrasound velocity and thickness of soft tissue.
The objective of the present work has been to study some aspects of bone and intestinal compartments in rats with Walker 256 carcinosarcoma, an experimental model of humoral hypercalcemia of malignancy (HHM). The results have been compared to those obtained in control animals and, also, to those obtained in Yoshida sarcoma-bearing rats, which were used as tumoral controls without hypercalcemia. Urinary hydroxyproline/creatinine ratio (OHProl/creat) is increased, in both Walker 256 and Yoshida tumor-bearing animals, showing the nonspecifity of this bone marker. However, serum tar-trate-resistant acid phosphatase (TRAP) levels are increased in Walker 256 tumor-bearing animals, but they are normal in Yoshida tumor-bearing animals, indicating that TRAP is a better index of bone resorption than OHProl/ creat in the HHM syndrome. The decrease of bone calcium content in Walker 256 tumor-bearing rats, not shown by Yoshida-bearing rats, also reflects an increased bone resorption due to HHM. Serum and bone osteocalcin levels are similar in control, Walker 256 and Yoshida tumor-bearing rats, but we observed a decrease in serum alkaline phosphatase levels in Walker 256 and Yoshida tumor-bearing animals, which could also be a nonspecific tumor effect, due to the presence of the neoplasia. Our results support the convenience of the employment of a nonhypercalcemic tumor group as control in the HHM study, in addition to the healthy controls. We have also observed higher 1,25-dihydroxyvitamin D serum levels in Walker 256 tumor-bearing rats than in control and Yoshida tumor-bearing rats. On the other hand, we have found normal levels in the fractional rate of intestinal calcium absorption in Walker-256 tumor-bearing rats, in spite of their high calcium levels, and a significant decrease of this parameter in Yoshida sarcoma-bearing animals. These results support the concomitant contribution of intestinal compartment to hypercalcemia, in the experimental model of HHM studied.
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