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Current research into the treatment of osteoporosis suggests that high, pulsatile concentrations of PTH could be effective at building bone. It is hypothesized that this may occur by inducing negative feedback of endogenous PTH with a subsequent increase in both calcitonin levels and calcitonin-mediated effects. Which of the following, if true, would disprove this hypothesis?
A. A patient treated with high, pulsatile levels of PTH fails to demonstrate an increase in bone density.
B. A patient treated with high, pulsatile levels of PTH demonstrates an increase in bone density as well as increased renal absorption of calcium.
C. A patient treated with calcitonin fails to demonstrate an increase in bone density.
D. Several patients treated with high, pulsatile levels of PTH demonstrate varying increases in bone density.
Correct answer is B. I can't seem to figure out why A isn't correct. Can somebody explain this?
A. A patient treated with high, pulsatile levels of PTH fails to demonstrate an increase in bone density.
B. A patient treated with high, pulsatile levels of PTH demonstrates an increase in bone density as well as increased renal absorption of calcium.
C. A patient treated with calcitonin fails to demonstrate an increase in bone density.
D. Several patients treated with high, pulsatile levels of PTH demonstrate varying increases in bone density.
Correct answer is B. I can't seem to figure out why A isn't correct. Can somebody explain this?