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So, what is the precise mechanism of this? I've got a couple of thoughts.
1. Simply steroid induced break down of bone matrix
2. A bit more complex, but it makes sense. Long term therapy can result in luid retention, and hypokalemia, producing a metabolic alkalosis, which as we have discussed before can give rise to a hypocalcemia-->increased PTH secretion, and that eventually giving rise to increased osteoclast activitiy with resultant osteoporosis. Any thoughts?
1. Simply steroid induced break down of bone matrix
2. A bit more complex, but it makes sense. Long term therapy can result in luid retention, and hypokalemia, producing a metabolic alkalosis, which as we have discussed before can give rise to a hypocalcemia-->increased PTH secretion, and that eventually giving rise to increased osteoclast activitiy with resultant osteoporosis. Any thoughts?