A recent article by The New England Journal of Medicine, entitled “ Glucocorticoid Induced Bone Disease ” was really eye-opening and shocking, for anyone who is reading it. It stated that patients who are on at least 10 mg/day of Prednisone (corticosteroid) for 90 days have a 75% increased chance of developing a hip fracture due to osteoporosis.
A 75% increase. That is quite scary. And I think that a scarier part of that, is many patients that we, as student clinicans, see at various clinics that we help out at, can be put on upwards of 90mg of Prednisone/90 days. Imagine what those effects of suppression are at the bone-level. Thinking about this makes me shudder just sitting here in my seat.
So what does this increased risk for bone fracture have to do with corticosteroid treatment? Corticosteroids, like prednisone, are synthetic hormones that deal with immune regulation and the stress responses, to act in a suppressive manner, shutting down inflammatory pathways and the like. Prednisone in particular can be used for many inflammatory conditions like chronic obstructive pulmonary disease (COPD = chronic bronchitis, emphysema, bronchiectasis, or asthma), rheumatoid arthritis, or Crohn’s disease, for example, to act in an anti-inflammatory manner.
In relation to osteoporosis, glucocorticoids and other corticosteroids, induce osteoblast (bone forming cells) destruction, osteocyte (bone cells) destruction, and minimal osteoclast (bone resporbing) destruction. So, if we take that equation, there is not enough bone forming cells, not enough bone cells in general, and increased destruction of bone cells that are present, with no replacement mechanism ensue. This is the mechanism that increases bone porosity and increased risk (75%) of bone fracture, particularly in the hip bones and vertebral disks.
One method of determining bone mineral density that is often used ( FRAX = bone density algorithm) to determine bone density is unable to be applied to patients with glucocorticoid induced bone disease. The reason for this is that FRAX does not take into account the use of glucocorticoid usage, as well as the fact that his algorithm only measures femoral head bone density, which is not affected in high glucocorticoid usage. The bones that ARE affected in glucocorticoid over-use are the vertebral bones and hip bones, which are not assessed in FRAX.
Typical conventional treatments are bisphosphonates (which decrease activity of osteoclasts that destroy bone), teriparatide (recombinant human parathyroid hormone approved by the FDA), and denosumab (humanized monoclonal antibody to the receptor activator of nuclear factor-κB ligand, RANKL, which was just approved by the FDA).
Other things to keep in mind are blood calcium levels and Vitamin D levels.
If you or someone you know has been put on more than 10mg of Prednisone for more than 90 days, please see your primary care physician immediately. This is a serious matter, that needs to be addressed.
Reference:
http://www.nejm.org/doi/full/10.1056/NEJMcp1012926
A recent article by The New England Journal of Medicine, entitled “ Glucocorticoid Induced Bone Disease ” was really eye-opening and shocking, for anyone who is reading it. It stated that patients who are on at least 10 mg/day of Prednisone (corticosteroid) for 90 days have a 75% increased chance of developing a hip fracture due to osteoporosis.
A 75% increase. That is quite scary. And I think that a scarier part of that, is many patients that we, as student clinicans, see at various clinics that we help out at, can be put on upwards of 90mg of Prednisone/90 days. Imagine what those effects of suppression are at the bone-level. Thinking about this makes me shudder just sitting here in my seat.
So what does this increased risk for bone fracture have to do with corticosteroid treatment? Corticosteroids, like prednisone, are synthetic hormones that deal with immune regulation and the stress responses, to act in a suppressive manner, shutting down inflammatory pathways and the like. Prednisone in particular can be used for many inflammatory conditions like chronic obstructive pulmonary disease (COPD = chronic bronchitis, emphysema, bronchiectasis, or asthma), rheumatoid arthritis, or Crohn’s disease, for example, to act in an anti-inflammatory manner.
In relation to osteoporosis, glucocorticoids and other corticosteroids, induce osteoblast (bone forming cells) destruction, osteocyte (bone cells) destruction, and minimal osteoclast (bone resporbing) destruction. So, if we take that equation, there is not enough bone forming cells, not enough bone cells in general, and increased destruction of bone cells that are present, with no replacement mechanism ensue. This is the mechanism that increases bone porosity and increased risk (75%) of bone fracture, particularly in the hip bones and vertebral disks.
One method of determining bone mineral density that is often used ( FRAX = bone density algorithm) to determine bone density is unable to be applied to patients with glucocorticoid induced bone disease. The reason for this is that FRAX does not take into account the use of glucocorticoid usage, as well as the fact that his algorithm only measures femoral head bone density, which is not affected in high glucocorticoid usage. The bones that ARE affected in glucocorticoid over-use are the vertebral bones and hip bones, which are not assessed in FRAX.
Typical conventional treatments are bisphosphonates (which decrease activity of osteoclasts that destroy bone), teriparatide (recombinant human parathyroid hormone approved by the FDA), and denosumab (humanized monoclonal antibody to the receptor activator of nuclear factor-κB ligand, RANKL, which was just approved by the FDA).
Other things to keep in mind are blood calcium levels and Vitamin D levels.
If you or someone you know has been put on more than 10mg of Prednisone for more than 90 days, please see your primary care physician immediately. This is a serious matter, that needs to be addressed.
Reference:
http://www.nejm.org/doi/full/10.1056/NEJMcp1012926