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Sunday, December 8, 2013

Prevention and Treatment of Steroid Induced Osteoporosis in SLE in a nutshell

Posted by Dr Prahallad Panda on 5:25 PM Comments

Long term glucocorticoid (GC) therapy may cause osteopenia or osteoporosis in patients suffering from SLE (Systemic Lupus Erytematosus). Osteopenia and osteoporosis are conditions, where there occurs rarification of bone due to less availability of calcium for bone health. In other wards the bone mass is decreased.
The frequency of osteoporosis in SLE ranges from 4.0 to 48.8% and that of osteopenia from 1.4 to 68.7%.
There are several ways in which this can happen:
1.       Inhibiting calcium absorption from the gastrointestinal track.
2.       Decreasing the renal tubular reabsorption of calcium and consequent secondary hyperparathyroidism.
3.       Glucocorticoids reduce growth hormone (GH) secretion and may alter the GH/insulin‐like growth factor (IGF)‐I axis. But, this may play a minor role.
4.       There is also an alteration in hypothalamic gonadotrophin‐releasing hormone secretion with subsequent reduction in serum testosterone and oestradiol levels.
5.       Inhibiting IGF‐I transcription in osteoblasts (Bone forming cells).
6.       Reducing the replication, differentiation and function of osteoblasts and increase the apoptosis rates of mature cells, thereby depleting the osteoblastic cell population and inhibiting the function of mature cells.
7.       In the presence of GCs, bone marrow stromal cells do not differentiate into osteoblasts; instead, these cells differentiate toward an adipocyte cell lineage.
8.       GCs increase the expression of macrophage colony stimulating factor (M‐CSF) and receptor activator of Nuclear factor kappa beta ( NF‐kB) ligand (RANK‐L).
9.       In addition, GCs decrease the expression of osteoprotegerin in stromal and osteoblastic cells.
Through these mechanisms, GCs can induce the formation of osteoclasts (Act opposite Osteoblasts) to and favour bone resorption. GCs also reduce the rate of apoptosis among mature osteoclasts.
Bone mineral density (BMD) can be tested by DXA (Dual-energy X-rays Absorptiometry). Results are scored compared with the BMD of young, healthy people and is expressed in a measure called a T-score. The scoring is as follows:

Dual-energy X-ray absorptiometry (DEXA) assess...
Dual-energy X-ray absorptiometry (DEXA) assessment of bone mineral density of the femoral neck (A) and the lumbar spine (B): T scores of - 4.2 and - 4.3 were found at the hip (A) and lumbar spine (B), respectively in a 53 year-old male patient affected with Fabry disease. Courtesy: Dr Caroline LEBRETON, CHU Raymond Poincaré, Garches, France. (Photo credit: Wikipedia)
DXA T-Score
Bone Mineral Density (BMD)
Not lower than –1.0
Between –1.0 and –2.5
Osteopenia (mild BMD loss)
–2.5 or lower
To prevent osteopenia and osteoporosis in the first place, some preventive measures can be taken.
  • Be physically active and do weight-bearing exercises, like walking, most days of each week.
  • Change lifestyle choices that raise your risk of OP, such as quitting smoking.
  • Implement strategies to help decrease your risk of falling, which raises the risk of fractures.
  • Get DXA testing of your BMD.
Treatment of established osteoporosis:
Vitamin D increases intestinal calcium absorption and increases its reabsorption in distal renal tubules. Serum levels of at least 30 ng/mL (82 nmol/L), and optimally of 40–60 ng/mL, of 25‐hydroxyvitamin D should be the target treatment regimen for GIO management. To achieve these levels, 1,000 to 2,000 IU of oral vitamin D daily or 50,000 to 60,000 IU per week may be necessary.
Bisphosphonates are indicated for the prevention and treatment of GIO (Glucocorticoid Induced Osteoporosis) and most guidelines recommend the use of these drugs. The prevention and treatment goals of bisphosphonate use are stabilizing or increasing bone mineral density, as well as reducing frequency of fractures.
Currently, alendronate (70 mg/week or 10 mg/day) and risedronate (35 mg/week or 5 mg/day) are the some of the oral antiresorptive drugs that are recommended in GIO. Zoledronic acid, in injection form had been approved for the prevention and treatment of GIO.
Caution needs to be exercised when considering the use of bisphosphonates in women of childbearing age with GIO, given that bisphosphonates have an extended half‐life and may cross the placenta with potentially unfavourable effects on foetal skeletal development. The adverse effect like osteonecrosis of jaw (ONJ) has to be kept in mind, while prescribing it.
Teriparatide a synthetic parathormone had also been approved by USFDA for treatment of GIO. It is taken as subcutaneous injection daily. It may not be continued for more than 2 years at a time. The injection comes in pre-filled syringes containing 30 doses.
In a randomized multicenter trial, it had been seen that subcutaneous teriparatide (20 µg/day) is more effective in comparison to the use of oral alendronate (10 mg/day) over 18 months in patients with established GIO.
The key to prevent and treat Glucocorticoid Induced Osteoporosis are adequate weight bearing physical exercise, calcium and vitamin D intake in adequate doses.  
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