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How does prednisone work?

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Ulcerative Colitis
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Posted 2/17/2015 6:22 PM (GMT 0)
I've been thinking about this for a few months now. For patients not on prednisone your body makes approximately 10mgs of cortisol per day. If you take that much or more of prednisone per day then your adrenal glands shut down and no longer produce their own cortisol. But, the prednisone theoretically replaces the cortisol that your own body used to make. Let's use the example that a UC'r started on the usual dosage of 40mgs per day and has now tapered down to 10mgs. How is that different than not being on prednisone at all, since you are just replacing your own body's manufacture of cortisol with an artificial source - prednisone (I'm not sure how they actually make prednisone)? In other words, what is different about not taking prednisone at all and taking 10mgs of pred per day? I'm thinking there is a clue in there somewhere that could be helpful in understanding UC and the treatment of UC, like maybe the body's andrenal glands are doing more than just producing 10mgs per day of cortisol and when they are shut down we get better because of this. I realize that prednisone is also an anti-inflammatory but not quite sure on how prednisone makes that happen because if you take other anti-inflammatories such as Ibuprofin - we get worse.
Posted 2/17/2015 6:44 PM (GMT 0)
Let's use the example that a UC'r started on the usual dosage of 40mgs per day and has now tapered down to 10mgs. How is that different than not being on prednisone at all,

The difference is that 10 mg is still a synthetic dose of cortisol and it will shut down all adrenal production of cortisol if taken permanently. This means the HPA axis gets unwired - the pituitary gland, hypothalamus and adrenal glands stop doing their job (ACTH production). This opens up a can of worms and increases the risk of other issues (see prednisone side-effects).

There are those with primary addison's disease (see John F. Kennedy's bio) where the adrenal glands don't produce cortisol, and this is where synthetic cortisol is needed to keep the body alive or the heart will stop beating. The dosage is around 5 mg of pred or time-released hydrocortisone (which better mimics adrenal function). Sometimes hydrocortisone is used to "shock" the adrenals back into functioning after long courses of prednisone.

Prednisone works because it is synthetic stress. Stress (or cortisol) suppresses immune function at the cost of long term damage to the adrenal glands. Think fight or flight response - the body recognizes a threat and it temporarily increases blood flow to the areas of the body needed for survival (legs, brain, heart, etc), while minimizing blood flow to the colon and other secondary organs. Chronic stress will also do the same and it's one of the major risk factors in disease risk (see studies on HPA axis). There was an interesting study done on medical school students - those who were more stressed had higher risk of colds and other infections.
Posted 2/17/2015 6:44 PM (GMT 0)
the adrenal glands do much more than just produce cortisol. that's why we need them to survive. it's terrible for them to be steroid dependent. why would we want our body to become dependent on artificial prednisone when our own adrenals have the capacity to produce our own cortisol? our adrenal glands also produce DHEA and norepinephrine. that's why when people suffer from adrenal fatigue, their body basically shuts down and they suffer from depression, fatigue, and low libido.
Posted 2/17/2015 6:45 PM (GMT 0)
Cortisol is synthesized in the body from cholesterol, which I find of interest,since many with UC are on the low

end of cholesterol levels, as am I. Perhaps I should start to eat lots of eggs and liverwurst.

But to answer part of your question pred is 5 times stronger in activity, while some others are up to 120.

ANyhow 10mg of pred = about 50mg of cortisol.

Old Mike

http://www.merckmanuals.com/vet/pharmacology/anti-inflammatory_agents/corticosteroids.html

Post Edited (Old Mike) : 2/17/2015 12:01:03 PM (GMT-7)

Posted 2/17/2015 6:51 PM (GMT 0)

Old Mike said...
Cortisol is synthesized in the body from cholesterol, which I find of interest,since many with UC are on the low
end of cholesterol levels, as am I.



But to answer part of your question pred is 5 times stronger in activity, while some others are up to 120.

ANyhow 10mg of pred = about 50mg of cortisol.

Old Mike

http://www.merckmanuals.com/vet/pharmacology/anti-inflammatory_agents/corticosteroids.html

When I separated myself from the dietary illusions of cholesterol and started eating cholesterol rich foods like eggs, butter, full fat milk, my adrenals started functioning better. My libido increased by about twenty fold as well. I'd like to think of cholesterol as the body's natural prednisone.

I suspect the cholesterol guidelines are responsible for the high sales of viagra and other erectile dysfunction medications.
Posted 2/17/2015 7:16 PM (GMT 0)
What is it that prednisone actually does to help UC? I'm talking more about nuts and bolts here instead of generalities. If it helps UC by shutting down the adrenal glands, then what is it about the andrenal glands that is bad for UC?
Posted 2/17/2015 7:46 PM (GMT 0)
It isn't the "shutting down of the adrenal glands" that makes UC better with pred, it's the suppression of the immune response (inflammatory cascade) that improves UC.

DRs give prednisone for all kinds of inflammation: asthma, swollen joints from reactive arthritis, regular arthritis, even the throat swelling that comes with mononucleosis....

www.mayoclinic.org/steroids/art-20045692

en.wikipedia.org/wiki/Prednisone

www.drugs.com/monograph/prednisone.html:

Actions

  • Principally an anti-inflammatory or immunosuppressant agent.
  • Exhibits anti-inflammatory activity and minimal mineralocorticoid properties.
  • Has approximately half the mineralocorticoid activity of hydrocortisone and cortisone.
  • Decreases inflammation by stabilizing leukocyte lysosomal membranes, preventing release of destructive acid hydrolases from leukocytes, or reducing leukocyte adhesion to capillary endothelium.
  • Inhibits macrophage accumulation in inflamed areas.
  • Reduces capillary wall permeability and edema formation.
  • Antagonizes histamine activity and release of kinin from substrates.
  • Reduces fibroblast proliferation, collagen deposition, and subsequent scar tissue formation.
  • Stimulates erythroid cells of bone marrow, prolongs survival time of erythrocytes and platelets, and produces neutrophilia and eosinopenia.
  • Promotes gluconeogenesis, redistribution of fat from peripheral to central areas of the body, and protein catabolism, which results in negative nitrogen balance.
  • Reduces intestinal absorption and increases renal excretion of calcium.
  • Suppresses the immune response by reducing activity and volume of the lymphatic system, producing lymphocytopenia.
  • Decreases immunoglobulin and complement concentrations and passage of immune complexes through basement membranes.
  • Depresses reactivity of tissue to antigen-antibody interactions.
Posted 2/17/2015 8:48 PM (GMT 0)
If it's the anti-inflammatory effect then why can we take prednisone but we can't take anti-inflammatories such as Ibuprofen and others? They actually make us worse.
Posted 2/17/2015 9:01 PM (GMT 0)
Two different sets of drug actions.
Pred mostly goes after the immune system.
Where NSAIDS go after enzymes cox1 and cox2,different pathways, in the body.
Messing with the bodies biochemical pathways with drugs can have all kinds of
results that you don't want.

Google is your friend, all kinds of info,on the subject.
Old Mike
Posted 2/17/2015 9:03 PM (GMT 0)
Exactly. I don't know whether it's the NSAID action on cox1 & cox2 that makes them especially bad for us, but they damage the lining of the digestive tract in everybody, just faster for IBDers.
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