New Member, 19, Female, LC
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Thanks everyone!
She's been on budesonide for 7 days now and no change in D. We are holding off with the cholystyramine for now. We are extremely concerned with the latest thyroid test values and hypothyroid symptoms, and we have doctor visits lined up to try to rebalance the thyroid meds. She is very afraid that if the D stops she will once again become extremely bloated and backed up. When her thyroid meds were working better, she felt her gut moved better and better able to pass formed stools and she felt better so she wants to prioritize thyroid first, then the D.
We are concerned the D is interfering with medicine absorption - what a chicken/egg dilemma!
One of her doctors has been suggesting Myers' Cocktail infusion treatments, but darn if we can find a place willing to do it.
Did have a question - she started taking budesonide 3mg 3 times a day, just to watch for reactions, but we've read to take them all at once, so we were wondering why, if it makes a difference.
She's been on budesonide for 7 days now and no change in D. We are holding off with the cholystyramine for now. We are extremely concerned with the latest thyroid test values and hypothyroid symptoms, and we have doctor visits lined up to try to rebalance the thyroid meds. She is very afraid that if the D stops she will once again become extremely bloated and backed up. When her thyroid meds were working better, she felt her gut moved better and better able to pass formed stools and she felt better so she wants to prioritize thyroid first, then the D.
We are concerned the D is interfering with medicine absorption - what a chicken/egg dilemma!
One of her doctors has been suggesting Myers' Cocktail infusion treatments, but darn if we can find a place willing to do it.
Did have a question - she started taking budesonide 3mg 3 times a day, just to watch for reactions, but we've read to take them all at once, so we were wondering why, if it makes a difference.
Strange that they make her take budesonide 3 times a day. Normal procedure is to start take the full dose once daily in the morning. This will have the least interference with cortisol levels. Taking the maximum dose at once definitely makes a difference. It’s three times as strong! When I have a serious flare 3 or 6 mg entocort at once is not enough. Let her try the 9mg in the morning for a couple of days and see if she improves.
Thanks! Actually spacing it out was her idea as she's so afraid of trying anything new, if she reacted to anything in the capsule (as she's sensitive to many so-called inactive ingredients) she figured a smaller dosage at one time would be better, and was planning on shifting to all at once in the morning.
Yes, budesonide works best if you take it all at once (with food -- have her eat something first and then take then take the medication).
Also, I think you're smart to hold on the cholestyramine. Your doctor probably explained this, but cholestyramine can bind to medications, so you need to be careful about the timing. Your doctor or pharmacist can explain the details, but you would need to take the cholestyramine x hours before and y hours after you take other medications. Otherwise some of her other drugs may become less effective.
Cholesturamine worked for me, but I had to work with my pharmacist and make a fancy, color-coded medication scheduling chart :) (I'm on a few different medications)
Good luck!
Also, I think you're smart to hold on the cholestyramine. Your doctor probably explained this, but cholestyramine can bind to medications, so you need to be careful about the timing. Your doctor or pharmacist can explain the details, but you would need to take the cholestyramine x hours before and y hours after you take other medications. Otherwise some of her other drugs may become less effective.
Cholesturamine worked for me, but I had to work with my pharmacist and make a fancy, color-coded medication scheduling chart :) (I'm on a few different medications)
Good luck!
Thanks y'all. Now for a more hypothetical question. While NSAID use is contraindicated for MS, how about specific COX-2 inhibitors? While it has become apparent that COX-2 inhibitors are not the long-term magic bullet for avoiding gastro damage while providing anti-inflammatory relief, it's gotten me to wondering if they might have some short term use with reducing the bloating and pain that starts when the diarrhea does finally slow down and stop and things start accumulating in the gut.
Several times in the past she received several days of IV Toredol which seemed to magically reduce her various weird symptoms, so there's obviously prostaglandins at work. It's been a very long while since she took any NSAID, but right now we're still using prednisone apparently for the same goal and we've got to get off that stuff.
FYI We will be starting 25 mcg Levothyroxine hopefully on Monday to help with the low thyroid numbers, and that we hope will help get the gut moving a little better. Our PCP feels low thyroid hormones can negatively affect virtually everything in the body and we need to do something about that if we want to make progress with the other issues as well.
Several times in the past she received several days of IV Toredol which seemed to magically reduce her various weird symptoms, so there's obviously prostaglandins at work. It's been a very long while since she took any NSAID, but right now we're still using prednisone apparently for the same goal and we've got to get off that stuff.
FYI We will be starting 25 mcg Levothyroxine hopefully on Monday to help with the low thyroid numbers, and that we hope will help get the gut moving a little better. Our PCP feels low thyroid hormones can negatively affect virtually everything in the body and we need to do something about that if we want to make progress with the other issues as well.
Cox-2 inhibitors are uncharted waters as far as I'm aware. I agree with your PCP that not just thyroid hormones but all hormones have an effect on MC, some more than others, obviously.Tex
It is suspected that some of the hardest material known to science can be found in the skulls of GI specialists who insist that diet has nothing to do with the treatment of microscopic colitis.
Thanks henrym for inquiring. We've had no change so far with the Entocort. We haven't tried the cholestyramine yet. She's afraid if the d stops then she's going to get horribly bloated, constipated and a lot of pain. Latest thyroid numbers were low (her thyroid's a moving target right now, we don't know why) and we've added more thyroid medicine but now waiting for it to start working (which takes forever with thyroid dosing). She thinks her gut will move better once she gets enough thyroid hormones. We see the Rheumy next week (with lots of questions), a new Endo in mid March and a new Gastro beginning of April. Hurry up and wait for us, I wish we can stumble onto at least one tiny little thing that can make her feel a tiny little bit better.
Jane,
Glucocorticoids (including budesonide) suppress the production of TSH by the pituitary gland. That tells the thyroid gland to produce less T4. The hormone levels will return to their previous levels when the budesonide treatment is ended.
Tex
Glucocorticoids (including budesonide) suppress the production of TSH by the pituitary gland. That tells the thyroid gland to produce less T4. The hormone levels will return to their previous levels when the budesonide treatment is ended.
Tex
It is suspected that some of the hardest material known to science can be found in the skulls of GI specialists who insist that diet has nothing to do with the treatment of microscopic colitis.
While we're waiting to see if our gastro will switch to mesalamine from sulfasalazine (and looking into stool testing in case we're missing something), we were wondering if anyone's tried Azathioprine (Imuran)? Imuran has my curiosity piqued as I read an article how it can cause T lymphocytes in the gut to die off. Mesalamine inhibits T lymphocyte proliferation, activation and differentiation. My thinking is that Mesalamine reduces the number of T lymphocytes entering the system while Azathioprine would reduce the current population of T lymphocytes.
Going one step further is extending the "histamine bucket" idea to a "lymphocyte bucket" idea - that managing both the rate of lymphocyte creation and death to keep the lymphocyte bucket from tipping and causing a flare. Also got me to wondering if ordinary immune system insults like colds, flu, minor infections, add to the bucket which would make it easier to tip and cause a MC flare.
Going one step further is extending the "histamine bucket" idea to a "lymphocyte bucket" idea - that managing both the rate of lymphocyte creation and death to keep the lymphocyte bucket from tipping and causing a flare. Also got me to wondering if ordinary immune system insults like colds, flu, minor infections, add to the bucket which would make it easier to tip and cause a MC flare.
Hi Jane,
This is just my opinion, but I think the medical community is missing the boat with using lymphocytes as inflammation markers. It's not lymphocytes that are causing most of the inflammation — it's mast cells. Lymphocytes are present of course, but they're not the primary drivers of inflammation. Histamine is just one of many pro-inflammatory agents released by mast cells. I discuss this in more detail in my new book (which will be available in a few days). Here's a quote from page 165:
190. Forbes, E. E., Groschwitz, K., Abonia, J. P., Brandt, E. B., Cohen, E., Blanchard, C., . . .Hogan, S. P. (2008). IL-9– and mast cell–mediated intestinal permeability predisposes to oral antigen hypersensitivity. The Journal of Experimental Medicine, 205(4), 897. Retrieved from http://jem.rupress.org/content/205/4/897
This viewpoint is unproven speculation of course, but it would indeed fit the "histamine, cytokine, etc., bucket" analogy.
Azathioprine generally works for suppressing the symptoms of MC. We have 2 or 3 members who are using Imuran successfully to control their MC. They still have to avoid their main food sensitivities (if they want to remain symptom-free), but they don't have to be as meticulous with their diet. Of course azathioprine carries an increased cancer risk, but the increased risk is relatively low. If one want's to go the route of the immune system suppressants, Imuran is far safer (IMO) than the anti-TNF drugs.
At any rate, these are my views on the subject. Whether or not future medical research proves me right, remains to be seen.
Tex
This is just my opinion, but I think the medical community is missing the boat with using lymphocytes as inflammation markers. It's not lymphocytes that are causing most of the inflammation — it's mast cells. Lymphocytes are present of course, but they're not the primary drivers of inflammation. Histamine is just one of many pro-inflammatory agents released by mast cells. I discuss this in more detail in my new book (which will be available in a few days). Here's a quote from page 165:
The reference to the research by Forbes et al. (2008) was cited earlier in the book:Not only MC, but all other IBDs, and all autoimmune-type diseases may be due to mast cell-based inflammation, rather than lymplocyte-based inflammation.
What if the inflammation that triggers or perpetuates the clinical symptoms associated with MC is caused by too much histamine or inappropriate mast cell activity that results in the release of histamine, cytokines and other proinflammatory immune system agents? We know from published research that mast cells (in the presence of IL-9) can create a condition of increased intestinal permeability (leaky gut) to promote food sensitivities (Forbes et al., 2008). Unfortunately this does not appear to be generally understood by most gastroenterologists because most GI specialists are not trained to recognize the role of mast cells in inflammatory bowel diseases. Rheumatologists often have a much better understanding of mast cell-based inflammation.
But there is compelling epidemiological evidence to suggest that mast cell-induced inflammation sufficient to cause or perpetuate an MC flare may indeed be the driving force behind inflammatory diseases. Perhaps this is why physicians have had so little success in trying to treat autoimmune-type diseases. This could explain why so many cases do not respond to treatment. The most effective treatment found so far is to disable the immune system, putting the patient at the mercy of the pharmaceutical industry, and imposing the risk of developing a fatal infection or cancer. Sadly, instead of treating the cause of the disease, many medical professionals (and patients) choose to simply disable the patients' immune system.
190. Forbes, E. E., Groschwitz, K., Abonia, J. P., Brandt, E. B., Cohen, E., Blanchard, C., . . .Hogan, S. P. (2008). IL-9– and mast cell–mediated intestinal permeability predisposes to oral antigen hypersensitivity. The Journal of Experimental Medicine, 205(4), 897. Retrieved from http://jem.rupress.org/content/205/4/897
This viewpoint is unproven speculation of course, but it would indeed fit the "histamine, cytokine, etc., bucket" analogy.
Azathioprine generally works for suppressing the symptoms of MC. We have 2 or 3 members who are using Imuran successfully to control their MC. They still have to avoid their main food sensitivities (if they want to remain symptom-free), but they don't have to be as meticulous with their diet. Of course azathioprine carries an increased cancer risk, but the increased risk is relatively low. If one want's to go the route of the immune system suppressants, Imuran is far safer (IMO) than the anti-TNF drugs.
At any rate, these are my views on the subject. Whether or not future medical research proves me right, remains to be seen.
Tex
It is suspected that some of the hardest material known to science can be found in the skulls of GI specialists who insist that diet has nothing to do with the treatment of microscopic colitis.