Budesonide Quick Question

[Pebbledash]

Hi all,

I was going to get back to you later this week, but thanks for your concern Carol. So . . .

The breaking news is that the Budesonide seems to have kicked in!! It took about 13 days to feel any effect. Early days, and I don't want to count my chickens, but the last 2 days have been ah-hum "solid."

Early days, I don't want to get over-confident. But it feels beautiful.

I am taking cholestyramine too. Yesterday dropped the imodium, and will try today without Pepto Bismol.

Lisa, thanks for the advice. I have to say, from the bottom of my heart, I read, re-read, and read again the messages on here, taking hope from others' experiences and advice.

A big take-home for me is that Budesonide can take time . . . despite what I have read at times, and what my gastro seemed to think.

I'll update later this week.

Paul

PS in my worst days I have been taking about 12 imodium a day and half a bottle of Pepto Bismol, to no real effect. This cannot be a good thing.

PPS I can't say enough about this forum and the people on it: you were there when I was at my lowest.

[Pebbledash]

Hi Paul,

Mesalamines are a class of drugs that can help with inflammation. Lialada is a brand of Mesalamine. I took 4 pills of Lialda in addition to 3 pills of Entocort in the middle of a flare to get things under control.

At my worst, I was also taking Imodium daily (my doctor OK'd up to 6 Imodium a day -- thankfully I never got to that, but would always keep a stash in my bag).

Prednisone is a steroid that is stronger than Entocort and I imagine would take care of your flare. My understanding is that Prednisone does come with some more side effects that you'd want to consider.

Wishing you all the best.

Hi Lisa--I have some questions for you I'll post later in the week, if that is okay.

Cheers
Paul

[carolm]

Great Paul! happy dance!

Wishing you continued improvement.

C.

[tommyboywalker]

This is the BEST news of the day, Paul!

How great does it feel to get some relief? I can remember how I felt when my Budesonide kicked in at day 10. So day 13 is right in that same ballpark. And I had steady improvement after that.

So now to develop a plan on moving forward. This forum helped me do just that. And I know it can help you do the same. So much good information within these threads from good folks that have been and are in the MC trenches.

Advice/recommendations/support is the trifecta in my book! We're all learning here.

All the best for a continued healing process and keep us updated!

[brandy]

[tex]

Tex

[Pebbledash]

This is the BEST news of the day, Paul!

How great does it feel to get some relief? I can remember how I felt when my Budesonide kicked in at day 10. So day 13 is right in that same ballpark. And I had steady improvement after that.

So now to develop a plan on moving forward. This forum helped me do just that. And I know it can help you do the same. So much good information within these threads from good folks that have been and are in the MC trenches.

Advice/recommendations/support is the trifecta in my book! We're all learning here.

All the best for a continued healing process and keep us updated!

Honestly, Tommy, I feel euphoric. I really do. I feel like taking a photograph of my "success" and framing it!!

That said, I am also cautious about counting my chickens. I know what happened last time, so I am taking this one step at a time, and also thinking very much of the long-term; I never want to go back to the half-life I have been maintaining.

BTW, the fact that you had been "there" (waiting on the Budesonide) helped me no-end.

I am not out of the woods yet, I am scared of being disappointed again, to be honest . . . but for now I am so happy!

[Pebbledash]

Carol, Brandy, Tex, Tommy, Jari, Lisa, Kilt: thank you big time.

[Pebbledash]

Tommy,

a few questions:

1. I presume you intend to come off Budesonide completely? If you are good just taking it every 4 days, is there a valid case for staying on this unobtrusive maintenance dose?

If you have a bad day or flare-up once you have cut the chains with Budesonide, would you have to go back to the full course again?

2. During your course, did you ever have days when, though better, you wouldn't call yourself "normal" (by non-colitis standards)? Did you ever take an additional supplement like immodium or a prescription drug?

3. Neuropathy: do you feel your neuropathy gets better or worse as your colitis improves--or perhaps there is no correlation for you?

Cheers
Paul

[Pebbledash]

Hi Paul,

Mesalamines are a class of drugs that can help with inflammation. Lialada is a brand of Mesalamine. I took 4 pills of Lialda in addition to 3 pills of Entocort in the middle of a flare to get things under control.

At my worst, I was also taking Imodium daily (my doctor OK'd up to 6 Imodium a day -- thankfully I never got to that, but would always keep a stash in my bag).

Hi Lisa,

So I gather that you were still on your starting dose of Budesonide (9mg) when you added Lialada? For how long?

Now you are (presumably) off Budesonide, do you ever have either Budesonide or Lialada on hand for emergencies--can they be used as "stop-gaps" or are they only valid in the context of long-term courses?

Thanks
Paul

[tommyboywalker]

Tommy,

a few questions:

1. I presume you intend to come off Budesonide completely? If you are good just taking it every 4 days, is there a valid case for staying on this unobtrusive maintenance dose?

If you have a bad day or flare-up once you have cut the chains with Budesonide, would you have to go back to the full course again?

2. During your course, did you ever have days when, though better, you wouldn't call yourself "normal" (by non-colitis standards)? Did you ever take an additional supplement like immodium or a prescription drug?

3. Neuropathy: do you feel your neuropathy gets better or worse as your colitis improves--or perhaps there is no correlation for you?
-------------------------------------------------------------------

Hey Paul!

1. Yes, the goal is for me to completely come off of Budesonide, then continue with a gluten free / dairy free diet. There is a theory that a very slow Budesonide taper is worth consideration. I don't know if it is backed up with actual research but with the amount of it being so minimal over time, I feel I have nothing to lose with going with it and my GI doc agreed. Could be a little "placebo effect" at play as well with the comfort of taking a little bit of the drug that (helped) give me my life back I suppose! As for the second part of this question, I hope that it doesn't occur but it is my understanding that if you have what is considered an actual "relapse", (not a flare) then it is recommended to go back to the full dosage of the drug (3 mg three times a day).

2. I have a day about every couple of weeks or so where things aren't so great. I would not call it an actual MC flare; just a bad day and to be honest, I had a couple of days a month before Colitis, so not that much different. When that happens, I take a dose of Pepto and a couple of Imodium and that takes care of it.

3. As for my Neuropathy and Complex Regional Pain Syndrome, I honestly can say that it hasn't changed much from before I developed Microscopic Colitis. There are some day to day week to week changes with it but that has always been there. So I would say no correlation there.

Hope this helps; hope things continue to go well with you and keep us updated!

[tex]

Paul,

For what it's worth, I agree with Tommy. I don't notice any correlation between my peripheral neuropathy and MC. I blame the original onset and development of peripheral neuropathy on MC (because the malabsorption issue caused me to become deficient in vitamins B-12, B-9, B-6, D, and the mineral magnesium, plus iron and potassium. In my opinion, the extended deficiency of B-12 and magnesium was the primary cause of the peripheral neuropathy. And once initiated, the damage seems to be very persistent, but there's no continuing connection that I can detect. Of course my MC is rarely active these days — only if I slip up on my diet.

I take the active forms of vitamins B-12, B-9, and B-6 to keep the peripheral neuropathy from getting any worse. This is the equivalent of the prescription supplement known as Metanx, which is prescribed to diabetics to treat peripheral neuropathy. I took Metanx for about 6 or 7 years, before switching to a generic non-prescription supplement It did reduce my symptoms significantly (I regained reflexes in my knees and ankles). It hasn't reversed all the damage, of course, but my peripheral neuropathy is now only a shadow of what it used to be.

Tex

[Pebbledash]

My stool calprotectin came back as 1026 ug/g (normal is > 50). That's a bit scary. I read on here that MC is usually not that high, while Crohn's is. But I have had a number of endoscopies/colonoscopies that have confirmed MC.

[tex]

That's probably rare, but I can recall another member who also had a very high result.

Calprotectin is a protein released by a type of white blood cell called a neutrophil. When there is inflammation in the GI tract, neutrophils move to the area and release calprotectin, resulting in an increased level in the stool. Neutrophils are the most abundant white blood cells in humans.

So here's my opinion: I never had a calprotectin test, but i can recall my neutrophil levels being consistently high back when I was reacting, and for many years during my recovery. When questioned, my doctors usually attributed it to pollen or other allergies (which may be correct). I have a hunch that those of us who have mast cell/histamine issues tend to have elevated neutrophil levels whenever our mast cell/histamine activity is higher than normal. I don't know if you have ever looked at any of my books, but in Understanding Microscopic Colitis, I devote many pages to discussing how mast cell/histamine problems can exacerbate and perpetuate the symptoms of MC. Here are a couple of quotes that shed some light on this topic:

From page 46:

In retrospect, it seems very likely that the failure of gastroenterology specialists to recognize the significance of mast cells in inflammatory bowel disease may be a primary reason why so little real progress has been made in the options available for treating MC and other IBDs during the past quarter century. Diagnosis of MC cases has increased significantly during this period of time due to the increased use of colonoscopy exams and especially due to the increased use of biopsies to identify the disease. But the types of medical treatments available have changed little during all those years.

The primary reason why this is so important is because the association of mast cell activity with MC suggests that many environmental factors can affect the disease. These can range from food or other dietary allergens to classic allergy issues such as seasonal pollen. Some patients even react to mild chemical vapors (such as cleaning agents ), molds, and heat (even exercise-based heat increases).

Consider the fact that many MC patients complain that 10 to 20 minutes after they begin eating a meal, they have to run to the bathroom. According to the official medical understanding of the disease, this type of reaction cannot be explained. Conventional thinking says that the inflammation associated with MC is due to the infiltration of inflammation-promoting lymphocytes into the mucosal lining of the colon. But this is a relatively slow reaction, because it must first be initiated by the production of IgA antibodies as the immune system reacts to antigens in the diet, and then the IgA antibodies must subsequently promote the infiltration of additional lymphocytes and other pro-inflammatory mediators This typically results in approximately a 3–6-hour lag between the ingestion of food and an episode of secretory diarrhea (watery diarrhea). for most MC patients.

From pages 164–165

Could mast cell-based inflammation be the primary mode of inflammation associated with MC?
If this theory can be verified, it appears to define a mechanism by which MC can be triggered independently of white cell inflammation. Currently, white cell-based inflammation is generally accepted as the cause of the inflammation. that's associated with the disease. Because lymphocyte-induced inflammation is a diagnostic marker for the disease (LC), this raises an interesting question. "Are there any undiagnosed cases of MC that involve only mast cell-induced inflammation (apart from mastocytic enterocolitis), or do all cases involve white cell-based inflammation?"

The medical description of microscopic colitis attributes the inflammation associated with both lymphocytic colitis and collagenous colitis to increased white cell infiltration into the mucosal and submucosal layers of the epithelial lining of the colon. While thickened collagen bands in the submucosal layer known as the lamina propria are diagnostic markers of collagenous colitis, it's not clear whether the increased thickness is a direct result of inflammation or merely a coincidental marker of CC. But the basic question here is “What if the increased level of white cells is not always the primary source of inflammation?”

If all cases of MC involve lymphocyte-promoted inflammation (by definition), then either all cases initiated by mast cell inflammation soon lead to lymphocytic infiltration, or mast cell-based inflammation (as described above) is concurrent with lymphocyte-based inflammation typically attributed to MC. Otherwise, there is no way that mast cell-based MC cases could be diagnosed under the current diagnostic criteria. Could this be why some symptomatic patients show elevated lymphocyte counts that are not high enough to meet the diagnostic requirement of a minimum of 20 lymphocytes per 100 enterocytes in order to qualify for a diagnosis of LC?

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.

The bottom line is that I believe that for those of us who have excessive mast cell activity/histamine issues, lymphocytic infiltration may be secondary as the driving force behind our flares. And allergic reactions tend to promote neutrophil activity, which may explain why some of us test uncharacteristicly high on calprotectin tests. The calprotectin test result (and therefore the level of mast cell inflammation) would reflect the degree of mast cell activity in the intestines (but this is just my opinion, it's not verified by medical documentation).

Tex

[tommyboywalker]

For what it's worth Paul, my Calprotectin number was around 600 when it was tested after being symptomatic for a couple of months. After diagnosis and treatment with Budesonide and with me responding well to it, I was never retested for this.

My GI doctor was not concerned about my 600 as he said that a high Calprotectin number is not unusual with my GI condition/inflammation level.

I would think that your Calprotectin number will come down as your GI settles down and the inflammation backs off.