High neutrophils, very low lymphocytes ?

[Alysia]

Hi. Thank you for being here ♡

I had my labs today. My neutrophils are always high but today they came even more, higher 10 points more then the usual high. The lymphocytes also came extremly low, much lower then the usual low. Closer to zero.

I always understand the high neutrophils and low lymphocytes as a reaction to pred and rtx. Is it correct ?

This time they are much extreme. I got rtx on January 3 and on March 31, 1000mg each time. Wg was flaring in the last months. It is less active but still smoldering: coughing, eyes still aching & red, ears aching only once a week now, less diarhea (but maybe because of strict diet), joints still aching (joints pains are like a lesson in anatomy, isn't it ? You say, oh here, I didn't know that there is a joint over there as well... ) .
Very tired all the time, aching all over. Every other day taking pain killers pills. Also itchy skin. Taking also fenystil drops every other day or so.

So, if the new extreme results reflect the activity of rtx, why do I still have wg symptoms ? Or maybe it reflects something else ??

P.s. I have a new symptom: when I am totally tired I feel my heartbeats in my chest. Not more fast or slow just more strong. Like the heart is jumping with force. The dr. Heard a heart murmur. I will do ECG tomorow and heart echo on Friday. The dr. Think that it is my broken heart. He knows that I miss my beautiful Phil. Can a broken heart become literaly so ?

I attach the labs. Hope it is clear enough. Sorry for the length of the post. I need my beautiful dr. Phil very much and this place still feels like it is his in a certain way.

Thanks ♡

2419

[Pete]

I can't really add anything by way of explanation. When I tried to enlarge the lab report, it became unreadable (on my phone). You may have something else going on. I hope your docs can figure it out. Good luck...

[Dirty Don]

Yes, a 'broken heart' can affect your health as much as anything else...it's the stress. I can hear my heart beat due to permanently enlarged Eustachian tube...causes an echo, can hear my heart beat, and the ocean is ever present! Hang tough kiddo...much love to you.

[crowneagle]

Alysia, mine are the same. High neutrophils low lymphocytes. What's your blood count? I believe that is more important. It would be worse if your neutrophils crashed. That would be neutropenia, which raises your risk of infection.



Hi. Thank you for being here ♡

I had my labs today. My neutrophils are always high but today they came even more, higher 10 points more then the usual high. The lymphocytes also came extremly low, much lower then the usual low. Closer to zero.

I always understand the high neutrophils and low lymphocytes as a reaction to pred and rtx. Is it correct ?

This time they are much extreme. I got rtx on January 3 and on March 31, 1000mg each time. Wg was flaring in the last months. It is less active but still smoldering: coughing, eyes still aching & red, ears aching only once a week now, less diarhea (but maybe because of strict diet), joints still aching (joints pains are like a lesson in anatomy, isn't it ? You say, oh here, I didn't know that there is a joint over there as well... ) .
Very tired all the time, aching all over. Every other day taking pain killers pills. Also itchy skin. Taking also fenystil drops every other day or so.

So, if the new extreme results reflect the activity of rtx, why do I still have wg symptoms ? Or maybe it reflects something else ??

P.s. I have a new symptom: when I am totally tired I feel my heartbeats in my chest. Not more fast or slow just more strong. Like the heart is jumping with force. The dr. Heard a heart murmur. I will do ECG tomorow and heart echo on Friday. The dr. Think that it is my broken heart. He knows that I miss my beautiful Phil. Can a broken heart become literaly so ?

I attach the labs. Hope it is clear enough. Sorry for the length of the post. I need my beautiful dr. Phil very much and this place still feels like it is his in a certain way.

Thanks ♡

2419

[annekat]

I can't enlarge your lab results at all on my old laptop. But I'm glad you brought this up, because I have always wondered about those, and my doc never says anything about them. I can't seem to find my lab reports right now, so will have to tell you later what the values for those two things are. I don't take RTX.

[MaxD]

Alysia,

The RTX effectively kills B cells (one of the two types of lymphocytes - B and T). So, depending on what the lymphocyte count is measuring, having low count may be expected with RTX treatment. Also, ANCA (the bad guys) are produced by plasma cells which are themselves produced by B-cells. ANCA are harmful because they make neutrophils clump into granulomas, essentially removing them from the blood stream and onto blood vessel walls. So perhaps high neutrophil and low lymphocyte may simply be RTX doing its job? See: https://www.rituxanforgpampa.com/about-rituxan-gpa-mpa-treatment/how-rituxan-is-thought-to-work.html (https://www.rituxanforgpampa.com/about-rituxan-gpa-mpa-treatment/how-rituxan-is-thought-to-work.html)

A common (often undiagnosed) risk of RTX is hypogammaglobulinemia (low gamma globulins), resulting in low immunity to infections. In my 3-monthly blood tests, my docs check for IgA, IgG, IgM (the immunoglobulin panel) to make sure I'm not too low. So far, I've been just below the low threshold but not enough for the docs to worry or treat for it. You may want to ask your docs about that in case you're down with some low-grade chronic infection. Also, if you tire quickly - check your hemoglobin (I'm sure it's in your tests, I couldn't read them).

Good luck with the ECG tests. You have people cheering for you.

[mishb]

I'm so glad you are getting the tests done to check the heartbeats. As I have said previously, it's better to be safe than sorry.
Or. better to know, one way or another.

I also believe that, this time, the double dose of RTX is doing the trick and has knocked those B cells out of the park, or for a six, as we Aussies say.
Fingers crossed that this is so

Take it easy lovely lady

[Alysia]

Yes, a 'broken heart' can affect your health as much as anything else...it's the stress. I can hear my heart beat due to permanently enlarged Eustachian tube...causes an echo, can hear my heart beat, and the ocean is ever present! Hang tough kiddo...much love to you.

Thank you so much, Don. I missed you.. your friendship is dear to my heart..

I don't hear my hear beats through the ears but feel them in the chest. like drums in the chest.
EKG was ok today. echo will be on Friday.

[Alysia]

Alysia,

The RTX effectively kills B cells (one of the two types of lymphocytes - B and T). So, depending on what the lymphocyte count is measuring, having low count may be expected with RTX treatment. Also, ANCA (the bad guys) are produced by plasma cells which are themselves produced by B-cells. ANCA are harmful because they make neutrophils clump into granulomas, essentially removing them from the blood stream and onto blood vessel walls. So perhaps high neutrophil and low lymphocyte may simply be RTX doing its job? See: https://www.rituxanforgpampa.com/about-rituxan-gpa-mpa-treatment/how-rituxan-is-thought-to-work.html (https://www.rituxanforgpampa.com/about-rituxan-gpa-mpa-treatment/how-rituxan-is-thought-to-work.html)

A common (often undiagnosed) risk of RTX is hypogammaglobulinemia (low gamma globulins), resulting in low immunity to infections. In my 3-monthly blood tests, my docs check for IgA, IgG, IgM (the immunoglobulin panel) to make sure I'm not too low. So far, I've been just below the low threshold but not enough for the docs to worry or treat for it. You may want to ask your docs about that in case you're down with some low-grade chronic infection. Also, if you tire quickly - check your hemoglobin (I'm sure it's in your tests, I couldn't read them).

Good luck with the ECG tests. You have people cheering for you.

Thank you for this wonderful explanation and for the good link. I can see from it why my body is aching all over.
then, I guess it means that the rtx is already working. it means that I can expect to feel better soon. this is what Michelle also says. I will try to post the lab results in a different way.... my hemoglobin is low. maybe some things that I feel are not wg but other issues like the lack of enough Iron and aching all over from the rtx.

[Alysia]

Thank you from the bottom of my heart, Pete, Don, Tom, Max, Anne, Micelle and all the others. I feel better today just because I have you. I love you ♡
2420

[Alysia]

first line is what the test is. second line is my results. third line is the 2 edges of the norms.


Glucose (B)
86
100 יחידות: mg/dl 70

Urea (B)
32
43 יחידות: mg/dl 17

Creatinine (B)
0.94
0.95 יחידות: mg/dl 0.51

eGFR
72
200 יחידות: ml/min/1.73m² 60

K+ Potassium (B)
4
5.1 יחידות: mmol/l 3.5

Na- Sodium (B)
139
146 יחידות: mmol/l 136

Ca-Calcium (B)
10.2
10.4 יחידות: mg/dl 8.1

Fe - Iron
41
180 יחידות: micg/dl 60

Ferritin
14
120 יחידות: ng/ml 10

WBC-Leucocytes
8.6
11 יחידות: 10*3/micl 4.5

RBC-Red Blood Cells
4.24
5.2 יחידות: 10*6/micl 4

Hemoglobin
12.4
16 יחידות: g/dl 12.5

Hematocrit
35.2
46 יחידות: % 36

MCV-Mean Cell Volume
83
97 יחידות: fl 79

MCH-Mean Cell Hemoglobin
29.2
34 יחידות: pg/cell 27

MCHC-M.Cell Hb cont.
35.2
36 יחידות: g/dl 31

RDW-Red Cell Distri.Width
13.7
15 יחידות: % 11.6

Platelets
273
450 יחידות: 10*3/micl 150

MPV-Mean Platelet Volume
11
12.9 יחידות: fl 8.5

Neutrophils %
85.9
75 יחידות: % 40

Lymphocytes %
8.8
43 יחידות: % 22

Monocytes %
4.2
13 יחידות: % 3

Eosinophils %
0.6
6 יחידות: % 0

Basophils %
0.5
2 יחידות: % 0

Neutrophils #
7.43
7.7 יחידות: # 1.8

Lymphocytes #
0.76
4.8 יחידות: # 1

Monocytes #
0.36
1.1 יחידות: # 0

Eosinophils #
0.05
0.6 יחידות: # 0

Basophils #
0.04
0.2 יחידות: # 0

[Jaha]

Alysia,
I think that maybe you should ask your doctor about the exhaustion and other symptoms you are having. I had a Rtx infusion in Feb and my neutrophils are a little high and lymphocytes are high, not sure what that means. I would think that by now I would be a professional on them lab tests, but I'm not, because I forget. I hope all is well with you and wish you all the best to you on your heart testing.

[Mark76]

Alysia,
I think that maybe you should ask your doctor about the exhaustion and other symptoms you are having. I had a Rtx infusion in Feb and my neutrophils are a little high and lymphocytes are high, not sure what that means. I would think that by now I would be a professional on them lab tests, but I'm not, because I forget. I hope all is well with you and wish you all the best to you on your heart testing.
Jaha
Yep Im in the same boat. Ritiximab in feb and my neutrophils and lymphocytes are elevated. Immunologist told me most likely prednisone in my case elevating them. Remember theres more to just the numbers or % of the cells...in particular the chemicals (cytokines and interleukins) released or not released thats important. If you have no signs or symptoms particularly pain the medication is most likely working. As for the fatigue you may be slightly anemic looking at your rbc and haem levels. Everything else looks good. Also remember your neutrophils are normally first line of defense in infection so you still have immune system in your favour

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[drz]

Which ones do they consider abnormal? I ask about any that fall outside normal range and usually get some explanation about why that is expected for me and often a good sign that the Wegs is under control. Our treatment meds are supposed to suppress some things and increase others.

[Alysia]

Thank you very much for your comments & caring, Jana, Mark & drz. Mark, I think that indeed I am a bit anemic. Fe iron is only 41 while the lower border of the norm is 60. Also hemoglobin and hematocrit are lower then the norm.
As for lymphocyts, yours Mark & Jana, are elevated after rtx while mine are very low: 8.8 while the norm is 22-43. It was never that low and I am on rtx since 2013. Also on pred. So no idea what it means ??
Thank you all for being here. I love you. God bless you ♡

[Alysia]

Pr3 came back. Still positive.

I dont need it to know that my wg is active.

Still joints aching, coughing etc. And this morning also crazy nose bleeding. Fountain. 30 min or so untill it calmed down. I didnt have such bleeding since 2013. My sweet Dr. Phil used to say that it is not a good sign.

So it is now a weired combination: wg is still active although the rtx is in the blood. I hope that it doesnt mean that rtx cant help me anymore ??? I dont mind dying but I am not good in sufferings.

And my heart is still beating with force. If I put my hand on the chest I can almost feel it knocking. It is calling to my sweetie.. echo results should come next week.

End of venting.

Thanks for being here. I love you ♡♡♡

[Mark76]

Oh dear...when was your last ritiximab infusion?

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[Alysia]

Oh dear...when was your last ritiximab infusion?

Sent from my SM-G900I using Tapatalk

First 1000mg on January 4. Second 1000mg on March 31. I thought that the first 1000mg will be enough.

[annekat]

Alysia, this is so disheartening to hear. Maybe you need a higher dose of RTX? Very naive of me to say, since I have no experience with it and don't know what the variations are in typical doses. I wonder what your doctor has to say about all this. How about more prednisone, too? I wish I had something to say that would help. I wish there was another med that would work for you, maybe in tandem with the RTX. I think you said your doc consults with Dr. Jayne. I wonder what he would say. All I can say is my warm thoughts are with you and I pray for a solution.
Also you should see a heart doctor, as the pounding in the chest sounds unusual for anyone on here that I remember. Please get better, somehow.....:wub:

Sorry, just re-read, and it sounds like you already saw a heart doctor.

[Alysia]

Thank you so much Anne. You are very kind & caring & sweet. We are so blessed to have you here. I love you ♡♡

I dont have the energy right now to set another meeting with my wg dr. And drive there.
I guess he will say that I can still wait for the full influence of the second rtx which should be in 3 months since I got it, so its about month and half from now. He might also suggest what he tried to add to my treatment in the past: a med called Arava or Leflunomide. I think I saw someone here who was on it. But it also take about 6 weeks until it works. As I know myself, being very sensitive it might be a disaster like the Imuran was for me. and then if it will work (mtx never worked for me) once I am too much immune compromised the UTI's starting to come. And they are even worse then nose bleedings, red eyes, ears aching and joints pains together. And they come with diarhea too because of the antibiotics.

More pred is an option that I contemplate everyday. I even have enough and can take on my own. Just being so many years constantly on the 5mg makes me afraid that once I will take more I will not be able to taper and will have to stay on higher dose for life. Not sure if it is true.

So waiting for the rtx to come to its full influence although it seems in the blood tests that it is there... :unsure:

And maybe I will take more pred meantime.

I dont have a cardio dr. But I did echo test and waiting for the results. Next week.

[annekat]

I would sure be tempted to take more pred, even 5mg. more could make a difference. I have done that occasionally when not feeling so good, and it has helped. I would understand your reservations, though, as I have them, too. I am afraid of what pred is doing to my bones. I got a bone density scan yesterday and don't know when I'll get the results. But it would probably be OK for you to increase a little if you are only at a low dose, like 5mg., to begin with. If it helps you through your day and makes it possible to drive to see the doctor, it is worth it. Or if it just helps you until RTX kicks in again. It will not be as hard to taper if you have not been doing it for very long. Best of luck with what you decide.

[mishb]

I agree, take another 5mg for a couple of days and see if it helps. You should be fine to go back to the usual 5 after that

[Pete]

I agree with Anne and Michelle. Bumping your pred up to 10 mg/day may be what you need to chase the symptoms away. Maybe your body needs help making more cortisol. Low dose pred shouldn't cause you any problems.

[Alysia]

Thank you so much, dear Anne, Pete & Michelle. I love you ♡♡♡ I thought about bigger dose, something like 40-30-20-15-10 for 5 days. But maybe 5mg more can be enough. I am still contemplating... might take more tomorow morning. I will see how I feel..
Any way dr. Phil said that if you take more pred for 5 days or less you dont need to taper. So I prefer to take only for 5 days...

[Alysia]

Thank you so much, dear Anne, Pete & Michelle. I love you ♡♡♡ I thought about bigger dose, something like 40-30-20-15-10 for 5 days. But maybe 5mg more can be enough. I am still contemplating... might take more tomorow morning. I will see how I feel..
Any way dr. Phil said that if you take more pred for 5 days or less you dont need to taper. So I prefer to take only for 5 days...

[Alysia]

Not sure why I posted twice although I tried to delete one...

[annekat]

Well, if you are on 5mg. now, 10mg. will be doubling your dose. I'm on 10mg. and found that taking 15mg. for a few days did help me. However, my symptoms were not as bad as yours are currently. I guess it is worth a try, but I wonder if your doc would suggest taking even more. So try the extra 5mg. and see what happens.

[drz]

Can you call or message your Weg treating doctor (s) and discuss increasing your pred med or adding other meds to help control the Weg symptoms? Often that is all that is need to make some change to help relieve symptoms. Do you have any option available like telemedicine consultation? We all know pred can be tough med to take, but we also all know without it very few of us would still be here.

[mishb]

It's been a couple of days now. Did you increase the pred by 5mg or a little bit more?
Are you feeling any better, or just the same? worse is not an acceptable answer :wink1:

[Alysia]

Thanks Michelle & drz. I love you ♡

I did increase my pred from 5mg to 10mg. Feeling better with it. Joints less aching. No nose bleeding. No ears aching. Diarhea now 3-4 times a day instead of 7-8. Still tired. But eyes are still red and aching in the corners. Maybe 10mg is not enough for the eyes. The eye doc suggested to take 30x5, 20x5, 10x5. Problem is that I also have new issue with my heart (I wrote on another thread) and I need to see a cardiologist now. But I wonder if the pred might mask things, so not sure how to continue... still trying to set a date, not easy, all dates are for around July. Looking for cancellations. Max wrote on the other thread that pred should work. So it seems that I need higher pred but it will prob depends on the date of meeting with the cardio dr.

Drz, I can always send email to my wg dr. He answers in few hours. But I am careful to use this option only in more severe cases and when I am lost. So far I do have some plans.

Thank you for being here, and being so caring and thoughtful. God bless you all ♡♡♡

[drz]

Thanks Michelle & drz. I love you ♡

I did increase my pred from 5mg to 10mg. Feeling better with it. Joints less aching. No nose bleeding. No ears aching. Diarhea now 3-4 times a day instead of 7-8. Still tired. But eyes are still red and aching in the corners. Maybe 10mg is not enough for the eyes. The eye doc suggested to take 30x5, 20x5, 10x5. Problem is that I also have new issue with my heart and I need to see a cardiologist now. But I wonder if the pred might mask things, so not sure how to continue... still trying to set a date, not easy, all dates are for around July. Looking for cancellations. Max wrote on the other thread that pred should work. So it seems that I need higher pred but it will prob depends on the date of meeting with the cardio dr.

Drz, I can always send email to my wg dr. He answers in few hours. But I am careful to use this option only in more severe cases and when I am lost. So far I do have some plans.

Thank you for being here, and being so caring and thoughtful. God bless you all ♡♡♡

I think your treating doctor would like to know this: "I did increase my pred from 5mg to 10mg. Feeling better with it. Joints less aching. No nose bleeding. No ears aching. Diarhea now 3-4 times a day instead of 7-8. Still tired. But eyes are still red and aching in the corners. Maybe 10mg is not enough for the eyes. The eye doc suggested to take 30x5, 20x5, 10x5. Problem is that I also have new issue with my heart (I wrote on another thread) and I need to see a cardiologist now. But I wonder if the pred might mask things, so not sure how to continue... still trying to set a date, not easy, all dates are for around July. Looking for cancellations. "

And he might have some ideas about your plans and maybe can help you with them too. I would contact my doctors in this situation and hope for some quick feedback and help.

[annekat]

Alysia, I think it is very encouraging that you are feeling so much better on the 10mg. pred, even though everything is not responding equally well. If your eyes are still really bad, I would guess that you could go with his suggested pred schedule since you would not be on each of the higher amounts for more than 5 days. I think under those conditions, tapering would not be too hard, not like when you were first treated and had been on high amounts for a lot longer. As for the 'masking' of the heart issues, I don't know, and sort of doubt it, but would ask one of your docs. I hope it goes well.

[Alysia]

Thanks drz & Anne, from the bottom of my heart ♡
Drz, I know that you are right and that I need to consult seriously with my wg doc. I will prob do it eventually, after going to the cardio doc. Just thinking how he will scratch his head (metaphorically) and express his disapointment from my stubborn wg .. not such fun.. cardio doc should be on June 2. Maybe earlier in case of cancellation.

Anne, more few days here on 10mg, continue to feel even better. It feels so much better with the joints. Even the eyes are less aching. So maybe it will do.

Thank you all for being here. I love you all. God bless you ♡♡♡

[annekat]

Thanks drz & Anne, from the bottom of my heart ♡
Drz, I know that you are right and that I need to consult seriously with my wg doc. I will prob do it eventually, after going to the cardio doc. Just thinking how he will scratch his head (metaphorically) and express his disapointment from my stubborn wg .. not such fun.. cardio doc should be on June 2. Maybe earlier in case of cancellation.

Anne, more few days here on 10mg, continue to feel even better. It feels so much better with the joints. Even the eyes are less aching. So maybe it will do.

Thank you all for being here. I love you all. God bless you ♡♡♡ That's great about the 10mg making such a difference. Maybe that's the problem, you needed to be on more than 5mg all along and it finally caught up with you. That's how I felt when I tried to go to 7.5mg. It didn't turn out to be enough and I've been on 10mg. ever since. Might be time for me to try going a little lower, though. I do hope you can drop the extra 5mg.

[marta]

So I had this epiphany a few weeks ago in the middle of the night (3am) based on my lab results and high neutrophils.

My epiphany is that we're treating the wrong point of the disease process, and that perhaps we should be looking at the neutrophils and their activity for the answers.

When my flare just started my ESR, CRP and liver enzymes (unique but for me, my liver is a marker as it gets involved in the game) were through the roof. I went on high doses of pred and within a week all my markers went to within normal range but my neutrophils went through the roof. This is what triggered my thought process in that the current treatment paradigm focuses on the 'adaptive immune system' - killing the B's (RTX) or the B's and T's (CTX) - which is quite late in the disease process. So what's going on with the neutrophils I wondered. They are the most prevalent and early immune responders in the body and are part of the 'innate immune system'. Why aren't researchers looking there? Do the answers lie there?

There are a few elements upon closer examination, specifically with Wegener's that really got my goosebumps going.

There is chemotaxis, which is what stimulates the neutrophills into action. Is there some sort of chemotaxis misfire that is triggering an over the top response from the neutrophills, which then feel overwhelmed and call in the adaptive immune system. Another interesting factoid is that the endothelial cells are connected with the whole chemotaxis/neutrophill freakout and those are the cells that are completely lining the entire system that WG affects, and I think more precisely the respiratory epithilum is the underlying culprit for all our problems (WG problems).

I think this is a crazy new way of looking at the disease process, and I actually mentioned it to the pulminologist I had to see the very next day, and it triggered a few moments of thoughtful contemplation (didn't feel like he was patronizing - ha ha) and it made me feel like maybe my 3am epiphany might have come from somewhere higher than the apex of my brain.

Just thought I'd share this with you, because I saw the word 'neutrophils' in the header. Play around with the idea if you like. I used 'muscle testing' to callibrate the truth of some of these ideas, and they test pretty positive, but that's a little out there for most people (not for my crazy brain though.)

[Alysia]

So I had this epiphany a few weeks ago in the middle of the night (3am) based on my lab results and high neutrophils.

My epiphany is that we're treating the wrong point of the disease process, and that perhaps we should be looking at the neutrophils and their activity for the answers.

When my flare just started my ESR, CRP and liver enzymes (unique but for me, my liver is a marker as it gets involved in the game) were through the roof. I went on high doses of pred and within a week all my markers went to within normal range but my neutrophils went through the roof. This is what triggered my thought process in that the current treatment paradigm focuses on the 'adaptive immune system' - killing the B's (RTX) or the B's and T's (CTX) - which is quite late in the disease process. So what's going on with the neutrophils I wondered. They are the most prevalent and early immune responders in the body and are part of the 'innate immune system'. Why aren't researchers looking there? Do the answers lie there?

There are a few elements upon closer examination, specifically with Wegener's that really got my goosebumps going.

There is chemotaxis, which is what stimulates the neutrophills into action. Is there some sort of chemotaxis misfire that is triggering an over the top response from the neutrophills, which then feel overwhelmed and call in the adaptive immune system. Another interesting factoid is that the endothelial cells are connected with the whole chemotaxis/neutrophill freakout and those are the cells that are completely lining the entire system that WG affects, and I think more precisely the respiratory epithilum is the underlying culprit for all our problems (WG problems).

I think this is a crazy new way of looking at the disease process, and I actually mentioned it to the pulminologist I had to see the very next day, and it triggered a few moments of thoughtful contemplation (didn't feel like he was patronizing - ha ha) and it made me feel like maybe my 3am epiphany might have come from somewhere higher than the apex of my brain.

Just thought I'd share this with you, because I saw the word 'neutrophils' in the header. Play around with the idea if you like. I used 'muscle testing' to callibrate the truth of some of these ideas, and they test pretty positive, but that's a little out there for most people (not for my crazy brain though.)

Wow marta. Very interesting. Lets see.

Not sure I understood you all the way, but this is what I got: do you say that maybe the activity of the neutrophiles is what causing wg ?

I wondered about my high neutrophiles and what it might mean. Maybe it is just caused by pred and rtx ?

But now after reading your post I went to check old papers. From 22.9.08 and few days after, when I was addmited to hospital in acute wg flare. Almost dying. Not yet any pred and rtx.
I checked my neutrophiles in the labs from those days. 10 times higher then now ! (I was deadly sick, ESR was above 110 or so). So, high neutrophiles are not necessary because of pred & rtx.

BUT, maybe they were just extremely high because the body identified an inflamation going on, so it cant help us much.. ??

Or maybe I missed something in your explanation ?

Thanks for always thinking about the processes, finding the common thread and cure. One day you will get there. Sending my love & prayers for your recovery ♡♡♡

[marta]

I know, it's a hard concept to verbalize, but it makes sense in my pea brain, I just don't have the words for it.

I think the neutrophil activation is directly related not only to WG, but all autoimmune disease (and also heart and stroke, cancer, and mental health among other chronic illness, but that's a much bigger picture.) I think that perhaps issues/pathologies in our epithelial cells might be triggering some sort of chemotaxis that stimulates an over-the-top reaction from our neutrophils, and this might be where the answer to the cure might lie. I think that if we focus on our search in the direction of the innate immune system, rather than the adaptive immune system, diagnosis, treatment and side effects, might be minimized and much less invasive than the current paradigm associated with significant risks (as we are all sadly aware.)

I'm putting it out there because I certainly can't do anything about it myself, but maybe someone will stumble on this who can do something and move the idea forward.

Best of luck buddy. Take care of yourself.

[annekat]

I will have to read this over again to better understand, and have my attention on other things today, but I will say that you don't have a pea brain, Marta, you are brilliant!

[Pete]

Marta, have you shared your epiphany with your wegs doc? I'd like to think it's very worthy of further investigation. If you don't want to, would you be upset if I passed it on to Dr Villa Forte at Cleveland Clinic?

Thanks!!

[Alysia]

I know, it's a hard concept to verbalize, but it makes sense in my pea brain, I just don't have the words for it.

I think the neutrophil activation is directly related not only to WG, but all autoimmune disease (and also heart and stroke, cancer, and mental health among other chronic illness, but that's a much bigger picture.) I think that perhaps issues/pathologies in our epithelial cells might be triggering some sort of chemotaxis that stimulates an over-the-top reaction from our neutrophils, and this might be where the answer to the cure might lie. I think that if we focus on our search in the direction of the innate immune system, rather than the adaptive immune system, diagnosis, treatment and side effects, might be minimized and much less invasive than the current paradigm associated with significant risks (as we are all sadly aware.)

I'm putting it out there because I certainly can't do anything about it myself, but maybe someone will stumble on this who can do something and move the idea forward.

Best of luck buddy. Take care of yourself.

I agree with Anne. You are brilliant.

I try to play more with your ideas.

Will the following question can guide us more? :

Is it the neutrophils activation that cause the flare or is it the flare that cause the high neutrophils ?

If this question is connected to your questions, maybe we can check it by going to our labs and checking what came first, the flare or the high neutrophils.... ??

[Mark76]

Ok marta your epiphany is what drives scientific research. As some of you may know I am a pilot by trade but I did my PhD in Immunology particularly in the area of cytokines so I know a bit or two on Immunology and what you are saying regarding neutrophils makes perfect sense. Allow me to describe in a little more detail what the current understanding of the pathogenisis is. Alot is still not known however current thinking is that autoantibodies to pr3 or mpo proteins, found in neutrophils, cause the neutrophils to release cytokines (resulting in more neutrophils hence the higher neutrophil count), oxygen radicals, endothelium binding proteins and pr3 (these proteins/enzymes along with free radical oxygen cause the inflammation). Now t cells also play a part in all of this but I wont confuse you with this for time being. So current treatment is cyclophosphomide which is a broad acting chemo drug that halts all rapidly dividing cells such as white blood cells. Ritiximab targets the b cells in particular a subclass of b cells that has been found to produce the autoantibodies to pr3 and mpo. Prednisone action is to dampen the volume if you like in the cytokine or pro inflammatory proteins released by the neutrophils and other cells. Now, if I understand you correctly you are proposing targeting the neutrophils instead. The problem with this is that our neutrophils are essentially our first line of defense and it isnt the neutrophils per se that is the problem. It is the activation of the neutrophils by the autoantibodies to release the range of chemicals from the neutrophils granules which is the problem. So targeting the autoantibodies is a good target eg ritiximab. Other targets might be antagonists to cell adhesion proteins or cytokines or somehow inhibiting the release of pr3. There is so much complexity with the immune system and still so much not known. For example it has only recently been determined at least in rats that staph aureus shares similar homology or structure to pr3 and also determined that if you take bactrim as a prophylaxis it can reduce your relapse rate by up to 60%.

Like you Im intrigued by the disease and always thinking of what else can be done to cure this shitty disease. Infact I live in Australia and wish to establish a research centre focusing on vasculitis so that more research and support can go into this area. Hopefully this answers your question and thanks for your critical thinking.

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[Pete]

This line of research could be the route to the breakthrough we've been hoping and praying for.

[annekat]

Wow, this forum is full of super-smart people. Wouldn't it be interesting if Weggies were the ones who found the answers we are waiting for.

[marta]

I will have to read this over again to better understand, and have my attention on other things today, but I will say that you don't have a pea brain, Marta, you are brilliant!

very pea indeed, but thanks for the vote of confidence Anne... like I said, it was a bizarre download in the middle of the night, had nothing to do with anything from me... it came from somewhere else, and I had to spend a bunch of time looking things up not the Google machine, that I had no idea about, it just kept coming.

[marta]

Marta, have you shared your epiphany with your wegs doc? I'd like to think it's very worthy of further investigation. If you don't want to, would you be upset if I passed it on to Dr Villa Forte at Cleveland Clinic?

Thanks!!

Pass it on Pete. I believe it all happens for a reason. If someone on here can do something with it, then great. I'm the messenger of something over my head, but once I thought it through and looked into it further, it sure made a lot of sense. You go brotha! Do with it what you can. I hope it can lead to something good. Godspeed.

[Mark76]

Marta yep keep questioning things unfortunately targeting neutrophils is not the answer as noted in my previous message. As someone else mentioned prednisone can also cause increase in neutrophils. It is kind of irrelevant though if you have slight neutrophilia (high neutrophils ). Its the chemicals released that is the issue.

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[marta]

Ok marta your epiphany is what drives scientific research. As some of you may know I am a pilot by trade but I did my PhD in Immunology particularly in the area of cytokines so I know a bit or two on Immunology and what you are saying regarding neutrophils makes perfect sense. Allow me to describe in a little more detail what the current understanding of the pathogenisis is. Alot is still not known however current thinking is that autoantibodies to pr3 or mpo proteins, found in neutrophils, cause the neutrophils to release cytokines (resulting in more neutrophils hence the higher neutrophil count), oxygen radicals, endothelium binding proteins and pr3 (these proteins/enzymes along with free radical oxygen cause the inflammation). Now t cells also play a part in all of this but I wont confuse you with this for time being. So current treatment is cyclophosphomide which is a broad acting chemo drug that halts all rapidly dividing cells such as white blood cells. Ritiximab targets the b cells in particular a subclass of b cells that has been found to produce the autoantibodies to pr3 and mpo. Prednisone action is to dampen the volume if you like in the cytokine or pro inflammatory proteins released by the neutrophils and other cells. Now, if I understand you correctly you are proposing targeting the neutrophils instead. The problem with this is that our neutrophils are essentially our first line of defense and it isnt the neutrophils per se that is the problem. It is the activation of the neutrophils by the autoantibodies to release the range of chemicals from the neutrophils granules which is the problem. So targeting the autoantibodies is a good target eg ritiximab. Other targets might be antagonists to cell adhesion proteins or cytokines or somehow inhibiting the release of pr3. There is so much complexity with the immune system and still so much not known. For example it has only recently been determined at least in rats that staph aureus shares similar homology or structure to pr3 and also determined that if you take bactrim as a prophylaxis it can reduce your relapse rate by up to 60%.

Like you Im intrigued by the disease and always thinking of what else can be done to cure this shitty disease. Infact I live in Australia and wish to establish a research centre focusing on vasculitis so that more research and support can go into this area. Hopefully this answers your question and thanks for your critical thinking.

Sent from my SM-G900I using Tapatalk

Zowee. This is cool stuff.

It was interesting because while I was having my first consult with a new pulminologist, I mentioned this crazy idea to him (as I had it in the middle of the night before seeing him, and it was fresh and exciting in my, as I said before, pea brain) and he actually stopped to ponder it and his reaction was similar to yours.

He was intrigued but his first reaction was that it would be a dangerous game since it is our first line of defence. I agree. But isn't our current treatment paradigm also a dangerous game? I think so. Isn't that how they killed the aliens in War of The Worlds - they had no B-cells (immune history.)

But what I'm thinking is that it's something before the neutrophils even... what is the chemotaxis that is triggering them? Is it some sort of endothelial or epithelial pathology... is it Interluken-8 or some other chemokine that is triggering such a response and if so can we treat it genetically rather than in an immune suppressing way? Could it be something as simple as glucose which has shown to alter chemotaxis and has not been part of our million years of evolution? Is there a connection between vascular endothelial cell pathology, neutrophil recruitment and hormone trafficking and the onset of autoimmune disease? Is autoimmune disease related to excessive or prolonged permeability of the endothelial monolayer? The questions are endless, and I have a feeling there might be some good answers hiding there, because, I don't know that these questions have been asked regarding this particular subject. I also think that within the answers to this subject (vasculitis in specific, but autoimmune disease as a whole) lie a whole bunch of other answers to questions people have actually been asking for a long time - we're the newbies on the block, but by searching for our answers, we might come up with some really- really big ones as well.

I am glad this crazy little moment in the middle of the night has got the talk going.
It was a similar moment in the night that got us published in a medical journal, so who knows....

Who knows.

Let's keep asking questions... and thanks for playing along.

I am writing some chapters down - while in my universe imposed sequestering, and this forum plays a big role in a lot of the events that have gone on for me since diagnosis. Once again, you never fail in being awesome.

[Mark76]

Zowee. This is cool stuff.

It was interesting because while I was having my first consult with a new pulminologist, I mentioned this crazy idea to him (as I had it in the middle of the night before seeing him, and it was fresh and exciting in my, as I said before, pea brain) and he actually stopped to ponder it and his reaction was similar to yours.

He was intrigued but his first reaction was that it would be a dangerous game since it is our first line of defence. I agree. But isn't our current treatment paradigm also a dangerous game? I think so. Isn't that how they killed the aliens in War of The Worlds - they had no B-cells (immune history.)

But what I'm thinking is that it's something before the neutrophils even... what is the chemotaxis that is triggering them? Is it some sort of endothelial or epithelial pathology... is it Interluken-8 or some other chemokine that is triggering such a response and if so can we treat it genetically rather than in an immune suppressing way? Could it be something as simple as glucose which has shown to alter chemotaxis and has not been part of our million years of evolution? Is there a connection between vascular endothelial cell pathology, neutrophil recruitment and hormone trafficking and the onset of autoimmune disease? Is autoimmune disease related to excessive or prolonged permeability of the endothelial monolayer? The questions are endless, and I have a feeling there might be some good answers hiding there, because, I don't know that these questions have been asked regarding this particular subject. I also think that within the answers to this subject (vasculitis in specific, but autoimmune disease as a whole) lie a whole bunch of other answers to questions people have actually been asking for a long time - we're the newbies on the block, but by searching for our answers, we might come up with some really- really big ones as well.

I am glad this crazy little moment in the middle of the night has got the talk going.
It was a similar moment in the night that got us published in a medical journal, so who knows....

Who knows.

Let's keep asking questions... and thanks for playing along.

I am writing some chapters down - while in my universe imposed sequestering, and this forum plays a big role in a lot of the events that have gone on for me since diagnosis. Once again, you never fail in being awesome.
Wow alot of questions alright and like most scientists don't know the answers to alot of your questions. The question relating to what cytokines cause neutrophil and monocytes too by the way is again complex but the main cytokines are interleukin 4 and tumour necrosis factor alpha. Infact clinical trials are currently being undertaken on entacept which binds to the tnf-a. The thing with tnf is that it is a pro inflammatory cytokine meaning it causes inflammation by recruiting more cells but it also assists in tissue healing.

Other research is looking into t cells in particular t cell 17 (Tch17). There is a drug also undergoing clinical trials called halofumide. Th17 has been shown to be involved in other autoimmune diseases such as IBD etc.

Somehow silencing the genes is an obvious choice but again not enough is known. There is evidence of genes DLPB1 and a retenoid RXB alleles (variants) think it is that may predisposes someone along with a pathogen or environmental (eg silicon dust ) to cause the autoimmune response. This gets into gene therapy etc...but would silencing those genes stop the autoimmune response once it has been initiated...hmmm im not sure. Most of the current drugs are effective especially at induction. There is speculation that one reason why people relapse is that there remains some autoantibodies stuck somewhere eg granulomas in lungs etc.

Some very thought provoking points and look forward to more discussion. I have a meeting with my Immunologist next week and may ask him some of these questions too.[emoji1]

Oh just to give you all an update im 4 months from diagnosis and treatment and latest crp was 1 yay. No pain anywhere only issue is blocked left ear still. Chest scan yesterday showed almost complete resolution with few minor ground glass opacities. Compared to before treatment had 4 granulomas in left lung ranging in size from 1cm to 6cm.

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[marta]

Mark, I would love to be a fly on the wall when you have a visit with your immunologist.
That would be probably the coolest visits he has with a patient - EVER.

Neat stuff, the immune system, and so wide open for all kinds of discussions, since it seems to be the last vestige for scientific exploration within the human body, and the biggest possible treasure trove for some significant breakthroughs (on all fronts of chronic illness, not just our flavour.)

I love that there's a PhD in Immunology on the forum. Totally dig it! Sorry you had to drop in in the manner that you did, but the universe works in mysterious ways, and it sounds like you're totally on top of 'the beastie' - continued success with recovery and then onward ho - time to find us some answers...

:w00t::w00t: (woot woot)

[me2]

Well, this discussion is certainly way over my head... but I'll jump in anyway. Maybe I'll get taller.

First of all congrats Mark on the solid improvements. I have not been following people here much lately so it is good to see some good news right off the bat.

I'm not sure if my info is relevant but I tried the anti-TNF drug Etanercept a long time ago. Before there were any studies. I was on it over a year and it didn't help. Later there was a trial done (2005) that concluded it was not helpful. I wasted 17 grand of my own money (insurance wouldn't pay) and more importantly it didn't help. Here is a bit of info from that study:

RESULTSThe mean follow-up for the overall cohort was 27 months. Of the 174 patients who could be evaluated, 126 (72.4 percent) had a sustained remission, but only 86 (49.4 percent) remained in remission for the remainder of the trial. There were no significant differences between the etanercept and control groups in the rates of sustained remission (69.7 percent vs. 75.3 percent, P=0.39), sustained periods of low-level disease activity (86.5 percent vs. 90.6 percent, P=0.32), or the time required to achieve those measures. Disease flares were common in both groups, with 118 flares in the etanercept group (23 severe and 95 limited) and 134 in the control group (25 severe and 109 limited). There was no significant difference between the etanercept and control groups in the relative risk of disease flares per 100 person-years of follow-up (0.89, P=0.54). During the study, 56.2 percent of patients in the etanercept group and 57.1 percent of those in the control group had at least one severe or life-threatening adverse event or died (P=0.90). Solid cancers developed in six patients in the etanercept group, as compared with none in the control group (P=0.01).
Full Text of Results... (http://www.nejm.org/doi/full/10.1056/NEJMoa041884#Results)


CONCLUSIONSEtanercept is not effective for the maintenance of remission in patients with Wegener's granulomatosis. Durable remissions were achieved in only a minority of the patients, and there was a high rate of treatment-related complications.


-- Me2 here again. Thankfully I have not had complications from that treatment. Or the many others I have tried. I don't know of a WG treatment that I have NOT tried. Methotrexate, Cytoxan, Rituxan, IVIG, Myfortic, etc. Amazing I am still here.
I am super impressed that you have an advanced degree in immunology. I got some basic books from the university I go to for treatment and it was wildly complex. I understood very little.

I have been a guinea pig for many treatments. I took Rituxan long before it was approved. My illness likes to keep me on the cutting edge I guess. Right now, on my own initiative, I am well into experimenting with cannabis. It is a subject that is a horrible quagmire of mis-information and chaos BUT there are massive personal accounts of healing that I can't ignore. I have been working on this for some time.

I have found a ND recently that I think is well informed and is helping me with dosages. She is also having me get genetic testing - but I haven't looked into why yet. I've been super, super busy lately.

If I come up with any useful results or info I plan on sharing it with the forum.

It's great to see Marta here too.

[me2]

Oh, about neutrophils. My scientist doc up at the University of Washington told me some time ago that he thought the next break through would involve cytokines. His studies were on neutrophils so I'm guessing he is talking about cytokine production by neutrophils.

[Mark76]

Well, this discussion is certainly way over my head... but I'll jump in anyway. Maybe I'll get taller.

First of all congrats Mark on the solid improvements. I have not been following people here much lately so it is good to see some good news right off the bat.

I'm not sure if my info is relevant but I tried the anti-TNF drug Etanercept a long time ago. Before there were any studies. I was on it over a year and it didn't help. Later there was a trial done (2005) that concluded it was not helpful. I wasted 17 grand of my own money (insurance wouldn't pay) and more importantly it didn't help. Here is a bit of info from that study:

RESULTSThe mean follow-up for the overall cohort was 27 months. Of the 174 patients who could be evaluated, 126 (72.4 percent) had a sustained remission, but only 86 (49.4 percent) remained in remission for the remainder of the trial. There were no significant differences between the etanercept and control groups in the rates of sustained remission (69.7 percent vs. 75.3 percent, P=0.39), sustained periods of low-level disease activity (86.5 percent vs. 90.6 percent, P=0.32), or the time required to achieve those measures. Disease flares were common in both groups, with 118 flares in the etanercept group (23 severe and 95 limited) and 134 in the control group (25 severe and 109 limited). There was no significant difference between the etanercept and control groups in the relative risk of disease flares per 100 person-years of follow-up (0.89, P=0.54). During the study, 56.2 percent of patients in the etanercept group and 57.1 percent of those in the control group had at least one severe or life-threatening adverse event or died (P=0.90). Solid cancers developed in six patients in the etanercept group, as compared with none in the control group (P=0.01).
Full Text of Results... (http://www.nejm.org/doi/full/10.1056/NEJMoa041884#Results)


CONCLUSIONSEtanercept is not effective for the maintenance of remission in patients with Wegener's granulomatosis. Durable remissions were achieved in only a minority of the patients, and there was a high rate of treatment-related complications.


-- Me2 here again. Thankfully I have not had complications from that treatment. Or the many others I have tried. I don't know of a WG treatment that I have NOT tried. Methotrexate, Cytoxan, Rituxan, IVIG, Myfortic, etc. Amazing I am still here.
I am super impressed that you have an advanced degree in immunology. I got some basic books from the university I go to for treatment and it was wildly complex. I understood very little.

I have been a guinea pig for many treatments. I took Rituxan long before it was approved. My illness likes to keep me on the cutting edge I guess. Right now, on my own initiative, I am well into experimenting with cannabis. It is a subject that is a horrible quagmire of mis-information and chaos BUT there are massive personal accounts of healing that I can't ignore. I have been working on this for some time.

I have found a ND recently that I think is well informed and is helping me with dosages. She is also having me get genetic testing - but I haven't looked into why yet. I've been super, super busy lately.

If I come up with any useful results or info I plan on sharing it with the forum.

It's great to see Marta here too.

Great read...shame the trial didn't work. Yes immunology is complex whats more what occurs in one person may be different in another same with drugs. The problem with cytokine targeting is its another band aid fix which is why prednisone on its own isnt very effective for wg. In order to cure one needs to know what causes the initiation. I firmly believe that in many wg cases it is pathogen in nature eg staph so along comes a macrophage or t cell and presents it to a b cell and binds or whats called neutralizes the antigen (eg staph) and it remembers what staph looks like. So even after the staph has been eliminated neutrophils are swimming around the blood along with monocytes and heap of chemicals released including vcam, monocytes adhesion protein, cytokines (interleukins and tnf etc) all resulting in more white blood cells and adhesion to endothelium of blood vessels. Once the neutrophils are primed from cytokines the pr3 and mpo which are normally in the granules and lysozomes of neutrophils move to cell surface. Along come the b cells still floating in blood as well and pr3 (not sure about mpo) looks very similar to the staph the antibodies from b cell recognised a little while back and therefore binds forgetting of course that its our own cells...and voila inflammation cycle kicks off again!.

But again finding a drug candidate to fit all wg cases is extremely difficult.

Love this discussion and would love to form a research and support group here in Australia. Problem is getting the funding to get this moving. Also a shame that drug clinical trials takes so long before coming onto market.

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[Alysia]

I understand very little from what you, great minds, wrote above.. you are so amazing ♡♡ I wonder if any of the hypothesis can be checked here among us - maybe something like a poll, comparing certain labs at given times of the illness ??

[Gab122]

Hi Marta, I'm late to this thread... New to this disease. I just got diagnosed 8/1/16. Not a month ago. Trying to understand it all and wondered about why B cells were being killed instead of ANCA. Alysia suggested I read some of your posts and I found this. (Thank you Alysia.) I was mistakenly thinking neutrophils were B cells but I now see they are both just types of WBC.

Am I correct in thinking that ANCA changes the neutrophils and that change somehow in turn causes B cells to attack the blood vessel walls? Can you explain it to me?

Prior to GPA treatment I was on 10 day pred taper plus antibiotic not sure if that skews labs. Before I started high pred and ritux my neutrophils were not super high (11) but my ANCA against PR3 was 1178(!) my sed rate got up to 93 and my crp was 126. I had a lung biopsy that further confirmed GPA. I'm on 60 pred and ritux. Being treated by Mass Genl RA (MGH) in Boston. (My symptoms started early May with ear problems.)

Alysia mentioned her neutrophils were really high but other markers down and (I think) you wondered if the neutrophils were the place to focus treating this disease. I love how your brain is churning its best in the middle of the night 😊 (Am I confusing your post with someone else's post?)

Could it be that there is a chain of events. Different bloodmarkers rising and falling in a sequence of events in an active disease? So depending on when we have a blood draw we may see a certain portion of that chain of events?

Maybe that could explain why sometimes ANCA correlate and sometimes it doesn't?

Would love any insight you and anyone has!
Thanks
Gab

[Gab122]

Hi Max D

You mentioned on page one of this thread: "Also, ANCA (the bad guys) are produced by plasma cells which are themselves produced by B-cells. ANCA are harmful because they make neutrophils clump into granulomas, essentially removing them from the blood stream and onto blood vessel walls."

So B cells-->plasma cell ---> ANCA ---> effects neutrophils to clump and attack vessel walls? Is that right? It's not B cells attacking walls?

Thanks for any help!
Gab

[Mark76]

Hi Gab

Thanks for your response and hopefully your treatment is going well. The pathogenicity of GPA is extremely complex and there are various models of what occurs. Most likely there is more than one process that occurs leadibg to disease. For example there is one model that suggests and research indicates a slight homology or similar structure of staphylococcus aureus bacteria carried in a high %of population abd proteinase 3 (pr3). So in this model some form of antigen eg bacteria and it is detected by cells called antigen presenting cells as they present antigen eg bacteria or viruses to other immune cells such as b cells. So when the b cells bind it recognises it and for unknown reasons (faulty gene silencing perhaps) recognises the antigen as being a self antigen eg pr3 or mpo. So the b cells then mature in the bone marrow and expand and are called plasma cells. So b cells have antibodies but they stay intact to the b cells whereas plasma cells are mature b cells and the antibodies are able to detach.
Ok now there are antibodies to pr3 or mpo floating around. At the same time neutrophils which reside near blood vessels as they are one of the first line of wbc to encounter a foreign object or antigen. So the antigen presentibg cells also release chemicals that stimulate neutrophils and recruit more and they also make pr3 and mpo inside the cells which when activated express pr3 and or mpo onto cell surface. The free antibodies released from plasma cells (anca) and also more b cells bind to the pr3 on neutrophils and this then through various chemical mechanisms cause the b cells to release chemicals including reactive oxygen species. These reactive oxygen species causes oxidative damage to the blood vessel walls and hence vasculitis.

Very simplified explanation but hope it gives some sort of explanation. Check out my website www.vasculitisoz.com and go to immune tab and it explains it more there

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[Gab122]

Wow! Thank you mark76!

That's the simplified explanation?! 🤔 I started to be able to follow along a bit the 2nd time I read it... I think if I sit down and draw it I'll better understand what you said tho.... My project for tomorrow. 👍😊

You mentioned this as one model of how the disease works. I'm assuming it's believed to be the most current consensus of the medical community? Or a front runner in any case?

I'm tempted to go back to school and get a graduate degree in Rhrumatology now. I'm only 49. 😏
I haven't been in school since 1989! 😳

I will check out your website! Thank you for the link!!

Almost 3 weeks in and my treatment has helped me feel somewhat better already. I have my 2nd infusion this Thursday. I am not on any pain meds for ear pain anymore. My biggest complaint currently is a cough and tight feeling in my lungs. The ct scan did show 3 granulomas (3+ cm in size) and two smaller nodules. So I'm guessing they aren't gone yet.

I know I'm VERY fortunate to not have my kidneys involved or damaged at all (though I read that only 20% present with renal involvement, 80% develop renal involvement) so I know I am not necessarily out of the woods with that.

I'm astonished that my c-ANCA to pr3 was 1178. What do you make of that? Any theory on why it was so high? I know ANCA is not always correlated with disease activity - yet they use it as part of making a diagnosis. I'm confused on its true importance. Any thoughts?

My RA last week said I'm "moderate to severe" when I asked him to label my disease. And yet I'm also most likely an early diagnosis. And I was on high pred dose and first infusion within a week of dx. (3 months of symptoms before dx) ~ Side note: I did have chest X-ray confirmed pneumonia twice last year but both became resolved symptomatically with antibiotics. Wondering now if GPA was "simmering" back then.

Thanks again for sharing your knowledge with this newbie.
Gabrielle

[Mark76]

You sound almost identical to me...diagnosed in jan but had blocked ear nose bleeds severe sinus pain and lung nodules in november. Lung biopsy proved gpa. Yes thankfully no renal involvement and detected early which is normally good. Mine too was moderate to severe. Believe it or not often the greater the severity the greater the effectiveness of treatment. Yes anca shows only slight correlation of disease activity however significant titre changes often shows when a flare is about to occur possibly. They are looking at better markers inclyding mettaloprotein and cd8 t cells believe it or not.

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[Gab122]

Hi Alysia,
Decided to reply to your message in one of the threads... In case you still have difficulties

My message to you was that I thought you might find this post interesting. I did. [emoji4]