Very worried. I have Mixed Connective Tissue Disease, Shortens and Raynaud's and me latest ESR was 109. Anyone else had this result? Not on medication as have bad reaction to most drugs. Look forward to hearing others have had similar result.
Richer2
Richer, no, I haven’t had the result you’ve had and hopefully someone who has will see your post and answer up. I just wanted to tell you I’m sorry you are going through this. I’m sure someone in here can help.
I, like you am not on meds. Not because of a bad experience with them, but because I don’t want a bad experience from them. I feel we have enough to deal with, I don’t need more problems. But it’s a personal choice. I don’t judge anyone who is on meds and some seem to be doing well on them.
Best of luck and keep us posted. Again, hopefully someone with experience in this will answer up.
Hi Richer! That’s a pretty high ESR. Any ESR greater than 100 would make me worry about an infection or hypergammaglobulinemia (making too many antibodies). Another thought is something called giant cell arteritis which is inflammation of larger arteries. This can also cause high high ESR in the setting of autoimmune picture. Do you have any visual problems and jaw stiffness?
What did your doctors say about the ESR? I can’t imagine that is something they would just ignore.
I too mentioned Hypergammaglobulemia on the other post because my PV/ ESR is similarly high. But I think Richer would know if it was GCA as the symptoms are pretty severe. Hypergammaglobulemia like I have sounds more likely as not on any meds makes my PV plasma viscocity/ ESR very similarly high too I would think? I’m told it is quite common with Sjögren’s.
That’s why I ask what his doctor’s said about ESR. It’s not something that they typically ignore when over 100. GCA doesn’t always present in a terrible way. Some people don’t know until they get an angiogram or it’s found incidentally after elevated ESR and vague symptoms.
Just some quick info that goes along with what I’ve seen/been taught:
GCA should always be considered in the differential diagnosis of a new-onset headache in patients 50 years of age or older with an elevated erythrocyte sedimentation rate.
An ESR greater than or equal to 100 was found in 101 (12%) patients. Infection (46 patients) was the commonest cause, followed by malignancy (25), connective tissue disease (17), renal disease (8) and liver disease (5). ... Pneumonia was the commonest infection diagnosed and the commonest cause of a markedly elevated ESR.
Just wondering what his work up has been following high ESR? As I’m sure you know, docs tend to attribute abnormalities like this to our AI illnesses when other causes should be ruled out. Esp infection in someone with a dysfunctional immune system.
Well I defer to your medical knowledge of course. I was hospitalised with what was thought to be GCA 5 years ago because of facial pain and high ESR. It turned out that the facial pain was trigeminal neuralgia and small fibre neuropathy.
Since then every new doctor I see looks startled by my very high plasma viscocity. They did once phone about it but then they were told by a vascular dr not to be concerned - “just” high immunoglobulins and my normal. Mycophenolate, Methotrexate, Hydroxy and steroids all take it down to just above range.
I did seek an expert second opinion on this and the Sjögren’s rheumatologist confirmed Hypergammaglobulemia but that’s all I’ve been told. My ANA is positive but otherwise my autoantibodies are mostly normal.
Does this make sense to you? I’m sure I don’t have GCA but I still don’t think having such high viscocity is normal or healthy?
I could see why they were worried about GCA. Having high viscosity is not normal either even if caused by hypergammaglobulinemia. I would imagine any immunosuppressant would help even if just a little. Anything that knocks out your antibody making cells would be helpful. I’d wonder what something like rituximab would do for you.
As mentioned before, I think you’d benefit from a good hematologist TT. Something isn’t right. Maybe it’s not within the rheumatologic arena and could be a blood cell problem which does mimic rheum illnesses. Although exhaustive, it is a docs responsibility to rule everything out even if it takes months/years.
Thanks JM - I know you're in the US so I will just say that here in UK we usually have to go through our GP for all referrals unless the consultant refers us internally to a different specialist.
I do have a pretty definitive diagnosis of Sjogrens by lip biopsy (100%) and also am treated for hypothyroidism and acknowledged as having Raynauds, SFN and Erythromelagia. But it's taken me nearly 9 years to find out that I have Hypergammaglobulemia - and as you know I think there may be more to this than a seronegative rheumatic disease.
You really helped me when you suggested that I ask my new rheumatologist if I might not benefit from seeing a haematologist. I accept that I have hypergammaglobulemia but I'm just not sure what the underlying cause is other than my seronegative Sjogrens.
As I think you know I did have a high reading for this rare antibody, Image result for anti fibrillarin antibodyabcam.com
Anti‐fibrillarin (or anti‐U3‐RNP) antibody, but I think it probably wont show up next time. I also have a nucleolar pattern for my ANA and carried a weakly positive anti Th&To so it could all point to an unusual manifestation of Scleroderma overlapping my Sjogrens. But this wouldn't explain my consistently raised RBC count.
Life felt much more straight forward when I was just misdiagnosed and treated for RA I must say! They won't offer me Rituximab here in UK unless I turn seropositive for RA or possibly Sjogren's - and even then...?! I don't think immunesupression or Biologics have so much of a role to play in Scleroderma but we will see. x
But, TT, you do seem to be transitioning, don’t you think? I don’t know how they know when to use medications « off label, « as I was just discussing with Paul Howard but it may be a whole host of things. I really feel for you. Glad you have a new rheumatologist to maybe look at things afresh.
XK
I won’t be offered Rituximab but I don’t think I’m transitioning that much really.
I think we just get used to certain forms of pain over years or even a lifetime. I recall someone at an RA symposium saying that she had suffered JIA and was so used to pain that it came as a terrible shock to learn that, despite little pain she was aware of, she needed a double hip replacement aged 30.
Whereas others who haven’t endured much pain previously will find sudden onset inflammatory arthritis or SFN or dry eyes or mouth an absolute nightmare.
Pain doesn’t always equate to damage and that’s why having a very high ESR/ PV is a worry. In my case I have learnt to look hard at potential causes of it going over the high threshold into hyperviscocity - including UTIs and simmering dental abscesses - which I may not be that aware of but which can drive it up into numbers which for others would mean something very serious indeed.
My CRP is a much more reliable marker because it sits at an average of 12 and can go down to 4 (once on steroids!) but when I had pancreatitis it was 160. Certain antibiotics can lower mine which is interesting.
By getting copies of our blood results we can learn out own normal ranges.
Fatigue is a constant enemy and is a direct result of Hypergammaglobulemia for me because my body is always fighting these antibodies. SFN is mostly just numbness for me now. The only things that are getting worse are Raynaud’s and Erythromelagia. Other stuff relapses and remits or progresses very slowly eg ulnar drift.
Fatigue is life-sapping, isn’t it? You endure a lot, I know. You have so many varied symptoms with little relief.
That is amazing about the woman who needed her hips replaced. She must have, like you, endured too much.
XK
Interesting to read your reply Jmiller623 . I am almost on the floor with malaise and disability/pain if my ESR rises to 50 yet my rheumatologist will curl a disparaging lip and tell me that ‘these are not big numbers’ and, as such, is insignificant evidence of disease activity.
Hi Fennella. Just a disclaimer. I wouldn’t take what I say as etched in stone since I’m not anyone’s provider.
An ESR of 50 is moderately elevated but I think this level is common for many on this forum from the labs others have posted. I’d worry when it’s over 100 and make sure there aren’t other causes beyond CTD. Each person is different and even certain environment/situations have been shown to raise ESR - smoking being one of them.
Docs rely too much on labs when treating patients. My ESR is always near undetectable but this is because my total immunoglobulins are always low. Even during my worst times, it doesn’t budge unless I get an infection.
Jmiller: for interest’s sake only, you may find the alternative test to ESR my lab use quite interesting because it isn’t very susceptible to age, gender, weight or smoking apparently. labtestsonline.org.uk/tests...
“Unlike the ESR, the plasma viscosity is not raised in anaemia or decreased with polycythaemia (too many red cells). It increases slightly with age but less so than the ESR. The ESR may occasionally decrease again with very high levels of some paraproteins, leading to misleading results, while PVs accurately reflect protein levels”
PV is essentially the same as ESR but a more technical measurement on thickness. ESR is estimated sedimentation rate. It’s basically putting blood in a tube and counting how long it takes (in seconds) for red blood cells to settle out of plasma. It’s a rough rough estimate but a quick and dirty test that can tell you a lot. Antibodies and platelet activation make blood cells stickier and harder to settle hence higher ESR. PV is most assuredly more accurate than ESR but much more expensive. Here in the US, it’s not a commonly run lab because it’s ordered separately, mostly for polycythemia vera patients and is quite expensive. ESR is much cheaper and quicker to obtain. ESR and CRP are more commonly measured. CRP is more accurate for acute inflammation whereas elevated ESR can mean near past or present inflammation.
Is PV always measured with blood counts in the UK or is it also a separate test?
It is run instead of ESR in my area of Scotland - which has a large medical student population. I know about both because I started this autoimmune journey on an island nhs health board further north where ESR and CRP were the main inflammation markers used - never heard of PV until I relocated. Here in this one area of eastern Scotland they are a bit proud of their lab tests generally - including PV. But in Glasgow, the largest Scottish city, and Edinburgh, only the ESR is used and an old rheumy I saw last year in Glasgow took up at least 5 minutes of my 30 minute private consultation explaining that he didn’t know how to interpret my PV scores of over 2.00 and wasn’t going to bother trying to learn at his age! He then described my PV as mildly elevated jn his clinical letter - while disclaiming it as an unnecessarily exclusive marker which he didn’t understand!
But when I told my endocrinologist that my PV is usually over 2 he exclaimed “surely not? You must be wrong! (Checks his computer screen and) oh yes so it is! Well that’s outside my specialist remit for sure!”
High C3 and C4 results?
High potassium level and lupus nephritis
What does \"High\" mean really?
High pulse
High body temperature in the early am
