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I need some help

Discussion in 'Tests and Procedures' started by Michael Garhart, Sep 30, 2018.

  1. Michael Garhart

    Michael Garhart New Member

    So I have been going to specialists for a long while. You all know the story. Mine was Fibro + Hypothyroidism + Hypoglycemia, and the "fun" food and pain ailments that go along with that. I thought Keto would fix it, but it doesn't. It makes you feel better, even though you can't think as powerfully as before, but it doesn't resolve the issues. So off to the specialists again, but this time was different.

    2 vials of blood and a week later, I get these results:

    ANA: 23 Units, Positive. (Range: 0-20=Neg, 20-59-Pos, 60+=Strong Pos.)
    Anti-dsDNA: 360 IU/mL, Positive. (Range: Under 302=Neg, Over 302=Pos.)
    Anti-cardiolipin IgG: 27 CU, Positive. (Range: Under 20=Neg, Over 20= Pos.)

    I have read somewhere between 20-30 studies, ranging from 1970s to 2018, since I got the lab on Thursday. I felt it was pretty F'd up, to let a patent have to read and figure this out on their own. I can read a lot of the studies. I have courses passed in graduate statistics, but its not a picnic to try to decipher some of these things. They just said they would re-test in December? And that was via phone. What kind of answer is that?

    One of the things I read was that a CLIFT (Crithidia l. inflorescence) is considering a coin flip of 47-63% confidence. I had a CLIFT that said negative, but I don't understand why it was included. If it itself is positive, I can see why it is added, since its additional verification for the Anti-dsDNA, but the most recent ELISAs are the highest standard of specificity and avidity possible for such a lab. Studies I read commended that any other of the older methods from the 70s and on are superior than using a CLIFT. Maybe the CLIFT is just super cheap to do? They included the pattern as too obscure, and the studies also say these are meaningless, and that their prior hypothesis for them does not stack up statistically. They originally through they meant type of SLE, but that the idea should be thrown out the window. So why was that included?

    I am grateful this Rheum was thoughtful enough to actually give a lab for this, but I am concerned the lab has irrelevant information that could lead to a bad conclusion by the Rheum. I am so unsure, and very nervous. I'm tired of seeing specialists. I am worried that they could come to a false conclusion and my kidneys could be harmed, or that I become disabled and the information is bad.

    Am I overthinking this? Can someone experienced help me decipher what I am seeing?

    Recently, my AST tested high. The first time ever. I did stumble on studies that SLE can reduce insulin sensitivity and cause hypoglycemia. That would explain my unexplainable, non-diabetic results since 2010. They thought I had insulinoma, but that was negative, despite having the glucose and insulin pattern for it. SLE could explain my weakness in sunlight, but I don't get the rashes at all. I get massive joint and neural pain. I wake up every day with my head feeling like an inferno, with major brain fog. If I use a ladder, my entire feet and calves feel like they're burning. If I don't feel well, it feels like water is running over my legs. The list goes on, but I don't have any rashes. I do have dark urine, but no blood.

    Thank you. Sorry for rambling.
  2. lazylegs

    lazylegs Moderator

    Welcome Michael,

    In the general population there are people with a positive ANA, especially those with family members with some type of autoimmune disease and they themselves do not have Lupus. Yours is a low positive without a positive Anti-dsDNA and no specific pattern. The Anti-dsDNA isn't positive in all Lupus patients but it helps to point the doctor in that direction if it is. Unless you meet enough of the criteria in other ways your doctor is left being unsure if it is Lupus or not. The criteria for a Lupus diagnosis can be found on our main site https://www.thelupussite.com/lupus_diagnosis_tests/diagnosing_lupus.html.

    The positive Anti-cardiolipin IgG also leaves questions. It may or may not be significant since it is not specific to Lupus. Usually the test is done a second time if the result is high. It may just take time before the picture becomes clearer which is frustrating especially when you feel so poorly. If you do not feel confident in the results you can always get a second opinion.

    Take care,
    Michael Garhart likes this.
  3. Michael Garhart

    Michael Garhart New Member

    Hi! Thanks for the response. My anti-dsDNA was positive on the test of high specificity and high avidity, but not on the CLIFT version, which is old.

    I found this table in a 2011 study, where they compared the ELISA with high specificity and avidity in conjunction with each of the older lab tests, and this was the statistical conclusion:


    A negative agreement is the ratio in which a test can properly identify the analyte in obscuring serum, so a positive agreement is the ratio where it can properly identify the analyte in an obscured serum.

    The Spearman's rho is where a score closest to 1 is a perfect positive correlation.

    So this means CLIFT should not be used at all. It's old, and it requires a person to look at it physically and qualify it with their eyes. I thought it was odd to see it included after looking up these studies. But, yeah, my ELISA for it was positive.

    I forgot to add that my AST was also elevated, which I found very bizarre. I don't drink. I don't do anything remotely negative for my liver, so that was odd to me.

    On the link you provided, I could #5, 6, 8, 10, and 11.

    There is no history of familial autoimmunity, but my grandmother was schizophrenic, although she began life as fine. I thought she was pretty cool, but apparently it caused relationship issues. I was too young to understand those things. So I'm not sure if schizophrenia counts.

    Thanks again!
  4. lazylegs

    lazylegs Moderator

    Research has been done on the possibility of schizophrenia being an autoimmune disease. In my reading it does has some of the same hallmarks such as inflammation and in a few people studied autoantibodies. The studies are wordy and far over my head but it looks like further research will need to be done to find out if schizophrenia is to be included or if some of the people have been misdiagnosed and have it as part of another disease.

    Take care,
    Michael Garhart likes this.
  5. Michael Garhart

    Michael Garhart New Member

    Yeah, I should try to research it. My brain is pretty much dead today, but I'll get to it for sure.

    I do know that I score in the 99th percentile for the Inquisitiveness in the Openness factor for the Big 5. I know that factor is statistically significant, and it uses hundreds of thousands of people for the psychometric data. I had always wondered if that was because my grandmother was schizophrenic. There is no way to currently know yet. Only extraversion/introversion of the psychological traits is understood to any meaningful degree. Well, and neuroticism to a degree, too. Maybe I rolled the wrong genetic dice.

    My PCP messaged me back, because I sent him a PDF of the lab via the printer function, and his nurse said they may have to review false positives from this year all the way back when I was 19. And told me to sit tight until then. I have had a lot of labs like a lot of people here, so I thought that was considerate and thorough.
  6. x_claire_x

    x_claire_x Moderator

    Just quickly...my liver enzymes rose when my disease was most active as the liver was trying to deal with my muscle damage /enzymes etc ,that was occurring due to MCTD on the rampage...since meds correct they have reverted to normal despite rattling with meds...……...just a thought....Claire
    Michael Garhart likes this.
  7. Michael Garhart

    Michael Garhart New Member

    I think its an important consideration. Thank you! I will try to research any related studies.
  8. Michael Garhart

    Michael Garhart New Member

    I found this:

    6.2.10. Antibody to Histone and Double-Stranded DNA (dsDNA)
    Antibodies to dsDNA have been detected in patients with AIH type 1. The presence of these antibodies has been associated with high immunoglobulin G (IgG) levels and a poor immediate response to corticosteroid treatment compared to anti-dsDNA-negative patients [137].

    6.3. Elevated Serum Immunoglobulin G (IgG)
    The elevated levels of serum IgG and low C3- and C4-complement levels in AIH patients were first described by Thompson et al. in 1973 [114]. High levels of IgG can be found in both AIH type 1 and type 2 patients [10, 11, 36, 142, 143], although 25% of the AIH type 2 patients may demonstrate normal IgG levels [25]. In our previous report comparing serum IgG levels between AIH patients and patients with other chronic liver diseases, we found that the mean serum IgG level was 30.6 g/L in AIH patients. Moreover, this level demonstrated a sensitivity of 90–98% and a specificity of approximately 96% for the diagnosis of AIH [144]

    6.2.1. Anti-Nuclear Antibody (ANA)
    ANAs exhibit nuclear staining in the kidney, stomach, and liver because ANAs are specific for nuclear antigens (first described by Miescher and Fauconnet in 1954) [77]. Although no specific ANA nuclear antigen has been identified in AIH type 1 [75], a variety of nuclear molecular targets have been detected, including centromeres, histones, double-stranded DNA, chromatin, and ribonucleoprotein complexes [78]. Moreover, no single ANA pattern is dominant in AIH, although a homogenous pattern is typical [79]. In addition, ANAs are not specific to AIH because ANA staining can also be observed in patients with chronic viral hepatitis B and C [80]. ANAs are also detected in patients with drug-induced hepatitis [13, 50, 51, 55] and other nonliver disorders. However, ANAs represent the sole marker of AIH disease in 13–15% of the patients [78, 81].

    Other autoimmune diseases may coexist in 20% of the AIH patients, including type 1 diabetes, thyroid disorders, systemic lupus erythematosus, rheumatoid arthritis, and primary sclerosing cholangitis [16, 18, 75, 149, 150].

    The colored numbers are just links to the studies done, which doesn't copy/paste over.

    I found a study on what happens with liver involvement in SLE, and it was too depressing to link. But, I also found this chart:


    I am sitting at a 5 now, because I have not had a histology, SLA, or LKM taken, so I'm either a 5 or 7+.

    I just accidently stumbled upon a study that shows smoking increases the risk of elevated anti-dsDNA by 4x, but cessation over time decreases the risk to 1.4x. Maybe it is methylating DNA? I dunno. I don't and never did smoke though, and I don't live in an air polluted area.

    Another study concludes that a positive for anticardiolipin often indicates Lupus at a more active time. Although other studies indicate they anticardiolipin can stand alone without Lupus. So its possible for that autoimmune antibody to wax and wane in someone with confirmed Lupus.

    re: schizophrenia:

    They found a patient that had both, and found that Azathioprine halted schizophrenic traits. They say its psychoneurological cross-relating at the central nervous system. They couldn't conclude anything, but seemed to hypothesize that it's related in atypical cases, and that immunosuppressants seem to work for both disorders concurrently. Although, in that case, she had discoid form, and I do not have discoid. Another study seems to imply that Lupus variants tend to aggravate Schizophrenia into full psychosis. Another study concludes this: "...the demonstration that such antibodies can exert functional effects in vitro constitute compelling evidence in support of the hypothesis that autoantibodies may play a role in the development of schizophrenia."

    So they are at a crossroad between "we're not sure" and "are they linked by predisposition at a neural and autoantibody level?".
    wolf1 likes this.

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