#also I have positive autoimmune titers

[gingersnapwolves]

great news! my labs say that something is definitely wrong with me!

[osddid-i-do-that]

For years, I’ve been telling doctors (rheumatologists in particular…) that I feel Amazingly Normal when they put me on steroids for acute illness things. I don’t get mood swings. I don’t feel shitty when I start the meds. I can function and think and get out of bed.

I have also had a stupid high ANA titer for years without any explanation (they test a few specific antibodies, nothing else comes back positive, I get told off for not having a “real” autoimmune disorder), POTS, chronic fatigue, and I’m underweight no matter what I do.

And now I’m finding that, based on this information, SOMEONE should have told me, “Huh, we should really test your adrenal glands!!”

I fucking swear, if all my remaining issues could be solved with a little bit of prednisone for the rest of my life, I’m gonna use all my newfound energy to level the entire medical establishment.

[normal-with-adhd-is-a-joke]

Love when I have blood tests actually come back showing something and the something is showing is possibly kidney stones or kidney disease /s. My doctor wants me to get a kidney ultrasound but I can't because I'm extremely ticklish. It sounds stupid but it's a valid barrier to treatment for me, I always have ECG techs be like "am I hurting you?" because I move so much. Literally one of the reasons I'm not having kids is because I know I can't sit still for an abdominal ultrasound. I've had an ultrasound on my throat before and it was horrible. One of the possible things that could be causing all this is an asymptomatic/unnoticed UTI so I'm on antibiotics and I'm going to have a retest done when the antibiotics are over.

Also my sed rates and c-reactive proteins are still bad and an ANA Pattern and Titer test came back that I probably have an autoimmune disease, possibly lupus. This test generally doesn't come back positive for ppl w/ CFS so while I definitely do have CFS I might have something else as well. And the doc who ordered all of these (rheum) is a pushy bitch who I don't want to keep working with but now I probably have to. Also she hasn't gotten back to me about these results yet so I'm just sitting here losing my mind trying to figure out what all the positive test results mean.

[eschynite]

The elevated ANA might just be from my chronically reactivated EBV honestly. But I do have malar rash and the painful/swollen joints, I think there are other tests (including a skin biopsy?) they'd have to do to confirm lupus. I'd have to meet other symptoms pretty strictly to qualify for a diagnosis bc my titer was 1:40 (weakly positive, occurs in healthy people and preclinical autoimmune syndromes). I also did some more research on fibromyalgia and apparently the idea that fibro pain is only in certain spots is outdated, it's general widespread pain, so that's a possibility even tho I never thought it was. Idt fibro causes stiff/swollen joints, though, so idk. I'll just have to wait for the rheumatologist to tell me I'm fine and to go home I guess <3

My bloodwork is consistent with lupus

[justmelagain]

Autoimmune Journey of Discovery:

Did some blood work on 12/20 to start autoimmune testing. Nurse took 12 vials of blood!

Do these people just FORGET that I'm chronically anemic too?! I have enough trouble keeping what I have without everyone taking it from me. lol I have 2 more sets of blood work scheduled in January. 😯

12/21 results: negative for Epstein-Barr & RA ✔

12/23 results: negative for Sjogren’s

Probability of lupus?! (I don’t know how to really read these things but ANA SCREEN, IFA is positive, ANA PATTERN is nuclear, homengenous - Homogeneous pattern is associated with systemic lupus erythematosus (SLE), drug-induced lupus and juvenile idiopathic arthritis, & ANA TITER is 1:40 where 

<1:40        Negative 1:40-1:80    Low Antibody Level >1:80        Elevated Antibody Level

Also, my sed rate is high (51; normal is below 20) & C-reactive protein is high (28.6; normal is below 8.0), which are other indicators for lupus.

Soooo...I guess...lupus it is.

[mcatmemoranda]

I don't like the way the rheumatology lectures from this past week were given. There are too many powerpoints and too many notes. It could've been much better organized. So I'm just skimming the notes and putting the stuff that was bolded here. Special serologic tests (FANA tests) that are used to help confirm the diagnosis are helpful, but biopsy gives the definitive diagnosis! Immunologic features include: Positive LE phenomenon, high titer antinuclear antibodies (most often it is the diffuse or homogeneous non-specific pattern on IF with the peripheral or rim pattern beings more specific and highly suggestive of active SLE). Antibodies against the SM antigen are highly indicative of SLE. While not specific for SLE, a depressed serum compliment level suggests activity of the disease process. Renal involvement is associated with deposition of immunoglobulin and complement along glomerular basement membrane (“lumpy-bumpy pattern”) while with skin manifestations there is deposition at the dermal-epidermal junction of the involved skin as well as the uninvolved skin. Numerous autoantibodies are at times present other than ANA and ds-DNA (see below).One should be suspicious of an autoimmune disease when the following antibodies are present: ANA, anti-dsDNA, anti-Sm, ant-Ro (= to anti-SSA), anti-La (= to anti-SSB), anti-RNP, antiphospholipid antibodies. A negative ANA is strong evidence against a diagnosis of SLE! Lymphocytotoxic antibodies (against primarily T lymphocytes) in the presence of complement can kill T cells. Evidence points to the fact that there is an imbalance in which Ts (suppressor) cell activity is depressed and B-cell activity is enhanced (thus the hypergammagobulinemia that is present); delayed hypersensitivity may also be impaired as a result of the lymphocytotoxic antibodies. Thus antibody formation (IgG) is excessive with unusual and high-titer antibody responses occurring. A female disposition in SLE (as well as other rheumatic diseases) may be related to the fact that estrogens enhance anti-DNA antibody formation with the androgens having an opposite effect. The cell used in the LE cell prep test is the Polymorphonuclear leukocyte (PMNs). The LE cell test has largely been replaced by the ANA (anti-nuclear antibody) test; the LE cell test is more specific but less sensitive than the ANA test; yet an understanding of the LE phenomenon and the LE test enables one to understand the disease process in SLE. All classes of antibodies may form antinuclear antibodies. Homogeneous ("diffuse","solid",”non-specific”): The expression of anti-deoxyribonucleoprotein is suggestive of active SLE. The entire nucleus fluoresces with the Ab nonspecific for a variety of nucleoproteins. This pattern is the pattern most frequently seen in SLE and is non-specific and much less specific than the rim pattern. Speckled pattern is associated with scleroderma and mixed connective tissue disease (MCTD). Nucleolar: Homogenous staining of the nucleolus and represents antibody to ribosomal protein. Most commonly seen in scleroderma and Sjögren's syndrome. Cytoplasmic: Mitochondrial staining often indicative of primary biliary cirrhosis with autoantibody against tissue in chronic hepatitis. Anti-RNA (I'm pretty sure it's supposed to be DNA, not RNA. The lecture slides didn't even mention RNA). Antibodies Anti-double-stranded RNA (ds-RNA) is seen in 70% of patients with SLE, and while not as specific as anti-ds-DNA antibodies they are more specific than anti-ss-DNA. They suggest a viral infection may have an etiologic role in SLE since they are often associated with viral types. Drug induced lupus rarely shows renal involvement. 2. Skin Almost 90% of patients with SLE have immunoglobulin and complement deposited in the dermal-epidermal junction of skin, which is not involved with an active lupus rash. The presence of this “butterfly rash” is frequent in SLE but not necessary for the diagnosis and can occur in other conditions e.g. MCTD. Patients with discoid lupus show deposition of Ig and C only in involved skin; this is the Lupus Band Test. A diagnosis of Systemic lupus is virtually made by the finding noted in both the involved skin and non-involved skin i.e. the pattern seen in both the involved and uninvolved skin would indicate systemic lupus while if only in the involved skin and not in the uninvolved skin it would indicate discoid lupus. Joints: elbow; synovitis and small joint involvement. Often there is deformity without erosion or bone destruction (unlike RA where there is often deformity with bone destruction). The arthritis of SLE is rarely destructive, and we do not see articular erosions and destructive bone changes. One can see a deformity called “Jaccoud’s deformity”. In Jaccoud’s deformity there is a symmetric deformity of the hands with ulna deviation at the metacarpophalangeal joints, but unlike RA it is reducible and there is no bone erosion as seen on x-ray. There is an unusual sensitivity to sunlight in SLE patients. The rash may vary from an erythematous blush, lesions of discoid lupus, or a maculopapular eruption. In white and Asian patients the rash is usually bright red, but in African Americans it may show up as a depigmentation or hyperpigmentation. Hair loss as well as ulcerations of oral or vaginal mucosa are fairly common. The Lupus Band Test will show the typical findings of systemic lupus (lumpy bumpy distribution along the basement membrane of immunoglobulin and complement) in the involved and uninvolved skin while in discoid lupus it will be present only in the involved skin, and thus it is used to differentiate systemic lupus from the localized discoid lupus. A depressed total hemolytic complement (CH50, C3, or C4) usually indicates immune complex activation, and is seen in conditions other than SLE (RA, vasculitis, etc.) When a congenital deficiency is not present, C4 is the most sensitive component of the complement in the diagnosis of SLE. Complement level rises with remissions and falls with exacerbations of the disease. The proposed classification is based on 11 criteria. For the purpose of identifying patients in clinical studies, a person shall be said to have systemic lupus erythematosus if any four or more of the 11 criteria are present, serially or simultaneously, during any interval of observation. It is strongly advised to review and know the current classification and the following differential diagnosis of SLE. If you suspect SLE a complete physical and history should be carried out looking for signs and symptoms of a multi-system disease. Screen with CBC including platelets, Westergren ESR, ANA, Rheumatoid factor, and urinalysis. Remember that a negative ANA is strong evidence against SLE. Although it is doubtful that SLE can be prevented, we can increase the life span and quality of life of the patient by proper diagnosis and therapy. Complications must be avoided (cardiovascular, osteoporosis, infections, cancers, etc.) by the careful use of indicated drugs. Thus a true holistic Osteopathic approach is indicated. A FULL OSTEOPATHIC APPROACH INCLUDES: LIFE STYLE CHANGES MANIPULATIVE AND PHYYSIOTHEAPY DRUG THERAPY FOR SLE ANALGESICS FOR PAIN NSAIDS Opioids (caution) CORTICOSTEROIDS DISEASE-MODIFYING ANTIRHEUMAIC DRUGS (DMARDS). Plaquenil (Hydrochlorquine). Immunosuppresents (e.g. cyclophosphamide, methotrexate and azathioprine). IMMUNOSUPPRESSIVE DRUGS. Belimumab (Benlysta): a monoclonal antibody that inhibits cell activating factor. Mycophenolate (CellCept). INTRAVENOUS IMMUNOGLOBULIN (reduces antibody production) PLASMAPHERESIS PSYCHIATRIC CARE RENAL TRANSPLANTATION

[pedrop61]

Serological Association of Measles Virus and Human Herpesvirus-6 with Brain Autoantibodies in Autism

Vijendra K. Singh, Sheren X. Lin, Victor C. Yang, , In Clinical Immunology and Immunopathology, Volume 89, Issue 1, 1998, Pages 105-108, ISSN 0090-1229, https://doi.org/10.1006/clin.1998.4588.

(http://www.sciencedirect.com/science/article/pii/S0090122998945883)

Abstract: Abstract Considering an autoimmunity and autism connection, brain autoantibodies to myelin basic protein (anti-MBP) and neuron–axon filament protein (anti-NAFP) have been found in autistic children. In this current study, we examined associations between virus serology and autoantibody by simultaneous analysis of measles virus antibody (measles-IgG), human herpesvirus-6 antibody (HHV-6-IgG), anti-MBP, and anti-NAFP. We found that measles-IgG and HHV-6-IgG titers were moderately higher in autistic children but they did not significantly differ from normal controls. Moreover, we found that a vast majority of virus serology-positive autistic sera was also positive for brain autoantibody: (i) 90% of measles-IgG-positive autistic sera was also positive for anti-MBP; (ii) 73% of measles-IgG-positive autistic sera was also positive for anti-NAFP; (iii) 84% of HHV-6-IgG-positive autistic sera was also positive for anti-MBP; and (iv) 72% of HHV-6-IgG-positive autistic sera was also positive for anti-NAFP. This study is the first to report an association between virus serology and brain autoantibody in autism; it supports the hypothesis that a virus-induced autoimmune response may play a causal role in autism.

giusto per ribadire che non è che il discorso sia concluso e tutto chiarito...come spesso accade in medicina.