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  1. #1
    Senior Member FunkOdyssey's Avatar
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    Default From adrenal fatigue to hypothyroidism to lyme to CFS to APS

    In my seven year journey to figure out just what the hell is wrong with me, I've been through several diagnoses, from Adrenal Fatigue, to ADHD, to Idiopathic Thrombocytopenic Purpura (ITP), to Subclinical Hypothyroidism, to Chronic Lyme, to Chronic Fatigue Syndrome. Out of a thousand different things I've tried over these years, and the thousands of dollars I've spent, the only thing I can say without doubt helped me at all is escitalopram at the 5mg dose. I finally saw a very very good rheumatologist and it turns out I have two separate types of antiphospholipid antibodies: beta 2 glycoprotein and phosphatidylserine. According to the doc, these lab results, along with my low platelet count and symptoms and medical history etc, are consistent with

    Antiphospholipid Syndrome!


    So, I finally have a concrete diagnosis with established treatments that are likely to improve my condition! I was prescribed hydroxychloroquine, which reduces autoantibody production, reduces the binding of autoantibodies to their targets, reduces inflammation in all kinds of ways, reduces the risk of thrombosis in this condition by 70%, and is basically exactly what the doctor ordered. I was told I can expect this drug to improve my fatigue, brain fog, random pains, and normalize my low platelet count. If it does half of those things I will be so thrilled. Let's hope I tolerate it well and don't get any deal-breaking sides.

    WOOOOOOOOOT

    Regimen

    ($45 monthly including drugs)

    Upon Awakening:
    5mg Escitalopram

    Breakfast:
    1g Source Naturals Perilla Oil (550mg ALA)
    1000iu Jarrow Vitamin D3
    100mcg Bluebonnet Selenium
    200mg Hydroxychloroquine

    Lunch:
    1g Source Naturals Perilla Oil
    81mg Bayer Enteric-Coated Aspirin
    1 cap Jarrow FamilE
    2857iu NOW Vitamin A (two 10k gelcaps weekly)

    Dinner:
    1g Source Naturals Perilla Oil
    1000iu Jarrow Vitamin D3
    90mcg Jarrow MK-7
    200mg Hydroxychloroquine

    Bedtime:
    400mcg Solgar Methylfolate

    Diet:
    Omega-6 restricted, arachidonic acid restricted, whole foods. 96% lean beef, lean chicken, oats, wild blueberries, apples, oranges, broccoli, carrots, red/yellow/orange peppers, almonds, macadamia nuts, whole milk, whey isolate.
    Last edited by FunkOdyssey; February 20th, 2012 at 03:49 PM.
    "Also, can I rig some sort of enema out of household items?" -Tussman

    "I don't have the stamina for a 3-some, and I am a one-pump chump" -Ubiyca

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    Senior Member kassem23's Avatar
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    Very excited for you. It's about time for Shawn to Shine!

  3. #3
    Senior Member FunkOdyssey's Avatar
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    Also my mom almost surely has the same thing (she has sjogren's, low platelet count, fibromyalgia, migraines, etc) so this discovery may save her life. She's getting in to see my doctor next week. She is at extremely high risk for stroke and will be able to get on antiplatelet therapy and etc. The only bad thing about this news is that, since the propensity to develop antiphospholipid antibodies is hereditary, I have a significant chance of passing it on to children if I have any.
    "Also, can I rig some sort of enema out of household items?" -Tussman

    "I don't have the stamina for a 3-some, and I am a one-pump chump" -Ubiyca

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    Senior Member Tussmann's Avatar
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    yeah dawg change that avatar

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    Member ProphetofProfit's Avatar
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    Do you get into the M&M hall of fame when you're fixed? Because this:

    "I finally have a concrete diagnosis"

    I the holy fucking grail.

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    Quote Originally Posted by FunkOdyssey View Post
    Also my mom almost surely has the same thing (she has sjogren's, low platelet count, fibromyalgia, migraines, etc) so this discovery may save her life. She's getting in to see my doctor next week. She is at extremely high risk for stroke and will be able to get on antiplatelet therapy and etc. The only bad thing about this news is that, since the propensity to develop antiphospholipid antibodies is hereditary, I have a significant chance of passing it on to children if I have any.
    My mom had all of the same symptoms as your mom in particular (and you as well), same misleading diagnoses, same misleading tests. I wish someone had thought about this APS before it was too late.

    I'm thrilled for ya, man.

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    Senior Member adreno's Avatar
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    Very exciting. My fingers crossed it works for you, man.

    No wonder you felt like shit on phosphatidylserine, lol.

    Any idea as to the cause of this? Is it genetic (congenital)? Or immune dysregulation due to infections?

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    Wow, congrats Funk. I hope this is the right answer after so many years of searching.

    Please keep us updated on your results with the medication.

  9. #9
    Senior Member FunkOdyssey's Avatar
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    Quote Originally Posted by superfob View Post
    Wow, congrats Funk. I hope this is the right answer after so many years of searching.

    Please keep us updated on your results with the medication.
    Thanks man. I'm already three 200mg pills into the therapy and the only side I've had was very brief nausea with my first pill and a strange feeling in my head around the tmax of the first dose (CNS, meet hydroxychloroquine, your new ever-present companion). Nothing since then. The catch with hydroxychloroquine is always "this drug should be very helpful IF you can tolerate it," and if there was going to be any severe or allergic reaction it would have happened by now, so I'm pretty excited.

    Quote Originally Posted by adreno View Post
    Very exciting. My fingers crossed it works for you, man.

    No wonder you felt like shit on phosphatidylserine, lol.

    Any idea as to the cause of this? Is it genetic (congenital)? Or immune dysregulation due to infections?
    lol the same thing occurred to me about phosphatidylserine. The HPA suppressive effect is plausible as an explanation but I couldn't help wonder if this was involved too. I don't know if human phosphatidylserine is similar enough to soy-derived phosphatidylserine for the antibodies to attack it. It's an interesting thought though.

    It is unknown what causes APS but a two-hit model has been proposed where you need a genetic component combined with an environmental trigger, much like theories that explain other autoimmune diseases and CFS. Environmental triggers are your standard fare: stress, infections, vaccinations, etc. I do think it is possible that the genetic component is actually a vertically transmitted retrovirus. This may not matter much because for many intents and purposes a retrovirus integrated into your genome is now "your genetics". Also, hydroxychloroquine has shown very positive results in preliminary trials of HIV patients, by preventing the activation of the immune system that drives replication of the virus and the progression toward AIDS, so it almost seems like the right drug no matter what is going on.

    Quote Originally Posted by GaWd View Post
    My mom had all of the same symptoms as your mom in particular (and you as well), same misleading diagnoses, same misleading tests. I wish someone had thought about this APS before it was too late.

    I'm thrilled for ya, man.
    There is speculation from researchers that with improved awareness and screening APS will overtake other diseases as the most common autoimmune disease. Unfortunately for many people their first warning is a fatal clotting event. The presence of antiphospholipid antibodies in CFS (94% positive for anticardiolipin) and Lyme patients is very interesting to me, and especially with the recent positive results of rituximab in CFS, I can't help but wonder what would happen if you treated all these patients from an autoimmune perspective using plaquenil, rituximab, etc. Additionally, plaquenil is known among rheumatologists to be particularly effective at resolving fatigue and brain fog when these are mediated by an autoimmune process, so it seems like it could be a great fit for CFS if it turns out to be an autoimmune condition as many suspect it may be.

    Quote Originally Posted by ProphetofProfit View Post
    Do you get into the M&M hall of fame when you're fixed? Because this:

    "I finally have a concrete diagnosis"

    I the holy fucking grail.
    lol I know. The trouble with all the previous diagnoses is that none of them ever quite fit correctly or could explain everything. This really feels to me like a bullseye. The doctor was so certain my lab results would be positive based on my history and my mom's, at the previous appointment he promised he'd eat my chart if they weren't. Then yesterday, he was so excited when the beta 2 glycoprotein and phosphatidylserine antibodies showed up that he called his wife (who is a doctor and practices with him) and son (don't know why he was there) into the exam room to celebrate the diagnosis with me. I think he even started to cry a little bit. It was a pretty special moment.
    Last edited by FunkOdyssey; February 18th, 2012 at 05:27 PM.
    "Also, can I rig some sort of enema out of household items?" -Tussman

    "I don't have the stamina for a 3-some, and I am a one-pump chump" -Ubiyca

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    Senior Member adreno's Avatar
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    Wow, a doctor who cares. That's a first.

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    FunkOdyssey, do you have a list of all the blood tests your doc has done?

  13. #12
    Senior Member FunkOdyssey's Avatar
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    Quote Originally Posted by xdopamine View Post
    FunkOdyssey, do you have a list of all the blood tests your doc has done?
    I do but I left it on my desk at work so it'll have to wait until Monday.
    "Also, can I rig some sort of enema out of household items?" -Tussman

    "I don't have the stamina for a 3-some, and I am a one-pump chump" -Ubiyca

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    Senior Member Azx's Avatar
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    Congrats yo, hope you can recover.

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    i read about this syndrome in "Autoimmune Epidemic" it can be very dangerous, it's good to hear that you caught it before something life-threatening happened.

    since it is autoimmune, maybe it will be helpful for you to focus on keeping your diet clean and limit chemical exposure. it would make sense that escitalopram has helped, ive read here and there about some anti-inflammatory effects although the findings have been a bit yes/a bit no in that area. but im glad it helps.

  16. #15
    Senior Member FunkOdyssey's Avatar
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    Quote Originally Posted by Julez View Post
    i read about this syndrome in "Autoimmune Epidemic" it can be very dangerous, it's good to hear that you caught it before something life-threatening happened.

    since it is autoimmune, maybe it will be helpful for you to focus on keeping your diet clean and limit chemical exposure. it would make sense that escitalopram has helped, ive read here and there about some anti-inflammatory effects although the findings have been a bit yes/a bit no in that area. but im glad it helps.
    SSRI's also inhibit platelet aggregation which should benefit the disease. I've actually resumed the 5mg escitalopram as I've done well on that previously. The doctor also wants me on an antiplatelet drug, either aspirin or plavix, which we're going to decide on at my next appointment. This was after I told him that aspirin bothered my gut in the past, however looking through my journal now I'm not sure if that was fair as I only documented problems at higher doses.

    As far as diet goes I've drastically reduced my omega-6 and overall fat intake which are steps that have been shown to help lupus patients in a clinical trial as well as animal models of autoimmune disease. I've also increased my daily consumption of fruits and vegetables quite a bit.
    Last edited by FunkOdyssey; February 18th, 2012 at 11:17 PM.
    "Also, can I rig some sort of enema out of household items?" -Tussman

    "I don't have the stamina for a 3-some, and I am a one-pump chump" -Ubiyca

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    Hey Funk,

    Glad you found what's been going on!

    Out of curiosity did you ever have elevated antibody titres to stuff like EBV, HHV-6, etc.?

  18. #17
    Senior Member FunkOdyssey's Avatar
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    Quote Originally Posted by daerus View Post
    Hey Funk,

    Glad you found what's been going on!

    Out of curiosity did you ever have elevated antibody titres to stuff like EBV, HHV-6, etc.?
    I had high IgG titers to HHV-6 and EBV. I don't know how to interpret the results though, whether the titer is elevated compared to healthy controls or whether it just reflects exposure like the vast majority of the population. I'm leaning toward it not meaning anything clinically significant.
    "Also, can I rig some sort of enema out of household items?" -Tussman

    "I don't have the stamina for a 3-some, and I am a one-pump chump" -Ubiyca

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    Wow that is certainly profound. And yeah, I always myself had nasty reactions to racetams, choline derivatives, GPC, CDP, etc. Makes you wonder. The fibro connection is a HUGE vindication for understanding how these diseases work.

    Fibro nerve symptoms just absolutely scream autoimmune. The virus or pathogen connection combined with genetic suceptability when under a stress event is also the theory I subscribe to. And I also think that the presence of some variety of pathogens plays a role in the development of the autoimmune syndrome. (As with RA and ankylosing spondylitis).

  20. #19
    Senior Member FunkOdyssey's Avatar
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    I'm going to see about getting on 20mg of fluvastatin at my next appointment as I have borderline high LDL cholesterol anyway.

    Ann N Y Acad Sci. 2009 Sep;1173:736-45.
    Statins for the treatment of antiphospholipid syndrome?

    Jajoria P, Murthy V, Papalardo E, Romay-Penabad Z, Gleason C, Pierangeli SS.
    Source

    Department of Internal Medicine, Antiphospholipid Standardization Laboratory, University of Texas Medical Branch, Galveston, Texas 77555-0883, USA.

    Abstract

    Fluvastatin has been shown to revert proinflammatory/prothrombotic effects of antiphospholipid antibodies (aPL) in vitro and in mice. Here, we examined whether fluvastatin affects the levels of proinflammatory/prothrombotic markers in antiphospholipid syndrome (APS) patients. Vascular endothelial growth factor (VEGF), soluble tissue factor (sTF), tumor necrosis factor-alpha (TNF-alpha), soluble intercellular adhesion molecule-1 (sICAM-1), sE-selectin (E-sel), C-reactive protein (CRP), and soluble vascular cell adhesion molecule (sVCAM-1), were measured in the sera of 93 APS patients and 60 controls and in the sera of nine patients with APS before and after 30 days of treatment with fluvastatin. Elevated levels of VEGF, sTF, and TNF-alpha were found in APS patients. Fluvastatin significantly reduced those markers in the majority of treated subjects. The data from this study show that statins may be beneficial in aPL-positive patients and warrant larger clinical trials to confirm the efficacy of the drug for the treatment of APS clinical manifestations.

    PMID: 19758223
    Ann Rheum Dis. 2011 Apr;70(4):675-82. Epub 2010 Dec 20.
    Global effects of fluvastatin on the prothrombotic status of patients with antiphospholipid syndrome.

    López-Pedrera C, Ruiz-Limón P, Aguirre MÁ, Barbarroja N, Pérez-Sánchez C, Buendía P, Rodriguez-García IC, Rodriguez-Ariza A, Collantes-Estevez E, Velasco F, Khasmahta M, Cuadrado MJ.
    Source

    IMIBIC, Hospital Reina Sofía, Avenida Menéndez Pidal s/n, E-14004 Córdoba, Spain. rosario.lopez.exts@juntadeandalucia.es

    Abstract

    OBJECTIVE:

    Numerous mechanisms have been proposed to explain the thrombotic/proinflammatory tendency of antiphospholipid syndrome (APS) patients. Prothrombotic monocyte activation by antiphospholipid antibodies involves numerous proteins and intracellular pathways. The anti-inflammatory, anticoagulant and immunoregulatory effects of statins have been aimed as a therapeutic tool in APS patients. This study delineates the global effects of fluvastatin on the prothrombotic tendency of monocytes from APS patients.
    METHODS:

    Forty-two APS patients with thrombosis and 35 healthy donors were included in the study. APS patients received 20 mg/day fluvastatin for 1 month. Blood samples were obtained before the start, at the end and 2 months after the end of treatment.
    RESULTS:

    After 1 month of treatment, monocytes showed a significant inhibition of tissue factor, protein activator receptors 1 and 2, vascular endothelial growth factor and Flt1 expression that was related to the inhibition of p38 mitogen-activated protein kinase (MAPK) and nuclear factor kappa B/Rel DNA-binding activity. Proteomic analysis showed proteins involved in thrombotic development (annexin II, RhoA and protein disulphide isomerase) with altered expression after fluvastatin administration. In-vitro studies indicated that the inhibition of 3-hydroxy-3-methylglutaryl coenzyme A reductase by fluvastatin might inhibit protein prenylation and MAPK activation.
    CONCLUSION:

    The data from this study support the belief that fluvastatin has multiple profound effects in monocyte activity, which might contribute to thrombosis prevention in APS patients.

    PMID:21173016
    Curr Rheumatol Rep. 2012 Feb;14(1):87-94.
    Potential use of statins in the treatment of antiphospholipid syndrome.

    Lopez-Pedrera C, Ruiz-Limon P, Aguirre MA, Rodriguez-Ariza A, Cuadrado MJ.
    Source

    Unidad de Investigación, Hospital Universitario Reina Sofía e Instituto Manimónides de Investigación Biomédica de Córdoba (IMIBIC), Córdoba, Spain. rosario.lopez.exts@juntadeandalucia.es

    Abstract

    Antiphospholipid syndrome (APS) is a disorder characterized by the association of arterial or venous thrombosis and/or pregnancy morbidity with the presence of antiphospholipid antibodies (anticardiolipin antibodies, lupus anticoagulant antibodies, and/or anti-β2-glycoprotein I antibodies). Several studies have contributed to uncovering the basis of antiphospholipid antibody pathogenicity, including the targeted cellular components, affected systems, involved receptors, intracellular pathways used, and the effector molecules that are altered in the process. Therapy for thrombosis traditionally has been based on long-term oral anticoagulation; however, bleeding complications and recurrence despite high-intensity anticoagulation can occur. Based on all the data obtained, new potential therapeutic agents have been proposed. Statins have a variety of direct effects on gene expression and the function of cells of both the innate and adaptive immune systems, many of which are related to blockade of GTPase isoprenylation. In APS, statins have multiple profound effects on monocyte, lymphocyte, and endothelial cell activities, all of which may contribute to thrombosis prevention in APS patients. Nevertheless, larger randomized trials are needed to validate the role of statins in the treatment of this autoimmune disease.

    PMID: 22105548
    "Also, can I rig some sort of enema out of household items?" -Tussman

    "I don't have the stamina for a 3-some, and I am a one-pump chump" -Ubiyca

  21. #20
    Senior Member FunkOdyssey's Avatar
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    I'm turning this into a log of sorts, and I updated the first post to include my regimen which I will update as changes occur.

    Plaquenil has been interesting so far. Sides have included insomnia, feeling slightly high or out-of-it, mild gut cramping, and some exaggeration of orthostatic hypotension which is most noticeable when exercising. The insomnia and high feeling seem to be diminishing. I'm told most side effects disappear by the three week mark. On the plus side, I usually have mild acne and it's clearing right up. I'm guessing this is some early anti-inflammatory activity in action.

    I promised to post all the labs Dr. Greco ran so here we go. If you have any questions about the results or why certain tests were ordered feel free to ask. Format is (Name of test) - (My result/value) - (normal range or result), abnormal results in bold.

    Antithyroid Ab
    Antithyroid Ab | Negative | Negative
    Thyroglobulin Ab | Negative | Negative


    Protein Electrophoresis, Serum
    Total Protein Elec. | 7.5 | 6.1-7.9 g/dL
    Albumin, Electro |4.34 | 2.9-4.9 g/dL
    Alpha1 | 0.18 | 0.1-0.4 g/dL
    Alpha2 | 0.88 | 0.3-1.0 g/dL
    Beta Globulin | 0.84 | 0.6-1.2 g/dL
    Gamma | 1.26 | 0.5-1.7 g/dL
    Comment: Essentially normal pattern seen on serum electrophoresis. No M-component seen.
    Monoclonal Protein | 0.00 | 0 g/dL

    Vitamin D
    25 Hydroxy Vit D3 | 54 | 25-80 ng/mL

    Extractable Nucl Ag Eval
    SS-A/RO AB, IgG | <0.2 | <1.0
    SS-B/LA AB, IgG | <0.2 | <1.0
    SM AB, IgG | <0.2 | <1.0
    RNP AB, IgG | 0.4 | <1.0
    SCL 70 AB, IgG | 0.7 | <1.0
    JO 1 AB, IgG | <0.2 | <1.0

    Platelet antibody
    Platelet AB, Serum | Negative | NA

    Complement, Total | 52 | 30-75 U/mL

    Viscosity, Serum | 1.2 | <=1.5 cpoise

    Cryoglobulins | Negative | Negative

    ANA Screen | Negative | Negative (I did have this turn up positive a few years ago)

    Cardiolipin AB Panel
    Anticardiolipin IgG | 1 | <23
    Anticardiolipin IgA | 3 | <22
    Anticardiolipin IgM | 8 | <11

    Beta 2 Glycoprotein
    B2GPI IgG | 3 | <20
    B2GPI IgA | 5 | <20
    B2GPI IgM | 20 | <20
    Phosphatidylserine
    Phosphatidylserine Ab IgG | 4 | <22 U/mL
    Phosphatidylserine Ab IgM | 18 | <16 U/mL
    Phosphatidylserine Ab IgA | 5 | <20 U/mL

    Anti DNA Antibody | Negative | Negative

    Lupus/Phospholipid AB Panel
    Lupus Anticoagulant | Negative
    Lupus AN, APTT (Baseline) | 33
    DRVVT Interpretation | Negative

    Anticentromere AB | Negative | Negative

    Cold Agglutinins | Negative | 0-32

    Urinalysis, Reflex to Microscopy
    Urine Color | Yellow | Yellow
    Urine Appearance | Clear | Clear
    Specific Gravity | 1.015 | 1.001-1.035
    Urine Leukocytes | Negative | Negative
    Urine Nitrite | Negative | Negative
    Urine pH | 7.0 | 5.0-8.0
    Urine Protein | Negative | Negative
    Urine Glucose | Normal | Normal
    Urine Acetone | Negative | Negative
    Urine Bilirubin | Negative | Negative
    Urine Blood | Negative | Negative

    Urine Macro
    Status | Completed

    Vitamin B12 | >1500 | 180-914 pg/ml (this after taking 2mg hydroxycobalamin for an extended period of time, have since discontinued it)

    C3 Complement | 117 | 79-152 mg/dL

    C4 Complement | 26 | 16-38 mg/dL

    Comprehensive Metabolic Panel
    Sodium | 139 | 136-144 MEQ/L
    Potassium | 4.0 | 3.6-5.5 MEQ/L
    Chloride | 102 | 101-111 MEQ/L
    CO2 | 30 | 22-32 mmol/L
    Glucose | 98 | 74-118 mg/dl
    Blood Urea Nitrogen | 19 | 8.0-20.0 mg/dl
    Creatinine | 1.0 | 0.7-1.2 mg/dl
    Albumin | 4.6 | 3.5-4.8 g/dl
    Bilirubin, Total | 0.6 | 0.3-1.2 mg/dL
    Calcium | 9.9 | 8.9-10.3 mg/dl
    Alkaline Phosphatase | 48 | 38-126 U/L
    Total Protein | 7.5 | 6.1-7.9 g/dL
    SGOT | 24 | 15-41 U/L
    SGPT | 29 | 17-63 U/L
    Anion Gap | 7 | 5-14 MEQ/L
    Estimated GFR | >60.0

    TSH Ultrasensitive | 2.09 | 0.34-5.60 uIU/mL

    Free Thyroxine | 0.69 | 0.58-1.64 ng/dL

    Immunoglobulin IgG, IgA, IgM
    Immunoglobulin G | 1139 | 791-1643 mg/dL
    Immunoglobulin A | 190 | 66-436 mg/dL
    Immunoglobulin M | 181 | 43-279 mg/dL

    Complete Blood Count
    WBC Count | 3.60 | 4.0-10.5 K/UL
    RBC Count | 4.80 | 4.7-6.0 M/UL
    Hemoglobin | 14.7 | 13.5-18.0 g/dL
    Hematocrit | 42.1 | 40-54 %
    MCV | 37.7 | 78-100 fL
    MCH | 30.7 | 27-31 PG
    MCHC | 35.0 | 32.0-36.0 g/dL
    Platelets | 136 | 150-450 K/UL
    Few giant platelets present checked on smear
    RBC Distribution Width | 12.7 | 11.5-14.5 %
    MPV | 12.7 | 6.0-9.5 fL

    Differential
    Segmented Neutrophil | 60 | 25-62 %
    Basophil | 1 | 0-2 %
    Eosinophil | 2 | 0-6 %
    Lymphocyte | 30 | 20-48 %
    Monocyte | 7 | 2-12 %
    ABS Neutro | 2.2 | 1.8-7.8 K/UL
    ABS Baso | 0.0 | 0.0-0.2 K/UL
    ABS Eos | 0.1 | 0.0-0.5 K/UL
    ABS Lymph | 1.1 | 1.0-4.8 K/UL
    ABS Mono | 0.3 | 0.0-0.8 K/UL

    Erythrocyte Sedimentation Rate | 5 | 0-15 MM/HR
    Last edited by FunkOdyssey; February 20th, 2012 at 04:43 PM.
    "Also, can I rig some sort of enema out of household items?" -Tussman

    "I don't have the stamina for a 3-some, and I am a one-pump chump" -Ubiyca

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