The Marshall Protocol Study Site > ABOUT THE MARSHALL PROTOCOL > Marshall Protocol FAQs (Required Reading) > What do my lab tests mean?
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The Marshall Protocol Study Site > ABOUT THE MARSHALL PROTOCOL > Marshall Protocol FAQs (Required Reading) > What do my lab tests mean? |
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Foundation Staff . 
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What do my lab tests mean? Organs, like the liver and kidneys, that have Th1 inflammation may show diminished function in blood test results while that inflammation is being cleared during the MP. This is an unavoidable result of the immune system reaction but it can be controlled by slowing down immunopathology. See My immune system reaction is too strong. What should I do? The result of any blood test must be considered in its clinical context. "You can all expect your WBC and differential, the balance of neutrophils, monocyctes, % lymphocytes, NK cells, and etc, to change a lot as the Th1 bacteria are killed. It is best not to get fixated on any expectation of "bad figures" and "good figures". If Doc gets too concerned about the numbers then, IMO, you should back off your antibiotic dose and take the therapy a bit slower." Dr. Marshall. ............................... Following are simple explanations and brief summaries of some of the expected lab results due to Th1 inflammation both before and during treatment with the Marshall Protocol. Complete Blood Count (CBC) A complete blood count (CBC) measures the following: * Red blood cells (RBCs) These cells (also called erythrocytes or haematids) deliver oxygen throughout the body and make blood look red. A low RBC can indicate anemia Ref. range 4.20 - 5.70 * Hemoglobin (Hgb) Hemoglobin is a protein used by red blood cells to distribute oxygen to other tissues and cells in the body. Low levels indicate anemia. Normal results vary, but in general are: -Male: 13.8 to 17.2 gm/dL (140-174g/l) -Female: 12.1 to 15.1 gm/dL (123-157g/L) * Hematocrit (Hct) is the percent of your blood that is occupied by red blood cells and is an indicator of anemia. Ref. Range 38.5 - 49.0% * Mean corpuscular volume (MCV) measures the size of the red blood cells. Larger or smaller than normal red blood cells may indicate anemia. Ref. Range 80 - 97 Mean corpuscular volume is decreased in anemia of chronic disease. The CBC also includes information about the red blood cells that is calculated from the other measurements: * MCH (mean corpuscular hemoglobin) Measures the amount of hemoglobin in red blood cells. Both hemoglobin and hematocrit are used to calculate this number. Low levels indicate anemia. Ref. range 27.5 - 33.5 * MCHC (mean corpuscular hemoglobin concentration) neasures the amount of hemoglobin in red blood cells. Both HGB and HCT are used to calculate this number. Low level indicates anemia. Ref. range 32.0 - 36.0% *RDW Red cell distribution width is a calculation of the variation in the size of your RBCs. The RDW blood test reports whether all the red cells are about the same width, size, and shape. This helps further classify types of anemia. In some anemias, such as pernicious anemia or polycythemia vera, the amount of variation in RBC size (along with variation in shape) causes an increase in the RDW. Packed cell volume (PCV, haematocrit index) A low PCV indicates anemia. A high PCV usually indicates the presence of dehydration. Anemia of chronic disease is common is Th1 inflammatory diseases and may be diagnosed by specific tests. Anemia of chronic disease equals: -ferritin normal or high -iron low -normal to low soluble transferrin receptor (sTfR) -normal to low total iron-binding capacity (TIBC) For detailed info re essential differential tests and treatment, see My doctor says I’m anemic. What should I do? The red blood count and hemoglobin may go up if the body lacks oxygen, as in severe pulmonary disease. This is a compensatory mechanism and may indicate the need for oxygen supplementation. Hemoglobin A1c Hemoglobin A1c or glycosylated hemoglobin is a form of hemoglobin used to monitor blood sugar levels over a long period of time in diabetics. A high A1c represents poor glucose control. The International Diabetes Federation recommends the A1c be below 6.5%. Several factors may alter the accuracy of this test. It is not used to diagnose diabetes. White Blood cells White blood cells (WBCs) Ref. Range 4.5-11.0x10 3 /mm 3 or 4.5-11.0x10 9 These immune cells (leukocytes) form in the bone marrow to help fight infection. Elevated WBC, known as leukocytosis, may be due to inflammation, bacterial infection or steroid use. Low levels may result from treatment or disease. See WBC count The Differential (Diff) white count provides information on specific types of leukocytes (WBCs). Each differential always adds up to 100%. To make an accurate assessment, consider both relative and absolute values. For example a relative value of 70% neutrophils may seem within normal limits; however, if the total WBC is 20,000, the absolute value (70% x 20,000) would be an abnormally high count of 14,000. * Neutrophil Count (Ref. range between 38% and 80%) Absolute neutrophil count is 1.8 - 7 (x1-3uL) Neutrophils serve as the major defense of the body against acute bacterial and certain fungal infections. Neutrophils are attracted to sites of injury and infection. Neutrophils may increase in response to a number of conditions or diseases. The percentage is often increased during a bacterial infection. Inflammatory disorders, including autoimmune diseases such as rheumatoid arthritis, can cause an increase in the number and activity of neutrophils. Some drugs, such as corticosteroids, also lead to an increased number of neutrophils in the blood. Neutropenia is an abnormally low number of neutrophils in the blood. Neutropenia can develop if neutrophils are used up or destroyed in the bloodstream faster than the bone marrow can make new ones. With some bacterial infections, some allergic disorders, and some drug treatments, neutrophils are destroyed faster than they are produced. The bacteria living inside the phagocytes cause the phagocytes to emit the Th1 cytokines without the need for neutrophils, or indeed any other cells of the immune system, to be present. People with an enlarged spleen may have a low neutrophil count because the enlarged spleen traps and destroys neutrophils. A low number (neutropenia) increases risk of bacterial infection. *Eosinophils (Ref. range 1-6%) Absolute eosinophil count is 30 - 600) Eosinophils are associated with allergy and asthma. An increase in eosinophils, has many possible causes, including autoimmune diseases. A low eosinophil count may be caused by overproduction of certain steroids in the body. Hormone 1-25D is a steroid. *Monocytes (Ref. range 3-8%) mature into different types of macrophages at different anatomical locations. Absolute monocyte count is 40-900. Elevated monocytes (monocytosis) may be caused by chronic inflammation. * Basophils% (Ref. range 0.0 - 2.0) Absolute basophil count is 40-900. Basophils control inflammation and damage of tissues in the body. A low basophil count is not that uncommon, which is why the reference range goes down to 0 as normal. * Lymphocytes% Ref. range 15% and 40%. Absolute lymphocyte count is1000 - 3500. Lymphocytes includes T-cells, B-cells, and natural killer (NK) cells. Elevated absolute lymphocytes (lymphocytosis) occurs in response to acute infections. Graves' disease and Crohn's disease may result in an increase in the number of lymphocytes in the bloodstream. % Lymphocytes are often low in chronic inflammation because Th1 diseases are lymphopenic, which means a lack of T-cells. This is because the T-cells play only a minor role in Th1 disease. The bacteria living inside the phagocytes cause the phagocytes to emit the Th1 cytokines causing down-regulation of lymphocytes. The lymphocytes have little impact on chronic disease, except to the extent that they themselves are parasitized by the bacteria. This is the reason that Medicine has failed to understand these idiopathic diseases. They have focused on Lymphocytes and Natural Killer cells, whose behavior is secondary to the primary infectious process. In sarcoidosis this causes the lymphocytes to leave the area of highest inflammatory action (in the center of a granuloma) and migrate to the periphery. If you look at a Sarcoid granuloma under a microscope, it is 90% monocytes and immature macrophages. The down-regulation also reduces the number of lymphocytes being generated from stem cells. In less intense Th1 inflammation, that does not form granuloma, the down-regulation of the T-cells is observable primarily by the down-regulation of the lymphocytes. Lymphocytes are downstream, bystanders. Their level of expression is dependent on the nuclear receptors, which is dependent on the bugs. As you get rid of the bugs everything else comes back to normal. See My white count is low. What should I do? Lymphocyte Subset Panel This profile screens for immunodeficiencies, including percent and absolute cell counts for T-cell subsets (CD2, CD3), B-cells(CD19, HLA-DR), and NK-cells and CD4:CD8 ratio. "Until we see data to show otherwise or until we more precisely understand the role of infected Lymphocytes, CD expression is of little interest concerning the pathogenesis of Th1 inflammation." ..Trevor.. Natural Killer cells may be measured in a Lymphocyte subset panel. "NK cells have no role to play in the pathogenesis of the Th1 disease process. The opinion of anybody talking about NK cells in chronic disease should be immediately discounted. Apoptosis is delayed in Th1 infected cells, not accelerated. The NK theories tend to be just a variation on the old "autoimmunity" theories that delayed true progress in Medicine for so long...Believe me, you will not need any extra stimulus for your immune system when it becomes functional again. Indeed, damping down an over-exuberant response can be far more of a problem than stimulation." ..Trevor.. *Platelet count may be included in the CBC. Ref. range 140,000 - 390,000 (mm3) Platelets are cells produced by the bone marrow to help blood clot. Decreased platelet count is called thrombocytopenia. If Th1 inflammation involves the bone marrow, liver or spleen, immunopathology can cause a reduction in platelets. If this happens, MP meds should be adjusted to proceed to dampen the immune system reaction and proceed more slowly. A retest should reveal if immunopathology was the problem. A high platelet count is called thrombocythemia or thrombocytosis. Reactive or secondary thrombocytosis is caused by an underlying inflammatory disease process such as RA and sarcoidosis. "Treatment is aimed at the cause. If the treatment is successful, the platelet count usually returns to normal." *MPV - Mean Platelet Volume Ref. range 7.5 - 11.5 MPV Measures the average volume (size) of your platelets. Higher-than-normal MPV is associated with an increased risk of heart attacks and stroke. Erythrocyte Sedimentation (Sed) Rate (ESR) Sed rate is a test that can be done a couple of ways, but basically it involves letting a tube of blood sit upright and seeing how many cells precipitate to the bottom in a certain amount of time(sedimentation). The normal sedimentation rate (Westergren method) for males is 0-15 millimeters per hour, females is 0-20 millimeters per hour. The sedimentation rate can be slightly more elevated in the elderly. The Sed rate may be elevated in Th1 inflammatory disease but it may be normal. It is elevated in many other conditions, making it too general to be of much use in diagnosis. In sarcoidosis patients, the pathogens are so well secreted in the granuloma that the immune system does not touch them. There are no antibodies formed, and, since the pathogens delay apoptosis, the SED rate is almost always very low. When the immune system starts killing the pathogens, then the SED rate may shoot up, usually above the upper end of normal but a normal sed rate does not mean no immunopathology. Without before and after sed rates this can be hard to evaluate, as some folks have very low sed rates to begin with. Electrolytes Electrolytes are positively and negatively charged molecules, called ions, that are found within cells, between cells, in the bloodstream, and in other fluids throughout the body. Electrolytes with a positive charge include sodium, potassium, calcium, and magnesium; the negative ions are chloride, bicarbonate, and phosphate. The concentrations of these ions in the bloodstream remain fairly constant throughout the day in a healthy person. Changes in the concentration of one or more of these ions can occur during various acute and chronic disease states and can lead to serious consequences. Tests that measure the concentration of electrolytes are useful in the emergency room and to obtain clues for the diagnosis of specific diseases. Electrolyte tests are used for diagnosing dietary deficiencies, excess loss of nutrients due to urination, vomiting, and diarrhea, or abnormal shifts in the location of an electrolyte within the body. When an abnormal electrolyte value is detected, the physician may either act to immediately correct the imbalance directly (in the case of an emergency) or run further tests to determine the underlying cause of the abnormal electrolyte value. Electrolyte disturbances can occur with malfunctioning of the kidney (renal failure), infections that produce severe and continual diarrhea or vomiting, drugs that cause loss of electrolytes in the urine (diuretics), poisoning due to accidental consumption of electrolytes, or diseases involving hormones that regulate electrolyte concentrations. Potassium During the preparation of blood plasma or serum, health workers must take care not to break the red blood cells, especially when testing for serum potassium. Because the concentration of potassium within red blood cells is much higher than in the surrounding plasma or serum, broken cells would cause falsely elevated potassium levels. The normal levels of serum potassium are 3.5-5.0 mM. Note: Benicar has a potassium-sparing effect on the kidneys. If you have kidney disease, you may retain too much potassium which could be dangerous. You may not notice any symptoms so your doctor should do a blood test to check your potassium level periodically if you have this problem. Elevated serum potassium is called hyperkalemia. Treatment of hyperkalemia depends on individual circumstances. Kidney function tests may show inflammation which is to be expected with long-standing disease and immunopathology. This article, Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers: what to do if the serum creatinine and/or serum potassium concentration rises, explains that long-term benefits have to be the focus when using ARBs. See My potassium is elevated. What should I do? Sodium The normal level of serum sodium is in the range of 136-145 mM. High serum sodium levels (hypernatremia) occur at sodium concentrations over 145 mM, with severe hypernatremia over 152 mM. Hypernatremia is usually caused by diseases that cause excessive urination. In these cases, water is lost, but sodium is still retained in the body. The symptoms include confusion and can lead to convulsions and coma. Low serum sodium levels (hyponatremia) are below 130 mM, with severe hyponatremia at or below 125 mM. Hyponatremia often occurs with severe diarrhea, with losses of both water and sodium, but with sodium loss exceeding water loss. Hyponatremia provokes clinical problems only if serum sodium falls below 125 mM, especially if this has occurred rapidly. The symptoms can be as mild as tiredness but may lead to convulsions and coma. Decreased sodium levels (hyponatremia) need careful evaluation to determine what, if any, treatment is needed. See My sodium is low. What should I do? Calcium The normal concentration of total serum calcium (bound calcium plus free calcium) is in the range of 8.8-10.4 mg/dL. About 40% of the total calcium in the plasma is loosely bound to proteins; this calcium is referred to as bound calcium. The normal range of free calcium is 4.8-5.2 mg/dL. High levels of calcium ions (hypercalcemia) occur at free calcium ion concentrations over 5.2 mg/dL or total serum calcium above 10.4 mg/dL. Hypercalcemia usually occurs when the body dissolves bone at an abnormally fast rate, increasing both serum calcium and serum phosphate. Sudden hypercalcemia can cause vomiting and coma, while prolonged and moderate hypercalcemia results in the deposit of calcium phosphate crystals in the kidneys and eye. Hypocalcemia occurs when serum free calcium ions fall below 4.4 mg/dL, or when total serum calcium falls below 8.8 mg/dL. Hypocalcemia can result from (among other reasons) hypoparathyroidism (low parathyroid hormone), from failure to produce 1,25-dihydroxyvitamin D, from low levels of plasma magnesium, and from phosphate poisoning. Most sarcoidosis patients have normal blood levels of calcium, although some do develop hypercalcemia and/or hypercalciuria. However, it has been known for more than 25 years that sarcoidosis patients can have elevated levels of Hormone D (1,25-) even when they have normal calcium levels, and high levels of this hormone make a person feel very ill. It used to be thought that hypercalcemia was the only result of excess Vitamin D; we now know it is far more complex than that. Many normocalcemic sarcoidosis patients have suffered from kidney stones and calcium deposition into the soft tissue as a result of excess levels of 1,25D in their tissue. See Don’t I need to take a calcium supplement? and My 25-D is low. Should I be concerned about osteoporosis? Chloride The normal concentration range of chloride is 350-375 mg/dL or 98-106 mM. Serum chloride levels sometimes increase to abnormal levels as an undesirable side effect of medical treatment with sodium chloride or ammonium chloride. Renal failure may increase serum chloride. Low serum chloride may be caused by vomiting. Anion gap The anion gap is used to aid in the differential diagnosis of metabolic acidosis. See this reference for details. Carbon dioxide (CO2) Carbon dioxide testing may be ordered, usually as part of an electrolyte panel. When CO2 levels are higher or lower than normal, it suggests that your body is having trouble maintaining its acid-base balance or that you have upset your electrolyte balance, perhaps by losing or retaining fluid. Both of these imbalances may be due to a wide range of dysfunctions. Phosphorus The normal level of phosphate, as expressed as the concentration of phosphorus, is 2.0-4.3 mg/dL. Serum phosphorus levels are controlled by the parathyroid hormone (PTH) and 1,25-dihydroxyvitamin D. Hyperphosphatemia occurs at serum phosphate levels above 5 mg/dL. It can result from the failure of the kidneys to excrete phosphate into the urine, causing phosphate to accumulate in the bloodstream. Hyperphosphatemia can also be caused by the impaired action of parathyroid hormone and by phosphate poisoning. Hypophosphatemia occurs if serum phosphorus falls to 2.0 mg/dL or lower. It often results from a shift of inorganic phosphate from the bloodstream to various organs and tissues. This shift can be caused by a rise in pH (alkalization) of the bloodstream, which can occur during hyperventilation, a reaction in various disease states. Tests for abnormalities in phosphate metabolism also involve tests for serum calcium. Bicarbonate The normal concentration of bicarbonate is about 27 mM. Tests for bicarbonate are generally accompanied by tests for blood pH and possibly tests for kidney malfunction, abnormal hormone function, or gastrointestinal disorders. Magnesium The normal concentration of serum magnesium is in the range of 2.0-3.0 mg/dL. Hypermagnesemia occurs at serum magnesium levels over 25 mM (60 mg/dL). Hypermagnesemia is rare but can occur with the excessive consumption of magnesium salts. Hypomagnesemia occurs when serum magnesium levels fall below 0.8 mM, and can result from poor nutrition. PTH (parathormone) Elevated 1,25-D may lead to a depressed PTH. This hormone chart shows PTH cascading from 1,25-D. Serum phosphorus levels are controlled by PTH and 1,25-dihydroxy vitamin D. This transcript of the vitamin D presentation at our LAX conference, includes information information on hyperpararthyroidism. Blood Urea Nitrogen (BUN) BUN is often high because nitric oxide is one of the components given off by dying bacteria and apoptosing white cells, as nitric oxide is one of the byproducts of the endotoxin inflammation. It is reasonable for BUN to be elevated, as the bacterial endotoxins cause Nitic Oxide (NO) to be generated in the inflamed tissues. It will almost certainly go higher once the antibiotics start to kill off the bacteria. ARBs (Benicar) are renoprotective but the intracellular bacteria have to be killed off before creatinine or BUN improve. All infections and antibiotic courses for them can cause elevations in bun and creatinine. Urea is a by-product of protein metabolism. This waste product is formed in the liver, then filtered from the blood and excreted in the urine by the kidneys. The BUN test measures the amount of nitrogen contained in the urea. High BUN levels can indicate kidney dysfunction, but because blood urea nitrogen is also affected by protein intake and liver function, the test is usually done in conjunction with a blood creatinine, a more specific indicator of kidney function. Creatinine, 24 hour creatinine clearance, estimated glomerular filtration rate (eGFR) These tests assess kidney function. See My kidney function tests are worse since I started the MP. What should I do? CRP (C-reactive protein) CRP is generated by the body to help it fight bacterial infection. It being high in Th1 disease and atherosclerosis is really no surprise but folks with extensive inflammation may have a normal CRP. This abstract provides an accurate analysis of CRP and inflammation. Elevated C reactive protein is an inflammation marker, specific for infection and indicative of vascular inflammation. In sarcoidosis patients, the CRP is part of the body's reaction to infection, but it would not be generated until the body can recognize that it is dealing with infective pathogens. This often doesn't happen until you start killing the pathogens with the MP, and the DNA fragments start to enter the bloodstream. "CRP is one of those tests that medicine doesn't really understand. The body produces CRP in reaction to a bacterial pathogen. Doc thinks it is a sign of inflammation, it is actually a reaction to inflammation and it can be elevated by immunopathology. A normal CRP when on the MP does not mean bacteria are not being killed. C-Reactive Protein is upregulated by inflammatory cytokines, and reportedly enhanced by dexamethasone. Nobody really knows its function, but it is associated with Th1 inflammatory disease. Its being elevated is therefore not unusual in the MP, and I consider it a sign of activity." Dr. Marshall Normal CRP values vary from lab to lab. Generally, there is no CRP detectable in the blood. A positive test means you have inflammation in the body. The CRP gene is transcribed at the same time as one family of anti-microbials. There is some conjecture whether CRP itself is an anti-microbial. It's a good sign if your body is making it, because it means the CRP gene is being transcribed correctly. hs-CRP Your doctor may also use a highly sensitive test called hs-CRP to determine your risk of heart disease. According to the American Heart Association: -You are at low risk of developing cardiovascular disease if your hs-CRP level is lower than 1.0mg/L. -You are at average risk of developing cardiovascular disease if your levels are between 1.0 and 3.0 mg/L. -You are at high risk for cardiovascular disease if your hs-CRP level is higher than 3.0 mg/L. Angiotensin Converting Enzyme (ACE) ACE is a marker of the th1 inflammatory process. It is an intermediate biochemical and has no direct action in the inflammatory cycle other than to cause the release of quantities of Angiotensin II. That is probabbly why it is relatively insignificant in some patients; it depends on the Renin Angiotensin System activity level. ACE is an inexpensive test but it is often nonconclusive. Elevated ACE indicates the same as the elevated 1,25-D and therefore adds nothing to the interpretation, except an increased level of confidence. The more your ACE is initially elevated, the more ACE is being generated in your inflammation, and the higher the ACE wil go when the Angiotensin II receptors are blocked. We have had one report of ACE greater than 400. The serum ACE often rises to quite high levels when you have an Angiotensin Receptor Blockade in place with Benicar. This is because the inflamed tissue can't get any Angiotensin II binding at its receptors, so it puts out extra ACE to try and convert more Renin/A-1 into Angiotensin II (the Angiotensin-II level rises too). But even though all that Angiotensin II is manufactured, there are no receptors left for it to bind to, so it can do no harm. See Why has my ACE gone up since I started the MP? and Sarcoidosis Angiotensin II A-II elevates because the inflammation keeps pumping out ACE trying to get A-II to bind to the receptors. Because the receptors are blocked the inflammation never gets enough A-II even though it keeps trying to make more Albumin Albumin is low in many different diseases and disorders, including liver disorders, nephrotic syndrome and inflammation. Triglycerides Elevated Triglycerides indicates (most probably) liver inflammation which will drop with resolution of that inflammation by treatment with the MP. Analysis of the bacterial 'kete genome' which Dr. Marshall presented at the "30th Anniversy of Lyme" conference shows that these pathogens use an anaerobic glucose metabolism to produce energy, and that triglycerides are the waste product of this bacterial metabolism. Triglycerides are normally elevated in sarcoidosis patients, but they fall during the MP. Corticosteroids often cause triglycerides to jump when patients relapse while coming off the steroids. See My cholesterol and/or triglycerides are very high. Will the MP help? Homocysteine Elevated homocysteine levels have been implicated in atherosclerosis. Inflammation is thought to also contribute to atherosclerosis. Creatinine phosphokinase (CPK) CPK is a muscle enzyme that is found inside muscle cells. Normal levels of CPK in the blood range from about 35 to 190 units per liter. If the muscle cells are damaged from any cause the CPK enzyme will be released into the blood and the CPK test becomes elevated. There are many causes of CPK elevation. During a heart attack, the heart muscle is damaged and a high CPK level is often used to diagnosis an acute heart attack in the emergency room. Trauma to the muscle such as heavy exercise or accidents can elevate CPK. Drugs such as the statin colesterol medications can damage muscle and elevate CPK. High CPK may also occur due in chronic inflammatory conditions such as mixed connective tissue disease, dermatomyositis, polymyositis and muscular dystrophies. AST is found in high concentration in heart muscle, liver cells, and skeletal muscle cells. It is also found, to a lesser degree, in other tissues. Although elevated serum AST is not specific for liver disease, it is used primarily to diagnose and monitor the course of liver disease (in combination with other enzymes such as ALT, ALP, and bilirubin). The normal range is 10 to 34 IU/L. Anti-ccp or citrulline antibody is a blood test used to help in diagnosing rheumatoid arthritis (RA). Citrulline antibody is an immune protein (antibody) that binds to a non-standard amino acid (citrulline) that is formed by removing amino groups from the natural amino acid, arginine. Citrulline antibodies are measured with a blood test that is analyzed in laboratories. Last edited on Wed Aug 27th, 2008 10:00 by Foundation Staff |
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Antinuclear Antibody tests (filelink) I regard the ANA tests as largely irrelevant. They are not specific enough to be useful as Th1 disease markers. Indeed, ANA disappear as the infection progresses. Many of the sarcies have had ANA disappear over the years, to be replaced by biopsy-verifiable granuloma. Our paper at the International Autoimmunity Conference in Budapest basically argued that 'autoimmunity' does not exist. I argued that the body is reacting to pathogens, not to itself. There were many there who agreed with me. Which does explain, of course, why folks don't immediately collapse in a heap of antibodies when they are diagnosed with 'autoimmune disease'. I believe that it stands to reason that if the body were actually attacking itself, it would do a better job of it, and the patient would die pretty quickly. Antibodies are present in many of the diseases the MP addresses (eg RA, Lupus) and I never considered that they would be absent, once the SED rate rises as the bacteria start being killed. Antibodies are not the cause of the disease state, they are a by-product of the key inflammatory process. Hence the concept of 'autoimmunity' is meaningless. ..Trevor.. Marshall TG: VDR Nuclear Receptor Competence is the Key to Recovery from Chronic Inflammatory and Autoimmune Disease. Abstract presentation, Days of molecular medicine, 2006. Copy available from URL http://autoimmunityresearch.org/karolinska-handout.pdf Antinuclear ab’s Serum titre: < 1:40 ANAs are associated with a variety of conditions other than SLE including rheumatoid diseases, chronic active hepatitis, fibrosing alveolitis, viral infections and drug ingestion. Patterns of ANA are said to be significant: Nucleolar associated with scleroderma, centromere with CREST syndrome, and speckled pattern with MCTD, Sjögrens, SLE and Polymyositis. Rim or homogeneous has been associated with SLE but there is a considerable amount of pattern overlap. See also Lupus In 'Overlap' With Other Connective Tissue Diseases Last edited on Thu Jan 31st, 2008 04:24 by Foundation Staff |
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Using lab tests to track immunopathology (herxlabfilelink) Dr. Greg Blaney wrote: What ever the cause, transient decrease in Hgb and hematocrit are common in the early phases of the MP. My use of lab tests is to help determine pace of therapy especially if degree of Herx reaction is difficult for patient to interpret. With chronically ill patients, it is common to disassociate from one's feelings and therefore can be difficult to determine the sometimes subtle shifts associated with Herx reactions. As the old saying goes "I've been down so long, it is beginning to look like up." |
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