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    Complementary and Alternative Medical Lab Testing Part 14: Immunology
    Complementary and Alternative Medical Lab Testing Part 14: Immunology
    Complementary and Alternative Medical Lab Testing Part 14: Immunology
    Ebook201 pages2 hours

    Complementary and Alternative Medical Lab Testing Part 14: Immunology

    By Ronald Steriti

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    About this ebook

    Complementary and Alternative Medical Lab Testing (CAM Labs) contains summaries of the published research on lab tests, primarily from PubMed trials on humans. Each chapter (disease) begins with a brief summary of conventional lab tests, followed by additional lab tests, including diabetes, insulin resistance, metabolic syndrome, inflammation, etc. There are sections on endocrine hormones (thyroid, adrenal, sex steroids) and environmental medicine (toxic heavy metals). The nutritional assessments section includes minerals, vitamins and amino acids.

    CAM Labs 14 – Immunology

    1. Autoimmune Disease
    2. Chronic Fatigue Syndrome
    3. Common Cold
    4. Fever
    5. Gangrene
    6. Human Immunodeficiency Virus (HIV)
    7. Systemic Lupus Erythematosus (SLE)
    8. Stiff-Person Syndrome

    LanguageEnglish
    PublisherRonald Steriti
    Release dateJun 4, 2016
    ISBN9781311935564
    Complementary and Alternative Medical Lab Testing Part 14: Immunology
    Author

    Ronald Steriti

    Dr. Ronald Steriti is a graduate of Southwest College of Naturopathic Medicine and currently is researcher for Jonathan V. Wright at the Tahoma Clinic.

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      Book preview

      Complementary and Alternative Medical Lab Testing Part 14 - Ronald Steriti

      Complementary and Alternative

      Medical Lab Testing

      Part 14: Immunology

      By Ronald Steriti, ND, PhD

      ©

      Complementary and Alternative Medical Lab Testing Clinician’s Guide Part 14: Immunology

      By Ronald Steriti, ND, PhD

      Copyright © 2016

      All rights reserved. No part of this book may be reproduced in any form or by any means, including photocopying, including in a web site, or stored in a retrieval system, or transmitted in any form by any means, without expressed, written permission of the copyright owner.

      The contents of this document are the sole property of the author.

      Disclaimer

      This book has not been evaluated by the FDA and is not intended to diagnose, treat, cure or prevent any disease.

      The information contained in this book is for educational purposes only, and should not be construed as medical advice or instruction. No action should be taken based solely on the contents of this book. Readers should consult appropriate health officials.

      While extensive efforts have been made to ensure the accuracy of the information contained, the possibility of errors, omissions, and misinterpretations cannot be ruled out. The reader is advised to consult the original references for verification and clarification.

      Foreward

      This book is a summary the published research on lab tests, primarily from PubMed. The studies are limited to those with trials on humans. As such, some labs may be excluded due to the lack of published research. That is simply a reflection of the current state of research - much more work is needed!

      Although this book may be useful for differential diagnosis, lab tests are can also be used to identify inderlying causes and associated conditions.

      The sections on conventional lab tests are purposefully brief. These tests are typically used to confirm a diagnosis. There are other more comprehensive sources of information on conventional medical lab testing.

      Table of Contents

      1. Autoimmune Disease

      2. Chronic Fatigue Syndrome

      3. Common Cold

      4. Fever

      5. Gangrene

      6. Human Immunodeficiency Virus (HIV)

      7. Systemic Lupus Erythematosus (SLE)

      8. Stiff-Person Syndrome

      Chapter 1. Autoimmune Disease

      Conventional Lab Tests

      CBC with differential, comprehensive metabolic panel (Castro and Gourley, 2010)

      Inflammatory markers: ESR, CRP

      Rheumatoid Arthritis Factor (RA Factor)

      Antinuclear Antibodies (ANA): Lupus (SLE)

      Autoantibody testing

      Additional Lab Tests

      TH1/TH2 Ratio

      This review reconsiders how the Th1/Th2 paradigm can be applied to Th1-mediated autoimmune disease. Although there is evidence that autoimmune diseases such as multiple sclerosis, type 1 insulin-dependent diabetes mellitus, and posterior uveitis are Th1 mediated and that in some cases reduction of the Th1 response or a Th2 type shift may alleviate disease, many apparent exceptions are now well documented. These exceptions center around the contradictory actions of the Th1 cytokine IFN-gamma and the evidence that Th2 lymphocytes can also cause disease. Recent information on the regulation of Th1 and Th2 lymphocytes in terms of the innate immune response and by other T cells helps to clarify the reasons for some of these discrepancies and enables the Th1/Th2 concept to be accepted as an integral part of the complex interactions occurring as autoimmune disease develops. (Crane and Forrester, 2005)

      Many autoimmune diseases are caused by autopathogenic Th1 cells. Because in vitro Th1 and Th2 cells cross-regulate each other, it is likely that the induction of self-antigen-specific Th2 cells can prevent autoimmune disease. In the past year, investigators have further defined the role of Th1 and Th2 cytokines in the induction and regulation of autoimmunity. Furthermore, the role of MHC-antigen-T-cell avidity (strength of signal) in inducing such protective immune responses has been elucidated. (Nicholson and Kuchroo, 1996)

      CD4+ T cells play a key role in regulating immune system function. When these regulatory processes go awry, organ-specific autoimmune diseases may develop. Here, Roland Liblau, Steven Singer and Hugh McDevitt explore the thesis that a particular subset of CD4+ T cells, namely T helper 1 (Th1) cells, contributes to the pathogenesis of organ-specific autoimmune diseases, while another subset, Th2 cells, prevents them. (Liblau et al., 1995)

      CD4/CD8 (Treg) Ratio

      A study assessed Helper T-cell involvement and possibilities to quantify the cell-based immune response in systemic autoimmune diseases (SAID) in 14 systemic lupus erythematosus (SLE) and 7 rheumatoid arthritis (RA) patients. The goals of investigation were T-CD4+/T-CD8+ ratio, regulatory T cells (Treg) status and TH1/TH2 serum cytokine profiles (IFN-gamma and IL-2, respectively IL-4 and IL-6). SLE group proved significant decreased average Treg value as compared to RA group and controls and showed significant low Treg incidence (86% patients). The distribution of high T-CD4+/T-CD8+ ratio registered no significant distinction among LES and RA groups. SAID patients presented low serum IFN-gamma (86% RA, 60% SLE), high IL-2 (57% RA) and high IL-6 (53% LES), but no significant IL-4 modification. We conclude that Treg percentage remains the only cellular criterion for SAID immune evaluation. In the same time, different secretion mechanisms seem to be involved in SAID, i.e. TH2 in SLE and TH1 in RA. (Ursaciuc et al., 2010)

      Digestive Assessments

      The Digestive System in Systemic Autoimmune Diseases represents the state-of-the-art in the field of digestive disorders in the most common systemic autoimmune diseases. The volume consists of an introductory chapter on imaging techniques in digestive diseases, followed by eight chapters on digestive manifestations in specific systemic autoimmune diseases. The final five chapters deal with digestive diseases with an autoimmune pathogenesis and systemic manifestations. International in scope, the table of contents reads like a Who's who in clinical research on systemic autoimmune diseases. More than 20 contributors from the European Union, the United States, Mexico and South Africa share their knowledge in this detailed volume. (Asherson, 2011)

      In an autoimmune disease, the immune system attacks and harms the body's own tissues. The systemic autoimmune diseases include collagen vascular diseases, the systemic vasculitides, Wegener granulomatosis, and Churg-Strauss syndrome. These disorders can involve any part of the gastrointestinal tract, hepatobiliary system and pancreas. They can cause a variety of gastrointestinal manifestations that are influenced by the pathophysiologic characteristics of the underlying disease process. There is a wide variation of gastrointestinal manifestations from these autoimmune disorders including, but not limited to: oral ulcers, dysphagia, gastroesophageal reflux disease, abdominal pain, constipation, diarrhea, fecal incontinence, pseudo-obstruction, perforation and gastrointestinal bleeding. Clinical workup should be initiated by the patient's subjective complaints. This review analyzes the effects of autoimmune diseases on the gastrointestinal tract. (Cojocaru et al., 2011)

      Celiac Disease

      Celiac disease (CD) is frequently accompanied by a variety of extradigestive manifestations, thus making it a systemic disease rather than a disease limited to the gastrointestinal tract. This is primarily explained by the fact that CD belongs to the group of autoimmune diseases. The only one with a known etiology is related to a permanent intolerance to gluten. Remarkable breakthroughs have been achieved in the last decades, due to a greater interest in the diagnosis of atypical and asymptomatic patients, which are more frequent in adults. The known presence of several associated diseases provides guidance in the search of oligosymptomatic cases as well as studies performed in relatives of patients with CD. The causes for the onset and manifestation of associated diseases are diverse; some share a similar genetic base, like type 1 diabetes mellitus (T1D); others share pathogenic mechanisms, and yet, others are of unknown nature. General practitioners and other specialists must remember that CD may debut with extraintestinal manifestations, and associated illnesses may appear both at the time of diagnosis and throughout the evolution of the disease. The implementation of a gluten-free diet (GFD) improves the overall clinical course and influences the evolution of the associated diseases. In some cases, such as iron deficiency anemia, the GFD contributes to its disappearance. In other disorders, like T1D, this allows a better control of the disease. In several other complications and/or associated diseases, an adequate adherence to a GFD may slow down their evolution, especially if implemented during an early stage. (Lauret and Rodrigo, 2013)

      Autoimmune diseases are characterized by tissue damage and loss of function due to an immune response that is directed against specific organs. This review is focused on celiac disease (CD), an autoimmune enteropathy, and type 1 diabetes (T1D), a hyperglycosaemia caused by a destructive autoimmune process targeting the insulin-producing pancreatic islet cells. Even if environmental factors and genetic susceptibility are clearly involved in the pathogenesis of autoimmunity, for most autoimmune disorders there is no or little knowledge about the causing agent or genetic makeup underlying the disease. In this respect, CD represents a unique autoimmune disorder because a close genetic association with HLA-DQ2 or HLA-DQ8 haplotypes and, more importantly, the environmental trigger (the gliadin fraction of gluten-containing grains wheat, barley, and rye) are known. Conversely, the trigger for autoimmune destruction of pancreatic ss cells in T1D is unclear. Interestingly, recent data suggest that gliadin is also involved in the pathogenesis of T1D. There is growing evidence that increased intestinal permeability plays a pathogenic role in various autoimmune diseases including CD and T1D. Therefore, we hypothesize that besides genetic and environmental factors, loss of intestinal barrier function is necessary to develop autoimmunity. In this review, each of these components will be briefly reviewed. (Visser et al., 2009)

      The clinical spectrum of celiac disease continues to evolve. What was once thought to be a rare disorder affecting young children is now recognized to be very common with a range of symptoms from asymptomatic disease to severely affected persons. Screening for celiac disease has become relatively easily with reliable antibodies against self-antigens (TG) and modified environmental antigens (DGP). Diagnosis is confirmed by small intestinal biopsy with characteristic changes graded by the Marsh score. Elimination of gluten from the diet has been the standard of care for the last half century. Patients often have difficulty adhering to a gluten-free diet, and the failure of symptoms, antibody levels, or pathologic changes to improve after initiating the diet may be largely due to this difficulty. The genetic risk for celiac disease is largely related to HLA genotypes, with over 90% of subjects with celiac disease positive for DQ2 and the remainder positive for DQ8. The HLA association with celiac disease is largely accountable for its link to other autoimmune diseases, including type 1 diabetes and autoimmune thyroid disease, and the majority of risk for celiac disease in these populations is related to HLA genotype. Celiac disease also carries an increased risk for type 1 diabetes and autoimmune thyroid disease. Genetic syndromes such as Turner and Down syndromes are associated with an increased risk for celiac disease. Practitioners can identify groups of subjects at high risk for celiac disease and perform screening with celiac disease-related antibodies. (Barker and Liu, 2008)

      Celiac disease is an immune-mediated disorder clinically characterized by a multitude of symptoms and complications. The comorbidity between celiac disease and other autoimmune disorders has been clearly established. Two main theories have been postulated to explain this comorbidity: (1) linkage disequilibrium between the genes responsible for celiac disease and those responsible for the coexpressed autoimmune diseases or (2) untreated celiac disease leading to the onset of other autoimmune diseases. This article reviews the current literature supporting either theory and places the current knowledge in the field within the context of the most recent data on the pathogenesis of celiac disease. The current literature did not clearly establish which of the two theories explain the comorbidity between celiac disease and other autoimmune disorders. There is, however, growing evidence that the loss of the intestinal barrier function typical of celiac disease could be responsible of the onset of other autoimmune disease. This concept implies that the autoimmune response can be theoretically stopped and perhaps reversed if the interplay between autoimmune predisposing genes and trigger(s) is prevented or eliminated by a prompt diagnosis and treatment. (Fasano, 2006)

      Intestinal Permeability

      Autoimmune diseases are characterized by tissue damage and loss of function due to an immune response that is directed against specific organs. This review is focused on the role of impaired intestinal barrier function on autoimmune pathogenesis. Together with the gut-associated lymphoid tissue and the neuroendocrine network, the intestinal epithelial barrier, with its intercellular tight junctions, controls the equilibrium between tolerance and immunity to non-self antigens. Zonulin is the only physiologic modulator of intercellular tight junctions described so far that is involved in trafficking of macromolecules and, therefore, in tolerance/immune response balance. When the zonulin pathway is deregulated in genetically susceptible individuals, autoimmune disorders can occur. This new paradigm subverts traditional theories underlying the development of these diseases and suggests that these processes can be arrested if the interplay between genes and environmental triggers is prevented by re-establishing the zonulin-dependent intestinal barrier function. Both animal models and recent clinical evidence support this new paradigm and provide the rationale for innovative approaches to prevent and treat autoimmune diseases. (Fasano, 2012)

      The primary functions of the gastrointestinal tract have traditionally been perceived to be limited to the digestion and absorption of nutrients and electrolytes, and to water homeostasis. A more attentive analysis of the anatomic and functional arrangement of the gastrointestinal tract, however, suggests that another extremely important function of this organ is its ability to regulate the trafficking of macromolecules between the environment and the host through a barrier mechanism. Together with the gut-associated lymphoid tissue and the neuroendocrine network, the intestinal epithelial barrier, with its intercellular tight junctions, controls the equilibrium between tolerance and immunity to nonself-antigens. When the finely tuned trafficking of macromolecules is dysregulated in genetically susceptible individuals, both intestinal and extraintestinal autoimmune disorders can occur. This new paradigm subverts traditional theories underlying the development of autoimmunity, which

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