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home:publications:benediktsson_autoimmunity_2010 [06.14.2010] – created paulalberthome:publications:benediktsson_autoimmunity_2010 [07.04.2022] (current) – external edit 127.0.0.1
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-====== Presentation Olmesartan medoxomil & treatment of autoimmune disease======+====== Poster Bipolar disorders and autoimmune disease share a similar etiology======
  
  
 **Type:** Conference presentation\\ **Type:** Conference presentation\\
-**Presenter:**  Dr. Greg Blaney\\+**Presenter:**  Chris Benediktsson, Janet Raty, Trevor Marshall, PhD\\
 **Conference:**  7th International Congress on Autoimmunity\\ **Conference:**  7th International Congress on Autoimmunity\\
 **Location:** Ljubljana, Slovenia\\ **Location:** Ljubljana, Slovenia\\
 **Date:**  May 2010\\ **Date:**  May 2010\\
 +**Additional Content:**  [[https://mpkb.org/_media/home/publications/ica2010_benediktsson.pdf|PDF of poster]]
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 ===== Abstract ===== ===== Abstract =====
  
  
-Recent research highlights the importance of VDR integrity and responsiveness on innate immune functionVDR knock out mice show both an increased frequency and severity of autoimmune disease and reduced ability to cope with bacterial infection and persistence. We have found that autoimmune disease in humans is associated with elevated levels of 1,25 OH Vitamin D indicating VDR resistance. Co-morbid conditions such as colitis, sinusitisvasculitis and recurrent infections, reflecting intracellular or biofilm bacterial persistence, have been found by ourselves and others in autoimmune diseasesIn silico modeling and clinical observation show that olmesartan medoxomil, an angiotensin receptor blocker, acts as a VDR agonist. Selected patients with significant and advanced autoimmune disease, including inflammatory arthropathy, autoimmune thyroiditis, ankylosing spondylitis, sarcoidosis,  were treated with olmesartan at dosing levels sufficient to activate the VDR along with bacteriostatic antibiotics at sub-inhibitory dose levels. During treatment, temporary exacerbation of symptoms and worsening of clinical markers were seen reflecting immune response. Physical manifestations included inflammation and swelling of jointsdermatitiscentral and peripheral nervous system dysfunctionfever and fatigueLaboratory changes included reduction in red and white blood cells, platelets; elevation in serum potassium, creatinine; and reduction in eGFR. After sufficient time of treatment, positive therapeutic responses that manifested included reversal of late-stage autoimmune conditions including carotid artery calcification, inflammatory joint disease, neuropathy, and osteoporosis. In addition normalization of clinical markers such as CRP,SED rate, kidney function were observed +Since the mid 1800s we have known that some infectious agents can cause dramatic personality changes, for example in diseases such as syphilis, rabies, toxoplasmosis and neurologic lyme diseaseTreatment was dominated for many years by psychological theorizing, much of it Freudian; biological approaches were essentially limited to genetics. Recently both persistent viruses and antibodies to pathogens have been detected in samples from patients with bipolar disease. “Autoantibodies” to brain proteins, nuclear material, and brain lipids, among others, have been detected in both schizophrenic and bipolar populations. Higher levels of interleukin (IL1, IL 2, IL RA)CD 4CD 8 and Th1 and Th2 cytokines have been found in bipolar patients before, during and after medical treatment, strongly suggesting that bipolar disorders and autoimmune disease share a similar etiology. 
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 +We have been conducting an observational study since 2002 of a VDR agonist along with pulsed low dose antibiotics for treatment of chronic inflammatory diseases. Intriguinglymany of the study subjects had initially reported comorbid symptoms of cognitive impairment, including brain fog and major depressionconsistent with advanced chronic disease. Four patientswho had noted prior diagnoses of bipolar disorder 1 and IIreported significant improvement in bipolar symptoms after therapyThe improvement in mental function was concurrent with improvements in the symptoms of the comorbid autoimmune disease. This is consistent with a shared etiology and strongly suggestive of the involvement of bacterial pathogens. 
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 +{{tag>posters Chris_Benediktsson Janet_Raty Trevor_Marshall_PhD 2010}}
  
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