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home:publications:benediktsson_autoimmunity_2010 [06.14.2010]
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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:​** ​ [[http://​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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