16.04.2016, 19:10
Cimetidine as a Novel Adjunctive Treatment for Early Stage Lyme Disease
D.C. Justin Shemenski, April 09, 2016
http://dx.doi.org/10.1016/j.mehy.2016.03.015
In dieser Studie wird diskutiert, ob das H2-Antihistaminikum Cimetidin, das in der Regel zur Verminderung der Magensaftproduktion bei Magen- oder Zwölffingerdarmgeschwüren eingesetzt wird in der frühen Phase einer Borreliose hilft. Die Idee ist, dass eine Therapie mit Cimetidin angeblich immunmodulierend wirkt.
- Die TH1-assozierten Zytokine IL-12, TNF-α, and IFN-γ werden erhöht und
- das TH2-assozierten Zytokin IL-10 gesenkt.
Shemenski schlägt eine Cimentidin-Therapie vor, wenn ich es aus dem Abstract richtig verstehe begleitend zur Antibiotikumstherapie.
Der Volltext ist leider hinter der "pay wall".
"ABSTRACT: Lyme disease, caused by the spirochete Borrelia burgdorferi (Bb), is the most common vector-borne illness in the United States. It is a complex disease which may affect the skin, joints, heart, eyes, and central nervous system. Prompt diagnosis and treatment is curative in most instances. However, a significant percentage of patients experience ongoing symptoms after treatment. Currently, there is much controversy regarding the diagnosis, pathophysiology, and treatment of Lyme disease. Pathogen persistence despite treatment lies at the heart of this debate.
Many believe that the ongoing symptoms are due to factors such as autoimmunity or permanent damage that is incurred during the active infection. However, there is an emerging school of thought that states that ongoing symptoms are due to a persistent infection that is able to survive both the immune response and antibiotic therapy. Numerous studies have shown that Bb can indeed persist within the host despite treatment and several mechanisms have been proposed to explain Bb’s persistence capabilities. These include: polymorphism, antigenic variance, biofilm formation, persister cells, and immunomodulation.
There is evidence that Bb is able to alter cytokine profiles within the host which may allow the organism to survive the immune response. This immunomodulation follows a pattern of T-helper 1 (TH1) suppression in favor of T-helper 2 (TH2) processes. In contrast, it has been shown that the optimal immune response to Bb infection involves an early, robust TH1 response and a later conversion to TH2 dominance once the infection is controlled or cleared. It has been proposed that a reconstitution of proper immune-competency in the infected host may improve clinical outcomes in Lyme disease.
Cimetidine (CIM) is an over-the-counter histamine-2 (H2) antagonist that is primarily used to lower acid secretions in the stomach. T-regulatory (Treg) cells also possess the H2 receptor, which has spurred interest in CIM as a potential immunomodulator. CIM therapy has been shown to increase levels of the TH1 associated cytokines IL-12, TNF-α, and IFN-γ while decreasing levels of the TH2 associated cytokine IL-10. The author proposes a novel theory that CIM therapy during early Bb infection may promote a more appropriate immune response and increase the utility of antibiotic therapy during early stage Lyme disease, thus improving clinical outcomes of the disease."
D.C. Justin Shemenski, April 09, 2016
http://dx.doi.org/10.1016/j.mehy.2016.03.015
In dieser Studie wird diskutiert, ob das H2-Antihistaminikum Cimetidin, das in der Regel zur Verminderung der Magensaftproduktion bei Magen- oder Zwölffingerdarmgeschwüren eingesetzt wird in der frühen Phase einer Borreliose hilft. Die Idee ist, dass eine Therapie mit Cimetidin angeblich immunmodulierend wirkt.
- Die TH1-assozierten Zytokine IL-12, TNF-α, and IFN-γ werden erhöht und
- das TH2-assozierten Zytokin IL-10 gesenkt.
Shemenski schlägt eine Cimentidin-Therapie vor, wenn ich es aus dem Abstract richtig verstehe begleitend zur Antibiotikumstherapie.
Der Volltext ist leider hinter der "pay wall".
"ABSTRACT: Lyme disease, caused by the spirochete Borrelia burgdorferi (Bb), is the most common vector-borne illness in the United States. It is a complex disease which may affect the skin, joints, heart, eyes, and central nervous system. Prompt diagnosis and treatment is curative in most instances. However, a significant percentage of patients experience ongoing symptoms after treatment. Currently, there is much controversy regarding the diagnosis, pathophysiology, and treatment of Lyme disease. Pathogen persistence despite treatment lies at the heart of this debate.
Many believe that the ongoing symptoms are due to factors such as autoimmunity or permanent damage that is incurred during the active infection. However, there is an emerging school of thought that states that ongoing symptoms are due to a persistent infection that is able to survive both the immune response and antibiotic therapy. Numerous studies have shown that Bb can indeed persist within the host despite treatment and several mechanisms have been proposed to explain Bb’s persistence capabilities. These include: polymorphism, antigenic variance, biofilm formation, persister cells, and immunomodulation.
There is evidence that Bb is able to alter cytokine profiles within the host which may allow the organism to survive the immune response. This immunomodulation follows a pattern of T-helper 1 (TH1) suppression in favor of T-helper 2 (TH2) processes. In contrast, it has been shown that the optimal immune response to Bb infection involves an early, robust TH1 response and a later conversion to TH2 dominance once the infection is controlled or cleared. It has been proposed that a reconstitution of proper immune-competency in the infected host may improve clinical outcomes in Lyme disease.
Cimetidine (CIM) is an over-the-counter histamine-2 (H2) antagonist that is primarily used to lower acid secretions in the stomach. T-regulatory (Treg) cells also possess the H2 receptor, which has spurred interest in CIM as a potential immunomodulator. CIM therapy has been shown to increase levels of the TH1 associated cytokines IL-12, TNF-α, and IFN-γ while decreasing levels of the TH2 associated cytokine IL-10. The author proposes a novel theory that CIM therapy during early Bb infection may promote a more appropriate immune response and increase the utility of antibiotic therapy during early stage Lyme disease, thus improving clinical outcomes of the disease."