Lyme disease future or investigational therapies: Difference between revisions
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* A developing hypothesis is that the [[chronic]] secretion of [[Stress (medicine)|stress]] [[hormones]] (specifically [[glucocorticoids]] and [[catecholamines]]) as a result of ''[[Borrelia afzelii|Borrelia]]'' infection may reduce the effect of [[neurotransmitters]], or other receptors in the brain by cell-mediated pro-inflammatory pathways, thereby leading to the dysregulation of neurohormones.<ref>{{cite journal |author=Elenkov IJ, Iezzoni DG, Daly A, Harris AG, Chrousos GP |title=Cytokine dysregulation, inflammation and well-being |journal=Neuroimmunomodulation |volume=12 |issue=5 |pages=255-69 |year=2005 |pmid=16166805 |doi=10.1159/000087104}}</ref><ref>{{cite journal |author=Calcagni E, Elenkov I |title=Stress system activity, innate and T helper cytokines, and susceptibility to immune-related diseases |journal=Ann. N. Y. Acad. Sci. |volume=1069 |issue= |pages=62-76 |year=2006 |pmid=16855135 |doi=10.1196/annals.1351.006}}</ref> | * A developing hypothesis is that the [[chronic]] secretion of [[Stress (medicine)|stress]] [[hormones]] (specifically [[glucocorticoids]] and [[catecholamines]]) as a result of ''[[Borrelia afzelii|Borrelia]]'' infection may reduce the effect of [[neurotransmitters]], or other receptors in the brain by cell-mediated pro-inflammatory pathways, thereby leading to the dysregulation of neurohormones.<ref>{{cite journal |author=Elenkov IJ, Iezzoni DG, Daly A, Harris AG, Chrousos GP |title=Cytokine dysregulation, inflammation and well-being |journal=Neuroimmunomodulation |volume=12 |issue=5 |pages=255-69 |year=2005 |pmid=16166805 |doi=10.1159/000087104}}</ref><ref>{{cite journal |author=Calcagni E, Elenkov I |title=Stress system activity, innate and T helper cytokines, and susceptibility to immune-related diseases |journal=Ann. N. Y. Acad. Sci. |volume=1069 |issue= |pages=62-76 |year=2006 |pmid=16855135 |doi=10.1196/annals.1351.006}}</ref> | ||
* This process is mediated via the [[hypothalamic-pituitary-adrenal axis]]. | * This process is mediated via the [[hypothalamic-pituitary-adrenal axis]]. | ||
* Additionally, [[tryptophan]], a precursor to [[serotonin]], appears to be reduced within the [[CNS]] in a number of patients with Lyme disease.<ref>{{cite journal |author=Gasse T, Murr C, Meyersbach P, ''et al'' |title=Neopterin production and tryptophan degradation in acute Lyme neuroborreliosis versus late Lyme encephalopathy |journal=European journal of clinical chemistry and clinical biochemistry : journal of the Forum of European Clinical Chemistry Societies |volume=32 |issue=9 |pages=685-9 |year=1994 |pmid=7865624}}</ref> | * Additionally, [[tryptophan]], a precursor to [[serotonin]], appears to be reduced within the [[CNS]] in a number of patients with [[Lyme disease]].<ref>{{cite journal |author=Gasse T, Murr C, Meyersbach P, ''et al'' |title=Neopterin production and tryptophan degradation in acute Lyme neuroborreliosis versus late Lyme encephalopathy |journal=European journal of clinical chemistry and clinical biochemistry : journal of the Forum of European Clinical Chemistry Societies |volume=32 |issue=9 |pages=685-9 |year=1994 |pmid=7865624}}</ref> | ||
* [[Antidepressants]] have been shown to be immunomodulatory and anti-inflammatory against pro-inflammatory [[cytokine]] processes, specifically on the regulation of IFN-gamma and [[IL-10]], as well as [[TNF-alpha]] and [[IL-6]] through a [[Psychoneuroimmunology|psycho-neuroimmunological]] process.<ref>{{cite journal |author=Kubera M, Lin AH, Kenis G, Bosmans E, van Bockstaele D, Maes M |title=Anti-Inflammatory effects of antidepressants through suppression of the interferon-gamma/interleukin-10 production ratio |journal=Journal of clinical psychopharmacology |volume=21 |issue=2 |pages=199-206 |year=2001 |pmid=11270917}}</ref> | * [[Antidepressants]] have been shown to be immunomodulatory and anti-inflammatory against pro-inflammatory [[cytokine]] processes, specifically on the regulation of IFN-gamma and [[IL-10]], as well as [[TNF-alpha]] and [[IL-6]] through a [[Psychoneuroimmunology|psycho-neuroimmunological]] process.<ref>{{cite journal |author=Kubera M, Lin AH, Kenis G, Bosmans E, van Bockstaele D, Maes M |title=Anti-Inflammatory effects of antidepressants through suppression of the interferon-gamma/interleukin-10 production ratio |journal=Journal of clinical psychopharmacology |volume=21 |issue=2 |pages=199-206 |year=2001 |pmid=11270917}}</ref> | ||
* Antidepressants have also been shown to suppress Th1 upregulation.<ref>{{cite journal |author=Diamond M, Kelly JP, Connor TJ |title=Antidepressants suppress production of the Th1 [[cytokine]] interferon-gamma, independent of monoamine transporter blockade |journal=European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology |volume=16 |issue=7 |pages=481-90 |year=2006 |pmid=16388933 |doi=10.1016/j.euroneuro.2005.11.011}}</ref> | * Antidepressants have also been shown to suppress Th1 upregulation.<ref>{{cite journal |author=Diamond M, Kelly JP, Connor TJ |title=Antidepressants suppress production of the Th1 [[cytokine]] interferon-gamma, independent of monoamine transporter blockade |journal=European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology |volume=16 |issue=7 |pages=481-90 |year=2006 |pmid=16388933 |doi=10.1016/j.euroneuro.2005.11.011}}</ref> | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Anmol Pitliya, M.B.B.S. M.D.[2]
Overview
Future and investigational therapies of Lyme disease are directed towards decreasing the pro-inflammatory immune process and decreasing Th1 upregulation. Studies have also been conducted to test the role of neurohormones in neuropsychiatric complications of Lyme disease. Other therapies including hyperbaric oxygen therapy, antifungal medications and use of bee venom are also under investigation.
Future or Investigational Therapies
Psycho-neuroimmunological therapies
- A developing hypothesis is that the chronic secretion of stress hormones (specifically glucocorticoids and catecholamines) as a result of Borrelia infection may reduce the effect of neurotransmitters, or other receptors in the brain by cell-mediated pro-inflammatory pathways, thereby leading to the dysregulation of neurohormones.[1][2]
- This process is mediated via the hypothalamic-pituitary-adrenal axis.
- Additionally, tryptophan, a precursor to serotonin, appears to be reduced within the CNS in a number of patients with Lyme disease.[3]
- Antidepressants have been shown to be immunomodulatory and anti-inflammatory against pro-inflammatory cytokine processes, specifically on the regulation of IFN-gamma and IL-10, as well as TNF-alpha and IL-6 through a psycho-neuroimmunological process.[4]
- Antidepressants have also been shown to suppress Th1 upregulation.[5]
- These studies warrant investigation of antidepressants for use in a psycho-neuroimmunological approach for optimal pharmacotherapy of antibiotic refractory Lyme patients.
Hyperbaric oxygen therapy
- The use of hyperbaric oxygen therapy (which is used conventionally to treat a number of other conditions), as an adjunct to antibiotics for Lyme has been discussed.[6]
- Though there are no published data from clinical trials to support its use, preliminary results using a mouse model suggest its effectiveness against B. burgdorferi both in vitro and in vivo.[7]
Antifungal medications
- Anecdotal clinical research has shown potential for the antifungal azole medications such as fluconazole for the treatment of Lyme disease, but this has yet to be repeated in a controlled study or postulated a developed hypothetical model for its use.[8]
Alternative medicine
- One approach in the field of alternative medicine is the use of bee venom to treat Lyme disease because it contains the peptide melittin, which has been shown to exert inhibitory effects on Lyme bacteria in vitro; however, no clinical trials of this treatment have been carried out.[9]
References
- ↑ Elenkov IJ, Iezzoni DG, Daly A, Harris AG, Chrousos GP (2005). "Cytokine dysregulation, inflammation and well-being". Neuroimmunomodulation. 12 (5): 255–69. doi:10.1159/000087104. PMID 16166805.
- ↑ Calcagni E, Elenkov I (2006). "Stress system activity, innate and T helper cytokines, and susceptibility to immune-related diseases". Ann. N. Y. Acad. Sci. 1069: 62–76. doi:10.1196/annals.1351.006. PMID 16855135.
- ↑ Gasse T, Murr C, Meyersbach P; et al. (1994). "Neopterin production and tryptophan degradation in acute Lyme neuroborreliosis versus late Lyme encephalopathy". European journal of clinical chemistry and clinical biochemistry : journal of the Forum of European Clinical Chemistry Societies. 32 (9): 685–9. PMID 7865624.
- ↑ Kubera M, Lin AH, Kenis G, Bosmans E, van Bockstaele D, Maes M (2001). "Anti-Inflammatory effects of antidepressants through suppression of the interferon-gamma/interleukin-10 production ratio". Journal of clinical psychopharmacology. 21 (2): 199–206. PMID 11270917.
- ↑ Diamond M, Kelly JP, Connor TJ (2006). "Antidepressants suppress production of the Th1 cytokine interferon-gamma, independent of monoamine transporter blockade". European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology. 16 (7): 481–90. doi:10.1016/j.euroneuro.2005.11.011. PMID 16388933.
- ↑ Taylor R, Simpson I (2005). "Review of treatment options for Lyme borreliosis". J Chemother. 17 Suppl 2: 3–16. PMID 16315580.
- ↑ Pavia C (2003). "Current and novel therapies for Lyme disease". Expert Opin Investig Drugs. 12 (6): 1003–16. PMID 12783604.
- ↑ Schardt FW (2004). "Clinical effects of fluconazole in patients with neuroborreliosis". Eur. J. Med. Res. 9 (7): 334–6. PMID 15337633.
- ↑ Lubke LL, Garon CF (1997). "The antimicrobial agent melittin exhibits powerful in vitro inhibitory effects on the Lyme disease spirochete". Clin. Infect. Dis. 25 Suppl 1: S48–51. PMID 9233664.