摘要
Pediatric autoimmune neuropsychiatric disorders associated with or without streptococcal and other bacterial infections (PANDAS/CANS) are emerging as a featured pediatric disorder. Although there is some controversy regarding treatment approaches, especially related to the behavioral sequelae, we have hypothesized in other published work that it is characterized by the rapid onset of Reward Deficiency Syndrome (RDS) in children. We propose utilizing a multi-systems biological approach involving the coupling of genetic addiction risk testing and pro-dopamine regulation (KB220/POLYGEN®) to help induce “dopamine homeostasis” in patients with PANDAS, especially those with known DNA-induced hypodopaminergia. This case study examines a 12-year-old Caucasian male with no prior psychiatric issues who presented with a sudden onset of severe anxiety, depression, emotional liability, and suicidal ideation. The patient underwent genotyping and the genetic addiction risk score (GARS) testing, which revealed risk polymorphisms in the dopamine D2 (-DRD2/ANKK (Taq1A), OPRM1 (A/G), DRD3 (C/T), and MAOA (4R) genes. These polymorphisms have been linked to hypodopaminergia. The patient was subsequently placed on research ID-KB220ZPBMPOLY (POLYGEN®), and albeit the possibility of bias, based upon self and parental assessment, a marked rapid improvement in psychiatric symptoms was observed. In the second phase of treatment (102 days utilizing KB220), the patient received standard antibody testing, which was positive for Lyme. Antibacterial therapy started immediately, and KB220z was discontinued to provide a wash-out period. A monotonic trend analysis was performed on each outcome measure, and a consistently decreasing trend was observed utilizing antibacterial therapy. Our recommendation, albeit only one case, is to utilize and further research a combined therapeutic approach, involving precision-guided DNA testing and pro-dopamine regulation along with antibacterial therapy, as well as glutathione to address offensive enhanced cytokines, in patients with suspected PANDAS/CANS.
Pediatric autoimmune neuropsychiatric disorders associated with or without streptococcal and other bacterial infections (PANDAS/CANS) are emerging as a featured pediatric disorder. Although there is some controversy regarding treatment approaches, especially related to the behavioral sequelae, we have hypothesized in other published work that it is characterized by the rapid onset of Reward Deficiency Syndrome (RDS) in children. We propose utilizing a multi-systems biological approach involving the coupling of genetic addiction risk testing and pro-dopamine regulation (KB220/POLYGEN®) to help induce “dopamine homeostasis” in patients with PANDAS, especially those with known DNA-induced hypodopaminergia. This case study examines a 12-year-old Caucasian male with no prior psychiatric issues who presented with a sudden onset of severe anxiety, depression, emotional liability, and suicidal ideation. The patient underwent genotyping and the genetic addiction risk score (GARS) testing, which revealed risk polymorphisms in the dopamine D2 (-DRD2/ANKK (Taq1A), OPRM1 (A/G), DRD3 (C/T), and MAOA (4R) genes. These polymorphisms have been linked to hypodopaminergia. The patient was subsequently placed on research ID-KB220ZPBMPOLY (POLYGEN®), and albeit the possibility of bias, based upon self and parental assessment, a marked rapid improvement in psychiatric symptoms was observed. In the second phase of treatment (102 days utilizing KB220), the patient received standard antibody testing, which was positive for Lyme. Antibacterial therapy started immediately, and KB220z was discontinued to provide a wash-out period. A monotonic trend analysis was performed on each outcome measure, and a consistently decreasing trend was observed utilizing antibacterial therapy. Our recommendation, albeit only one case, is to utilize and further research a combined therapeutic approach, involving precision-guided DNA testing and pro-dopamine regulation along with antibacterial therapy, as well as glutathione to address offensive enhanced cytokines, in patients with suspected PANDAS/CANS.
作者
Kenneth Blum
Igor Elman
David Han
Colin Hanna
David Baron
Ashim Gupta
Shan Kazmi
Jag Khalsa
Debasis Bagchi
Thomas McLaughlin
Rajendra D. Badgaiyan
Edward J. Modestino
Drew Edwards
Catherine A. Dennen
Eric R. Braverman
Abdalla Bowirrat
Keerthy Sunder
Kevin Murphy
Nicole Jafari
Foojan Zeine
Paul R. Carney
Mark S. Gold
Kai-Uwe Lewandowski
Alireza Sharafshah
Aryeh R. Pollack
Panayotis K. Thanos
Kenneth Blum;Igor Elman;David Han;Colin Hanna;David Baron;Ashim Gupta;Shan Kazmi;Jag Khalsa;Debasis Bagchi;Thomas McLaughlin;Rajendra D. Badgaiyan;Edward J. Modestino;Drew Edwards;Catherine A. Dennen;Eric R. Braverman;Abdalla Bowirrat;Keerthy Sunder;Kevin Murphy;Nicole Jafari;Foojan Zeine;Paul R. Carney;Mark S. Gold;Kai-Uwe Lewandowski;Alireza Sharafshah;Aryeh R. Pollack;Panayotis K. Thanos(Division of Addiction Research & Education, Center for Sports and Mental Health, Western University of Health Sciences, Pomona, CA, USA;Department of Psychiatry, Boonshoft School of Medicine, Wright State University and Dayton VA Medical Centre, Dayton, OH, USA;Division of Nutrigenomics, Victory Nutrition International, Lederoch, PA, USA;Institute of Psychology, ELTE Etvs Lornd University, Budapest, Hungary;Department of Psychiatry, School of Medicine, University of Vermont, Burlington, VT, USA;The Kenneth Blum Behavioral & Neurogenetic Institute, LLC., Austin, TX, USA;Department of Molecular Biology, Adelson School of Medicine, Ariel University, Ariel, Israel;Division of Neuromodulation Research, Karma Doctors & Karma TMS, Palm Springs, CA, USA;Division of Personalized Interventions, Peak Logic, Del Mar, CA, USA;Division of Personalized Medicine, Cross-Cultural Research & Educational Institute, San Clemente, CA, USA;Awareness Integration Institute, San Clemente, CA, USA;Division of Personalized Pain Therapy, Center for Advanced Spine Care of Southern Arizona, Tucson, AZ, USA;Department of Psychiatry, Harvard School of Medicine, Cambridge, MA, USA;Department of Management Science and Statistics, University of Texas, San Antonio, TX, USA;Behavioral Neuropharmacology and Neuroimaging Laboratory, Clinical Research Institute on Addictions, Department of Pharmacology and Toxicology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, NY, USA;Future Biologics, Lawrenceville, GA, USA;Department of Microbiology, Immunology, & Tropic Diseases, School of Medicine, Georgetown University, Washington DC, USA;Department of Pharmaceutical Sciences, College of Pharmacy, Texas Southern University, Houston, TX, USA;Department of Psychiatry, School of Medicine, Case Western University, Cleveland, OH, USA;Brain and Behavior Laboratory, Curry College, Milton, MA, USA;The Neurogenesis Project, Jacksonville, FL, USA;Department of Family Medicine, Jefferson Health Northeast, Philadelphia, PA, USA;Department of Psychiatry, UC Riverside School of Medicine, University California, Riverside, CA, USA;Department of Human Development, California State University at Long Beach, Long Beach, CA, USA;Department of Health Science, California State University at Long Beach, Long Beach, CA, USA;Division Pediatric Neurology, School of Medicine, University of Missouri, Columbia, MO, USA;Department of Psychiatry, School of Medicine, Washington University, St. Louis, MO, USA;Cellular and Molecular Research Center, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran)
