多态多巴胺 D2 (-DRD2/ANKK (Taq1A))、OPRM1 (A/G)、DRD3 (C/T) 和 MAOA (4R) 基因受损的青春期前男性假定 PANDAS/CANS 患者神经精神症状的首次表观遗传类型改善试验:通过精确引导的 DNA 检测和多巴胺调节剂 (KB220) 及抗菌疗法取得积极临床结果。

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引用次数: 0

摘要

伴有或不伴有链球菌和其他细菌感染的小儿自身免疫性神经精神障碍(PANDAS/CANS)正在成为一种主要的儿科疾病。尽管在治疗方法上存在一些争议,尤其是在行为后遗症方面,但我们在其他已发表的研究中提出了一个假设,即这种疾病的特点是儿童奖赏缺失综合征(RDS)发病迅速。我们建议利用多系统生物学方法,将遗传成瘾风险检测和促多巴胺调节(KB220/POLYGEN®)结合起来,帮助诱导 PANDAS 患者,尤其是已知 DNA 诱导的多巴胺功能减退症患者的 "多巴胺稳态"。本病例研究的患者是一名 12 岁的白种男性,以前没有精神病史,但突然出现严重焦虑、抑郁、情感障碍和自杀倾向。该患者接受了基因分型和遗传成瘾风险评分(GARS)测试,结果显示其多巴胺 D2 (-DRD2/ANKK (Taq1A)、OPRM1 (A/G)、DRD3 (C/T) 和 MAOA (4R) 基因存在风险多态性。这些多态性与多巴胺功能减退症有关。患者随后接受了 ID-KB220ZPBMPOLY (POLYGEN®) 研究,尽管可能存在偏差,但根据患者本人和家长的评估,精神症状得到了明显快速的改善。在治疗的第二阶段(使用 KB220 102 天),患者接受了标准抗体检测,结果显示莱姆抗体阳性。随即开始抗菌治疗,并停用 KB220z,以提供一个冲淡期。我们对每项结果指标进行了单调趋势分析,发现使用抗菌治疗后,结果呈持续下降趋势。尽管只有一个病例,但我们建议在疑似 PANDAS/CANS 患者中使用并进一步研究联合治疗方法,包括精确引导的 DNA 检测和多巴胺调节,以及抗菌治疗和谷胱甘肽,以解决进攻性细胞因子增强的问题。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The First Pilot Epigenetic Type Improvement of Neuropsychiatric Symptoms in a Polymorphic Dopamine D2 (-DRD2/ANKK (Taq1A)), OPRM1 (A/G), DRD3 (C/T), and MAOA (4R) Compromised Preadolescence Male with Putative PANDAS/CANS: Positive Clinical Outcome with Precision-Guided DNA Testing and Pro-Dopamine Regulation (KB220) and Antibacterial Therapies.

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.

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