Med Hypotheses. 2012 Jan;78(1):60-6. doi: 10.1016/j.mehy.2011.09.041. Epub 2011 Oct 13.
In endemic pemphigus foliaceus (EPF) or "fogo selvagem" the epidemiological evidence shows that all the described outbreaks occur on the banks of rivers where there is mercury contamination from alluvium gold mining and deforestation. Pathophysiological evidence shows a similarity to pemphigus induced by sulphydryl (SH-) drugs that act by denaturing cadherins at the desmosomal level, which are the pemphigus antigens. The sulfhydryl radical (SH-) call also thiol or mercaptans from the SH-drugs, act at the level of SH-groups of cystein as would the methyl mercury from the contaminated animals and fish in the diet of humans from endemic areas of pemphigus foliaceus. The methyl mercury would join the SH-groups from the cysteines amino acids from cadherin proteins in the skin. The autoimmune disease would only be triggered in genetically susceptible individuals with human leukocyte antigen HLA-DRB 1 haplotypes, just as Brown-Norway (BN) rats which are susceptible to develop Th2-dependent autoimmunity induced by metals. Immunological evidence from all the seroepidemiological studies could also be explained by binding mechanism of the methyl mercury to the SH-groups from the cysteines in the desmosomal cadherins proteins. The conclusion is that chronic methyl mercury poisoning is the most likely trigger of endemic pemphigus foliaceus "fogo selvagem". To reduce the contamination of methyl mercury in the animals of the polluted rivers is pertinent to the design of campaigns and education programs with the population. Implement reforestation and biological control measures like phytoremediation technologies using decontaminant plants to decrease the methylation, and the process of biomagnifications of the methyl mercury in the Latin-America EPF foci.
在地方性落叶型天疱疮（EPF）或“野火”中，流行病学证据表明，所有描述的暴发都发生在河流两岸，这些河流受到冲积金矿和森林砍伐导致的汞污染。病理生理学证据表明，它与巯基（SH）药物诱导的天疱疮具有相似性，后者通过在桥粒水平使钙黏蛋白变性而发挥作用，钙黏蛋白是天疱疮的抗原。SH-药物中的巯基自由基（SH-）也称为硫醇或硫氢化物，作用于半胱氨酸的 SH 基团，就像来自受污染动物和鱼类的甲基汞一样，进入 EPF 地方性流行地区人类的饮食中。甲基汞会与皮肤中钙黏蛋白蛋白的半胱氨酸氨基酸的 SH 基团结合。只有在具有人类白细胞抗原 HLA-DRB1 单倍型的遗传易感个体中，这种自身免疫性疾病才会被触发，就像对金属诱导的 Th2 依赖性自身免疫敏感的 Brown-Norway（BN）大鼠一样。所有血清流行病学研究的免疫学证据也可以通过甲基汞与桥粒钙黏蛋白蛋白中的半胱氨酸的 SH 基团的结合机制来解释。结论是，慢性甲基汞中毒是地方性落叶型天疱疮“野火”最有可能的触发因素。减少受污染河流中动物的甲基汞污染对于设计与人群相关的运动和教育计划非常重要。实施重新造林和生物控制措施，例如使用去污植物的植物修复技术来减少甲基化，以及降低拉丁美洲 EPF 焦点中甲基汞的生物放大过程。
