Beburishvili A G, Burchuladze N Sh, Mikhin V S, Kitaeva A V, Mikhin I V
Volgograd State Medical University, Volgograd, Russian Federation.
Khirurgiia (Mosk). 2022(7):58-63. doi: 10.17116/hirurgia202207158.
To study the literature data on pancreatogenic encephalopathy in patients with destructive pancreatitis.
Searching for Russian- and English-language literature data was carried out in electronic databases: elibrary, PubMed, the Cochrane Library. We planned a systematic review if studies with evidence level 1 and 2 were available. If these trials were absent, descriptive review was considered.
No studies with evidence level 1 and 2 were found in available literature. Therefore, a descriptive review was carried out. Analysis of primary sources showed that the incidence of pancreatogenic encephalopathy is 9-35% and has no direct correlation with etiology of destructive pancreatitis. Major factors of pathogenesis are high serum enzymes, activation of proinflammatory cytokines and hypoxemia, which are accompanied by damage to myelin sheath of the white matter and cytotoxic brain edema. Clinical manifestation of pancreatogenic encephalopathy occurs within two weeks. Acute onset and various symptoms are typical. Possible laboratory predictors of encephalopathy are persistent hyperglycemia, increased hematocrit, fibrinogen-like protein 2 (FPB-2), proinflammatory cytokines TNF-αand interleukin-1-beta. Pancreatogenic encephalopathy is a factor of unfavorable prognosis of treatment. Mortality in patients with pancreatogenic encephalopathy is 57-70%. Favorable course of pancreatic necrosis is followed by regression of cerebral disorders in most cases while residual cognitive disorders are possible in elderly patients.
Pancreatogenic encephalopathy accompanies severe destructive pancreatitis. It is an unfavorable factor for treatment outcomes requiring further research.
研究坏死性胰腺炎患者胰源性脑病的文献资料。
在电子数据库（elibrary、PubMed、Cochrane图书馆）中检索俄语和英语文献资料。如果有证据等级为1和2的研究，我们计划进行系统评价。如果没有这些试验，则考虑进行描述性综述。
在现有文献中未发现证据等级为1和2的研究。因此，进行了描述性综述。对原始资料的分析表明，胰源性脑病的发病率为9% - 35%，与坏死性胰腺炎的病因无直接相关性。发病机制的主要因素是血清酶升高、促炎细胞因子激活和低氧血症，这些因素伴有白质髓鞘损伤和细胞毒性脑水肿。胰源性脑病的临床表现发生在两周内。急性起病和症状多样是其典型表现。脑病可能的实验室预测指标为持续性高血糖、血细胞比容升高、纤维蛋白原样蛋白2（FPB - 2）、促炎细胞因子TNF-α和白细胞介素 - 1β。胰源性脑病是治疗预后不良的一个因素。胰源性脑病患者的死亡率为57% - 70%。大多数情况下，胰腺坏死病情好转后脑部病变也会随之消退，但老年患者可能会遗留认知障碍。
胰源性脑病伴随严重的坏死性胰腺炎。它是影响治疗结果的一个不良因素，需要进一步研究。
