Brankov O, Shivachev Kh, Drebov R, Dumanov K
Department of Pediatric Surgery, Emergency Hospital N.I.Pirogov - Sofia, Bulgaria.
Khirurgiia (Sofiia). 2007(3):5-8.
For a 10 years period (1996-2005) 66 children with severe caustic injuries of the esophagus and stomach were admitted at the Department of Pediatric Surgery. Subject of this article are 17 children with clinical, laboratory and intraoperative proven acute pancreatitis. The patients were admitted at the clinic 12 hours to 12 days after the ingestion of the corrosive agent. Fifteen of them underwent surgery and different surgical procedures were performed - gastric resection, transhiatal esophagectomy, gastrectomy, gastrostomy. In all patients were found elevated levels of alpha-amilase in blood serum and urine as well as elevated CRP in blood serum. Clinically manifested acute pancreatitis was diagnosed on ultrasound studies and laparotomy. The newest theories about the genesis of acute pancreatitis emphasize on the role of oxidative stress. Experimental models suggest that burn trauma (thermal or chemical) cause critical increase of free oxygen radicals and lipid peroxydation products in the tissue of the damaged organ and the bloodstream. The local tissue damage leads to release of inflammatory mediators which enter the bloodstream and cause distant organs damage of - lung, liver, kidneys and pancreas. In this preliminary report the authors discuss the pathogenesis of acute pancreatitis in children with acute corrosive ingestion injury of the esophagus and stomach. We call this phenomenon " caustic " oxidative stress. This is the first scientific report on this topic in the reviewed literature.
在10年期间（1996 - 2005年），小儿外科收治了66例食管和胃严重腐蚀性损伤的儿童。本文的研究对象是17例经临床、实验室及术中证实为急性胰腺炎的儿童。这些患者在摄入腐蚀性物质后12小时至12天被收治入院。其中15例接受了手术，实施了不同的手术操作——胃切除术、经裂孔食管切除术、胃大部切除术、胃造瘘术。所有患者血清和尿液中的α淀粉酶水平以及血清CRP均升高。通过超声检查和剖腹手术诊断出临床表现为急性胰腺炎。关于急性胰腺炎发病机制的最新理论强调氧化应激的作用。实验模型表明，烧伤创伤（热烧伤或化学烧伤）会导致受损器官组织和血液中游离氧自由基及脂质过氧化产物急剧增加。局部组织损伤会导致炎症介质释放，这些介质进入血液并导致远处器官如肺、肝、肾和胰腺受损。在这份初步报告中，作者探讨了食管和胃急性腐蚀性摄入损伤患儿急性胰腺炎的发病机制。我们将这种现象称为“腐蚀性”氧化应激。这是综述文献中关于该主题的首篇科学报告。
