Khan S
Department of Surgery, Nepalgunj Medical College, Teaching Hospital, Nepalgunj, Nepal.
Kathmandu Univ Med J (KUMJ). 2006 Jul-Sep;4(3):281-9.
Hyperbilirubinemia is the result of imbalance between production and excretion of bilirubin by the liver. It may be because of hepatocellular, cholestatic or haemolytic diseases. Liver receives blood mainly through portal venous system, which receives blood from abdominal organs. Portal blood carries nutrients and other substances absorbed from gut including bacteria and its product (toxins). In small percentage, even in normal healthy people, bacteria are found in portal blood. It is commonly cleared by detoxification and immunological action of reticuloendothelial (RES) system of liver that act as first line defence in clearing toxic substances, bacteria and it's products. But when bacterial load overwhelms the Kuffer cell function, may cause dysfunction or damage to the hepatocytes (liver parenchyma). It reflects, rise in serum bilirubin (SB) alone or in combination with liver enzymes depending upon the type, severity and site of lesion. Recently, another substance known as Cytokines e.g. IL-6, Tumour necrosis factor (TNF), have also been labelled to be responsible for depressed excretory function of liver and may lead to increase in SB level without rise in liver enzymes.
To evaluate hyperbilirubinemia associated in acute inflammation of appendix (acute appendicitis and its complication).
This is a prospective study conducted at NGMC Teaching hospital Nepalgunj, Nepal during Oct.2004-Oct.2005. 45 Consecutive cases of acute appendicitis admitted in surgical unit III, were recruited for this study. Clinically suspected cases were subjected to investigations to confirm the diagnosis. Investigations included total leucocytes count, differential leucocytes count, urine analysis and ultrasound. These cases were also subjected to routine liver function tests. Subsequently these cases were operated and clinical diagnosis was confirmed per-operatively and post operatively by histopathological examination of the specimen. Their clinical and investigative data were compiled and analyzed and following observations were obtained. Routine liver function test results were compared with laboratory reference values given in Table- 1, 2 and 3.
Case with acute appendicitis and its complication with test negative for HBSAg and no past history of jaundice.
Case with acute appendicitis and its complication with test positive for HBSAg and /or past history of jaundice.
Total number cases were 45. Of 45, 25 were males and 20 were females. Their age ranged from 11 years to 60 years. The average was 27.2 years. Duration of symptoms ranged from 5 hours to maximum 9 days. Among 45 cases diagnosed as acute appendicitis clinically (preoperatively), per operatively, 36 cases had inflamed appendix, 3 cases had gangrene, 5 cases had perforation with peritonitis (4 localized and 1 generalized peritonitis) and only a single case was noted to be of normal appendix (Table 4). Liver function tests (LFT) analysis revealed following results, Among 45 cases, SB was raised in 39 cases where as 6 cases had normal SB level. The raised SB ranged from 1.2 mg/dL to 8.4 mg/dL. The average level of SB was 2.38 mg/dL. All the cases had indirect fraction of SB above 15%. (Table 4). The rise in SB was without concomitant much rise in liver enzymes.
Following conclusion can be drawn from the present study. Firstly, There was Hyperbilirubinemia in 86.6% of the patients of acute inflammation of appendix (i.e. acute appendicitis and its complications). Secondly, Raised SB ranged from 1.2mg/dL - 8.4 mg/dL. Thirdly, The rise in SB was mixed in type (both indirect and direct). Finally, The hyperbilirubinemia was intra hepatic cholestatic in type due either to abnormality in permeability of hepatocyte or ductular membrane enzyme inhibition as the liver enzymes were not much elevated.
高胆红素血症是肝脏胆红素生成与排泄失衡的结果。其可能由肝细胞性、胆汁淤积性或溶血性疾病引起。肝脏主要通过门静脉系统接受血液,门静脉系统从腹部器官接收血液。门静脉血携带从肠道吸收的营养物质和其他物质,包括细菌及其产物(毒素)。即使在正常健康人群中,门静脉血中也有少量细菌。肝脏的网状内皮系统(RES)通过解毒和免疫作用通常可清除这些细菌,该系统在清除有毒物质、细菌及其产物方面起一线防御作用。但当细菌负荷超过库普弗细胞的功能时,可能导致肝细胞(肝实质)功能障碍或损伤。这表现为血清胆红素(SB)单独升高或与肝酶一起升高,具体取决于病变的类型、严重程度和部位。最近,另一种称为细胞因子的物质,如白细胞介素 - 6、肿瘤坏死因子(TNF),也被认为与肝脏排泄功能降低有关,可能导致SB水平升高而肝酶不升高。
评估阑尾急性炎症(急性阑尾炎及其并发症)相关的高胆红素血症。
这是一项于2004年10月至2005年10月在尼泊尔尼泊尔根杰的NGMC教学医院进行的前瞻性研究。连续45例入住外科三室的急性阑尾炎患者被纳入本研究。临床疑似病例接受检查以确诊。检查包括全血细胞计数、白细胞分类计数、尿液分析和超声检查。这些病例还接受了常规肝功能检查。随后对这些病例进行手术,并通过标本的组织病理学检查在术中及术后确认临床诊断。收集并分析了他们的临床和检查数据,得到以下观察结果。将常规肝功能检查结果与表1、2和3中给出的实验室参考值进行比较。
急性阑尾炎及其并发症患者,乙肝表面抗原(HBSAg)检测阴性且无黄疸病史。
急性阑尾炎及其并发症患者,乙肝表面抗原(HBSAg)检测阳性和/或有黄疸病史。
病例总数为45例。其中男性25例,女性20例。年龄范围为11岁至60岁,平均年龄为27.2岁。症状持续时间为5小时至最长9天。在45例临床诊断为急性阑尾炎(术前)的病例中,术中发现36例阑尾发炎,3例坏疽,5例穿孔伴腹膜炎(4例局限性腹膜炎和1例弥漫性腹膜炎),仅1例阑尾正常(表4)。肝功能检查(LFT)分析结果如下,45例中,39例SB升高,6例SB水平正常。升高的SB范围为1.2mg/dL至8.4mg/dL,SB平均水平为2.38mg/dL。所有病例间接胆红素比例均高于15%(表4)。SB升高但肝酶没有相应大幅升高。
从本研究中可以得出以下结论。首先,86.6%的阑尾急性炎症患者(即急性阑尾炎及其并发症)存在高胆红素血症。其次,升高的SB范围为1.2mg/dL - 8.4mg/dL。第三,SB升高为混合型(间接胆红素和直接胆红素均升高)。最后,由于肝细胞通透性异常或胆小管膜酶抑制,导致肝酶升高不明显,高胆红素血症为肝内胆汁淤积型。