急性胰腺炎合并肝损害32例临床分析

目的探讨急性胰腺炎肝损害的临床特点。方法收集59例既往无肝病史及近期服用损肝药物的急性胰腺炎病人，通过测定血清总胆红素(TBIL)、直接胆红素(DBIL)、白蛋白(ALB)、丙氨酸转氨酶(ALT)、门冬氨酸转氨酶(AST)实验室指标，对肝损害发生率、肝损害程度、病程进行分析。结果重症急性胰腺炎(SAP)较轻症急性胰腺炎(MAP)肝损害发生率高(P＜0．025)。32例急性胰腺炎合并肝损害中，SAP与MAP相比肝损害指标无差异性(P＞0．05)。胆源性诱因与肝损害程度无关(P＞0．05)。SAP肝损害者比MAP肝损害者住院天数明显延长(P＜0．05)。结论急性胰腺炎肝损害的发生率与胰腺炎的程度成正相关，肝损害延长了胰腺炎的病程。     

急性胰腺炎肝损害与血清肿瘤坏死因子-α的水平

目的:探讨血清肿瘤坏死因子-α水平与急性胰腺炎肝损害的关系.方法:急性胰腺炎组63(男44例,女19例),正常对照组30(男20名,女10名),应用7600-020型自动分析仪(日本日立)测定治疗前后血清白蛋白、谷草转氨酶(AST)、谷丙转氨酶(ALT)、碱性磷酸酶(ALP)、总胆红素(STB)水平,应用放射免疫分析法测定治疗前后血清肿瘤坏死因子-α(INF-α)水平.结果:在63例急性胰腺炎中,合并肝损害38例(60.3%);45例轻症急性胰腺炎(MAP)有21例发生肝损害(发生率46.7%),18例重症急性胰腺炎(SAP)有17例发生肝损害(94.4%).肝损害的表现:AST升高31例(MAP 14例,SAP17例),ALT升高31例(MAP14例,SAP17例),ALP升高18例(MAP5例,SAP13例),STB升高29例(MAP13例,SAP16例).与MAP患者比较,治疗前SAP患者的血清白蛋白明显降低(P＜0.01),血清AST,ALT,ALP,STB,TNF-α水平显著增高(P＜0.01).治疗后SAP患者血清白蛋白升高(P＜0.05),MAP和SAP血清AST,ALT,ALP,STB,TNF-α水平均明显下降(P＜0.05或P＜0.01),SAP组的AST,ALT,TNF-α仍明显高于MAP组(P＜0.01).急性胰腺炎肝损伤组和非肝损伤组的TNF-α水平在治疗前均显著高于对照组(P＜0.01),治疗后均明显低于治疗前(P＜0.01),且与对照组比较无显著差异.治疗前肝损伤组的TNF-α明显高于非肝损伤组(P＜0.01),治疗后二者之间无显著性差异.MAP肝损伤患者和SAP肝损伤患者的TNF-α水平均显著高于对照组,治疗后TNF-α水平均低于治疗前(P＜0.01),但SAP患者仍高于对照组(P＜0.01),而MAP组已接近正常.急性胰腺炎肝损伤患者的血清TNF-α水平与血清AST、ALT正相关(r=0.68,P＜0.01;r=0.64,P＜0.01),与碱性磷酸酶、总胆红素无相关性.结论:急性胰腺炎的肝脏损害发生率较高,SAP肝损伤的发生率明显高于MAP,急性胰腺炎肝损伤患者血清TNF-α水平明显升高,且升高程度与病情严重程度正相关.     

轻型急性胰腺炎并急性肝损害的临床分析

目的探讨轻型急性胰腺炎(MAP)并急性肝损害的特点及其对胰腺炎病程的影响、与病因的相关性及可能的机制。方法 186例MAP患者,统计肝功指标的特点,并在不同病因胰腺炎间进行比较;分析肝损害与MAP病程中的其他临床指标的关系;从血淀粉酶复原时间、腹痛恢复时间及住院天数分析肝损害对MAP病程的影响。结果急性肝损害的发病率为65.6%;以转氨酶和胆红素同时升高常见且升高程度不一;在不同病因所致的胰腺炎间肝损害发生率不全相同(P<0.05),以胆源性MAP伴发的急性肝损害较重(P<0.05)。伴发急性肝损害者入院查体存在腹膜刺激征的比例、发病24 h血淀粉酶水平以及血糖升高的比例均较同期无肝损害者高(均P<0.05)。伴发肝损害者血淀粉酶复原时间、腹痛缓解时间以及住院时间均延长(P<0.05)。结论 MAP患者较常发生急性肝损害,肝损害的程度与胰腺炎病因有关,肝损害会延长MAP的病程;肝损害的发生机制是多方面的。     

急性胰腺炎合并肝损害的影像学表现

目的探讨急性胰腺炎(AP)合并肝损害的影像学表现及临床意义。方法选取该院2012-01~2015-02收治的40例临床确诊为AP的患者,分为轻型胰腺炎(MAP)25例和重型胰腺炎(SAP)15例,并随机选取同期就诊的查体健康者15名作为对照组,进行平扫肝/脾CT值比值测量,对肝功能实验室检查的各项指标进行回顾性分析,观察肝/脾CT值比值与肝功能损害的关系,比较各组间差异性。结果 25例MAP中肝功能损害指标升高18例,出现肝/脾CT值比值倒置72%(13/18);肝功能指标正常7例,出现肝/脾CT值比值倒置57%(4/7),未出现倒置43%(3/7);SAP患者肝功能损害指数上升且肝/脾CT值比值倒置93.3%(14/15)。MAP、SAP肝功能损害指标升高组肝/脾CT值比值分别为(0.85±0.21)、(0.69±0.31),与正常组肝/脾CT值比值(1.25±0.15)比较差异有统计学意义(P0.05)。结论肝脏CT值降低程度与胰腺炎程度有一定的相关。     

胸腔积液联合血液浓缩对急性胰腺炎严重度评估的临床价值

目的探讨胸腔积液、血液浓缩和二者的联合应用对急性胰腺炎疾病严重程度的评估价值,并观察胸腔积液与急性胰腺炎病因、并发症及死亡率的关系.方法对136例急性胰腺炎住院患者作回顾性分析,急性胰腺炎及其严重度评估的标准依据患者的临床表现,实验室检查及增强CT检查.记录患者的胸片和红细胞压积检测结果,并分析胸腔积液与急性胰腺炎患者的病因、并发症及预后的相关性.结果轻型急性胰腺炎(MAP)96例,重症急性胰腺炎(SAP)40例.SAP患者合并胸腔积液者18例(45%),有血液浓缩现象者6例(15%),胸腔积液和血液浓缩同时存在者5例(12.5%);MAP患者合并胸腔积液者10例(10.4%),血液浓缩者2例(2.1%),无胸腔积液和血液浓缩同时存在者,两者相比有显著性差异(P<0.01);此外,胆源性急性胰腺炎合并胸腔积液者11例(14.4%),酒精性急性胰腺炎合并胸腔积液者5例(48.1%),P<0.05.结论胸腔积液、血液浓缩均可作为SAP的独立预测指标,但以胸腔积液联合血液浓缩最为准确.胸腔积液与酒精性急性胰腺炎的病因具有明显的相关性,但未发现胰腺局部并发症如胰腺假性囊肿以及患者死亡率与胸腔积液的关系.     

急性胰腺炎患者外周血内毒素核心抗体及TNF-α水平与病情严重度的关系

目的探讨内毒素核心抗体水平及TNF-α水平与AP病情严重度之间的关系。方法应用ELISA方法测定30例AP患者(SAP15例,MAP15例)入院第1天、第7天与第14天的外周血内毒素核心抗体和TNF-α水平,并以20例健康自愿者作为对照。结果MAP患者和SAP患者在入院第1天的外周血内毒素核心抗体水平都明显低于对照组(P<0.01)。SAP患者第1天的外周血内毒素核心抗体水平明显低于MAP患者(P<0.01),但第7、第14天的水平却高于同期MAP患者(P<0.01)。伴有脏器功能损害的SAPⅡ级患者在第1天的内毒素核心抗体水平也较没有脏器损害的SAPⅠ级患者低,但在第7、第14天的内毒素核心抗体水平则高于SAPⅠ级患者(P<0.01)。MAP与SAP患者在入院第1、7、14天的外周血TNF-α水平均高于正常对照组(P<0.01),SAP患者的水平高于MAP患者,SAPⅡ级患者又高于SAPⅠ级患者。结论早期测定内毒素核心抗体和TNF-α水平可能是评估胰腺炎严重程度的有价值指标。     

血清白细胞介素-6和细胞间黏附分子-1对急性胰腺炎严重程度的早期判断价值

目的:研究血清白细胞介素-6(IL-6)和细胞间黏附分子-1(ICAM-1)对急性胰腺炎严重程度的早期判断价值.方法:收集临床确诊的28例急性胰腺炎(AP)患者,分为重症急性胰腺炎(SAP)13例和轻症急性胰腺炎(MAP)15例两组,另选择10例体检健康人群作对照组(CG),分别测定血清IL-6和ICAM-1的浓度、并进行比较.结果:(1)发病24 h 内入院的SAP患者血清IL-6和ICAM-1浓度与MAP患者及对照组之间有显著性差异(P＜0.01);而MAP患者与CG之间无显著性差异(P＞0.05)(2)入院时SAP患者血清IL-6浓度与MAP患者及对照组之间有明显差异(P＜0.01);入院后SAP患者的血清IL-6浓度逐渐下降,5 d后与MAP比较无显著性差异(P＞0.05).(3)入院2 d后 SAP患者血清ICAM-1的浓度升高最明显,以后逐渐下降,但与MAP比较均有显著性差异(P＜0.05).讨论:血清IL-6和ICAM-1对急性胰腺炎病情严重程度有早期判断价值.     

血清基质金属蛋白酶9在急性胰腺炎严重程度早期评估中的价值

目的探讨血清基质金属蛋白酶9(MMP-9)定量测定对急性胰腺炎严重程度早期评估的价值。方法2004年1月~2005年6月住院治疗的急性胰腺炎(AP)患者24例,男11例,女13例,其中轻症急性胰腺炎(MAP)12例,男4例,女8例,平均年龄55.2岁;重症急性胰腺炎(SAP)12例,男7例,女5例,平均年龄43.6岁。所有患者均符合急性胰腺炎的诊断标准。选择12名军检健康者作为对照组,分别测定MAP、SAP患者及健康对照者的血清MMP-9浓度,并进行比较分析。结果入院后24h内SAP组血清MMP-9为(421.72±32.99)ng/ml,MAP组为(284.87±25.14)ng/ml,两者比较,差异显著(P<0.001),MAP组与对照组间也存在显著差异(P<0.001)。结论血清MMP-9水平在急性胰腺炎严重程度早期评估中具有一定价值。     

血清基质金属蛋白酶9在急性胰腺炎严重程度早期评估中的价值

目的探讨血清基质金属蛋白酶9(MMP-9)定量测定对急性胰腺炎严重程度早期评估的价值.方法 2004年1月～ 2005年6月住院治疗的急性胰腺炎(AP)患者24例,男11例,女13例,其中轻症急性胰腺炎(MAP)12例,男4例,女8例,平均年龄55.2岁;重症急性胰腺炎(SAP)12例,男7例,女5例,平均年龄43.6岁.所有患者均符合急性胰腺炎的诊断标准.选择12名军检健康者作为对照组,分别测定MAP、SAP患者及健康对照者的血清MMP-9浓度,并进行比较分析.结果入院后24 h内SAP组血清MMP-9为(421.72 ± 32.99)ng/ml,MAP组为(284.87 ± 25.14)ng/ml,两者比较,差异显著(P < 0.001),MAP组与对照组间也存在显著差异(P < 0.001).结论血清MMP-9水平在急性胰腺炎严重程度早期评估中具有一定价值.     

急性胰腺炎合并肝脏损伤43例并文献复习

目的了解急性胰腺炎(acute pancreatitis,AP)合并肝脏损伤的临床特点并复习相关文献。方法对柘城县人民医院2013年8月-2016年7月43例AP伴肝脏损伤临床资料进行回顾性分析。结果 43例AP合并肝脏损伤患者中,轻症急性胰腺炎(MAP)33例(6.7%),重症急性胰腺炎(SAP)10例(3.3%),胆源性(46.5%)为AP主要病因。与MAP相比,SAP时肝酶(ALT和AST)升高、TBIL升高、ALB下降、PT延长、PTA降低,差异有统计学意义(P0.05),肝脏损伤程度更严重。结论 AP并发肝脏损伤程度与胰腺炎症程度密切相关,且以胆源性多发,须加强临床重视。     

急性胰腺炎时的肝功能损害

对47例急性胰腺炎患者的肝功能进行了分析，并探讨了其临床意义。结果显示；肝功能损害发生率在急性水肿型胰腺炎66．67％（18／27），在急性出血坏死型胰腺火100％（20／20），P＜0．025，且Child分级越低，胰腺炎程度越重。本文还讨论了急性胰腺炎时发生肝功能损害的柚是。结果提示：肝功能损害程度与急性胰腺炎程度相关，并有助于判断其预后。     

Hepatic Histopathological Changes in Biliary Pancreatitis

Objectives : Elevation of scrum transaminase has been shown to establish gallstone etiology in acute pancreatitis, but little has been reported regarding hepatic histopathological changes in biliary pancreatitis. The main purposes of this study were to observe hepatic histopathological changes in the acute stage of biliary pancreatitis and to elucidate the mechanism of transaminase elevation. Methods : Microscopic findings for liver biopsy specimens (26 patients) as well as gross pathological observations of the biliary tract at emergency operation were analyzed in 62 patients with biliary pancreatitis. Results : The main light microscopic findings were hepatocyte necrosis (96.2%) and acute cholangitis (65.4%). The main electron microscopic findings (two patients) were disorganized liver cell plate, retention of biliary material in the dilated canaliculi, and shedding of cytoplasm into the space of Disse in some areas. At laparotuim, impacted and floating bile duct stones were found in 35 (56.5%) and 13 (21.0%) patients, respectively, and acute inflammatory biliary diseases were encountered in 43 (69.4%) patients. Conclusions : The main hepatic histopathological changes in biliary pancreatitis were acute inflammatory hepatocyte necrosis, hepatocyte degeneration, and acute cholangitis caused by ampullary stones impacted during their trans papillary passage. Serum transaminase elevation might be a reflection of hepatocyte necrosis and/or degeneration.     

Acute pancreatitis complicating acute exacerbation of chronic hepatitis B infection carries a poor prognosis

The clinical outcome of acute pancreatitis complicating acute exacerbation of chronic hepatitis virus B (HBV) infection has never been studied. Ninety patients with acute pancreatitis were recruited. Five patients (5.6%) (Group 1) had acute pancreatitis superimposed on acute exacerbation of chronic HBV infection with no other causes of acute pancreatitis being identified. The clinical outcome of these five patients was compared to the 85 non-HBV infected patients (Group 2) with acute pancreatitis. A third group (Group 3) of patients ( n =406) with acute exacerbation of chronic HBV infections without acute pancreatitis was also recruited for comparison. Group 1 had a significantly higher mortality rate (4 out of 5, 80%) compared to those of Group 2 (13 out of 85, 15.3%, P =0.0041) and Group 3 (9 out of 406, 2.2%, P  < 0.0001). In Group 1 patients, the acute pancreatitis occurred during the initial rise of HBV DNA with relatively low or normal level of alanine aminotransferase (ALT) in two patients, during the rise of ALT with declining level of HBV DNA in one patient, and during the cholestatic phase of the acute exacerbation in one patient. The acute pancreatitis was clinically silent and only diagnosed by computerized tomography in the remaining patient. Direct viral damage and/or immunological attack to the pancreatic tissue were probably the underlying pathogenesis of the acute pancreatitis in these patients.
In conclusion, acute pancreatitis complicating acute exacerbation of chronic HBV infection carried an extremely poor prognosis with high mortality.     

Differential Determination of Serum Isoamylase Using an Amylase Inhibitor and Its Clinical Application

Diagnostic significance of a simple and rapid screening procedure for determining the relative amounts of pancreatic and salivary isoamylase using an amylase inhibitor was evaluated in 242 subjects (controls 84, acute pancreatitis nine, chronic pancreatitis 28, pancreatic cancer 14, peptic ulcer 25, liver cirrhosis 15, cholelithiasis 24, irritable colon syndrome 13, diabetes mellitus 13, mumps seven, and chronic renal failure 10). Electrophoretically separated isoamylases of saliva and pure pancreatic juice were all inhibited at similar degrees to the corresponding unfractionated amylases. Total amylase and pancreatic isoamylase were elevated in all nine patients with acute pancreatitis. Pancreatic isoamylase was decreased in 12 of 28 patients (43%) with chronic pancreatitis and increased in nine of 14 patients (64%) with pancreatic cancer. The mean pancreatic isoamylase activity in the patients with acute pancreatitis was significantly higher (p less than 0.01), while that of chronic pancreatitis was significantly lower (p less than 0.05) when compared with controls. The inhibition method offers simple, rapid, and specific analysis of serum isoamylase for the differential diagnosis of hyperamylasemia in cases of emergency.     

The specificity of peptide-PABA-test (author's transl)]

Exocrine pancreatic function was determined by oral administration of N-benzoyl-L-tyrosyl-p-aminobenzoic acid (peptic-PABA-test) in 120 controls, 74 patients with chronic pancreatitis, 35 patients with acute pancreatitis 2--6 weeks after recovery, 201 patients with a variety of gastro-intestinal diseases and in 10 patients with anorexia nervosa. In the control group, 70% +/- 18% of the oral administered dose of PABA was found within 6 hours in the urine. In contrast the group of chronic pancreatic patients excreted only 40% +/- 13% over the same period. "False negative" PABA excretion was found in 11 (9%) of the 120 persons with no pancreas disease. "False positive" PABA excretion was found in 13 (17,5%) of the 74 patients with chronic pancreatitis. The test was not influenced by age or sex. After stomach resection or cholecystectomy and in patients with ulcus duodeni, chronic hepatitis, functional diarrhea, Crohn's disease, colitis ulcerosa and acute pancreatitis 2--6 weeks after recovery the peptide-PABA-test was not distored. Diminished PABA excretion was encountered in some patients with toxic liver disease, inflammatory disease of the small intensine like M. Whipple, celiac disease and unspecific enteritis and in a few patients with cholelithiasis. Low PABA excretion was found in early all patients with partial small intestinal resection, terminal liver cirrhosis or liver metastasis with ascites and in all patients with anorexia nervosa.     

Pancreatitis associated with alcoholic liver disease

The prevalence with which alcoholic pancreatitis is associated with alcoholic liver disease is unclear. To investigate this association further, we have reviewed the autopsy findings of 1022 patients who died from alcoholic liver disease and compared these findings with those from 352 patients who died from cardiac or pulmonary disease. All patients who died from liver disease had a history of chronic alcoholism with clinical and biochemical evidence of severe liver damage. Death resulted from hepatic coma, gastrointestinal bleeding, or infection. Liver disease patients were classified into two groups: (1) those with cirrhosis (77%) and (2) those without cirrhosis but with acute and/or chronic sclerosing hyaline necrosis (23%). Anatomic and histopathologic changes characteristic of chronic pancreatitis were found in 203 patients in approximately the same frequency (20% and 18%, respectively) in both groups. Acute pancreatitis without chronic lesions was observed in 8% and 10% of both groups, respectively. In the control group of 352 autopsies (122 cardiac and 230 pulmonary patients), the overall prevalence of pancreatitis, at 2.6%, was significantly (P<0.001) lower than that observed in the alcoholic liver disease groups. A total of 22 cases (50%) dying from acute or chronic sclerosing hyaline necrosis had severe chronic calcifying pancreatitis compared to 29 patients (18%) (P<0.001) dying from cirrhosis. By contrast, dense fibrosis was significantly (P<0.001) more commonly observed in patients with cirrhosis. We conclude that pancreatitis occurs frequently in patients dying from alcoholic liver disease but is an uncommon finding in patients dying from other causes. Biliary tract pathology was more prevalent (P<0.05) in patients dying from cirrhosis without pancreatitis than those patients dying from liver disease with pancreatitis. In the control group of patients dying from pulmonary or cardiac disease, biliary pathology was far less frequently (P<0.01) observed.     

Associated liver disease in alcoholic pancreatitis

Two studies investigating the association of liver disease with acute and chronic pancreatitis in alcoholics are presented. In a retrospective study of 50 patients, no clinical liver disease was found in 9 patients with acute pancreatitis, while 23 (56%) of 41 patients with chronic pancreatitis had liver disease by clinical criteria. Of this latter group, 8 were confirmed histologically; thus 19% of patients with chronic pancreatitis had biopsy-proven cirrhosis. Fifty alcoholic patients with pancreatitis were prospectively evaluated. All who had clinical evidence of liver disease were biopsied. No cases of liver disease were encountered in the 4 patients with acute pancreatitis. Although 28 (60%) cases of clinically diagnosed liver disease were present in 46 patients with chronic pancreatitis, only 20 of these seemed significant (cirrhosis, alcoholic hepatitis, severe fatty liver), for an incidence of 43%. Thus, clinically significant alcoholic liver disease occurs quite frequently in association with alcoholic pancreatitis. This association is meaningful in more effective management of these patients in general and in preoperative assessment of the risk of surgery in particular.Presented in part, at the Annual Meeting of American Pancreatic Study Group held on November 7, 1975, in Chicage, Illinois.     

The effect of pancreatitis associated ascitic fluid on some functions of rat liver mitochondria. A possible mechanism of the damage to the liver in acute pancreatitis

The damage to the liver during acute pancreatitis (AP) could be partly dependent on depressive action of pancreatitis associated ascitic fluid (PAAF) on the energy metabolism of hepatocytes. The aim of the study was to assess the effect of PAAF from dogs with acute experimental pancreatitis (AEP) and from humans with AP on the respiratory function of isolated rat liver mitochondria (RLM). The mitochondrial oxygen consumption rate in state 3 respiration (with ADP) and in state 4 (without ADP) using sodium succinate as substrate and oxygen Clark's electrode was estimated. Respiratory control ratio (RCR) and P/O ratio were calculated. PAAF was collected after 6 h of AEP induced by Elliott's method in 8 dogs, and from 4 patients with AP, intraoperatively. Both animal and human PAAFs increase the oxygen consumption rate by RLM in state 4 dose dependently (by 65% with 50 microL to 150% with 200 microL of canine PAAF). This uncoupling effect of human PAAF was twice more potent than the canine. Dialysis of PAAF reduced this effect almost completely. The mitochondrial ATPase activity in RLM treated with PAAF was stimulated and this effect was also reduced by dialysis. The conclusion was that the damage to the liver in AEP could be partly dependent on the toxicity of dializable component(s) of PAAF on the energy metabolism of mitochondria. These findings may partly explain the beneficial effects of peritoneal lavage in acute pancreatitis.     

Clinical course of ulcerative colitis patients who develop acute pancreatitis

AIM To investigate the clinical course of ulcerative colitis(UC)patients who develop acute pancreatitis.METHODS We analyzed 3307 UC patients from the inflammatory bowel disease registry at Asan Medical Center from June 1989 to May 2015.The clinical course of UC patients who developed acute pancreatitis was compared with that of non-pancreatitis UC patients.RESULTS Among 51 patients who developed acute pancreatitis,13(0.40%)had autoimmune,10(0.30%)had aminosalicylate-induced,and 13(1.73%)had thiopurineinduced pancreatitis.All 13 patients with autoimmune pancreatitis(AIP)had type 2 AIP.Two(15.4%)patients had pre-existing AIP,and three(23.1%)patients developed AIP and UC simultaneously.Compared to non-pancreatitis patients,AIP patients had UC diagnosed at a significantly younger age(median,22.9 years vs 36.4 years;P=0.001).AIP and aminosalicylate-induced pancreatitis patients had more extensive UC compared to non-pancreatitis patients.All patients with pancreatitis recovered uneventfully,and there were no recurrences.Biologics were used more frequently in aminosalicylate-and thiopurine-induced pancreatitis patients compared to non-pancreatitis patients[adjusted OR(95%CI),5.16(1.42-18.67)and6.90(1.83-25.98),respectively].Biologic utilization rate was similar among AIP and non-pancreatitis patients[OR(95%CI),0.84(0.11-6.66)].Colectomy rates for autoimmune,aminosalicylate-induced,and thiopurineinduced pancreatitis,and for non-pancreatitis patients were 15.4%(2/13),20%(2/10),15.4%(2/13),and7.3%(239/3256),respectively;the rates were not significantly different after adjusting for baseline disease extent.CONCLUSION Pancreatitis patients show a non-significant increase in colectomy,after adjusting for baseline disease extent.     

Nonalcoholic fatty liver and the severity of acute pancreatitis

AimTo explore the effect of nonalcoholic fatty liver as a hepatic manifestation of metabolic syndrome on the severity of acute pancreatitis. We hypothesized that patients with nonalcoholic fatty liver would have a more severe form of acute pancreatitis.Patients and methodsWe retrospectively analyzed 822 patients hospitalized with acute pancreatitis. We diagnosed acute pancreatitis and determined its severity according the revised Atlanta classification criteria from 2012. We assessed nonalcoholic fatty liver with computed tomography.ResultsThere were 198 (24.1%) patients out of 822 analyzed who had nonalcoholic fatty liver. Patients with nonalcoholic fatty liver had statistically higher incidence of moderately severe (35.4% vs. 14.6%; p = 0.02) and severe acute pancreatitis (20.7% vs. 9.6%; p < 0.001) compared to patients without nonalcoholic fatty liver. At the admission patients with nonalcoholic fatty liver had higher values of C-reactive protein as well as at day three, higher APACHE II score at admission and significantly higher incidence of organ failure and local complications as well as higher values of computed tomography severity index compared to patients without nonalcoholic fatty liver. We found independent association between the occurrence of moderately severe and severe acute pancreatitis and nonalcoholic fatty liver (OR 2.13, 95%CI 1.236–3.689). Compared to patients without nonalcoholic fatty liver, patients with nonalcoholic fatty liver had a higher death rate, however not statistically significant (5.6% vs. 4.3%; p = NS).ConclusionPresence of nonalcoholic fatty liver at admission can indicate a higher risk for developing more severe forms of acute pancreatitis and could be used as an additional prognostic tool.