酒精性与胆源性慢性胰腺炎的临床特点的异同

目的：比较与分析慢性胰腺炎（CP）及不同病因之间的临床表现特点及治疗。方法：回顾性分析总结了1991－2000年北京协和医院110例慢性胰腺炎患者的临床表现。结果：（1）110例慢性胰腺炎患者中，腹痛占85．4％，腹泻占22．7％，糖尿病占27．3％，胰腺钙化占13．6％，假性囊肿占28．2％，有3例（2．7％）合并胰腺癌。（2）酒精性CP各种临床症状发生频率明显高于胆源性CP，但其腹痛程度较胆源性CP轻。（3）酒精性慢性胰腺炎的腹泻（29．1％），糖尿病（41．9％），胰腺钙化（22．6％）的发生率明显高于胆源性（分别为16．7％，19．1％和9．5％）。（4）内科保守治疗有效率为81．2％。结论：在临床表现上，酒精性较胆源性慢性胰腺炎的发生率高；前者的并发症多而早。在治疗上，目前采用内科治疗（44．5％）的比例略低于外科治疗（55．3％）。     

215例慢性胰腺炎病因学分析

目的：探讨我国慢性胰腺炎的病因。方法：回顾性分析1990－2000年北京协和医院215例慢性胰腺炎患者的病因。结果：215例慢性胰腺炎患者的病因中,胆道系统疾病占36．7％,酒精中毒占26．5％,特发性占30．2％,其他病因包括自身免疫性疾病、急性胰腺炎、外伤和遗传等。胆道系统疾病中以胆囊结石最为多见,其次为胆管结石和胆囊炎。结论：我国慢性胰腺炎的病因以胆道系统疾病为主,而酒精性因素呈上升趋势,自身免疫性疾病作为慢性胰腺炎的病因正逐渐受到重视。     

126例慢性胰腺炎病因学分析

目的 探讨我国慢性胰腺炎的病因。方法 回顾性分析1994～2002年我院共收治126例慢性胰腺炎病人病因。结果 126例慢性胰腺炎病人的病因中胆道系统疾病占32．5％。酒精中毒占28．6％。特发性占20．6％，其它病因包括自身免疫疾病、急性胰腺炎、外伤和遗传等。胆道系统疾病中以胆囊结石为最多见，其次为胆管结石和胆囊炎。结论 我国慢性胰腺疾病的病因，以胆道系统疾病为主，而酒精性因素有上升趋势。自身免疫系统疾病作为胰腺疾病的病因正渐受到重视。     

胆源性和酒精性慢性胰腺炎临床特点分析

背景：慢性胰腺炎作为一种常见疾病已引起广泛关注．但对其病因分布以及不同类型慢性胰腺炎的临床特征尚不十分明了。目的：了解慢性胰腺炎的临床特征，分析胆源性与酒精性慢性胰腺炎的异同。方法：回顾性分析武汉协和医院1991年1月～2005年12月收治的119例慢性胰腺炎患者的病因构成、临床表现和常规实验室检查结果。结果：本组119例慢性胰腺炎中，最常见的病因为胆系疾病和长期饮酒，分别占37．0％和18．5％。临床表现多样化，常见的除腹痛外，还包括上腹不适、腹胀、消化不良等。除与胆道梗阻相关的黄疸和相应生化改变外，胆源性胰腺炎与酒精性胰腺炎的其他临床表现无明显差异。胆源性胰腺炎的中性粒细胞计数和天冬氨酸氨基转移酶（AST）水平更高。结论：胆系疾病和长期饮酒是本组慢性胰腺炎的主要病因。单从症状和体征难以直接判断慢性胰腺炎的病因，淤胆相关指标以及中性粒细胞计数和AST水平对鉴别胆源性与酒精性胰腺炎有一定临床价值。     

酒精致胰腺炎的机制研究

慢性酒精中毒是西方发达国家慢性胰腺炎(CP)的首要原因,约占CP病因的40%~90%[1],男性多于女性,发病年龄多在40岁以上。急性胰腺炎(AP)约40%的病因是酒精。复发性胰腺炎患者57%的病因是酗酒。我国CP的病因中,急、慢性酒精中毒从10%~20%[2]上升到34.58%,从而取代慢性胆道系统疾病     

酒精致胰腺炎的机制研究

慢性酒精中毒是西方发达国家慢性胰腺炎(CP)的首要原因,约占CP病因的40% ～ 90%[1],男性多于女性,发病年龄多在40岁以上.急性胰腺炎(AP)约40%的病因是酒精.复发性胰腺炎患者57%的病因是酗酒.我国CP的病因中,急、慢性酒精中毒从10% ～ 20%[2]上升到34.58%,从而取代慢性胆道系统疾病(31.15%)成为首要病因[3].     

慢性胰腺炎294例的病因学及临床诊治

目的:研究我国慢性胰腺炎的相关因素及诊治特点方法:回顾分析长海医院近10 a确诊为慢性胰腺炎的294例住院患者,调查其相关病因、诊断方法及治疗措施. 结果:在294例患者中,胆源性89例(30.3%),酒精性84 例(28.6%),其他病因包括腹部手术后、胰腺外伤、胰管先天异常、自身免疫病、先天因素以及特发性等,均较少见.大部分患者表现为反复发作性腹痛,少数伴有脂肪泻及体重减轻等症状.49例患者通过组织学检查确诊,其他均通过影像学检查及BT-PABA试验诊断.大部分患者(81.0%)经非手术治疗症状缓解. 结论:慢性胆道系统疾病仍是我国慢性胰腺炎的主要致病因素,但其比例明显下降,而酒精性慢性胰腺炎明显增多.影像学检查在慢性胰腺炎诊断中具有重要作用,非手术治疗是目前治疗慢性胰腺炎的主要方法.     

重症高甘油三酯性急性胰腺炎的临床特征分析

目的分析重症急性高甘油三酯性急性胰腺炎(HTGP)的临床特点。方法收集2013年1月-2016年6月广西医科大学第一附属医院179例中度重症急性胰腺炎(MSAP)和重症急性胰腺炎(SAP)患者资料。按病因分为4组:重症胆源性急性胰腺炎68例、重症酒精性急性胰腺炎39例、HTGP 45例及其他重症急性胰腺炎组(其他组) 27例,记录前3组有明确病因患者的人口学资料、入院第1天TG水平、病因、胰腺坏死,全身并发症[急性呼吸窘迫综合征(ARDS)、急性肾功能损伤、低血压、弥散性血管内凝血],其他临床结果(是否入住ICU、住院时间、病死率)。为了进一步了解TG浓度对AP患者转归的影响,根据入院第1天TG水平不同分为血脂正常(82例)、轻度(52例)、中度(28例)、重度(17例) 4组,对不同水平组全身并发症、胰腺坏死、临床结果的发生率进行分析。计量资料多组间比较采用Kruskal-Wallis H检验,计数资料组间比较采用χ2检验,采用Spearman秩相关作相关分析。结果结果显示,胆道疾病仍然是SAP的第一大病因(38%),而高甘油三酯血症成为了SAP的第二大病因(25%)。全身并发症的比较中,高甘油三酯血症组较胆源性急性胰腺炎组及酒精性急性胰腺炎组更易出现ARDS(P值分别为0. 014、0. 022);各TG水平组间全身并发症如ARDS、急性肾功能损伤发生率与TG水平存在正相关(r值分别为0. 966、0. 982,P值分别为0. 004、0. 019)。结论HTGP较胆源性急性胰腺炎组及酒精性急性胰腺炎组出现ARDS的发生率更高,随着TG水平升高,更容易引起ARDS、急性肾功能损伤。     

胆石症与慢性胰腺炎

胰腺炎病因存在明显的地域特征，因地理环境、经济状况和生活习惯不同而存在较大差异，“国人急性胰腺炎(AP)以胆石症为主，西方国家以酒精性为主”的结论已成共识。尽管慢性酒精中毒已成为公认慢性胰腺炎(CP)的常见原因，但近20多年来，我国学者一直认为CP与同时存在的胆道疾患(胆石症、胆囊炎和胆总管疾病等)密切相关。胆石能否成为CP病因，我国学者与欧美以及亚洲一些学者存在不同观点，而分歧焦点在于胆石症是CP的病因，还是CP的伴发疾病或危险因素。     

慢性胰腺炎的病因

慢性胰腺炎的发病率地区间差别很大，欧美国家发病率较高，而我国发病率较低，但近年来有升高的趋势，目前尚无准确统计数字［１］。我国慢性胰腺炎的病因与两方国家有所不同。在西方国家的慢性胰腺炎病因中，酒精性高居首位，其他依次为遗传、热带性、损伤和自身免疫等因素。据我国文献及我院近１０年２１５例病例报道，我国慢性胰腺炎最常见的病因是胆道系统疾病，其次为酒精性，也有一部分患者无明显病因，称之为特发性。 胆源性疾病能否成为慢性胰腺炎的病因仍存在争议。我国学者与欧美，甚至亚洲的一些学者在这一问题上存在分歧。早在…     

Etiological analysis of chronic pancreatitis in 215 cases

OBJECTIVE: To investigate the etiology of chronic pancreatitis in China. METHODS: The causes of 215 cases of chronic pancreatitis treated at Peking Union Medical College Hospital between 1990 and 2000 were analyzed retrospectively. RESULTS: The causes of chronic pancreatitis were biliary diseases (36.7%), alcoholic (26.5%), idiopathic (30.2%), and other uncommon causes such as auto­immune disease, recurrent acute pancreatitis, trauma and heredity. Among biliary diseases, the most common cause was cholecystolithiasis, followed by bile duct stone and cholecystitis. CONCLUSIONS: The main cause of chronic pancreatitis in China is biliary disease. That caused by ethanol is increasing, and autoimmune disease is also receiving increasing attention.     

Analytical studies of both initial symptoms and clinical symptoms and signs of different etiologies of chronic pancreatitis: an approach by using odds ratios]

We conducted the statistical analysis of both initial symptoms and clinical symptoms and signs of different etiologies of chronic pancreatitis by using odds ratios which was one of the techniques of evidence-based medicine. The official report published by The Research Group of Intractable Pancreatic Diseases sponsored by the Welfare Ministry of Japan in 1986 was available as the data source of the present study. Nine items of initial symptoms and 25 items of 28 clinical symptoms and signs were compared in 4 different etiologies of the disease which were alcoholic, biliary, idiopatic and nonalcoholic (both biliary and idiopatic). In initial symptoms, 1.5 items were significantly more observed in alcoholic pancreatitis than in nonalcoholic, biliary and idioatic pancreatitis, 4 of which (abdominal pain, back pain, poor appetite and loss of body weight) were common items as might be related closely to the alcohol intake, 2. only one item of jaundice was significantly more observed in biliary pancreatitis than in alcoholic and idiopatic pancreatitis, 3.3 items of poor appetite, diarrhea and abdominal mass were more frequently observed in idiopatic pancreatitis than in biliary pancreatitis. In clinical symptoms and signs, 1. almost all items (21 to 24) were significantly more observed in alcoholic pancreatitis than in the other etiologies of the disease, and seemed to be related directly or indirectly to alcohol intake, 2.3 or 4 items which were related closely to gallstone and acute cholecystitis were significantly more observed in biliary pancreatitis than the other two etiologies of the disease, and 3.4 items consisting of diarrhea, loss of body weight, and pancreatic swelling were more frequently observed in idiopathic pancreatitis than in biliary pancreatitis.     

Pancreas divisum does not modify the natural course of chronic pancreatitis

Background Pancreas divisum is the most common congenital variant of the pancreas; however, its clinical significance remains controversial. The purpose of our study was to determine the role of pancreas divisum in the development of chronic pancreatitis. Methods We compared the clinical presentation, morphological findings, and course of disease of 30 patients with chronic pancreatitis associated with pancreas divisum (there was coexisting chronic alcohol abuse in 18 cases) to those of 57 patients with chronic pancreatitis and no evidence of pancreas divisum (15 with nonalcoholic pancreatitis and 42 with alcoholic pancreatitis). Results Sex distribution, age at onset of disease, clinical presentation, course of disease, and frequency of complications were not affected by the presence of pancreas divisum. Although the etiology of pancreatitis in patients with pancreas divisum may be attributed to impaired drainage of the majority of the gland through the minor papilla, we observed a relatively low frequency of isolated dorsal duct involvement in our patients irrespective of alcohol use (25% and 28% in patients with and without a history of alcohol abuse, respectively). However, involvement of the ventral duct was commonly observed (75% and 72%, respectively). Conclusions The presence of pancreas divisum in our study did not modify the natural course of chronic nonalcoholic or alcoholic pancreatitis. Pancreas divisum is not likely to play a dominant role in the etiopathogenesis of chronic pancreatitis.     

Nutritional data and etiology of chronic pancreatitis in Mexico

Alcoholism and malnutrition have been implicated commonly in the etiology of chronic pancreatitis (CP). The geographical distribution and clinical and nutritional features differ between the alcoholic and tropical forms of CP. This work presents the etiology and nutritional characteristics of CP in Mexico, a country in which both alcoholism and childhood malnutrition are common. Two well-defined groups of patients have been identified: an alcoholic group composed mainly of males with a mean age at clinical onset of 41 years and a high dietary intake of fat, protein, carbohydrates, and calories; and a nonalcoholic group with a female preponderance, a mean age at onset of 23 years, and a higher intake of protein than controls. We conclude that alcoholic chronic pancreatitis in Mexico is similar to that reported in other temperate countries. Although the nonalcoholic group resembles that observed in tropical countries in many ways, our patients are not malnourished, further questioning the role of childhood malnutrition in the pathogenesis of this type of chronic pancreatitis.     

Serum amylase and lipase concentrations and lipase/amylase ratio in assessment of etiology and severity of acute pancreatitis

We studied the behavior of serum amylase and lipase in 66 consecutive patients with acute pancreatitis in order to assess the ability of these tests and of the serum lipase-amylase ratio to establish the etiology and predict the severity of acute pancreatitis. Forty-two patients had biliary acute pancreatitis, 14 had alcoholic acute pancreatitis, and the remaining 10 nonbiliary, nonalcoholic (NBNA) acute pancreatitis. Serum amylase and lipase were abnormally high in all patients. The elevations of both serum amylase and lipase were significantly lower in patients with alcoholic pancreatitis than in those with biliary pancreatitis, although a considerable overlap was observed between the two groups. No statistically significant differences were found between NBNA patients and those with either biliary or alcoholic forms of the disease. The serum lipase-amylase ratios in patients with alcoholic pancreatitis ranged from 0.2 to 5.6, in those with biliary pancreatitis from 0.1 to 7.9, and in those with NBNA pancreatitis from 0.1 to 4.4. These differences were not statistically significant. No differences in serum enzyme levels were observed among patients without apparent imaging signs of acute pancreatitis (N=20), those with signs of Pancreatic edema (N=36), and those with necrotizing pancreatitis (N=10). The results indicate that serum amylase and lipase concentrations are not able to establish either the etiology or to predict the severity of acute pancreatitis as assessed by imaging techniques. Furthermore, the serum lipase-amylase ratio is not useful in distinguishing acute episodes of alcoholic from nonalcoholic acute pancreatitis.     

Prognosis and prognostic factors in chronic pancreatitis

To evaluate the prognosis and prognostic factors of chronic pancreatitis, 84 patients with alcoholic chronic pancreatitis and 51 with nonalcoholic chronic pancreatitis have been followed for 1-21 years (average of 7.1 years). The follow-up period was defined as the period from diagnosis to death in those who died and to the present in those still alive. The following conclusions were obtained. (1) Patients with alcoholic chronic pancreatitis showed a significantly higher mortality rate (26.2%) and cancer death rate (8.3%) than the age- and sex-matched population. In patients with nonalcoholic chronic pancreatitis, however, the difference did not reach the level of statistical significance, although both rates tended to be higher. (2) Patients with alcoholic chronic pancreatitis showed a significantly poorer prognosis than those with nonalcoholic chronic pancreatitis. (3) Frequent causes of death in chronic pancreatitis were cancer (11 cases) and diabetes-associated conditions (renal failure in three cases, intractable pneumonia in one, hypoglycemic shock in two, and myocardial infarction in two). Death directly from pancreatitis was observed in four. (4) Unfavorable prognostic factors in alcoholic chronic pancreatitis included heavy drinking, continuance of drinking after diagnosis, smoking, insulin-dependent diabetes, and an advanced age. In nonalcoholic chronic pancreatitis, however, patients' age was the only significant prognostic factor; smoking did not reach the level of statistical significance, although it tended to lead to a poorer prognosis.     

Modifications of pure human pancreatic juice induced by chronic alcohol consumption

Pure pancreatic juice has been collected from 25 humans by endoscopic retrograde catheterization of the papilla. Nine did not present with digestive diseases and their mean daily alcohol consumption had never exceeded 40 g (nonalcoholic controls). Sixteen drank more than 100 g alcohol per day for at least 5 years previously (alcoholic patients). Five of those presented with chronic pancreatitis and 11 were apparently normal (alcoholic controls). Juice was collected in 1-min fractions for 20 min. 0.5 CU/kg secretin was injected at the beginning and 3 CHR U/kg cholecystokinin-pancreozymin at the 10th min. Protein concentration was significantly greater in alcoholic patients than in nonalcoholic controls in the samples following both secretin and cholecystokinin-pancreozymin injections, and the highest observed protein concentration was significantly greater in alcoholic controls than in nonalcoholic controls. When it had returned to resting values after hormonal injections, protein concentration was significantly higher in alcoholic chronic pancreatitis patients than in alcoholic controls in six samples, and in two similar samples it was higher in alcoholic chronic pancreatitis patients than in nonalcoholic controls. Protein output was not significantly different in alcoholic controls than in nonalcoholic controls. Bicarbonate concentration was significantly lower in alcoholic patients than in nonalcoholic controls in two samples following secretin injection. Volume was similar in alcoholic controls and nonalcoholic controls, but lower in alcoholic chronic pancreatitis patients than in alcoholic controls in three samples. These results substantiate the assumption already put forward of a hypersecretion of protein not compensated for by a hypersecretion of water and bicarbonate as the origin of alcoholic pancreatitis.     

Exocrine Pancreatic Function in Chronic Liver Diseases

To confirm the respective influence of chronic alcoholism and liver disease on exocrine pancreatic function in cholecystokinin secretin (CS), tests were performed on patients with chronic liver cirrhosis (LC) and non-cirrhotic (nLC) disease of alcoholic (A) and nonalcoholic (nA) etiology. Results were compared in four subgroups (ALC, N = 26; AnLC, N = 45; nALC, N = 18; and nAnLC, N = 43). Volume of duodenal juice and bicarbonate output (BO) were increased and maximal bicarbonate concentration was decreased in ALC, compared with those in normal controls. Comparison of LC and nLC indicated that the volume, BO, and amylase output (AO) were greater in LC than in nLC of alcoholic etiology, but not in those of nonalcoholic etiology. The initial disappearance rate (KICG) of indocyanine green (ICG) excretion correlated with a parameter of CS test in alcoholic liver disease (vs. volume: r = -0.51, p less than 0.01 vs BO: r = -0.40, p less than 0.01), but not in nonalcoholic liver disease. Concurrent chronic pancreatitis with pain and definite exocrine insufficiency was observed in only one ALC patient and in four AnLC patients, but in none of the nonalcoholics. In alcoholic liver disease, exocrine pancreatic secretion tends to increase with severity of liver damage, but concurrence of definite chronic pancreatitis is not correlated with the severity.     

血清淀粉酶和脂肪酶浓度及其比值对急性胰腺炎诊断价值的研究

目的探讨血清淀粉酶、脂肪酶浓度及脂肪酶／淀粉酶浓度比值在急性胰腺炎的病因分类和指导疾病的分级诊断中的作用。方法收集急性胰腺炎患者128例,按照病因分为胆源性、酒精性、其他病因三组,按照病情严重程度结合CT检查结果分为轻、中、重三组,比较各组间血清淀粉酶、脂肪酶浓度,脂肪酶／淀粉酶浓度比值的差异。结果酒精性急性胰腺炎患者的血清淀粉酶水平低于胆源性和其他病因患者（P=0．005、0．026）,胆源性和其他病因组间淀粉酶浓度差异无统计学意义。各病因分组之间,脂肪酶浓度和脂肪酶／淀粉酶浓度比值的差异均无统计学意义。按照疾病严重程度分组研究中,淀粉酶、脂肪酶浓度以及脂肪酶／淀粉酶浓度比值在各组间的差异无统计学意义。结论血清淀粉酶浓度在鉴别酒精性和非酒精性急性胰腺炎方面有指示作用,而脂肪酶浓度及脂肪酶／淀粉酶浓度比值不足以用来鉴别急性胰腺炎的病因,也不能单独作为指示疾病严重程度的指标。