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酒精性慢性胰腺炎的病程:一项前瞻性临床形态学长期研究。

Course of alcoholic chronic pancreatitis: a prospective clinicomorphological long-term study.

作者信息

Ammann R W, Heitz P U, Klöppel G

机构信息

Division of Gastroenterology, Department of Internal Medicine, University Hospital, Zurich, Switzerland.

出版信息

Gastroenterology. 1996 Jul;111(1):224-31. doi: 10.1053/gast.1996.v111.pm8698203.

Abstract

BACKGROUND & AIMS: The pathogenesis of alcoholic chronic pancreatitis and its relationship to alcoholic acute pancreatitis are debated. According to our recent clinical long-term study, alcoholic chronic pancreatitis seems to evolve from severe acute pancreatits. The aim of this study was to correlate clinical findings to the pancreatic histopathology at early and advanced stages of the disease.

METHODS

Morphological changes (pseudocysts, autodigestive necrosis, calcification, and perilobular and intralobular fibrosis) were recorded in 37 surgical and 46 postmortem pancreas specimens of 73 patients from our long-term series, who progressed from clinically acute to chronic pancreatitis (mean follow-up, 12 years). Pancreatic function was monitored at yearly intervals.

RESULTS

Surgical interventions were performed at a mean of 4.1 years from onset. Histologically, focal necrosis (49%) and mild perilobular fibrosis (54%) predominated, Pseudocysts (n = 41, mostly postnecrotic) occurred in 88% within 6 years from onset. Autopsy specimens were obtained at a mean of 12 years. These pancreata often showed severe perilobular and intralobular fibrosis (85%) and calcifications (74%), but rarely necrosis (4%). Fibrosis correlated with progressive pancreatic dysfunction (P < 0.001), particularly in the 10 patients with two histological assessments (mean interval between biopsy and autopsy, 8 years).

CONCLUSIONS

The data support an evolution from severe alcoholic acute pancreatitis to chronic pancreatitis.

摘要

背景与目的

酒精性慢性胰腺炎的发病机制及其与酒精性急性胰腺炎的关系存在争议。根据我们最近的临床长期研究,酒精性慢性胰腺炎似乎由重症急性胰腺炎演变而来。本研究的目的是将疾病早期和晚期的临床发现与胰腺组织病理学相关联。

方法

在我们长期队列研究中的73例患者的37份手术切除胰腺标本和46份尸检胰腺标本中记录形态学变化(假性囊肿、自身消化性坏死、钙化以及小叶周围和小叶内纤维化),这些患者从临床急性胰腺炎进展为慢性胰腺炎(平均随访12年)。每年监测胰腺功能。

结果

平均在发病后4.1年进行手术干预。组织学上,局灶性坏死(49%)和轻度小叶周围纤维化(54%)占主导,88%的患者在发病后6年内出现假性囊肿(n = 41,大多为坏死性)。平均在发病12年后获取尸检标本。这些胰腺常表现为严重的小叶周围和小叶内纤维化(85%)和钙化(74%),但很少有坏死(4%)。纤维化与胰腺功能进行性减退相关(P < 0.001),特别是在10例接受两次组织学评估的患者中(活检与尸检的平均间隔时间为8年)。

结论

数据支持从重症酒精性急性胰腺炎向慢性胰腺炎的演变。

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