Intraductal papillary mucinous tumors of the pancreas confined to secondary ducts show less aggressive pathologic features as compared with those involving the main pancreatic duct.

Intraductal papillary mucinous tumors (IPMTs) of the pancreas are rare tumors characterized by a malignant potential. Because of the progress of imaging procedures, smaller cystic pancreatic lesions are now detected and some of them correspond to IPMTs that involve ectatic pancreatic branch ducts but spare the main pancreatic duct. To investigate differences in morphology and clinical behavior of branch and main duct types of IPMT, a surgical series of 43 cases was studied. All pathologic specimens of IPMT, surgically resected in our institution between October 1987 and July 1998, were analyzed. In all cases, the entire pancreatic specimen was systematically examined. IPMT of the branch type was found in 13 (30%) patients, whereas IPMT of main pancreatic duct type that involved the main pancreatic duct and branch ducts was observed in 30 (70%) patients. Patients with IPMT of the branch type were younger (median age, 55 yrs vs 64 yrs), and all but one of the lesions were located in the head and neck of the pancreas (vs 17 of 30 patients with the main duct type). The size of the cysts ranged from 4 to 55 mm, and the major duct showed a mild dilation in most cases. In contrast to the main pancreatic duct type, which showed invasive carcinoma and in situ carcinoma in 11 (37%) of 30 patients and 6 (20%) of 30 patients, respectively, IPMT of the branch type showed significantly less aggressive histologic lesions with five (39%) patients with simple hyperplasia, six (46%) patients with atypical hyperplasia, and two (15%) patients with in situ carcinoma. No invasive carcinoma was observed in this group. IPMT of the branch type occurs in younger patients and is associated with less aggressive histologic features than is the main pancreatic duct type. Our findings raise the difficult issue of clinical management of IPMT of the branch type as a distinctive group.

Squamous cell carcinoma and lipomatous pseudohypertrophy of the pancreas.

A 68-year-old woman who had been treated for non-insulin-dependent diabetes mellitus for the past 20 years was admitted to hospital because of abdominal pain and weight loss. Radiological investigation revealed a tumour in the body of the pancreas and numerous intraductal calcifications in both the tail and the head of the pancreas. Left-sided pancreatectomy was performed to remove the tumour. The resection specimen showed fatty enlargement of the parenchyma and numerous intraductal calcifications in the tissue adjacent to the tumour, which was 7 cm in diameter and was found to be a primary squamous cell carcinoma with a spindle cell component. There was also lipomatous pseudohypertrophy.

Localization of gastrinomas by endoscopic ultrasonography in patients with Zollinger-Ellison syndrome.

BACKGROUND: Preoperative localization of gastrinomas by current imaging techniques such as computed tomography (CT) scan and angiography is still difficult because of the small size of tumor(s) in most patients undergoing operation. This study evaluated the diagnostic value of endoscopic ultrasonography. METHODS: Twenty-two patients presenting with Zollinger-Ellison syndrome underwent exploratory laparotomy after preoperative attempts to identify the gastrinoma(s) by CT scan, upper gastrointestinal endoscopy, and endoscopic ultrasonography. Surgery included intraoperative ultrasonography and duodenal transillumination in all cases. The sensitivity and specificity of imaging techniques were then evaluated. RESULTS: At least one tumor was found in 19 patients (four had two tumors and one had multiple tumors). Duodenal, lymph node, and pancreatic gastrinomas were found in 42%, 38%, and 17% of the patients, respectively. Sensitivity of endoscopic ultrasonography was 50% for duodenal wall tumors (conventional endoscopy, 40%), 75% for pancreatic tumors (CT scan, 25%), and 62.5% for tumoral lymph nodes (CT scan, 0%). The specificity of all techniques was excellent. Correct diagnosis was made by endoscopic ultrasonography alone in 41% of the patients. The combination of conventional endoscopy and endoscopic ultrasonography provided correct diagnosis in 60% of the patients. CONCLUSIONS: Endoscopic ultrasonography should be considered as a first-choice imaging technique for preoperative detection of gastrinomas. Although small duodenal gastrinomas are still obviously difficult to detect, an accurate exploration of the pancreatic area was provided by this technique.

Intraductal papillary mucinous tumors of the pancreas: pancreatic resections guided by preoperative morphological assessment and intraoperative frozen section examination.

BACKGROUND: We undertook this study to assess the results of a policy of limited pancreatic resections for intraductal papillary-mucinous tumors (IPMT), guided by a standardized preoperative morphological assessment and the frozen section histologic examination of pancreatic resection margins. METHODS: From 1991 to 1998, there were 41 patients who underwent resection of IPMT in our center after standardized morphological preoperative assessment, including abdominal computed tomography scans, endoscopic retrograde cholangiopancreatography, and endoscopic ultrasonography. All patients but one underwent a partial pancreatic resection. RESULTS: Preoperative assessment had an 89% diagnostic accuracy for IPMT. It detected malignant transformation with a 67% sensitivity and a 95% specificity, but failed to correctly assess ductal extension of the disease in 17 cases (41%). The diagnostic accuracy of frozen section histologic examination of the pancreatic resection margin was 92%. There was no recurrence in case of in situ carcinoma when epithelial lesions were completely resected (8 cases) nor in lower grades of dysplasia (23 cases). Conversely, recurrence was constant in invasive carcinoma (10 cases) regardless of the status of the pancreatic margin. CONCLUSIONS: Frozen section histologic examination of the pancreatic resection margin is useful and reliable to ensure a complete resection of IPMT by a partial resection that prevents recurrence of noninvasive lesions.

A multidimensional case-control study of dietary, alcohol, and tobacco habits in alcoholic men with chronic pancreatitis.

This study compared diet, type of alcoholism, and smoking in three groups of alcoholic men, with chronic pancreatitis (n = 56), with histological cirrhosis (n = 50), and without pancreatitis or cirrhosis (controls; n = 50) by a multidimensional analysis. Only patients in whom the first symptom of pancreatitis or cirrhosis was present for < 1 year before the interview were included. Patients with pancreatitis consumed more nonalcohol calories than cirrhotics (p < 0.05). The percentage of calories taken as proteins (p < 0.0003) and lipids (p < 0.0001) was higher and the percentage of calories taken as alcohol (p < 0.0003) was lower in patients with pancreatitis than in cirrhotics and control patients. There was no difference among the three groups for total calories/basal energy expenditure ratio, total nonalcohol calories/basal energy expenditure ratio, mineral and vitamin intake, or tobacco consumption. The duration of excessive alcohol consumption and the total alcohol consumption in patients with pancreatitis was similar to that of controls but lower than that of cirrhotics (p < 0.002 and p < 0.05, respectively). Three parameters were found to be independently different in the three groups by discriminant analysis: percentage of calories taken as lipids (p < 0.0001), duration of excessive alcohol consumption (p < 0.002), and percentage of calories taken as proteins (p < 0.08). These three parameters explained 24% of the variance. We conclude that the reasons alcoholic men develop chronic pancreatitis may be explained partly by dietary habits.(ABSTRACT TRUNCATED AT 250 WORDS)

p53 protein expression and DNA ploidy in cystic tumors of the pancreas.

Cystic tumors of the pancreas form a heterogeneous group, with benign, premalignant, and malignant tumors. The molecular events that underlie their neoplastic transformation process are poorly understood. Our purpose was to study DNA ploidy by flow cytometry and p53 protein expression by immunohistochemistry in a large series of cystic tumors of the pancreas. The series of 51 surgical specimens included 18 serous cystadenomas, 20 mucinous cystic tumors (benign, n = 14; borderline, n = 1; malignant, n = 5), 10 intraductal papillary-mucinous tumors (benign, n = 4; borderline, n = 1; malignant, n = 5), and 3 papillary and cystic tumors. The p53 protein immunohistochemical study was done in all cases on deparaffinized sections stained with the monoclonal antibody DO7. DNA flow cytometry was performed in 31 cases on formalin-fixed and paraffinembedded material. Neither p53 protein immunoreactivity nor DNA aneuploidy was observed in any case of serous cystadenoma. p53 protein overexpression was present in four of five malignant mucinous cystic tumors but was absent in benign and borderline cases. Only one case of malignant mucinous cystic tumor was DNA aneuploid. All benign and borderline intraductal papillary-mucinous tumors were p53 negative, and two of five malignant cases were p53 positive. There was no DNA aneuploidy in any case of intraductal papillary-mucinous tumors. The three cases of papillary-cystic tumors showed neither p53 protein immunoreactivity nor DNA aneuploidy. In cystic tumors of the pancreas, p53 protein overexpression and DNA aneuploidy are rare events, restricted to malignant cases, mostly mucinous cystadenocarcinomas. Our results confirm that this group of tumors is heterogeneous and underline the need for earlier markers of an aggressive behavior.

Symptomatic duodenal stenosis in chronic pancreatitis: a study of 17 cases in a medical-surgical series of 306 patients.

The aim of this study was to assess the prevalence, presentation, cause, and location of symptomatic duodenal stenosis, and its relation to the natural course of chronic pancreatitis in a medical-surgical series of 306 patients (86% alcoholics). Mean follow-up of the series was 7.9 years. Symptomatic duodenal stenosis occurred in 17 patients (5.6%). Diagnosis was confirmed by a barium series. The cause of stenosis was compression by the pancreatic head in all patients, associated with a pancreatic abscess in two. No pseudocysts were found at the time of diagnosis. The location was the 1st and 2nd part of the duodenum or the entire duodenal loop in 4, 6, and 7 patients, respectively. Cholestasis due to common bile duct stenosis occurred in association with duodenal stenosis in 9 patients. Fifteen patients were treated surgically; 11 for gastroenterostomy, and 4 for duodenopancreatectomy. Two patients were not treated surgically. We conclude that during the course of chronic pancreatitis, symptomatic duodenal stenosis occurred in 5.6% of patients, mainly during the first years of the clinical course of chronic pancreatitis, was due to pancreatic head compression and not pseudocysts, usually involved the 2nd part of the duodenum and, was associated with biliary stenosis in half of the cases. Since these two complications require surgery, common bile duct stenosis should be investigated when symptomatic duodenal stenosis is diagnosed.

In vivo assessment of lipid peroxidation in experimental edematous and necrotizing rat pancreatitis.

Lipid peroxidation, which may be involved in the pathogenesis of acute pancreatitis, is usually assessed in vitro or indirectly using antioxidants or free radical scavengers. We assessed lipid peroxidation in an in vivo model by measuring ethane exhalation in two models of acute pancreatitis. Edematous acute pancreatitis was induced by a supramaximal intraperitoneal injection of cerulein. Necrotizing acute pancreatitis was induced by retrograde infusion of sodium taurocholate into the pancreaticobiliary duct. Rats were placed in closed chambers and ethane exhalation was measured in aliquots. Ethane exhalation was significantly increased (p < 0.002) in cerulein (n = 12)- but not in taurocholate (n = 6)-induced pancreatitis compared to controls (n = 12 and 6, respectively). Our results suggest that free radicals may play a role in the pathogenesis of edematous pancreatitis but do not play an important role in the progression to necrotizing pancreatitis.

Calcitonin-secreting tumors of the pancreas: about six cases.

Calcitonin release has rarely been reported in patients (pts) with neuroendocrine pancreatic tumors (NPT). The aim of this study was to describe the characteristics of calcitonin-secreting tumors (CST) of the pancreas. Serum calcitonin determination was part of the prospective evaluation of 66 pts with NPT referred to our institution over a 3-year period. Six pts (9%) had elevated calcitonin levels [at least twice the limit of the normal value (N)]. Abdominal ultrasonography, computed tomography scan, and endoscopic ultrasound were performed to identify the primary tumor(s) and metastases. Immunostaining using anticalcitonin and other antibodies was performed on the surgical resection specimen (four pts) or biopsy of liver metastases (two pts). Three of the six pts (four males, two females; median age, 51.5 years) had diarrhea. Serum calcitonin levels (median, range) were 17.5 N (6N-40N). Slight elevations in serum somatostatin (1.2N-2.3N) were associated in three pts. Pancreatic tumors were single in five of six pts and evenly distributed in the head and in the tail. Five pts had metastases, mainly in the liver. Multiple endocrine neoplasia type I was present in one pt. Immunostaining using calcitonin and somatostatin antibodies was positive in four pts each, respectively, and areas that were positive for one peptide were negative for the other. Diarrhea disappeared in the two pts who responded to treatment of the tumor(s). Three of the four pts with liver metastases died from tumor progression after 2, 10, and 24 months, respectively. CST of the pancreas are often malignant and can be considered as functional in half of the cases, irrespective of the serum calcitonin levels. Somatostatin secretion is often associated. Although rare, calcitonin secretion should be investigated in NPT pts presenting with diarrhea that cannot be explained by an increase in other hormone levels or in patients with nonfunctioning NPT.

Are endoscopic procedures able to predict the benignity of ampullary tumors?

BACKGROUND: Malignant ampullary tumors (AT) require pancreatico-duodenectomy (PD) for curative treatment whereas benign AT can be appropriately treated by local resection. This study evaluated the accuracy of endoscopic exploration combining side-viewing duodenoscopy (SVD) with forceps biopsies, endoscopic sphincterotomy (ES), and endoscopic ultrasonography (EUS) to distinguish benign AT from malignant one. PATIENTS AND METHODS: Twenty-six patients with AT had preoperative SVD with forceps biopsies, including 9 with ES, and EUS. Nodal status was evaluated by EUS in all patients, but could not evaluate parietal spread in 6 in whom ES was previously done. Results of endoscopic examination were compared with pathologic examination after resection (2 local excisions for 2 benign AT, and 24 PD for 20 malignant and 4 benign AT). RESULTS: Accuracy of histologic examination of the 26 biopsies of the papilla was 69%. After ES, accuracy of intra-ampullary biopsies was 77%. The EUS had a 75% accuracy for the parietal spread (tumor limited to ampulla or not) and a 69% accuracy for the nodal status. In 11 patients, all explorations were consistent with a benign lesion, but 6 of these patients had a histologically proven malignancy, including one with nodal metastases and two with duodenal involvement. CONCLUSIONS: Side-viewing duodenoscopy with biopsies, even after ES, combined with EUS is not accurate enough to preoperatively ensure that an AT is benign. Indication for a local resection based on these explorations alone is not safe.

Liver metastases of digestive endocrine tumours: natural history and response to medical treatment.

BACKGROUND: Few data are available about the natural history of liver metastases of digestive endocrine tumours. Moreover, results of studies on treatment with intravenous chemotherapy, hepatic arterial chemoembolization and somatostatin analogues are conflicting. AIMS OF THE STUDY: To assess the progression of liver metastases of digestive endocrine tumours before antitumoral treatment, and to evaluate a stepwise therapeutic strategy in these patients. PATIENTS AND METHODS: 22 patients with histologically-confirmed liver metastases were studied. Primary tumours were carcinoids in nine, gastrinomas in five, non-functioning pancreatic tumours in six and calcitonin-secreting tumours in two patients. The progression of liver metastases was assessed according to the World Health Organization criteria in 10 patients before treatment, and during treatment in all patients. Intravenous (i.v.) chemotherapy with streptozotocin and 5-fluorouracil was used in patients with more than 25% progression in tumour size or with more than 50% liver involvement. Hepatic arterial chemoembolization was performed if i.v. chemotherapy failed, or as a first-choice treatment after 1993. The somatostatin analogues octreotide or lanreotide were used as a third-choice treatment. RESULTS: Progression (+90%, range 28-600%) of liver metastases was identified in the 10 patients studied before treatment, after a median follow-up of 11.5 months. Objective and minor responses were obtained in 2/10 patients (20%) and 1/10 patients (10%) receiving i.v. chemotherapy. Corresponding figures were 3/7 (43%) and 2/7 (29%) for hepatic arterial chemoembolization. No objective response was observed with somatostatin analogues, although 2 patients experienced a minor response. CONCLUSION: Untreated liver metastases of digestive endocrine tumours show an objective increase (their size approximately doubles after 1 year of follow-up). Among the currently available therapeutic modalities, hepatic arterial chemoembolization provides the highest response rates. An increase in patient survival as a result of this procedure remains to be determined.

Diagnostic value of CA 72-4 and carcinoembryonic antigen determination in the fluid of pancreatic cystic lesions.

OBJECTIVE: Mucinous cystic tumours of the pancreas need to be distinguished from other cystic lesions because of their malignant potential. The aim of this study was to assess prospectively the reliability of CA 72-4 and carcinoembryonic antigen analysis in the fluid of cystic lesions of the pancreas obtained by fine-needle aspiration for pathological diagnosis. METHODS: CA 72-4 and carcinoembryonic antigen were measured in cyst fluid obtained preoperatively by fine-needle aspiration. The 91 lesions consisted of 16 serous cystadenomas, 16 mucinous cystadenomas, 14 cystadenocarcinomas and 45 pancreatic pseudocysts complicating well documented chronic pancreatitis. RESULTS: A CA 72-4 level of >40 U/ml had a 63% sensitivity and 98% specificity for distinguishing mucinous cystadenomas and cystadenocarcinomas from serous cystadenomas and pseudocysts. A carcinoembryonic antigen level of >400 ng/ml had a 57% sensitivity and a 100% specificity for distinguishing mucinous tumours and cystadenocarcinomas from pseudocysts. A carcinoembryonic antigen level of <4 ng/ml had a 100% sensitivity and a 93% specificity for distinguishing serous cystadenomas from mucinous cystadenomas, cystadenocarcinomas and pseudocysts. CONCLUSION: Combined measurement of CA 72-4 and carcinoembryonic antigen may be used to distinguish accurately mucinous cystadenomas and cystadenocarcinomas from serous cystadenomas and pseudocysts.

Hepatic arterial chemoembolization with streptozotocin in patients with metastatic digestive endocrine tumours.

BACKGROUND: Hepatic arterial chemoembolization (CE) with anthracyclines is an effective treatment for progressive liver metastases of digestive endocrine tumours. Streptozotocin (STZ) is widely used for systemic chemotherapy, but its efficacy by the hepatic arterial route has not been evaluated. PATIENTS AND METHODS: Fifteen consecutive patients, mean age 57.8 years, were prospectively included between July 1993 and January 1997. All patients had progressive liver metastases from either a carcinoid tumour (eight patients) or an islet cell carcinoma (ICC) (seven patients) that had increased in size (> or = 25%) before CE. Five patients had the carcinoid syndrome. STZ was administered, as an emulsion with iodized oil, into the hepatic artery before embolization with gelatin sponge particles. Two to six procedures (median, 3) were performed in 12 patients (one in three patients). Changes in the size of the liver metastases were evaluated by CT scan or MRI according to WHO criteria. The median follow-up was 15 months (1-50). RESULTS: An objective response was achieved in 8/15 patients (53%; median duration of 10.5 months) whatever the primary tumour (carcinoid or ICC). The carcinoid syndrome disappeared in 3/5 patients for 10, 11 and 17 months, respectively. CE effectively controlled hypoglycaemic attacks (decrease of > 50%) in the patient with insulinoma. The biological response was complete in four patients for a median duration of 7 months. CE induced minor side effects, namely nausea, fever and abdominal pain. Acute and reversible tubular necrosis due to CE was observed in one patient who had previously undergone a nephrectomy. CONCLUSION: Hepatic arterial chemoembolization with STZ is an effective treatment for patients with liver metastases caused by digestive endocrine tumours.

[Conclusions concerning the symptomatic treatment of cancer of the pancreas]. / Conclusions sur le traitement symptomatique du cancer du pancréas.

Symptomatic treatment is the only possibility in the large majority of patients with pancreatic cancer since a curative surgical excision of the tumor is only possible in less than 5% of cases. In most cases, symptomatic treatment must take short survival rate into consideration. Symptoms managed, in the aim to improve the quality of remaining life include weight loss and anorexia, abdominal pain, jaundice secondary to biliary compression, and sometimes digestive consequences of pancreatic surgery. Weight loss can be treated with nutritional support (particularly enteral nutrition) but the indications of such a treatment are rare. Abdominal pain should be treated by potent analgesics (opiates) and sometimes by percutaneous block of the coeliac ganglion rather than abdominal radiotherapy. Jaundice can be treated by surgical biliary drainage or better still by palliative biliary endoprothesis. Finally, digestive consequences of pancreatic surgery require symptomatic treatment.

[Influence of bouts of acute pancreatitis on the course of chronic alcoholic pancreatitis in man]. / Influence des poussées de pancréatite aiguë sur l'évolution de la pancréatite chronique alcoolique de l'homme.

The purpose of this study was to ascertain the influence of acute pancreatitis upon the course of chronic pancreatitis, its complications, the need for surgical treatment, and mortality, in alcoholic men. The studied population was composed of 222 men; 110 had never had acute pancreatitis and 112 had presented at least once with acute pancreatitis. The cumulative probability to have a first bout of acute pancreatitis was 41.5 percent, 2 years after the onset of chronic pancreatitis. There was no difference in follow-up but clinical onset of chronic pancreatitis was earlier in the "acute pancreatitis" group. There was no difference in the prevalence of biliary strictures, non-alcoholic hepatic disease or need for surgery. On the contrary, diabetes mellitus, alcoholic hepatic disease were less frequent and pseudocysts were more frequent in the "acute pancreatitis" group. We observed 56 deaths. The comparison of mortality and cumulative survival rates showed a lower mortality in the "acute pancreatitis" group (p less than 0.02 and 0.05, respectively). The main causes of death were alcohol-related hepatic disease, postoperative mortality, and carcinoma Alcoholic cirrhosis was more frequent in patients who died in the "no acute pancreatitis" group. We conclude that: a) acute pancreatitis is an early complication of chronic pancreatitis in one case out of two; b) clinical onset of chronic pancreatitis occurs earlier in patients who presented with acute pancreatitis; c) need for surgery is not different; d) alcoholic hepatic disease is more frequent in the "no acute pancreatitis" group; e) mortality is lower in the "acute pancreatitis" group.(ABSTRACT TRUNCATED AT 250 WORDS)

[Cost of fibroscopy in gastroduodenal ulcer]. / Coût de la fibroscopie dans la maladie ulcéreuse gastroduodénale.

The assessment of mean cost of upper GI endoscopy is of critical importance if one wants to perform pharmacoeconomic studies, especially in peptic ulcer disease (PUD). The aim of this work was to calculate such costs, based on an inquiry conducted in December 1991 in a representative sampling of 94 French gastroenterologists (GEs) (i.e. 4.3% of the whole population). Thirty-nine percent of GEs work in their office; 25% work in private and 26% in public hospitals. GEs performed 70 +/- 5 (mean +/- SEM) upper GI endoscopies per month. Fifty-nine % are performed to investigate epigastric pain; PUD was found in nearly one patient out of four. Fifteen % of the endoscopies were performed for follow-up of PUD. Upper GI endoscopy modalities varied greatly according to whether performed in GEs' office, private or public hospital. The proportion of investigations performed with biopsies was 66, 71 and 50%, respectively. Neuroleptanalgesia (or general anesthesia), was performed in 8, 49 and 4% of cases, respectively, and a 24-hour hospitalization was required in 0, 7 and 2% of cases, respectively. Sources of expenditure were evaluated according to the current fares of the French Health Care System (for GEs' office and private hospitals) and to real costs (for public hospitals). Taking into account the differences in place and modalities of realization, mean cost of upper GI endoscopy was evaluated at 1,084 FF. This cost could be used in future cost or cost/effectiveness studies of diagnostic or therapeutic strategies.

[Does chronic pancreatitis promote duodenal ulcer in men?]. / La pancréatite chronique de l'homme favorise-t-elle la survenue d'un ulcère duodénal?

The aims of this study were to assess the prevalence of duodenal ulcer during chronic pancreatitis and the relationship between the occurrence of duodenal ulcer and the course of chronic pancreatitis. The population consisted of 264 men with chronic pancreatitis, 94 percent of which were of alcoholic origin. Duodenal ulcer occurred in 37 patients (14 percent). Fifteen patients with gastric or anastomotic ulcer were excluded. The 37 patients with duodenal ulcer were compared with 212 patients without ulcer. There was no significant difference between the two groups as regards the course of chronic pancreatitis except for insulin-dependent diabetes mellitus which was significantly more frequent in patients without duodenal ulcer (P less than 0.05). Eight patients with duodenal ulcer died but the cause of death was not related to their ulcer. All patients with duodenal ulcer and 92 percent of those without were smokers (not significant). Duodenal ulcer occurred in 25/37 patients (68 percent) before the clinical onset of chronic pancreatitis. The risk of duodenal ulcer occurrence was constant in 17-65 year old patients and independent of the time of chronic pancreatitis onset. We concluded that in men with chronic pancreatitis: a) prevalence of duodenal ulcer is 14 percent; b) duodenal ulcer occurred most often before clinical onset of chronic pancreatitis; c) duodenal ulcer occurs independently of the course of pancreatitis which cannot account for its high prevalence. Smoking may be a promoting factor.

[Does acute alcoholic pancreatitis always reveal chronic pancreatitis?]. / Les pancréatites aiguës alcooliques révèlent-elles toujours une pancréatite chronique?

OBJECTIVES: Whether acute alcoholic pancreatitis may occur without underlying alcoholic chronic pancreatitis is still a matter of debate. The aims of this study were to assess the frequency and delay of signs of alcoholic chronic pancreatitis in patients who had an alcoholic acute pancreatitis revealing a pancreatic disease. PATIENTS AND METHODS: From 1975 to 1993, all patients hospitalised for acute alcoholic pancreatitis as a first manifestation for a pancreatic disease and with follow-up > 2 years were included. Definite (pancreatic calcifications, mild to severe Wirsung duct abnormalities, histological or operative data) and probable (diabetes mellitus) diagnosis of chronic alcoholic pancreatitis was systematically searched for initially and during follow-up. RESULTS: Among 122 patients, 114 were included and 8 were excluded because of insufficient follow-up. A definite diagnosis of chronic pancreatitis was made in 101 patients (88.6%) (pancreatic calcifications: n = 71, mild to severe pancreatographic abnormalities: n = 19, histological data: n = 8, peroperative data: n = 3). In 61 patients, the diagnosis of chronic pancreatitis was made during the first year of follow-up and in 40 patients, the diagnosis was made after one year of follow-up. Diabetes mellitus occurred in 4 other patients (3.5%) in whom diagnosis of chronic pancreatitis was considered as probable. No signs of chronic pancreatitis were found in 9 patients (7.9%). CONCLUSION: Acute alcoholic pancreatitis is the hallmark of underlying chronic pancreatitis in 92.1% of patients. Acute alcoholic pancreatitis without underlying chronic pancreatitis either does not exist or is extremely rare.

[Diagnostic value of serum Ca 19-9 antigen in chronic pancreatitis and pancreatic adenocarcinoma]. / Valeur diagnostique de l'antigène sérique Ca 19-9 au cours de la pancréatite chronique et de l'adénocarcinome pancréatique. Influence de leurs complications.

OBJECTIVES: The value of serum Ca 19-9 dosage for pancreatic carcinoma diagnosis has been studied in heterogeneous series. The effect of the complications of chronic pancreatitis and pancreatic carcinoma on serum Ca 19-9 value has not been assessed precisely. The aims of this study were to assess: a) the value of Ca 19-9 to differentiate benign from malignant pancreatic disease; b) the influence of complications (particularly, cholestasis). METHODS: The studied population included 179 patients: 126 with chronic pancreatitis (25 females, 101 males, 45 with cholestasis) and 53 with pancreatic carcinoma (27 females, 26 males, 37 with cholestasis). RESULTS: At 37 UI/mL threshold, the specificity and sensitivity of Ca 19-9 were 53 and 95%, respectively. Cholestasis was associated with a significant increase of Ca 19-9 in patients with chronic pancreatitis but not in those with pancreatic carcinoma. At 300 UI/mL threshold, the specificity and sensitivity of Ca 19-9 were 95 and 81% in patients without cholestasis and 87 and 81% in those with cholestasis, respectively. Diabetes mellitus was associated with a significant increase of Ca 19-9 only in patients with chronic pancreatitis without cholestasis. Pancreatic calcifications, pseudocysts, cirrhosis, pleural effusion or ascites were not associated with significant variation of Ca 19-9. CONCLUSION: In patients with pancreatic disease, 300 UI/mL threshold is the most accurate to differentiate benign from malignant disease, whatever the presence of cholestasis.

[Natural history of non-alcoholic chronic pancreatitis. Study of 37 cases and comparison with 319 cases of alcoholic chronic pancreatitis]. / Histoire naturelle de la pancréatite chronique non alcoolique. Etude de 37 cas et comparaison avec 319 cas de pancréatite chronique alcoolique.

UNLABELLED: We studied the etiology, complications, need for surgical treatment and survival in patients with non-alcoholic chronic pancreatitis (n = 37, including 5 familial, 2 postradiation and 30 idiopathic cases of pancreatitis) and with alcoholic chronic pancreatitis (n = 319). The median follow-up was 6 years. There was a higher frequency of onset of the disease in the fourth decade in alcoholic patients and a more regular pattern with a peak in the third decade in the non-alcoholic patients. The comparison between the two groups showed, in non-alcoholic patients: a lower M/F ratio (non-alcoholics: 1, alcoholics: 9; P < 0.0001), less smokers (P < 0.0001), a lower cumulative probability for development of pancreatic calcification (P < 0.02), insulin-dependent diabetes mellitus (P < 0.02) and pseudocysts (P < 0.01). Frequency and type of surgery were not different in the 2 groups. The observed survival of non-alcoholic patients was better than the observed survival in alcoholic patients and than the expected survival in a matched French population. CONCLUSIONS: in this study, non-alcoholic chronic pancreatitis accounted for 10.4% of the disease; the comparison to alcoholic chronic pancreatitis shows that it is the same, however less evolutive, disease. Chronic pancreatitis by itself has no major influence on vital prognosis.