Of one hundred and forty-nine patients (101 male and 48 female) 4-67 years of age, 117 were alcoholics and underwent pancreatectomy because of episodic or continuous abdominal pain or complications or chronic pancreatitis. Nineteen patients underwent pancreaticoduodenectomy, seventy-seven 80-95% distal resection, anf fifty-three 40-80% distal pancreatic resection. There were 3 operative death and 30 late deaths 6 months to 11 years post pancreatectomy. Twenty-one patients were lost to followup, 1 to 11 years post pancreatectomy. Ninety-five patients are known to be alive, 4 of whom are institutionalized. Indications for pancreatectomy in addition to abdominal pain include recurrent or multiple pseudocysts, failure to relieve pain after decompression of a pseudocyst, pseudoaneurysm of the visceral arteries associated with a pseudocyst, recurrent attacks of pancreatitis unrelived by non-resective operations, duodenal stenosis and left side portal hypertension. The choice between pancreaticoduodenectomy or distal resection of 40-80% or 80-95% of the pancreas should be based on the principle site of inflammation whether proximal or distal in the gland, the size of the common bile duct, the ability to rule out carcinoma, and the anticipated deficits in exocrine and endocrine function. The risk of diabetes is very significant after 80-95% distal resection and of steatorrhea after pancreaticoduodenectomy. When the disease process can be encompassed by 40-80% distal pancreatectomy this is the procedure of choice. (+info)
High proportion of mutant K-ras gene in pancreatic juice of patients with pancreatic cystic lesions.
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BACKGROUND/AIMS: It was recently reported that the quantitative analysis of mutant K-ras gene in pancreatic juice could be useful for the diagnosis of pancreatic cancer. This methodology was applied to patients with pancreatic cystic lesions. METHODS: DNA was extracted from pancreatic juice collected at the time of endoscopy with injection of secretin. The ratio of the K-ras mutant allele to the wild-type allele was measured by two methods to detect and semiquantify mutant K-ras gene: polymerase chain reaction/preferential homoduplex formation assay and enriched polymerase chain reaction/enzyme linked mini-sequence assay. RESULTS: A high frequency of K-ras mutation was detected (more than 2% of all K-ras genes) in six of 14 patients (43%) with pancreatic cysts. This frequency was similar to those detected in patients with pancreatic adenocarcinoma and in intraductal papillary neoplasms of the pancreas. In contrast, the frequency of mutation was low (less than 2%) in patients without either pancreatic cysts or pancreatic neoplasms. CONCLUSIONS: K-ras gene mutation may be derived from duct cells in the pancreas with a high potential for tumorigenesis. Therefore careful follow up of patients with a pancreatic cyst is recommended if they are found to have a high level of the mutant gene in the pancreatic juice. (+info)
A case of lymphoepithelial cyst of the pancreas.
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We report a relatively rare case of lymphoepithelial cyst of the pancreas. The patient, a 43-year-old man with no subjective symptoms, was found to have a pancreatic tumor during a physical examination. Based on the ultrasonographic and abdominal computed tomographic findings, a pancreatic cystic tumor was diagnosed. Endoscopic retrograde pancreatography showed a normal duct system. Enucleation was easily performed. Macroscopically, the cyst resembled an atheroma. Histopathologic examination disclosed lymphoepithelial cyst of the pancreas. (+info)
Visualization of pancreatic pseudocyst.
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In a 44-year-old woman, a pancreatic pseudocyst was demonstrated on delayed images obtained up to 8 days after the intravenous administration of 0.250 mCi 75Se-selenomethionine. The initial routine pancreas image study failed to visualize both the pancreas and the pancreatic pseudocyst. The diagnosis was confirmed at surgery and the fluid of the pancreatic pseudocyst contained 0.73% of the injected dose of the radioselenium. (+info)
Molecular characterization of pancreatic serous microcystic adenomas: evidence for a tumor suppressor gene on chromosome 10q.
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Pancreatic serous microcystic adenomas (SCAs) are rare, benign tumors with a striking female preference. Virtually no information is available about chromosomal or genetic anomalies in this disease. We performed extensive molecular characterization of 21 cases of formalin-fixed, paraffin-embedded sporadic SCAs consisting in genome-wide allelic loss analysis with 79 microsatellite markers covering all 22 autosomes, assessment of microsatellite instability, and mutational analysis of the VHL, K-ras, and p53 genes in nine cases for which frozen tissue was available. Although no case showed microsatellite instability of the type seen in mismatch repair-deficient tumors, a relatively low fractional allelic loss of 0.08 was found. Losses on chromosome 10q were the most frequent event in SCAs (50% of cases), followed by allelic losses on chromosome 3p (40% of cases). Moderately frequent losses (>25% of cases) were found on chromosomes 1q, 2q, and 7q. The VHL gene, located on chromosome 3p, had somatic inactivating mutations in two of nine cases (22%), whereas no mutations were found in either K-ras or p53, in agreement with the finding that all 21 cases stained negative for p53 by immunohistochemistry. Our study indicates that the involvement of chromosomal arms 10q and 3p is characteristic of SCAs and that the VHL gene is involved in a subset of sporadic cases. (+info)
Neurogenic tumors of the digestive tract: report of two cases.
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We report two female patients with neurogenic tumors of the digestive tract. In the first patient, the tumor of 10 cm diameter originated in the stomach and at preoperative CT imitated a peripancreatic cyst. In the second patient, the tumor of 6 cm diameter originated in the duodenum. Despite large size, the tumors were clinically indolent and escaped detection at routine endoscopic evaluation. In both cases the neoplasm was removed and postoperative histopathology combined with immunohistochemistry was consistent with diagnosis of digestive Schwannoma. (+info)
Changing patterns in the management of pancreatic pseudocysts.
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The records of patients treated from 1938 through June, 1974, for pancreatic cysts have been reviewed. There was 205 cysts including 168 pseudocysts, 21 neoplastic, 13 retention, and 3 congenital pseudocysts. An analysis of two eras has been made: cysts treated prior to 1962 (56 patients) and cysts treated after 1962 (98 patients). In the earlier era 66.4% of patients were treated by external drainage and 34% by excision or internal drainage. By marked contrast in the more recent era only 27% were treated by external drainage and 73% by excision or internal drainage. The recurrence rate fell from 27% in the earlier era to 6% in the modern era. Improved morbidity was evidenced by a reduction from 32.2% to 15.3% in additional procedures required. Individualization in the treatment of pseudocyts with adherence to establish criteria for procedure selection with increased reliance on excision or internal drainage, as well as early diagnosis and timely intervention have improved the results of surgical therapy in this disease. (+info)
Comparison of Pkd1-targeted mutants reveals that loss of polycystin-1 causes cystogenesis and bone defects.
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A high level of polycystin-1 expression is detected in kidneys of all patients with autosomal dominant polycystic kidney disease (ADPKD). Mice that overexpress polycystin-1 also develop renal cysts. Whether overexpression of polycystin-1 is necessary for cyst formation is still unclear. Here, we report the generation of a targeted mouse mutant with a null mutation in Pkd1 and its phenotypic characterization in comparison with the del34 mutants that carry a 'truncation mutation' in Pkd1. We show that null homozygotes develop the same, but more aggressive, renal and pancreatic cystic disease as del34/del34. Moreover, we report that both homozygous mutants develop polyhydramnios, hydrops fetalis, spina bifida occulta and osteochondrodysplasia. Heterozygotes also develop adult-onset pancreatic disease. We show further that del34 homozygotes continue to produce mutant polycystin-1, thereby providing a possible explanation for increased immunoreactive polycystin-1 in ADPKD cyst epithelia in the context of the two-hit model. Our data demonstrate for the first time that loss of polycystin-1 leads to cyst formation and defective skeletogenesis, and indicate that polycystin-1 is critical in both epithelium and chondrocyte development. (+info)