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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The typical MRI features of the most common pancreatic diseases, such as pancreatitis and adenocarcinoma of the pancreas, have been established. However, even in these common pancreatic disorders, MRI correlation with the underlying pathology is limited for clinical reasons. We emphasize MR-pathological correlation of inflammatory and neoplastic pancreatic changes, including pancreatitis, adenocarcinoma, acinar cell carcinoma, rare cystic and solid pancreatic neoplasms, and islet cell tumors. By highlighting the correlation of key pathological features with MR findings, a better understanding of the MR appearance of pancreatic pathology can be provided. In addition, MRI may prove a powerful tool in detection and characterization of pancreatic tumors.
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PMID:[MRI of the pancreas: radiologic-pathologic correlation]. 877 27

Our objective was to assess the detection rate and the accuracy of tumor size determination in pancreatic ductal adenocarcinoma using dynamic computed tomography (CT). Preoperative dynamic CT was evaluated in 35 surgically resected pancreatic ductal adenocarcinomas and the findings were compared with the results of histopathological examination. Pancreatic adenocarcinoma was visualized by dynamic CT as a low-density mass in 97% of cases. All three lesions < or = 2 cm in size were demonstrated in good contrast to normal pancreatic parenchyma. The tumor size measured on dynamic CT showed a good correlation with that measured histopathologically, especially in small tumors. Dynamic CT was useful for evaluating the extent of pancreatic adenocarcinoma, especially for small tumors. The detectability of lesions by CT depended on the manner of tumor extension and the degree of associated pancreatitis as well as the tumor size.
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PMID:Computed tomography of pancreatic adenocarcinoma: comparison of tumor size measured by dynamic computed tomography and histopathologic examination. 888 42

To detect adenocarcinoma cells in the circulating peripheral blood, we "analyzed the presence of carcinoembryonic antigen (CEA) mRNA in the peripheral blood obtained from patients with pancreatic carcinoma (PC) or with gastric carcinoma (GC) and also, as controls, from pancreatitis or gastritis patients without carcinomas, a gastric lymphoma patient and four healthy volunteers. Because of the small number of carcinoma cells expected in the peripheral blood, the analysis was performed by the reverse transcription followed by an original two-step polymerase chain reaction. By this sensitive method, 3 of 9 PC patients and 2 of 9 GC patients were positive for CEA mRNA. Except for 1 highly advanced PC patient, 3 of 4 CEA mRNA-positive patients developed recurrence after curative resection or liver metastasis after palliative operation within 9 months after the analysis. None of the control patients was positive for CEA mRNA in the peripheral blood. The results suggest that our sensitive RT-PCR method for detecting CEA mRNA in the peripheral blood is practically useful to find the hematogenous spreading of adenocarcinoma cells.
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PMID:Identification of carcinoembryonic antigen mRNA in circulating peripheral blood of pancreatic carcinoma and gastric carcinoma patients. 895 Mar 23

Pancreatic adenocarcinoma is an important cause of death from cancer throughout the developed world. There are few established environmental risk factors, but a previous history of pancreatitis and exposure to tobacco and salted food appear to be the most important. A family history of pancreatic adenocarcinoma is not common in patients with this disease, but recent research has shown that pancreatic adenocarcinoma can be a feature of cancer susceptibility syndromes associated with germline mutations in p16, BRCA1, BRCA2, and APC. This highlights the need for a full family history in apparently sporadic cases. Somatic mutations in p16, BRCA2, and APC have also been reported in pancreatic cancer; however, K-RAS mutations appear to be the commonest oncogenic alteration. Recent advances in our understanding of the basis of hereditary cancer syndromes may be applicable to the diagnosis, treatment, and possibly prevention of pancreatic adenocarcinoma in the future.
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PMID:Pancreatic adenocarcinoma: epidemiology and genetics. 895 Jun 67

We have investigated a neural network classifier based on CT findings extracted by a radiologist for the differential diagnosis between the pancreatic ductal adenocarcinoma and mass-forming pancreatitis, and compared its classification performance with that of Bayesian analysis, Hayashi's quantification method II, and radiologists. The three computerized classification methods were designed to classify categorized CT findings extracted by a radiologist, and were trained and tested on 71 cases. There was comparable performance between the neural the network, the Bayesian analysis, Hayashi's quantification method II, and the radiologists, in classifying pancreatic carcinoma and inflammatory mass.
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PMID:Evaluation of a neural network classifier for pancreatic masses based on CT findings. 925 95

The rarest and hardly known complication of pancreas diseases is the subcutaneous nodular fat necrosis, a special type of panniculitides. It is mostly associated with pancreatitis and adenocarcinoma of pancreas. Its diagnostic criteria are (1) red painless or occasionally painful nodules showing a tendency of coalescence, emolition and fistulation on the lower extremities and later anywhere on the body, (2) alcoholic case-history, (3) tense, painful joints, (4) elevated pancreatic enzyme levels in the blood and urine. Since the underlying pancreas diseases may be asymptomatic, the pancreatogen panniculitis should be considered as a noteworthy marker of them. The histologic findings are pathognomic. In pancreatogen panniculitis in all likelihood the remote foci of adiponecrosis are due to the local action of pancreatic lipolytic enzymes carried by the blood. The question has not been settled yet. In this article there are presented two cases of pancreatogen panniculitis, recognized by the consultant dermatologist. Referral diagnoses of both cases were misleading: "erythema nodosum" in the first case and "drug eruption" in the second one. The determinant underlying pancreas disease in both cases was pancreatitis with pseudocyst resulted from alcoholic toxicomany.
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PMID:[Pancreatogenic panniculitis based on 2 cases]. 928 Aug 90

Pancreata with cancer also frequently have intraductal proliferative lesions, suggesting an association between pancreatic cancer and these lesions. We present three cases in which atypical papillary hyperplasia of the pancreas was documented 17 months to 10 years before the development of an infiltrating adenocarcinoma of the pancreas. The first patient was a 70-year-old woman who underwent pancreaticoduodenectomy for adenocarcinoma of the pancreas. Atypical papillary duct hyperplasia extended to the pancreatic neck margin of resection, but the margin was negative for infiltrating carcinoma. Nine years later, an infiltrating adenocarcinoma developed in the remaining pancreas. The second patient was a 58-year-old man who underwent distal pancreatectomy for chronic pancreatitis with pseudocyst. Histologic examination showed chronic pancreatitis and multiple foci of atypical papillary duct hyperplasia. Ten years later, the patient underwent a Whipple procedure for infiltrating adenocarcinoma of the pancreas. The third patient was a 46-year-old woman with recurrent pancreatitis who underwent a Whipple procedure. Histologic examination showed atypical papillary duct hyperplasia and chronic pancreatitis but no infiltrating carcinoma. At the time of surgery, the tail of the pancreas was grossly and radiographically normal. Seventeen months later, a malignant pleural effusion developed, and postmortem examination showed infiltrating adenocarcinoma in the tail of the pancreas. In the cases presented, atypical papillary hyperplasia was documented 17 months, 9 years, and 10 years before the development of infiltrating adenocarcinoma of the pancreas, supporting the concept that there is a progression from intraductal hyperplasia to infiltrating carcinoma of the pancreas, just as there is a progression from adenoma to infiltrating carcinoma in the colorectum. Based on evidence that these intraductal lesions are precursor lesions to infiltrating adenocarcinoma of the pancreas, we suggest that the term "hyperplasia" be replaced by the more specific term "pancreatic intraepithelial neoplasia."
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PMID:Progression of pancreatic intraductal neoplasias to infiltrating adenocarcinoma of the pancreas. 950 Feb 16

Medical records of 104 cats with diabetes mellitus were reviewed. Information from 54 cats that had multiple blood glucose concentrations evaluated at least 5 times over a minimum of 3 months, beginning at the time insulin treatment was initiated, was used to evaluate the efficacy of insulin in treating diabetes mellitus. Fourteen of 54 cats were treated with protamine zinc insulin (PZI), 26 with ultralente insulin, and 14 with lente insulin. Six, 29, and 19 cats had good, mediocre, and poor glycemic control, respectively, based on mean blood glucose concentrations, whereas 31, 21, and 2 owners thought clinical response was good, mediocre, and poor, respectively. No significant difference was found in glycemic control among cats treated with PZI, ultralente, or lente insulin. Glycemic control was significantly (P < .05) better in 33 cats without than in 21 cats with concurrent disease. All 104 cats were used to calculate survival data. Fifty-one of 104 cats were alive at the time of the study. Mean (+/- standard deviation [SD]) and median survival times were 24 (+/- 16) and 20 months, respectively, in the 51 cats still alive at the end of the evaluation, and 25 (+/- 4) and 17 months, respectively, in the 53 cats that had died during the period of evaluation. Pancreatic abnormalities identified in 37 cats that underwent necropsy included chronic pancreatitis (n = 17), acute to subacute pancreatitis (n = 2), exocrine pancreatic adenocarcinoma (n = 7) and adenoma (n = 1), islet cell atrophy and vacuolar degeneration (n = 27), and islet amyloidosis (n = 8). No association was found between glycemic control and islet amyloidosis or exocrine pancreatic neoplasia, or between survival time and chronic pancreatitis, islet amyloidosis, or exocrine pancreatic neoplasia. In conclusion, diabetic cats evaluated in this study showed a variable response to exogenously administered insulin, ranging from excellent to poor. By maintaining mean blood glucose concentrations under 300 mg/dL, clinical signs were improved, and owners were satisfied with insulin treatment. Concurrent potentially insulin-antagonistic diseases were common and deleteriously affected glycemic control and survival time.
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PMID:Response to insulin treatment and survival in 104 cats with diabetes mellitus (1985-1995). 950 53

We describe a case of mucosal bile duct carcinoma with superficial spread in a 69-year-old man with gallstone pancreatitis. The patient was seen at the hospital because of abdominal pain, fever, and jaundice. Endoscopic retrograde cholangiography (ERC) demonstrated a protruding lesion in the lower third of the common bile duct (CBD) showing wall irregularity suggestive of malignancy. Percutaneous transhepatic cholangioscopy (PTCS) disclosed a papillary tumor with granular mucosa extending continuously to the middle third of the CBD. Cholangioscopic biopsy specimens taken from both the papillary tumor and surrounding granular mucosa revealed papillary adenocarcinoma. After this assessment of extent of cancer by PTCS, we performed pancreatoduodenectomy with extrahepatic bile duct resection and regional lymph node dissection. Pathology examination revealed papillary adenocarcinoma limited to the mucosal layer. The resected margin of the bile duct was free of tumor. We also reviewed 25 cases of early mucosal bile duct carcinoma described in detail in the Japanese literature, and we discuss the diagnostic advantages of PTCS.
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PMID:Mucosal bile duct carcinoma with superficial spread. 974 93

The aim of this study was to document the natural history of chronic hereditary pancreatitis and to compare its evolution to that of chronic alcoholic pancreatitis. Twelve subjects with chronic hereditary pancreatitis were followed up for a mean duration of 15.8 years (range, 1-23) and compared to subjects with chronic alcoholic pancreatitis who were followed up from 1972 to 1980. The subjects with chronic hereditary pancreatitis, when compared to those with chronic alcoholic pancreatitis, were found to have an earlier onset of symptoms (10.5 vs. 46.0 years, p < 0.05); a significant delay in diagnosis (14.3 vs. 3 years); a similar prevalence of pancreatic calcification (58 vs. 57%); a similar amount of pancreatic insufficiency; both endocrine (50 vs. 70%) and exocrine 42 vs. 38%); and a higher prevalence of pseudocysts (33 vs. 10%, p < 0.05). Only one pancreatic adenocarcinoma was diagnosed in a patient with chronic alcoholic pancreatitis. Apart from the earlier onset and the delay in diagnosis, chronic hereditary pancreatitis has a natural history similar to that of chronic alcoholic pancreatitis. The disease is progressive with a high incidence of complications, but all subjects were alive after follow-up.
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PMID:The natural history of hereditary chronic pancreatitis: a study of 12 cases compared to chronic alcoholic pancreatitis. 978 40


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