Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Duodenal lesions are being reported in cases with familial polyposis of the colon. A case is described presenting with duodenal obstruction and pancreatitis complicating a peri-ampullary carcinoma in a patient with familial polyposis (adenomatosis of the colon and rectum). Upper gastrointestinal lesions notably in the duodenum include duodenal polyps and carcinoma and peri-ampullary malignancy. It is suggested that endoscopy and hypotonic duodenography be considered in patients with adenomatosis of the colon and rectum presenting with non-colonic alimentary symptoms.
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PMID:Pancreatitis and duodenal obstruction due to periampullary carcinoma associated with familial polyposis coli. 68 14

Patients with familial polyposis coli or Gardner's syndrome are at risk for a variety of extracolonic manifestations. In a series of patients followed at the University of Washington, we have found several recurring and unusual manifestations, including upper gastrointestinal polyposis, small bowel obstruction secondary to desmoid tumors or adhesions, recurring pancreatitis, and adenoma of the papilla of Vater. In one family with familial polyposis only, a set of twins had different manifestations; one twin had familial polyposis only, whereas the second had classic extracolonic manifestations of Gardner's syndrome. Multiple rectal adenomas developed in a woman with an ileorectal anastomosis with each of three pregnancies. Spontaneous regression occurred after each delivery. Multiple rectal adenomas developed in her daughter on two occasions while taking birth control pills. Physicians caring for these patients should look for such manifestations.
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PMID:Unfamiliar aspects of familial polyposis coli. 372 22

The majority of patients with Gardner's syndrome and familial polyposis coli develop duodenal adenomatous polyps. Duodenal cancer sometimes arises in this setting, but nonmalignant problems from duodenal polyps have not been described. This report presents a patient with Gardner's syndrome who developed hemorrhagic pancreatitis and was found to have a villous adenoma encasing the pancreatic duct at the duodenal papilla. The case is important because it suggests that patients with polyposis coli may be at risk for significant nonmalignant problems from duodenal polyps, particularly if polyps exhibit villous histology and occur at the duodenal papilla.
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PMID:Villous adenoma of the duodenal papilla presenting as necrotizing pancreatitis in a patient with Gardner's syndrome. 379 88

The incidence of periampullary carcinoma is increased in patients with familial polyposis coli or the Gardner syndrome. Patients with familial polyposis coli and ampullary tumors usually present with obstructive jaundice or abdominal pain. We report the case of a 41-year-old woman with the Gardner syndrome in whom relapsing acute pancreatitis was the presenting manifestation of an ampullary neoplasm. A diagnosis of ampullary neoplasm should be considered in any patient with familial polyposis coli or the Gardner syndrome and pancreatitis, even in cases of relapsing acute pancreatitis.
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PMID:Relapsing acute pancreatitis as the presenting manifestation of an ampullary neoplasm in a patient with familial polyposis coli. 402 80

We assessed the outcome of stapled ileal J-pouch-anal anastomosis with intersphincteric resection of the anal transition zone in 83 consecutive patients with ulcerative colitis (n = 71) or familial adenomatous polyposis (n = 12). There was no postoperative mortality. Two patients (2.4%) required permanent ileostomy for manifestation of unsuspected Crohn's disease. Major postoperative complications consisted of pelvic sepsis, anastomotic leakage, and pancreatitis with 3.6% each. Both, frequency of bowel movements and degree of continence improved with time. Two years after takedown of the diverting ileostomy 45 patients with ulcerative colitis and 12 with familial adenomatous polyposis were assessed with a frequency of bowel movements of 5.6 +/- 2 and 3.2 +/- 1 per 24 h, respectively (P < 0.05). At this time none of them had major daytime or nighttime incontinence. Minor incontinence was reported by 9% and 14% of the patients with ulcerative colitis during day-time and night-time, respectively. The patients with familial adenomatous polyposis demonstrated better results, without day-time seepage and intermittent nocturnal seepage in only 9%. It is concluded that direct ileal J-pouch-anal anastomosis is a safe procedure with excellent functional results for patients with ulcerative colitis and familial adenomatous polyposis.
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PMID:Stapled ileal pouch-anal anastomosis with resection of the anal transition zone. 856 12

The first case of a patient with familial adenomatous polyposis (FAP) who developed pancreatitis after routine screening and biopsy of the ampulla of Vater is described.
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PMID:Iatrogenic pancreatitis in familial adenomatous polyposis. 840 66

Familial adenomatous polyposis of the colon, or Gardner's syndrome, is often accompanied by adenomas of the stomach and duodenum. We experienced a rare case of Gardner's syndrome, with adenomas of the common bile duct, in a patient who presented with relapsing acute pancreatitis. Our findings indicate that adenoma in the common bile duct or pancreatic duct should be considered as a possible etiology when patients with familial polyposis or Gardner's syndrome present with pancreatitis, particularly relapsing acute pancreatitis.
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PMID:Adenoma of the common human bile duct in Gardner's syndrome may cause relapsing acute pancreatitis. 925 Sep 8

The optimal treatment of adenomas of the papilla of Vater has still not been definitively established, and the endoscopic excision of such lesions has received little attention in the literature. We report here the cases of two patients with familial adenomatous polyposis, in whom ampullary adenomas measuring 8 and 20 mm, respectively, were treated using one-piece snare excision of the lesion together with the papilla (snare papillectomy), followed by temporary biliopancreatic drainage. Procedure-related complications were an oozing-type hemorrhage and a mild pancreatitis, easily controlled by conservative measures. During the 18-month follow-up, one patient had a small recurrence that was successfully retreated. Further endoscopic and biopsy controls were negative. Although limited, our experience and the data in the literature indicate that snare papillectomy is a viable alternative to surgery for benign ampullary adenomas. Excising both the lesion and the papilla offers good oncological debridement and, unlike laser or thermal ablation, allows a complete histological evaluation of the pathological tissue. However, snare papillectomy should always be associated with temporary biliopancreatic drainage before or after the procedure in order to prevent ductal obstruction and serious pancreatitis. This maneuver should therefore preferably be performed by experienced endoscopists trained in therapeutic endoscopic retrograde cholangiopancreatography and hemostatic techniques.
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PMID:Endoscopic snare papillectomy in patients with familial adenomatous polyposis and ampullary adenoma. 936 Aug 85

The diagnosis of pancreatic cancer usually depends upon symptoms; consequently it is late when there is no chance for cure. At this point, pain, anorexia, early satiety, sleep problems and weight loss are present. Back pain also may be prominent, which predicts unresectability and shortened survival after resection. However, earlier recognition of symptoms of pancreatic cancer might improve early detection of the cancer. For example, 25% of patients have symptoms compatible with upper abdominal disease up to 6 months prior to diagnosis and 15% of patients may seek medical attention more than 6 months prior to diagnosis. These symptoms erroneously may be attributed to problems such as irritable syndrome. Symptoms, however, may be less common. For example a quarter of patients with pancreatic cancer may have no pain at diagnosis, and half, particularly those with pancreatic head tumors, may have little pain compared with patients with body-tail tumors. However, if the tumor is suspected because of predisposing conditions, earlier diagnosis may be possible. These conditions include diseases such as chronic pancreatitis, intraductal papillary mucinous tumor (IPMT), and recent onset of diabetes mellitus, particularly if the diabetes occurs during or beyond the sixth decade. In addition inherited syndromes also are associated with an increased risk of pancreatic cancer including familial pancreatic cancer, hereditary pancreatitis, familial adenomatous polyposis syndrome (FAP) and familial atypical multiple mole melanoma (FAMMM) syndrome (hereditary dysplastic nevus syndrome). Of these conditions, recent onset of diabetes may be the best clue and should be included in a clinical profile of patients prior to the onset of symptoms to identify a high-risk group to apply screening strategies for detection of early disease. Contrary to a clinical aphorism that pancreatic cancer patients are elderly, lean and recently may have developed diabetes, we found that patients who develop pancreatic cancer are overweight prior to onset of symptoms compared to controls (body mass index, 28 vs 25). Forty percent had the diagnosis of diabetes made at the time of diagnosis of pancreatic cancer and more patients with a resectable tumor had diabetes (58%) compared to patients with locally unresectable or metastatic disease (37%). Perhaps, screening overweight persons who have new-onset diabetes may lead to a diagnosis of asymptomatic, early, resectable pancreatic cancer.
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PMID:Pancreatic cancer: clinical presentation, pitfalls and early clues. 1043 7

Approximately 5% to 10% of patients with pancreatic cancer have one or more first-degree relatives with this disease. A subset of these individuals have a hereditary form of pancreatic cancer designated by association with such hereditary disorders as familial adenomatous polyposis, hereditary nonpolyposis colorectal cancer, hereditary pancreatitis, or familial atypical multiple mole melanoma (FAMMM) syndrome. A subset of those FAMMM kindred with the CDKN2A (p16) germline mutation that expresses both pancreatic cancer and malignant melanoma may constitute a new hereditary pancreatic cancer-prone syndrome.
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PMID:Update on familial pancreatic cancer. 1127 79


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