Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0000737 (abdominal pain)
 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Spontaneous rupture of the right upper ureter caused by metastatic ureteric tumor in an 80-year-old man is reported. He was admitted to our hospital with right lower abdominal pain. Ultrasonography showed mild right hydronephrosis and a low echogenicity mass under the right kidney. Drip infusion pyelography and abdominal computerized tomography showed extravasation of contrast medium around the right upper ureter. Retrograde pyelography was unsuccessful because of edema of the bladder wall. Right ureterocutaneostomy was performed under the diagnosis of spontaneous rupture of the right ureter. The right ureter was completely obstructed 3 cm below the point where it crossed the common iliac artery. At this site, the ureteric wall was hard, thickened, and adherent to the surrounding tissue. The lesion was a metastatic adenocarcinoma. The origin of the tumor could not be found, but pancreatic cancer was suspected on the basis of elevated CEA and PSTI levels. He died of peritonitis carcinomatosis at 8 months after surgery. Thirty three cases of spontaneous rupture of the ureter and 60 cases of metastatic ureteric tumor have been reported in Japan. However, our patient is the first reported case of spontaneous rupture of the ureter caused by a metastatic ureteric tumor in the Japanese literature.
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PMID:[Spontaneous rupture of the ureter caused by metastatic ureteric tumor: a case report]. 790 May 70

Hereditary chronic pancreatitis (HCP) is a very rare form of early onset chronic pancreatitis. With the exception of the young age at diagnosis and a slower progression, the clinical course, morphological features and laboratory findings of HCP do not differ from those of patients with alcoholic chronic pancreatitis. As well, diagnostic criteria and treatment of HCP resemble that of chronic pancreatitis of other causes. The clinical presentation is highly variable and includes chronic abdominal pain, impairment of endocrine and exocrine pancreatic function, nausea and vomiting, maldigestion, diabetes, pseudocysts, bile duct and duodenal obstruction, and rarely pancreatic cancer. Fortunately, most patients have a mild disease. Mutations in the PRSS1 gene, encoding cationic trypsinogen, play a causative role in chronic pancreatitis. It has been shown that the PRSS1 mutations increase autocatalytic conversion of trypsinogen to active trypsin, and thus probably cause premature, intrapancreatic trypsinogen activation disturbing the intrapancreatic balance of proteases and their inhibitors. Other genes, such as the anionic trypsinogen (PRSS2), the serine protease inhibitor, Kazal type 1 (SPINK1) and the cystic fibrosis transmembrane conductance regulator (CFTR) have been found to be associated with chronic pancreatitis (idiopathic and hereditary) as well. Genetic testing should only be performed in carefully selected patients by direct DNA sequencing and antenatal diagnosis should not be encouraged. Treatment focuses on enzyme and nutritional supplementation, pain management, pancreatic diabetes, and local organ complications, such as pseudocysts, bile duct or duodenal obstruction. The disease course and prognosis of patients with HCP is unpredictable. Pancreatic cancer risk is elevated. Therefore, HCP patients should strongly avoid environmental risk factors for pancreatic cancer.
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PMID:Hereditary chronic pancreatitis. 1720 47