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Query: UMLS:C0000737 (abdominal pain)
 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The case records of 69 patients who had pancreatic pseudocysts were reviewed retrospectively. All patients had abdominal pain and tenderness, 38 had nausea and vomiting, 9 had chills and fever and 5 had jaundice. Forty-eight patients had elevated body temperatures and 26 had elevated leukocyte counts. A history of alcoholism was obtained in 48 patients. Ultrasonography demonstrated 54 pseudocysts near the body of the pancreas, 8 near the tail and 7 near the head. Thirty-nine patients had internal drainage, 16 had laparotomy and external drainage and 14 had percutaneous catheter drainage. One of these 14 patients died of uncontrollable sepsis. Six of the 39 patients who had internal drainage had clinical evidence of sepsis (4 had septic complications postoperatively, and 2 died); the remaining 33 patients who had noninfected pseudocysts left hospital within 20 days of operation. However, only four of nine patients who had percutaneous drainage for noninfected pseudocysts left hospital within 20 days of the procedure. Thus, the authors recommend that infected pancreatic pseudocysts be managed by percutaneous catheter drainage and noninfected pseudocysts by internal drainage.
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PMID:Pancreatic pseudocysts: the role of percutaneous catheter drainage. 149 40

The cases of two patients with fulminant hepatic failure after intake of therapeutic doses (4-8 g) of paracetamol, and who were admitted to hospital for assessment for liver transplantation, are described. In both patients starvation, due to abdominal pain, nausea and vomiting or diarrhoea, was probably contributing to the toxic effect of the drug. One of the patients also had an excessive alcohol intake. Paracetamol should not be prescribed for patients with alcoholism or with low food intake.
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PMID:Hepatotoxicity due to repeated intake of low doses of paracetamol. 160 96

The serum amylase concentration reflects the balance between the rates of amylase entry into and removal from the blood. Hyperamylasemia can result either from an increased rate of entry of amylase into the circulation and/or a decreased metabolic clearance of this enzyme. The pancreas and salivary glands have amylase concentrations that are several orders of magnitude greater than that of any other normal tissue, and these two organs probably account for almost all of the serum amylase activity in normal persons. A variety of techniques are now available to distinguish pancreatic from salivary-type isoamylase. Pancreatic hyperamylasemia results from an insult to the pancreas, ranging from trivial (cannulation of the pancreatic duct) to severe (pancreatitis). In addition, loss of bowel integrity (infarction or perforation) causes pancreatic hyperamylasemia due to absorption of amylase from the intestinal lumen. Hyperamylasemia due to salivary-type isoamylase is observed in conditions involving the salivary glands. In addition, this type of hyperamylasemia occurs in conditions in which there is no clinical evidence of salivary gland disease, such as chronic alcoholism, postoperative states (particularly postcoronary bypass), lactic acidosis, anorexia nervosa or bulimia, and malignant neoplasms that secrete amylase. Hyperamylasemia can also result from decreased metabolic clearance of amylase due to renal failure or macroamylasemia (a condition in which an abnormally high-molecular-weight amylase is present in the serum). Patients with abdominal pain and a markedly elevated serum amylase (more than three times the upper limit of normal) usually have acute pancreatitis, and additional serum enzyme testing is not helpful. Patients with smaller elevations of serum amylase often have conditions other than pancreatitis, and measurement of a serum enzyme more specific for the pancreas (pancreatitic isoamylase, lipase or trypsin) is frequently of diagnostic value in such patients.
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PMID:Where does serum amylase come from and where does it go? 170 56

An analysis of postmortem investigations between 1980 and 1985 revealed 43 patients with acute pancreatitis. In 13 (30.2%) of them, the diagnosis was first established at autopsy. In eight of the latter patients, the diagnosis could have been present on admission. The etiology was alcoholism in three patients, hypothermia in one, biliary tract disease in one, and unknown in three patients. In five patients, acute pancreatitis developed after gastric, pancreatic, or biliary tract surgery. Abdominal pain was present in only one patient. Amylase levels had been estimated in 11 patients, but the level was in the diagnostic range (greater than or equal to 3 times of upper normal level) in only four. Consequently, ultrasound examination was performed in only two of the latter four patients, but failed to show the pancreas because of intestinal gas. To diagnose acute pancreatitis at an earlier stage and to improve therapy and prognosis, we recommend that serum amylase levels be measured and ultrasound examination be performed. If the results are inconclusive, this should be followed by computed tomography for all abdominal emergency cases and for patients who have undergone cardiopulmonary or upper abdominal surgery, especially when the patients deteriorate or fail to improve postoperatively.
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PMID:Undetected fatal acute pancreatitis: why is the disease so frequently overlooked? 180 1

The papilla of Vater and its sphincter of Oddi, lying at the confluence of the bile and pancreatic ducts in man, have long been suspected as a source of upper abdominal pain. Enlarging the opening of the transpapillary segment of the bile and major pancreatic ducts by using a transduodenal sphincteroplasty with transampullary septectomy resulted in death in a patient with a peripapillary diverticulum and pancreas divisum. Eight-six patients followed for 1 to 10 years experienced a 75% success rate. Thirty-six patients had a marked stenosis of their duct of Wirsung, suggesting that their pain was primarily from the pancreas. The remainder had either a generalized narrowing (40 patients) or a normal (7 patients) papilla. Pain was not satisfactorily resolved in patients with an associated pancreas divisum, chronic pancreatitis, and recurrent episodes of acute pancreatitis with alcoholism.
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PMID:Transduodenal sphincteroplasty with transampullary septectomy for stenosing papillitis. 199 Aug 74

Acute pancreatitis is a disease characterized by abdominal pain, low-grade fever, abdominal tenderness and rigidity, and moderate elevation of the white blood cell count. A widely used revised classification of pancreatitis is that proposed in 1984 at Marseille. It only distinguishes between acute and chronic pancreatitis. In 61 cases were 40 men and 21 women. The mean age in the total series was 52.5 years. The etiology of the acute condition was alcoholism in 32.8% and biliary tract disease in 23%. In 9.8% the acute pancreatitis is associated with alimentary tract diseases (adipositas, hyperlipidemia). The severity of acute pancreatitis is pathological anatomy determined by three stages. In pathogenesis the process of digestion is caused by activated pancreatic enzyme with acinar cell injury. The acinar cell is normally protected from the action of its own enzymes by elaborate intracellular compartmentation of enzymes. Acute pancreatitis is triggered by pancreatic phospholipase A leading to necrosis of lipolytically active fat cells with release of membrane-toxic fatty acids with following destruction of adjacent tissue. Fat necrosis initiates an acute inflammatory reaction with immigration of granulocytes and liberation of kinins, which activate pancreatic enzyme. Pancreatic enzymes are similar to lysosomal enzymes with regard to substrate specificity. Activation will be also triggered by lysosomal enzymes of necrotic acinar cells.
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PMID:[Acute pancreatitis--etiology, pathological anatomy and pathogenesis]. 226 Mar 61

We have made a comparative cross study of 30 patients with chronic pancreatitis and steatorrhea. The aim of the study has been to compare the effectiveness of a new galenic form of pancreatin, in pellets, with the common galenic presentation, in tablets. In all the cases the cause of pancreatic failure was alcoholism. In both groups the treatment was administered during seven days, after a period of wash out. We evaluated steatorrhea and clinical symptoms, including the typical abdominal pain. (The doses administrated were 12 tablets/day or 9 pellets/day.) Statistically there was a significant decrease of steatorrhea p less than 0.01.
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PMID:[A comparative cross-over study of pellet pancreatin and tablet pancreatin in chronic pancreatitis]. 263 38

Acute carbon tetrachloride poisoning in 19 patients was confirmed by means of laboratory analysis of blood specimens. The whole-blood carbon tetrachloride concentrations ranged from 0.1-31.5 mg/l. Vomiting (11 patients), abdominal pain (5), diarrhoea (4), and coma/drowsiness (6) were the commonest symptoms and signs. Out of 13 patients treated with intravenous acetylcysteine 7 showed mild hepatic damage, 1 had moderate hepatic damage, and 1 with a history of alcoholism sustained massive hepatorenal damage and needed haemodialysis. Of the 6 patients (1 lost to follow-up) who were not given acetylcysteine 3 had hepatorenal failure and needed dialysis, and 1 died. The possibility of carbon tetrachloride poisoning after ingestion of, or exposure to, chlorinated hydrocarbons and in patients presenting with hepatic or renal impairment without obvious cause should not be ignored. Prompt treatment with acetylcysteine may minimise subsequent hepatorenal damage.
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PMID:Acute carbon tetrachloride poisoning in 19 patients: implications for diagnosis and treatment. 285 73

Two patients with inflammatory bowel disease and no history of bilio-pancreatic disorders or alcoholism developed acute pancreatitis after therapy with sulfasalazine. The treatment lasted two months in the first case and four days in the second. The onset of pancreatic complications was heralded by jaundice; abdominal pain was a late symptom. The clinical course was dramatic in both cases, and one patient died. These findings agree with the hypothesis that sulfasalazine like other sulfonamidic compounds is a potentially pancreotoxic drug.
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PMID:Pancreatitis and pancreatic necrosis during sulfasalazine therapy. 287 81

Intratubular deposits of calcium oxalate crystals can be responsible for acute renal failure. The present report concerns two cases for which none of the known causes of oxalate nephropathy were found. Both patients had common features: chronic alcoholism and denutrition. Except for early lumbar and abdominal pain, the renal failure picture was without any peculiarity. Renal biopsy showed tubular epithelium alterations with marked luminal deposition of birefringent crystals consistent with calcium oxalate. In one patient serum oxalate level was high, and in the other urinary oxalate excretion rose above normal when diuresis resumed. Renal function recovered spontaneously (follow-up of four years for one patient). Neither intoxication nor intestinal disease could be detected. Given the key role of pyridoxine in oxalate metabolism, we suggest that vitamin B6 deficiency secondary to alcoholism and denutrition could cause a rise in oxalemia leading to oxalate nephropathy. Experiments in animals support this hypothesis.
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PMID:[Reversible acute renal failure with tubular oxalosis. Possible role of nutritional factors]. 323 1


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