Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 5-year-old mentally retarded child developed laboratory evidence of pancreatitis during accidental acute carbamazepine (CBZ) intoxication. He had been seizure-free with CBZ for 4 years for a seizure disorder with no obvious toxicity. CBZ had been discontinued 5 months before he was admitted to the hospital. After he accidentally ingested a CBZ overdose, he was found vomiting and lethargic. Serum amylase and lipase levels were increased for several days. With supportive treatment and no CBZ, he recovered and serum amylase and lipase levels returned to normal. No other causes of pancreatitis were identified. Therefore, most likely the chemical pancreatitis was associated with the acute CBZ intoxication.
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PMID:Acute chemical pancreatitis associated with carbamazepine intoxication. 842 54

The patient with acute pancreatitis requires constant assessments and interventions to minimize pancreatic inflammation and promote early detection and treatment of systemic complications. The onset of acute pancreatitis is most commonly initiated by biliary or alcohol disease, although many other causes have identified. The course of the disease may range from mild to fulminant based on the degree of pancreatic necrosis. Significant clinical symptoms include abdominal pain, nausea, and vomiting. The patient may present with signs of hypovolemic shock, with associated sequestration of fluid in the peritoneum as a result of inflammatory and mediated responses. Laboratory evidence of the disease includes increased levels of amylase and lipase, although a definitive diagnosis cannot be made without radiographic tests. Multisystem failure can occur in necrotizing acute pancreatitis as a result of mediators that are activated by the proteolytic enzymes, normally produced by the pancreas, and released into the peritoneum by injured cells. Collaborative management of the patient includes therapies directed at correcting initiating events, hemodynamic stabilization, and supportive measures to rest the pancreas and resolve presenting clinical symptoms. The management of multisystem organ failure that can result from necrotizing pancreatitis is a multidisciplinary challenge.
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PMID:Acute pancreatitis. 844 97

To determine the frequency of pancreatitis and to define risk factors for pancreatitis in patients with AIDS, we compared patients with pancreatitis to patients without pancreatitis in an urban infectious disease practice. Pancreatitis was defined as at least one clinical sign or symptom (nausea, vomiting, abdominal pain, or tenderness) accompanied by elevation of serum amylase or lipase. Twenty-four (22%) of 105 patients with AIDS, 2 (4%) of 46 patients with AIDS-related complex, 1 (3%) of 39 asymptomatic patients infected with HIV-1, and none of 9 uninfected patients at risk for HIV-1 developed pancreatitis as defined above. Fourteen patients experienced multiple episodes and three were symptomatic for more than 2 months. Pancreatitis was more likely to have occurred in patients with AIDS (P < .001), biliary tract disease (P = .013), and hypertriglyceridemia (P = .032). After matching for these factors and duration of current HIV disease, cryptosporidiosis, intravenous pentamidine, and isoniazid were each associated independently with pancreatitis (P < .05). Before didanosine (ddl) became available, 22% of the patients with AIDS in this practice had pancreatitis. Cryptosporidiosis, isoniazid, and intravenous pentamidine should be considered among the potential etiologies.
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PMID:Pancreatitis associated with human immunodeficiency virus infection: a matched case-control study. 882 75

We report a case of acute pancreatitis with diabetic ketoacidosis associated with increased serum myoglobin concentration, acute renal failure, and disseminated intravascular coagulation. A 49-year-old man suffering from diarrhea, vomiting, and somnolence was admitted to the hospital. He had had flu-like symptoms for 4 days prior to the onset of these symptoms. He was a habitual drinker and had been consuming 360 ml-900 ml of the drink "shochu" (distilled spirits containing 28% alcohol) daily for 30 years. Laboratory data on admission revealed elevated serum levels of pancreatic enzymes, including amylase, trypsin, lipase, pancreatic secretory trypsin inhibitor (PSTI), phospholipase A2 (PLA2), and elastase-1, as well as elevated levels of glucose (373 mg/dl), ketone bodies (3675 mumol/l), and myoglobin (229.8 ng/ml). Treatment with subcutaneous insulin and intravenous administration of electrolyte fluid and the systemic protease inhibitor, gabexate mesilate, was begun immediately. Early after the initiation of treatment, there was an increase in serum creatinine (4.9 mg/dl), and thromobocytopenia (15000/microliters) was observed. The patient completely recovered from renal failure and acute pancreatitis, but required insulin therapy. Alcohol ingestion and dehydration are thought to have played a major role in the triggering of the acute pancreatitis. We examined the relationship among acute pancreatitis, diabetic ketoacidosis, and hypermyoglobinemia in the literature.
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PMID:Acute pancreatitis with diabetic ketoacidosis associated with hypermyoglobinemia, acute renal failure, and DIC. 884 91

We report the case of a 61-year-old woman, who suffered from abdominal pain, nausea, vomiting and fever. She had a past medical history of acute rheumatism, pyelonephritis and systemic scleroderma. Since 1971 she was hospitalized many times because of recurrent abdominal pain with increased serum amylase and lipase values. On admission, she was in distress and demonstrated clinical signs of acute pancreatitis. The link between systemic lupus erythematosus and acute pancreatitis is discussed in view of the reported cases of the world literature.
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PMID:Pancreatitis in systemic scleroderma. 936 Feb 94

A six-year-old, spayed female Shetland sheepdog was presented with acute onset of anorexia and vomiting. An inflammatory leukogram and elevated serum amylase, lipase, alkaline phosphatase, alanine transferase, and triglycerides supported a diagnosis of severe acute pancreatitis. An enlarged, hypoechoic pancreas was visualized on abdominal ultrasonography. The patient clinically responded to medical therapy consisting of nothing per os, total parenteral nutrition, and supportive care. She presented again three weeks later with anorexia and vomiting. A large, anechoic mass was seen in the left limb of the pancreas on ultrasonographic examination of the abdomen. Differentials for this mass included abscess, focal peritonitis, and pancreatic pseudocyst. Clinical signs resolved with supportive care. The mass failed to resolve. Sterile fluid (35 ml) was removed via ultrasonographic-guided centesis 42 days after initial presentation. Ultrasonographic appearance, biochemical analyses, and fluid examination with negative cultures suggested pancreatic pseudocyst. The pseudocyst gradually resolved over the next seven months postcentesis.
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PMID:Resolution of a pancreatic pseudocyst in a dog following percutaneous ultrasonographic-guided drainage. 982 89

Despite the uncommon clinical diagnosis, cats frequently suffer from disorders of the exocrine pancreas. Pancreatitis is the most common feline exocrine pancreatic disorder. Pancreatitis can be acute or chronic and mild or severe. The etiology of most cases of feline pancreatitis is idiopathic. Some cases have been associated with severe abdominal trauma, infectious diseases, cholangiohepatitis, and organophosphate and other drug intoxication. The clinical presentation of cats with pancreatitis is nonspecific. Vomiting and signs of abdominal pain, which are the clinical signs most commonly observed in humans and dogs with pancreatitis, are only uncommonly observed in cats with pancreatitis. Routine laboratory findings are also nonspecific. Abdominal ultrasonography is a valuable diagnostic tool in feline patients with pancreatitis. Serum activities of lipase and amylase are rarely increased in cats with pancreatitis; however, these cats often have elevated serum fTLI concentrations. The goals of management are removal of the inciting cause, provision of supportive and symptomatic therapy, and careful monitoring for and aggressive treatment of systemic complications. Exocrine pancreatic insufficiency is a syndrome caused by insufficient synthesis of pancreatic digestive enzymes by the exocrine portion of the pancrease. The clinical signs most commonly reported are weight loss, loose and voluminous stools, and greasy soiling of the hair coat. Serum fTLI is subnormal in affected cats. Treatment of cats with EPI consists of enzyme supplementation with powdered pancreatic extracts or raw beef pancreas. Many cats with EPI have concurrent small intestinal disease. Most cats with EPI also have severely decreased serum cobalamin concentrations and may require parenteral cobalamin supplementation. Pancreatic adenocarcinoma is the most common neoplastic condition of the exocrine pancreas in the cat. At the time of diagnosis, the tumor has already metastasized in most cases, and the prognosis is poor. Pancreatic pseudocyst, pancreatic abscess, pancreatic parasites, pancreatic bladder, and nodular hyperplasia are other exocrine pancreatic disorders, that are less commonly seen in cats.
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PMID:Feline exocrine pancreatic disorders. 1020 2

A squirrel monkey (Saimiri sciureus) presented with wasting, vomiting and diarrhoea. Haematology revealed elevation of creatinine phosphokinase, lactic dehydrogenase, alanine aminotransferase, amylase and lipase, together with azotaemia and hypoalbuminaemia. Prominent findings were chronic pancreatitis with acinar and ductal plugs, granulomatous and necrotizing peripancreatic steatitis, degenerative myopathy, testicular atrophy, candidiasis and bacterial necrotizing glossitis. Antioxidant analyses revealed low concentrations of serum vitamin E (and apparently A), hepatic selenium and hair zinc. Pancreatitis may have caused malabsorption and maldigestion, associated with deficiency of multiple antioxidants.
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PMID:Antioxidant status in a squirrel monkey (Saimiri sciureus) with chronic pancreatitis and degenerative myopathy. 1103 77

The case is described of a 32-year-old man suffering from alcoholism who came to the Emergency Unit with vomiting, fever and sharp epigastric pain irradiating to the chest and upper abdomen. A diagnosis of acute pancreatitis was made after high amylase and lipase levels were observed and the results of computed tomography scan revealed images typical of acute pancreatitis. Findings upon admission and after the initial 48 hours did not correlate with a severe or complicated course according to Ranson's criteria. On the third day after admission he suddenly developed decreased vision. A fluorescein angiogram showed arteriolar occlusion, retinal and choriocapillary ischaemia. Purtscher's retinopathy was suspected. After 4 weeks, the patient had recovered from acute pancreatitis, ophthalmoscopic examination showed normal results, and visual acuity had almost returned to normal. Activation of complement in acute pancreatitis could account for many haematologic acute disorders due to leucocyte emboli or other complement-mediated aggregates. Coagulation abnormalities may range from isolated intravascular thrombosis to severe disseminated intravascular coagulation. Purtscher's retinopathy, due to microembolizations in the choroidal and retinal arterioles, should be included among the various systemic effects of acute pancreatitis. This visual disorder is a rare systemic manifestation of acute pancreatitis which was not correlated to a severe or complicated clinical course. Treatment of these ocular complications remains to be established and outcome, therefore, depends upon resolution of the pancreatic disease.
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PMID:Acute pancreatitis with Purtscher's retinopathy: case report and review of the literature. 1114 85

Twenty six (7.3%) of a total of 356 patients with acute renal failure were found to have acute pancreatitis as the primary disease. Seventeen (65.4%) of them were males. Their mean age was 35.6 years. Clinically epigastric pain and tenderness were seen in all (100%); nausea vomiting (73%), low grade fever (50%), left sided pleural effusion (38.4%), haemopericardium (26.9%), shock (26.9%), pseudocyst (19.3%) and adult respiratory distress syndrome (7.6%) were the other major presenting features. Serum amnylase (100%), lipase (53.8%), triglycerides (53.8%) and blood sugar (38.5%) were raised in majority whereas serum calcium was detected to be below normal in 46.2% patients. Blood urea and serum creatinine were raised in all and hyperkalacmia was found in 50% patients. CT scan and USG abdomen showed bilateral enlarged kidneys (100%), pancreatic oedema (80.7%), necrosis of pancreas (19.3%) and pseudocyst (19.3%). Management included repeated peritoneal dialysis in all (100%) and surgical intervention in 53.8% patients with severe necrotising and haemorrhagic pancreatitis. All patients recovered from acute renal failure, but 26.9% patients expired due to complications of acute pancreatitis other than acute renal failure.
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PMID:Renal failure in acute pancreatitis. 1125 2


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