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)

Hereditary Pancreatitis (HP), is an autosomal dominant trait, which presents with recurrent attacks of abdominal pain, and is the most common cause of chronic relapsing pancreatitis in children. In addition to recurring episodes of intense epigastric pain, patients have nausea, vomiting, and anorexia, and typically show elevated serum amylase levels during the acute episode that can rapidly decline in convalescence. Complications of long-standing disease include features of chronic pancreatitis, such as pancreatic pseudo-cyst, exocrine and endocrine failure, parenchymal calcification, and pancreatic cancer. A large family from Virginia, which was originally studied by Katwinkle and Lapey in 1973, was re-ascertained through a new proband. Linkage studies in this family mapped the gene to the 7q35 region, with similar results being reported simultaneously by two other groups. A pathogenic G to A transition mutation in exon 3 of the cationic trypsinogen (CT) gene, which had previously been mapped to this region, was found both in our family as well as other families from North America. Many other conditions can produce abdominal symptoms that are often mis-attributed to the disease in HP families. An affected member of our family in whom the mutation was confirmed by direct sequencing of exon 3 of the cationic trypsinogen gene requested diagnostic testing on his 4-year-old son because of onset of severe abdominal pain and vomiting. Screening for the mutation in this child did not reveal the pathogenic G to A change. These results prevented unnecessary invasive diagnostic procedures and treatment in this child. The pre-symptomatic testing of high risk individuals could, thus, have a significant impact on the well being of both affected and normal family members.
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PMID:Implications of molecular diagnostic testing in families with hereditary pancreatitis. 1046 47

Acute pancreatitis is one of the complications associated with severe primary and secondary hypertriglyceridemia. The frequency of hypertriglyceridemia in patients with pancreatitis ranges from 4 to 53%. The elevation in serum triglycerides probably induces the release of free fatty acids, responsible for the pancreatic damage. During a three year study, nine patients with acute pancreatitis due to hypertriglyceridemia were followed up at the University Hospital of Federal University and at the "Hospital Monte Sinai" (Juiz de Fora, MG, Brazil). Suggestive clinical manifestations, especially superior abdominal pain, nausea, vomiting and ileus, were found in all the patients; however, only three showed elevated serum amylase levels. All had triglyceride levels above 1000 mg/dl (11.3 mmol/L). The evolution after clinical treatment was good in eight patients (two needed parenteral nutrition). The only death observed was due to shock and acute respiratory distress, refractory to clinical management. The maintenance treatment aimed at withdrawing the predisposing conditions and reduction of the triglyceride levels prevented recurrence of acute pancreatitis episodes during the 23 months of follow-up.
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PMID:[Hyperlipemic pancreatitis: clinical course]. 1051 73

An aged male with a known history of abdominal aortic aneurysm suffered from epigastralgia, vomiting and cold sweating for one day. According to the physical examination, serum amylase level and computed tomographic examination, acute pancreatitis was diagnosed. Surgical intervention for the abdominal aortic aneurysm was not performed because of his age, and finally this patient died after three recurrent episodes. Acute pancreatitis co-existing with an intact abdominal aortic aneurysm has never been reported before. The possible pathogenesis of this recurrent acute pancreatitis was discussed.
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PMID:Abdominal aortic aneurysm compression is probably responsible for the recurrent episodes of acute pancreatitis: case report. 1052 53

BACKGROUND: Although unusual, but not rare, obstruction in the vicinity of the jejunojejunostomy in Roux-Y gastric bypass (RYGBP) can progress in a very short period of time to a life-threatening situation. METHODS: Over a 10-year period in 1,174 RYGBPs, we have seen seven instances of acute and subacute partial to complete small bowel obstructions in the vicinity of the jejunojejunostomy, which can lead to acute gastric dilatation due to obstruction of the bilio-pancreatic limb. Signs and symptoms of the obstruction may include tachycardia, oliguria, hypotension, severe epigastric pain with or without a palpable mass in the epigastrium, chronic bile regurgitation and bilious vomiting, and a possible increase in serum amylase. Laboratory data otherwise has not been helpful, and although a palpable abdominal mass may be diagnostic, the best tools have been radiologic, i.e. the acute abdomen series, limited upper GI series in the patients that appear to be only partially obstructed, abdominal ultrasound and probably most importantly, CT of the abdomen. RESULTS: In the seven cases presented, diagnoses included internal hernia, adhesions, an idiopathic spontaneous hematoma of the bowel wall and retrograde intussusception at the jejunojejunostomy. CONCLUSIONS: Since many surgeons who perform bariatric surgery are alone in their community, they should train their non-bariatric surgical colleagues and associates to be aware of these potential deadly problems.
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PMID:Biliopancreatic Limb Obstruction in Gastric Bypass at or Proximal to the Jejunojejunostomy: A Potentially Deadly, Catastrophic Event. 1072 97

Hereditary tyrosinemia results from an inborn error in the final step of tyrosine metabolism. Neurological manifestations have been reported in nearly half of patients during illness to have characteristics of altered consciousness, weakness, anorexia, vomiting, and pain in the extremities and abdomen. His physical findings and laboratory results pointed out acute pancreatitis. There have been some reports of acute and chronic pancreatitis in patients with metabolic diseases; however, this is the first case with tyrosinemia type I who exhibited clinical and biochemical findings of acute pancreatitis during neurological crisis. The presented case suggests the possibility that the pancreas is affected in neurological crisis. The determination of amylase concentration both in serum and urine samples of further cases will clarity the association between pancreatitis and neurological crisis.
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PMID:Neurological crisis mimicking acute pancreatitis in tyrosinemia type I. 1077 Jan 19

A case of erythropoietic protoporphyria associated with severe hepatic dysfunction and acute pancreatitis is reported. The patient, a 33-year-old man, was admitted to our hospital complaining of upper abdominal pain, nausea, and vomiting of 3 days' duration. Laboratory tests on admission demonstrated liver dysfunction, anemia, and thrombocytopenia. On the third hospital day, the intensity of the upper abdominal pain increased, concomitantly with elevated levels of serum amylase. Ultrasonography and computed tomography scanning revealed a slightly enlarged pancreas. During this episode, he also complained of various neurological symptoms, including reduced mental alertness, weakness of extremities, constipation, profound sweating, and urinary retention. Porphyrin studies demonstrated markedly elevated erythrocyte and fecal protoporphyrin levels. Laparoscopic findings obtained after the attack subsided were compatible with porphyric liver cirrhosis. We therefore concluded that neurologic disorders and acute pancreatitis could develop in patients with erythropoietic protoporphyria with severe liver dysfunction.
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PMID:Erythropoietic protoporphyria with severe liver dysfunction and acute pancreatitis. 1083 76

Cystadenomas of the pancreas are rare tumors. They represent about 10% of the pancreatic cystic masses. Several hundred cases seem to have been reported so far. These tumors appear as serous and mucinous. Over 13 years period (1983-1996) we treated 22 patients for cystadenoma of the pancreas. All patients were women. There were 6 serous and 16 mucinous cystadenomas. The average age in the serous group was 31 years (ranging from 23 to 42 years) and 43 years (ranging 17-64) in mucinous group. Two patients had tumor in the head, 20 others in the tail and body of the pancreas. The diameter of these tumors varied from 3.5 to 17.0 cm (average 9.6 cm). The leading symptoms were epigastric or left subcostal pain in 19 patients, palpable mass in 10, weight loss in 5, vomiting in 5, and melena in one patient. Tumor was accidentally found in a women undergoing abdominal operation for enteric fistula after hysterectomy. Serum amylase was moderately elevated in two patients. Diagnosis of pancreatic cystadenoma was proposed preoperatively in 16 patients (72.7%). In other cases, diagnoses of pancreatic cysts in 5 patients or hydatid cyst in 1 patient were made. An ideal operative removal (excision) was done in 7 patients, both excision of the tumor and splenectomy in 2, while distal pancreatectomy and splenectomy were carried out in 13 others. There was no mortality. One female patient developed left subphrenic abscess and left pleural effusion which were successfully treated by drainage and thoracocenthesis. One patient developed transient pancreatic fistula. All patients have been under close follow-up from 6 months to 13 years and all stayed symptom free so far.
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PMID:Cystadenomas of the pancreas. 1095 97

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

We present a patient with duodenal papillary carcinoma who repeatedly developed acute pancreatitis preoperatively. The patient was a 65-year-old male. In February 1997, the patient consulted a local hospital due to vomiting, high fever, and jaundice. With the diagnosis of obstructive jaundice, percutaneous transhepatic biliary drainage (PTBD) was performed, revealing a distal bile duct obstruction. Because duodenal papillary carcinoma was diagnosed based on endoscopic findings, the patient was admitted to Kurume University Hospital. Hypotonic duodenography (HDG) disclosed a protruding lesion with an irregular surface in the descending part of the duodenum, resulting in a diagnosis of positive duodenal invasion (du1). Because computed tomography (CT) demonstrated a protruding lesion on the medial side of the second portion of the duodenum, positive pancreatic invasion (panc2) was diagnosed. On March 18 and April 22, sudden abdominal pain, leukocytosis, and an increase in serum amylase were noted. CT revealed that the pancreas was diffusely enlarged, showing an ill-defined boundary between the pancreas and adipose tissue and fluid collection. On CT, the lesion was evaluated as Grade 3 and moderate. For treatment, pancreatic enzyme inhibitors and antibiotics were intravenously injected. Peritoneal perfusion was concomitantly performed during the second treatment. Because symptoms remitted thereafter, a pylorus preserving pancreatoduodenectomy (PpPD) was carried out. The postoperative histologic examination revealed negative pancreatic invasion. Concerning the etiology of acute pancreatitis, not pancreatic invasion, but impaction of the liberated tumor mass in the common canal was considered responsible for the repeated pancreatitis because the tumor showed a cauliflower-like shape.
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PMID:A case of duodenal papillary carcinoma complicated by repeated acute pancreatitis. 1105 25

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


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