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)

We report three patients with diabetic ketoacidosis (DKA) who presented with striking elevations of serum lipase levels and less striking elevations of amylase and trypsinogen. All three had nausea and vomiting, but none had objective evidence of abdominal pain, and computed tomography scans of the pancreas were unremarkable. These cases suggest the association of asymptomatic enzyme elevations with DKA. We review the literature on this subject.
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PMID:Marked hyperlipasemia in diabetic ketoacidosis. A report of three cases. 138 14

A 28-year-old woman with nausea, vomiting, and abdominal pain had been hospitalized elsewhere on 13 separate occasions over the year before this admission for similar episodes thought to be secondary to acute pancreatitis. She had undergone repeated work-ups including endoscopic retrograde cholangiopancreatography, computed tomographic scan, and exploratory laparotomy. There was a discrepancy between her unremarkable physical examination and extremely elevated amylase (3,210 U/L) which suggested nonpancreatic hyperamylasemia; normal serum pancreatic isoamylase, trypsinogen, and lipase confirmed this suspicion. The patient was noted to have self-induced vomiting in the hospital which she admitted was frequent behavior. her psychiatric disturbance was characterized as an atypical eating disorder. This case illustrates that hyperamylasemia in association with abdominal pain, nausea, and vomiting may not be secondary to pancreatitis and that use of a second serum marker (such as trypsinogen, lipase, or isoamylase) helps to establish a definitive diagnosis.
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PMID:Atypical eating disorder masquerading as recurrent acute pancreatitis: the value of multiple pancreatic serological markers. 168 31

Acute pancreatitis is characterized by clinical, morphological, and functional aspects. Severe abdominal pain with progression during the first hours after onset is the leading symptom. In the majority of patients acute pancreatitis had a "mild" clinical course, but 10 to 20% will develop severe local and systemic complications. Symptoms at the onset of disease are not specific and need consideration of several other diagnoses. Elevation of pancreatic serum enzymes is the main parameter in the diagnosis of acute pancreatitis. Besides the traditional parameter of total amylase, several specific pancreatic enzymes (e.g. pancreatic amylase, lipase, immunoreactive trypsin or elastase) are now widely used in clinical routine and guarantee a higher diagnostic specificity. The imaging procedures ultrasonography and computed tomography aid in identifying etiological factors in grading the severity of the disease and deciding therapeutic strategies. Endoscopic retrograde chol- angiopancreatography is most sensitive in detecting biliary lithiasis and can be successfully complemented by sphincterotomy if needed. Besides complex clinical and laboratory criteria, several biochemical markers (e.g. C-reactive protein, PMN-elastase, trypsinogen activation peptides) have been found to be valid for the detection of pancreatic necrosis and are of definite prognostic value. On the basis of such detailed information, the therapeutic strategy can be planned in a straight-forward manner.
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PMID:Clinical picture and diagnosis of acute pancreatitis. 185 80

We compared the diagnostic sensitivities of serum amylase, lipase (assayed enzymatically and immunologically), trypsinogen and elastase-1, the 2-h-timed urine amylase excretion and the ratio of amylase and creatinine clearances in the recognition of acute pancreatitis. Serial serum and urine findings from 39 patients with acute pancreatitis, and from 42 patients with non-pancreatic causes of abdominal pain (controls), as well as findings from 24 healthy subjects (normals) were studied. Decision thresholds were established for each parameter using either the control or the normal population, and the resulting diagnostic sensitivities determined. On hospital admission, all serum assays were equally sensitive, but on subsequent days lipase, trypsinogen and elastase-1 assays all significantly surpassed the sensitivity of the serum amylase assay. On the second and subsequent hospitalization days, determination of timed urine amylase excretion offered no advantage over the serum amylase, and the ratio of amylase and creatinine clearances lacked discrimination altogether.
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PMID:Comparative evaluation of the diagnosis of acute pancreatitis based on serum and urine enzyme assays. 232 64

The serum behavior of amylase, pancreatic isoamylase, lipase, trypsinogen, and elastase 1 was studied in 145 patients with pancreatic disease and in 66 patients with abdominal pain of nonpancreatic origin, for the purpose of evaluating the relative diagnostic utility of their assays. In 34 patients with acute pancreatitis, serum lipase, trypsinogen, and elastase 1 were elevated in all 34, pancreatic isoamylase in 33 (97%) and amylase in 30 (88%). Ten of these acute pancreatitis patients were followed sequentially for seven days: the variations in their serum enzyme levels were parallel, although the lipase, trypsinogen, and particularly the elastase 1 elevations persisted longer than did those of amylase and pancreatic isoamylase. Among the patients with chronic pancreatitis, either in painful relapse (N = 19) or with pancreatic cysts (N = 15), the respective percentages of enzymes elevations were: 79 and 80% for elastase 1, 68 and 67% for trypsinogen, 63 and 73% for pancreatic isoamylase, 58 and 60% for lipase, 53 and 60% for amylase. In the 52 chronic pancreatitis patients studied during clinical remission, serum enzyme behavior varied greatly, and a majority of the assays (60%) were normal; even in the case of severe pancreatic exocrine insufficiency, normal as well as abnormally high and low enzyme values were seen. Highly variable enzyme behavior was also seen in the 40 patients with pancreatic cancer, and elastase I was the most frequently (35%) elevated enzyme in this group as well. Among the patients with abdominal pain of nonpancreatic origin, abnormally high enzyme levels were present in percentages ranging from 6% for lipase to 21% for trypsinogen.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of serum pancreatic enzyme assays in diagnosis of pancreatic disease. 279 21

The sensitivity and specificity of five assays used to diagnose acute pancreatitis were studied: two amylase assays; one lipase; one trypsinogen; and one pancreatic isoamylase. Thirty-nine patients with acute pancreatitis were compared to 127 controls with abdominal pain. Using the upper limit of normal both amylase assays appeared sensitive but somewhat nonspecific (specificities of 88.9% and 86%, respectively). The trypsinogen and pancreatic isoamylase assays were also relatively nonspecific (specificity of 82.8% and 85.1%). Most nonspecific elevations occurred between a one- and twofold elevation of each assay. Lipase, however, maintained excellent specificity (99%) at its upper limit of normal. If the level of best cutoff is used instead (the level that best enhances sensitivity and specificity), the specificities of both amylase assays, as well as the trypsinogen and pancreatic isoamylase assays, exceed 95%. At the best cutoff level, trypsinogen maintains a qualitative advantage in sensitivity over lipase or pancreatic isoamylase (97.4% as compared to 86.5% and 84.6%).
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PMID:Diagnostic assays in acute pancreatitis. A study of sensitivity and specificity. 258 Apr 67

Chronic pancreatitis should be considered in all patients with unexplained abdominal pain. The importance of small duct disease without obvious radiographic abnormalities is an important new concept. Diagnostic evaluation should begin with simple, non-invasive, inexpensive tests (serum trypsinogen) to be followed by more complicated testing (hormone stimulation test) if needed. Enteric-coated pancreatic enzymes are the drugs of choice for treating steatorrhea, while conventional non-enteric coated enzymes are preferred for managing pain. The somatostatin analogue octreotide may become an important therapy for treating abdominal pain unresponsive to pancreatic enzyme therapy. Endoscopic approaches to the treatment of chronic pancreatitis are experimental and may cause damage to the pancreas. Surgical ductal decompression is appropriate in selected patients.
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PMID:Medical management of chronic pancreatitis. 777 9

Hereditary pancreatitis is an autosomal dominant disorder with incomplete penetrance. It is characterised by recurring episodes of severe abdominal pain and often presents in childhood. Recently, a mutation in the cationic trypsinogen gene was identified in this disease. Previously, only one mutation at residue 117 of the trypsinogen gene has been found in the five separate hereditary pancreatitis families, four from the USA and one from Italy. Alteration of the Arg117 site is believed to disrupt a fail-safe mechanism for the inactivation of trypsin, leading to autodigestion of the pancreas under certain conditions. Molecular analysis of the trypsinogen gene was carried out on a hereditary pancreatitis family from the UK. The same G to A mutation at residue 117 was identified in this family, suggesting that this is a common mutation in hereditary pancreatitis.
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PMID:Evidence for a common mutation in hereditary pancreatitis. 971 98

Chronic pancreatitis should be considered in all patients with unexplained abdominal pain. The importance of small duct disease without obvious radiographic abnormalities is an important new concept. It is meaningful for the clinician to define whether the patient with chronic pancreatitis has small duct or large duct disease. Diagnostic evaluations should begin with a simple, noninvasive, inexpensive test such as serum trypsinogen, to be followed by more complicated testing such as the secretin stimulation test, particularly in those patients with small duct disease. Non-enteric-coated pancreatic enzyme preparations are preferred for the treatment of pain whereas enteric-coated pancreatic enzyme preparations are the drugs of choice for treating steatorrhea. Octreotide may become an important therapy for treating abdominal pain unresponsive to pancreatic enzyme therapy. Endoscopic treatment of the pain of chronic pancreatitis should be used only in highly selected patients and may cause damage to the pancreas. Surgical ductal decompression is appropriate in selected patients.
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PMID:Update on diagnosis and management of chronic pancreatitis. 1098 Sep 31

Chronic pancreatitis should be considered in all patients with unexplained abdominal pain. Management of abdominal pain in these patients continues to pose a formidable challenge. The importance of small duct disease without radiographic abnormalities is now a well-established concept. It is meaningful to determine whether patients with chronic pancreatitis have small duct or large duct disease because this distinction has therapeutic implications. Diagnostic evaluation should begin with simple noninvasive and inexpensive tests like serum trypsinogen and fecal elastase, to be followed where appropriate by more complicated measures such as the secretin hormone stimulation test, especially in patients with suspected small duct disease. No universal causal treatment is available. Non-enteric-coated enzyme preparations are useful for treatment of pain, whereas enteric-coated enzyme preparations are preferred for steatorrhea. Octreotide is used increasingly for abdominal pain that is unresponsive to pancreatic enzyme therapy. When medical therapy for chronic pancreatitis pain has failed, endoscopic therapy, endoscopic ultrasound-guided celiac plexus block, and thoracoscopic splanchnicectomy, performed by experts, may be considered for a highly selected patient population. Surgical ductal decompression is appropriate in patients with considerable pancreatic ductal dilation. The role and efficacy of cholecystokinin-receptor antagonists, antioxidants, and antidepressant drugs remain to be defined.
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PMID:Medical therapy for chronic pancreatitis pain. 1263 50


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