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Query: UMLS:C0001339 (acute pancreatitis)
 10,593 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We evaluated three commercially available methods for determining lipase (EC 3.1.1.3) in serum--the Du Pont aca, Boehringer Mannheim Diagnostics (BMD), and Kodak Ektachem (EK) procedures--for their analytical properties and diagnostic efficiencies. Titrimetry was used as the comparative method. The BMD and EK methods showed better agreement with the titrimetric method, owing to the presence of the necessary cofactor, colipase, in their reagents. Colipase also increased the analytical sensitivity of the BMD and EK procedures as compared with the aca method. Determinations of serum lipase, by all methods, had a clinical sensitivity in excess of 80% for acute pancreatitis; the specificity of the lipase test was about 60%, or twice that of serum amylase. Serum lipase determinations with the current, simpler technology are superior to total amylase in the diagnosis of patients with acute pancreatitis. When a colipase-supplemented method is used, a serum lipase value greater than 10-fold the upper reference limit appears to be pathognomonic for acute pancreatitis or inflammation of organs close to the pancreas.
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PMID:Assays of serum lipase: analytical and clinical considerations. 242 37

A rapid procedure for determining salivary- and pancreatic-type amylase (EC 3.2.1.1) in serum by incorporating a wheat germ inhibitor (from Triticum aestivum) was developed for the Du Pont aca IV analyzer. Under optimal assay conditions, activities of salivary and pancreatic amylase were inhibited by 93% and 19%, respectively. The 95% central reference interval for the percentage of inhibition of serum amylase was 38-84%. Patients with acute pancreatitis showed less than 26% inhibition of amylase after addition of the wheat germ extract, reflecting the prevalence of pancreatic-type amylase in this disorder.
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PMID:Determination of amylase activity in serum by using a wheat germ inhibitor with the Du Pont aca. 242 9

Fifty-one patients, 35 men and 16 women, with acute pancreatitis were studied prospectively with early computed tomography (CT). Etiological factors for acute pancreatitis were alcohol abuse (n = 28), gallstones (n = 14), pancreas cancer (n = 3) and miscellaneous (n = 6). Admission serum amylase levels ranged between 68-5,856 U/L with a mean of 1,090 +/- 1,369 U/L. The mean serum amylase level was significantly different between patients with alcoholic pancreatitis (439 +/- 302 U/L) and gallstone pancreatitis (2,480 +/- 1,575) (p less than 0.001). The initial pancreatic CT findings and corresponding mean serum amylase levels were in CT grade A (pancreas normal) 1,499 +/- 1,569 U/L (n = 11), in CT grade B (pancreatic enlargement with inflammation confined to pancreas) 1,144 +/- 1,542 U/L (n = 18), in CT grade C (inflammatory extension into one peripancreatic space) 722 +/- 962 U/L (n = 13) and in CT grade D (inflammatory extension into two or more peripancreatic spaces) 590 +/- 369 U/L (n = 9). However, on separating the etiology subgroups, there was no increase or decrease in the serum amylase level with increasing pancreatic inflammatory involvement. Pancreatic complications (pseudocyst, abscess, necrosis) requiring surgical intervention developed only in patients with CT grades C and D. We conclude that within the etiologic subgroups there is no correlation between the initial serum amylase level and the extent of pancreatic involvement visualized by CT. These findings provide a pathological basis for the clinical observation that the initial serum amylase level cannot predict the outcome in acute pancreatitis.
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PMID:Correlation of serum amylase levels with pancreatic pathology and pancreatitis etiology. 245 72

Among 100 consecutive patients with pancreatic pseudocysts, a biliary cause for the preceding acute pancreatitis was found in 27, for a mortality rate of 22 percent. Patients with alcohol abuse as the cause had a more favorable prognosis, with a 5 percent mortality rate among 59 patients (p less than 0.05, chi-square test). Despite an age difference between the two groups, we consider that this feature of patients with pancreatic pseudocyst warrants attention and we make recommendations herein with respect to therapy. Pseudocysts developed in 86 patients consequent to an episode of acute pancreatitis, and all 12 deaths (14 percent) were in this group. None of the remaining 14 patients whose pseudocysts were a feature of chronic pancreatitis died. Of the 81 patients in whom amylase levels were measured, 76 percent had an increased level.
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PMID:Importance of cause in the outcome of pancreatic pseudocysts. 245 84

Recent longitudinal studies have improved the knowledge of the natural history of chronic pancreatitis. This disease is mainly induced by alcohol abuse. Mean age at onset of the disease is 40 years. First symptoms are generally pain, often related to acute pancreatitis. Over the first five years of course, complications as pseudocysts or common bile duct stenoses can occur, often necessitating surgical treatment. In the late course, the disease becomes less symptomatic but the risk of diabetes mellitus increases. Occurrence of pancreatic calcifications is observed with time in the majority of patients. Chronic pancreatitis is associated with overmortality but the causes of death are mainly extrapancreatic (alcoholic liver disease and cancers). Abnormalities of pancreatic secretion induced by alcohol abuse play an important role in the pathophysiology of the disease: it is possible that the decrease of concentration of the "pancreatic stone protein" promotes formation of calcifications. Direct toxicity of alcohol is another possible factor.
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PMID:[The natural history and physiopathology of chronic pancreatitis]. 248 15

Three patients with retinopathy associated with acute pancreatitis were observed. Each of them had a long history of alcohol abuse. The first patient was asymptomatic. Second one developed moderate visual loss in one eye (visual acuity 20/40), with a fascicular defect on Goldmann visual field registration. Third patient complained with bilateral and severe visual loss, with a large central scotoma. Cotton-wool patches and hemorrhages were present in the mild types of retinopathy. These cases had a good prognosis. An ischemic edema of posterior pole was associated in severe type of retinopathy. In this case, fluorescein angiography showed occluded macular retinal arterioles. Visual prognosis was poor. Pathogenesis of the lesions is still discussed. The main hypothesis are fat emboli or activated complement-induced granulocyte embolus formation. Efficacity of corticosteroids is not known.
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PMID:[Retinopathy in pancreatitis]. 262 70

Utilising incomplete data supplied by the Hospital Inpatient Analysis, the annual incidence of acute pancreatitis in Northern Ireland was estimated to be about 170 cases per million population. The annual mortality rate for the years 1974-1983, using figures obtained from the Registrar-General for Northern Ireland, was 12.3 cases per million. An increase in both incidence and mortality from acute pancreatitis was demonstrated during the study. There was 191 deaths from pancreatitis during the study period and in 27 of these the diagnosis was made only at postmortem examination. Of the undiagnosed fatalities, 10 occurred in individuals with a history of alcohol abuse. Eight of the 27 undiagnosed cases had not sought medical attention, five had presented with a systemic complication of acute pancreatitis, and a further five had only minor gastrointestinal tract symptoms prior to death. The diagnosis of acute pancreatitis requires a high index of suspicion and should be considered in acutely ill patients, particularly those with a history of alcohol abuse, who fail to respond to appropriate therapy.
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PMID:Acute pancreatitis as a cause of sudden or unexpected death in Northern Ireland. 278 46

Human acute pancreatitis results from an autodigestive process frequently associated with alcohol abuse, gall stone disease and shock. Peripancreatic fat necrosis was identified as one of the earliest visible lesions, whereas acinar cell necrosis and haemorrhage were regarded as secondary changes. To examine the alterations in acinar cells in more detail, their enzyme content and fine structural features were studied immunocytochemically using antisera against alpha-amylase, lipase, trypsin, chymotrypsin and pancreatic stone protein, and electronmicroscopically in pancreatic tissues from patients with severe acute pancreatitis. Peripheral acinar cells in the immediate vicinity of fat necrosis were found to be heavily degranulated, while acinar cells at some distance of necrosis fully retained their enzyme content. Other frequent changes of the acinar cells included cuboidal transformation, loss of microvilli, increased occurrence of autophagosomes, and formation of enlarged acinar lumina. As there was no apparent cell membrane leakage or rupture of duct lumina, it is concluded that the acinar cells adjacent to fat necrosis release their granules by undirected basolateral extrusion. The findings thus suggest that one of the basic defects in acute pancreatitis is the uncontrolled release of enzymes from peripheral acinar cells into the interstitial space which, in turn, presumably by the action of lipase, leads to autodigestive fat necrosis.
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PMID:Human acute pancreatitis: its pathogenesis in the light of immunocytochemical and ultrastructural findings in acinar cells. 309 41

The long-held tenet that a cause and effect relation exists between primary hyperparathyroidism and pancreatitis has recently been questioned. To clarify this association, records of 1475 patients seen with pancreatitis during a 10-year period were reviewed. Five patients (0.4%) were identified with primary hyperparathyroidism. The four men and one woman ranged in age from 31 to 57 years. Four had recurrent pancreatitis over a 2-10 yr period before hyperparathyroidism was diagnosed. One patient had hypercalcemia noted 1 year prior to developing pancreatitis. Four patients had associated potential causes of pancreatitis including alcohol abuse, gallstones, and hypotension. Pancreatitis was severe in each patient. Two patients had more than four admissions for acute pancreatitis, one patient underwent pseudocyst drainage and distal pancreatectomy for chronic pancreatitis, one patient underwent pancreaticojejunostomy for chronic pancreatitis, and one patient died from hemorrhagic pancreatitis. Four patients have undergone successful parathyroidectomy and have had no further attacks of pancreatitis on follow-up ranging from 1 to 4 years. Hyperparathyroidism is rarely associated with pancreatitis, but when this combination occurs, the pancreatitis is likely to be severe. Despite its rarity, a cause and effect relationship is still suggested by the fact that parathyroidectomy seems to prevent recurrence of pancreatitis.
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PMID:The association of primary hyperparathyroidism and pancreatitis. 399 75

Of 311 patients with primary acute pancreatitis, seven revealed major and seven minor lipid abnormalities on hospital admission. One pregnant woman suffered acute pancreatitis associated with Fredrickson type I hyperlipoproteinaemia. Twelve of the 13 men with types IV and V hyperlipoproteinaemia suffered alcohol abuse pancreatitis and represented 13.2 per cent of this aetiological group. However, only one of the 157 patients (0.6 per cent) with biliary disease had lipid abnormalities. Two of the 13 men died--the oldest, who had gallstones, and one with alcohol related disease. The remaining 11 were subject to follow-up (5-10 years). Six, who had improvement of their lipid abnormalities, had abstained from alcohol. The other five had a persistent lipid disorder, and all admitted continuing heavy alcohol ingestion. The clinical diagnosis of acute pancreatitis was supported by serum amylase elevation in only nine of the fourteen patients. Urinary amylase levels were consistent with the diagnosis in 11 of the 12 patients. Estimation of both serum and urinary amylase gave 100 per cent support to the clinical diagnosis of acute pancreatitis. Hyperlipidaemia associated with acute pancreatitis may be secondary to alcohol abuse but the possible role of HLP cannot be discounted. Urinary amylase is useful in diagnosing acute pancreatitis in the presence of hyperlipidaemia.
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PMID:Hyperlipidaemia, alcohol abuse and acute pancreatitis. 620 8


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