Cause Of Hyperamylasemia Research Articles

A rare cause of hyperamylasemia: A case with pneumothorax and subcutaneous emphysema around the parotid gland in a trauma patient

Amylase is a common laboratory test in emergency departments, especially in trauma patients. Although hyperamylasemia is mostly caused by injury to the pancreas in trauma patients, non-pancreatic causes of hyperamylasemia are not rare. Being aware of these causes may prevent unnecessary diagnostic tests. In this study, we presented a trauma patient with hyperamylasemia of non-pancreatic origin. Possible mechanisms of hyperamylasemia in our case are acute hypoxia-induced hyperamylasemia because of left lung pneumothorax and massage-like activity of subcutaneous emphysema around the parotid gland.

Makroamilazemija kao razlog hiperamilazemije u klinički nejasnim stanjima - prikaz slučaja

Macroamylasemia is a rare condition characterized by elevated serum amylase levels due to the existence of macromolecules - complex amylase that cannot be secreted normally by the kidneys due to their size. It is a benign condition that is usually free of marked clinical symptoms and signs. The prevalence of macroamylasemia in the population is between 1 and 2%. The main clinical significance of macromylasemia is that it is often a diagnostic problem because it requires differentiation of this condition from other causes of hyperamylasemia. Therefore, it is rational to avoid unnecessary diagnostics and treatment, which burden both the patient and the health system. Macromalasemia as a diagnosis should be considered in any patient with elevated serum amylase activity in whom serum lipase and urine amylase levels are normal. Laboratory confirmation of the diagnosis of amylasemia rests on tests: electrophoresis or polyethylene glycol precipitation test. This paper presents a patient who has been routinely treated clinically due to non-specific gastrointestinal problems. During laboratory treatment, the patient's serum was found to have elevated amylase values. Additional diagnostics did not identify organic pancreatic diseases or other diseases that may be related to hyperamylasemia, and by calculating the ratio of renal amylase clearance to creatinine clearance of less than 1%, we conclude that it is most likely a macroamylasemia. Specific treatment was not required. The patient comes for a check-up once every 6 months.

A rare cause of hyperamylasemia

abc.2012.0695 Auteur(s) : Hatim Nafil solhatim@hotmail.com, Illias Tazi, Lahoucine Mahmal Service d’hematologie, CHU Mohamed VI, Universite Cadi Ayyad, Marrakech, Maroc Une femme de 66 ans, d’origine maghrebine, est hospitalisee en fevrier 2008 pour des douleurs rachidiennes. L’examen clinique a montre une patiente pâle, asthenique ; il n’a pas ete note de masses palpables ni de signes infectieux. Les examens biologiques ont montre une vitesse de sedimentation (VS) [...]

Elevated Amylase and Lipase Mimicking Pancreatitis: Diagnostic Pitfall

Purpose: Introduction: Serum amylase and lipase levels are standard tests to diagnose acute pancreatitis. However, they can be elevated in various clinical settings, including acute gastroenteritis or chronic alcoholism. Recognition is particularly important because using an elevated amylase or lipase level to diagnose acute pancreatitis may not be appropriate. We herein present a case of elevated amylase and lipase levels in the absence of acute pancreatitis. Case Presentation: A 56-year-old male with chronic alcoholism presented with nausea and vomiting for 5 days. He denied abdominal pain, fever or diarrhea. His past medical history was insignificant. He admitted alcohol abuse, notably hard liquors, which constituted his major dietary intake. His vital signs were T 96.9F, HR 90 /min, BP 142/91 mmHg, SpO2 97% on room air. He appeared disheveled. His heart sounds were regular and lungs were clear to auscultation. His abdomen was soft, bowel sounds were diminished but no tenderness was present. His complete blood count and metabolic panel were normal. His liver panel showed a slightly elevated ALT level of 90 U/L with normal bilirubin, ALP and ALT level. Serum amylase and lipase level was found to be 216 mg/dL and 702 mg/dL respectively. His alcohol level was 404 mg/dL. Ultrasonography showed fatty infiltration in the liver with intact pancreas, spleen and gallbladder. Subsequent esophagogastroduodenoscopy (EGD) revealed nonerosive gastritis. He was treated with intravenous fluids and esomeprazole. The following day, amylase and lipase level went down to 123 mg/dL and 437 mg/dL respectively. Discussion: Serum amylase or lipase levels are recognized as a useful marker for pancreatic inflammation. However, there are several other conditions that can cause hyperamylasemia or hyperlipasemia, such as gut perforation and renal failure. In this case, elevated amylase and lipase was probably due to acute gastritis and chronic alcoholism, considering the totally benign abdominal examination as well as the EGD findings. Although gastroenteritis in not widely considered as a cause of hyperamylasemia or hyperlipasemia, numerous cases have reported with possible specific pathogenesis. It may result from pancreatic involvement in the inflammatory process or from increased absorption of pancreatic enzymes from the intestinal lumen. Also, according to the literature, elevated serum lipase levels have been found in 11 to 33% of asymptomatic alcoholics. Therefore, acute gastroenteritis and chronic alcoholism should be included in the differential diagnosis of hyperamylasemia or hyperlipasemia. Extra caution should be exercised when interpreting elevated amylase and lipase mimicking pancreatitis.

Low incidence of hyperamylasemia after proximal double-balloon enteroscopy: has the insertion technique improved?

Reported complications of double-balloon enteroscopy (DBE) include post-enteroscopy pancreatitis. Hyperamylasemia after proximal DBE is reported frequently, but the relationship to development of pancreatitis remains unclear. Hyperamylasemia may be related to balloon inflation in the pancreatic head region. The aims of the study were to identify risk factors for hyperamylasemia and to determine the incidence of hyperamylasemia and pancreatitis when a modified cautious DBE insertion protocol was used. In a prospective study, involving consecutive patients undergoing a proximal DBE, serum amylase activity was assessed immediately before and after the procedure. 135 patients were included (men 78, women 57; mean age 49 years [range 17 - 88]). The mean total procedure time was 73 minutes (range 30 - 150 minutes), and mean number of passes during the proximal DBE was 14 (6 - 24). While patients (17 %) developed hyperamylasemia after the DBE procedure, only one patient with hyperamylasemia had clinical symptoms indicating a mild acute pancreatitis (0.7 %). Total procedure time and number of passes correlated significantly with the occurrence of hyperamylasemia. We found a low incidence of hyperamylasemia and pancreatitis post-DBE. Theoretically, this could result from the modified insertion technique, with local strain and friction of the small bowel as remaining causes of hyperamylasemia, a notion supported by the significant relation between hyperamylasemia and duration of DBE and total number of passes. We therefore advise use of the cautious insertion technique and, if possible, reduction of duration and of number of passes in every proximal DBE.

Pancreatic-Type Hyperamylasemia and Hyperlipasemia Secondary to Ruptured Ovarian Cyst: A Case Report and Review of the Literature

Although salivary-type hyperamylasemia is known to occur with ovarian pathologies such as salpingitis and adenocarcinoma, pancreatic-type hyperamylasemia and hyperlipasemia are considered to be highly specific for pancreatitis. To discuss the interpretation of hyperamylasemia in the context of acute abdominal pain, implications for management, and to review the literature relating to non-pancreatic causes of hyperamylasemia and hyperlipasemia. We present the case of a 25-year-old woman who presented with an acute abdomen and a markedly elevated pancreatic-type amylase and lipase in whom acute pancreatitis was suspected. Further investigations showed that the underlying pathology was actually a ruptured ovarian cyst causing massive intra-abdominal hemorrhage and necessitating emergency laparotomy. This case represents an initial report of pancreatic-type hyperamylasemia and hyperlipasemia occurring with ovarian pathology and hemoperitoneum. Although these derangements may have been secondary to peritoneal irritation, this case raises the possibility that ovarian tissue is able to secrete large amounts of pancreatic-type amylase and lipase in addition to salivary-type amylase. Clinicians should be aware that simultaneous elevations of both enzymes are not necessarily pathognomic of acute pancreatitis.

Risk factors of hyperamylasemia in diabetic ketoacidosis

Risk factors of hyperamylasemia in 152 diabetic ketoacidosis(DKA)patients who had no acute pancreatitis were examined.Serum levels of hemodiastase,natrium,kalium,chlorine,calcium,phosphonium,creatinine,carbon dioxide combining power,osmotic pressure,blood glucose,blood lipids and uric acid were measured.With hemodiastase and other 14 factors as independent variables,the multiple linear regression analysis was performed and the partial regression coefficient was estimated.Blood glucose,serum natrium,osmotic pressure and triglyceride entered the regression equation,and their partial coefficients were 10.26,10.35,2.21 and 8.00,respectively.The constant quantitv was -2162.06.Compared with amylase-normal group,hyperamylasemia group showed statistically significant difference in blood glucose,serum natrium,osmotic pressure and triglyceride levels.Higher blood glucose and triglyceride might be the primary causes of hyperamylasemia. Key words: Diabetic ketoacidosis; Amylases

Hyperamylasemia Due to Ruptured Cerebral Aneurysm: A case report

Unexpected findings of hyperamylasemia have been observed in patients with primary neurosurgical abnormalities without abdominal trauma or evidence of pancreatitis. However, the causes of hyperamylasemia in abovementioned cases have not been clearly elucidated. We have experienced hyperamylasemia in a 66 year-old female patient with subarachnoid hemorrhage caused by ruptured cerebral aneurysms who had had 2 aneurysms in right pericallosal and left middle cerebral trifurcational artery. Among the 2 aneurysms, the one in right pericallosal artery was ruptured and subarachnoid, intraventricular and intracranial hemorrhage was observed on the initial brain CT scan. There was no specific problem during operation and patient's staying in recovery room. Seven hours after the operation finished, severe hypotension and metabolic acidosis were occurred. Vital signs and acidosis were corrected with fluid and bicarbonate therapy. We incidentally found marked hyperamylasemia in the first postoperative day and serum amylase level was decreased and thereafter normalized through the seventh postoperative day. There was no evidence of acute pancreatitis on either clinical examination or radiologic study of abdominal sonography and CT scan. On the brain CT scan which was taken on the third postoperative day, the increase in the amount of hemorrhage in bilateral frontal area was found and cerebral ischemia was observed in the territory of bilateral anterior cerebral artery.

Gastroenteritis-associated hyperamylasemia: prevalence and clinical significance.

Serum amylase levels can be elevated in various pathological conditions. However, acute gastroenteritis has not been widely recognized as a cause for hyperamylasemia. We conducted a retrospective study of amylase results for all patients hospitalized or discharged from the emergency department with a diagnosis of gastroenteritis from April through November 1999. Patients with other possible medical causes for elevated amylase levels were excluded. We also compared the clinical and laboratory parameters of hyperamylasemic vs. normoamylasemic hospitalized patients with gastroenteritis. A total of 1041 patients with acute gastroenteritis were identified. Serum amylase levels were determined in 701 patients and were abnormally elevated in 66 of them. In 15 patients, other possible causes of hyperamylasemia were present, and these patients were excluded. The mean serum amylase level among the remaining 51 patients (7.4% of the remaining 686 patients with gastroenteritis) was 1.32 of the upper normal level, with a range of up to 2.2 times the upper normal range. Clinicians tended to admit more hyperamylasemic patients than normoamylasemic patients (10 of 51 vs. 65 of 635; P =.03, 1 sided). However, the course of gastroenteritis in the hospitalized hyperamylasemic patients did not differ significantly from that in the hospitalized normoamylasemic patients, as judged by the clinical signs and symptoms, laboratory results, length of hospital stay, and need for antibiotics. Gastroenteritis is associated with a mild to moderate elevation of serum amylase levels in a significant portion of patients and should be included in the differential diagnosis of hyperamylasemia. Such elevation, however, does not seem to bear clinical significance in terms of the severity of disease.

Hyperamylasemia in bulimia nervosa and hyperemesis gravidarum

Objectives The exact causes of hyperamylasemia detected in bulimia nervosa are unknown but it is presumed to be due either to repeated binging or to vomiting. This study set out to investigate the importance of vomiting in producing the raised serum amylase and to clarify whether the amylase in pancreatic or salivary. Methods Patients suffering from hyperemesis gravidarum who were repeatedly vomiting in pregnancy but not binge eating had their total serum and pancreatic amylase measured. Bulimic patients and a control sample of nonvomiting pregnant women were similarly studied. An assessment of the frequency and duration of vomiting and binging was also made. Results Results show 45% (5) of bulimic patients had raised serum amylase, but none had a raised pancreatic amylase. Twenty-four percent (7) of the hyperemetic patients also had a raised serum amylase level, all with a normal pancreatic amylase level. None of the nonvomiting pregnant patients had a raised amylase. Discussion Of patients with hyperemesis gravidarum who repeatedly vomit but do not binge, a significant number had raised amylase. This suggests that it is the vomiting rather than the binge behavior that increases amylase in bulimic patients. This increased amylase probably comes from the salivary gland. © 1999 by John Wiley & Sons, Inc. Int J Eat Disord 26: 223–227, 1999.

Effect of diaspirin cross-linked hemoglobin on normal and postischemic microcirculation of the rat pancreas.

Microcirculatory alterations with reduced nutritive supply to the pancreas could be the cause of hyperamylasemia, which occurs in some patients receiving the vasoactive oxygen carrier diaspirin cross-linked hemoglobin (DCLHb) in clinical studies. Therefore, the effects of DCLHb on rat pancreas microcirculation were evaluated. Anesthetized Sprague-Dawley rats received one of the following treatments during baseline conditions (n = 7 rats/group): 10% hydroxyethyl starch (HAES) (0.4 ml/kg), DCLHb (400 mg/kg), or DCLHb (1,400 mg/kg). After 1 h of complete, reversible pancreatic ischemia, other animals received 10% HAES (0.4 ml/kg) or DCLHb (400 mg/kg) during the onset of reperfusion. The number of red blood cell-perfused capillaries (functional capillary density, FCD) and the level of leukocyte adherence in postcapillary venules in the pancreas were assessed by means of intravital microscopy during 2 h after treatment. In the nonischemic groups, FCD was 18% greater after DCLHb (1,400 mg/kg) than after 10% HAES treatment without any increase in leukocyte adherence. In the inschemia-reperfusion (I/R) 10% HAES group, FCD was significantly (P < 0.05) lowered, leukocyte adherence enhanced, and mean arterial pressure (MAP) reduced by 31% compared with nonischemic animals. DCLHb treatment in the I/R group resulted in a slight increase in FCD, a significant (P < 0.05) reduction of leukocyte adherence, and a complete restoration of MAP compared with the animals of the I/R control group. Thus our data provide no evidence for a detrimental effect on the pancreatic microcirculation or an enhanced risk of postischemic pancreatitis by DCLHb.

A Case of Amylase Producing Small Cell Lung Cancer

The majority of lung cancers associated with hyperamylasemia are adenocarcinomas. Here we report an unusual case of a 54-year-old male patient who complained of dyspnea, anterior chest wall discomfort and facial edema for one month, presenting with a huge mediastinal mass and hyperamylasemia complicated by pericardial effusion. Histological evaluation of mediastinal mass revealed small cell carcinoma and pericardium showed nonspecific inflammation with fibrosis. The serum amylase had an electrophoretic mobility similar to that of salivary gland enzyme. There were no evidence of a salivary or pancreatic causes of hyperamylasemia. After chemotherapy, parenchymal lung lesions improved and hyperamylasemia disappeared. For the management of pericardial effusion, a pericardial window was formed. We concluded that the striking increase in serum amylase was due to the ectopic production of this enzyme by the tumor.

Histological pancreatitis in end-stage renal disease.

To clarify a possible cause of hyperamylasemia in end-stage renal disease (ESRD), histological studies were performed on the pancreatic glands of twenty-seven autopsied patients with ESRD who had received long-term hemodialysis. The findings were compared with those in a similar number of age-matched control subjects. Histological evidence of pancreatitis was found in 51.9% of the ESRD patients as compared with 14.8% in the controls (p < 0.005). The pancreatitis was chronic in nature in 85.7% of the ESRD patients showing changes of pancreatitis. Secretin administration to an additional group of twelve patients with ESRD induced an elevation in the activities of both total and P-type serum amylase in only one patient. These findings suggest that although histological pancreatic alterations are common in patients with ESRD, they are probably not responsible for the P-type hyperamylasemia frequently found in such patients.

臨床分野におけるα‐アミラーゼ分別測定の現況

Amylase isoenzyme analysis in serum is widely used in clinical medicine for the differential diagnosis of hyperamylasemia. The major clinical application of amylase isozyme determination at the present time is the differentiation of salivary from pancreatic hyperamylasemia . In the present study, we evaluated the usefulness of the established means of amylase isozyme analysis; electrophoresis, the amylase to creatinine clearance ratio (ACCR) and the amylase inhibitor test. Isozyme analysis by electrophoresis has not been widely used in clinical laboratories because it is too technically complex and time-consuming for ready clinical use. In spite of these short comings, electrophoresis is a useful and sensitive tool for the identification of minor components of amylase isozyme observed in the serum of patients with acute pancreatitis, the variant amylase isozyme pattern seen in patients with lung cancer as well as in normal persons, macro amylasemia, and aged amylase in cases of pancreatic pseudocysts or pleural effusion . The ratio of the renal clearance of amylase to that of creatinine (ACCR) is a simple, rapid, readily available and reliable means of assessing the presence or absence of acute pancreatitis. In addition to in acute pancreatitis, recent studies have revealed a nonspecific increase in ACCR in normoamylasemic conditions such as burns, diabetic acidosis and Bence-Jones proteinemia, and in postoperative patients. In patients with conditions other than pancreatitis, however, hyperamylasemia and a high ACCR are likely to be unrelated phenomena. A cause of hyperamylasemia is not a cause of an increased ACCR and vice versa. At present, therefore, acute pancreatitis appears to be the only condition that causes elevation of both the serum amylase level and the ACCR. The assay method involving wheat inhibitor, which is a relatively specific inhibitor of salivary amylase, is a simple and accurate means of differentiating salivary from pancreatic hyperamylasemia. Except for very high or very low pancreatic amylase levels, the results obtained with the inhibitor assay show good correlation with the results as to amylase isozyme distribution determined by electrophoresis. Thus, the inhibitor assay can be reliably used to determine if a patient's hyperamylasemia or the aged amylase in biological fluids is of pancreatic or salivary origin. The inhibitor assay, however, leads to clinical confusion in patients with macroamylasemia or with variant amylase isoenzymes. Although all three techniques mentioned above can differentiate salivary from pancreatic hyperamylasemia, salivary amylases are known not to be specific to the salivary gland. At present, there is no method for determining the origin of the amylase. In addition to the knowledge that hyperamylasemia is of nonpancreatic origin, knowledge that hyperamylasemia is related to some specific organ may greatly improve the diagnostic accuracy.

Hyperamylasemia and S-type isozyme dominance in liver cirrhosis

To investigate the mechanisms of serum amylase abnormalities in liver disease, we determined serum amylase levels, S-type isozyme proportion, clinical symptoms, and laboratory data in 38 cases of histologically confirmed liver cirrhosis and 19 controls. Of the 12 patients who were hyperamylasemic (12/38, 32%), 5 showed S-type isozyme dominance (5/12, 42%), whereas in the 26 normoamylasemic cirrhosis patients, only 5 were S-type isozyme dominant (5/26, 19%). Isozyme percentages were significantly higher (P less than 0.01) in the dominant-S-type cases than in the controls, and S-type dominance was found more frequently in the hyperamylasemic than in the normoamylasemic cirrhosis cases. Only ascites and esophageal varices were observed more frequently as clinical symptoms in the dominant-S-type cases. Our results suggest that amylase is not produced in the human liver, but that the decreased clearance rate of amylase, especially the S-type isozyme, may be a cause of hyperamylasemia and S-type isozyme dominance in cirrhosis.

Upper gastrointestinal endoscopy an unrecognized cause of hyperamylasemia

The prevalence of hyperamylasemia 2 hr and 24 hr after upper gastrointestinal endoscopy without attempts to cannulate the ampulla of Vater was prospectively studied in 50 consecutive patients. In the 2-hr sample, hyperamylasemia was observed in nine patients (18%) (serum amylase range 59-191 units/liter with a mean value of 102 units/liter; reference range: 12-46 units/liter). Five of the nine patients still had an increased serum amylase (range 54-118 units/liter, mean 78.4) 24 hr after endoscopy. When hyperamylasemia occurred, it always appeared in and was higher in the 2-hr sample. The increased serum amylase activity was due to a rise of S-type isoamylase. The cause of hyperamylasemia after gastrointestinal endoscopy is speculative but is probably due to an hypersalivation.

Serum amylase isoenzyme alterations in acute abdominal conditions

To determine the accuracy of the serum amylase in identifying a pancreatic source, amylase isoenzymes were determined prospectively in 65 patients initially evaluated with a complaint of abdominal pain and associated hyperamylasemia. Isoenzyme patterns were demonstrated by an electrophoretic technique, and the results were correlated with clinical diagnoses. Patients were divided into two diagnostic groups. Group I consisted of 42 patients with clinical findings suggesting pancreatitis. P-type isoenzymes were normal or elevated in 31 of these patients (74%), and s-type isoenzymes were normal or elevated in 11 (26%). Group 2 consisted of 23 patients with abdominal pain attributed to causes other than pancreatitis. Four patients (17%) had elevation of p-type isoenzymes, and 19 patients (83%) had predominantly s-type patterns. We conclude that amylase isoenzymes cannot determine unequivocally the cause of hyperamylasemia, but they can enhance the diagnostic specificity of the serum amylase. Elevated serum amylase with a predominant p-type pattern suggests pancreatic disease; elevation of s-type isoenzymes suggests but is not conclusive for, diagnoses other than pancreatitis. Hyperamylasemia with a normal isoenzyme pattern occurred in a few patients in both groups, and it was nondiagnostic.

Cholangio-venous reflux as a cause of recurrent hyperamylasemia in choledochal dilatation with anomalous pancreaticobiliary ductal union: An experimental study

Cylindrical choledochal dilatation, associated with anomalous pancreaticobiliary ductal union, causes recurrent episodes of right hypochondrial pain, vomiting, and fever. The symptoms are very often accompanied by hyperamylasemia, which is generally considered to be due to acute pancreatitis. However, our clinical experience and experimental studies have led us to the conclusion that pancreatitis is not the sole cause of hyperamylasemia. In this paper we report our further investigations of the cause of the hyperamylasemia. In 22 mongrel adult dogs, intracholedochal infusion was performed under a continuous hydrostatic pressure of 20 cm H2O for 2 hours. Solutions of amylase from three different sources and a lipase were used in the range of concentrations found clinically in the bile within a cylindrical choledochal dilatation. In the 3 groups, hyperamylasemia was proven by quantitative estimation of serum amylase level and/or by the changes in specific amylase isozymes. Lipase was also shown to transfer into the blood stream. In an additional experiment on 5 dogs, only the extrahepatic biliary tree, including the gallbladder, was infused with a solution of amylase from Bacillus subtilis. This produced no increase in the serum amylase. Our experiments suggest that amylase passes from the hepatocholedochal system into the blood stream. This phenomenon has long been known as cholangiovenous reflux.

A Rapid and Simple Assay to Determine if Macroamylase Is the Cause of Hyperamylasemia

Macromolecules are known to precipitate selectively in concentrated solutions of polyethylene glycol. This report describes the use of polyethylene glycol 6000 to distinguish macroamylase from normal-sized serum amylase. Preliminary studies indicated that a PEG concentration of 12% and a 10-min incubation at 37 degrees C separated normal serum amylase from macroamylase. Using these conditions, study of 18 macroamylase-containing sera showed precipitation of at least 73% of the amylase activity. In contrast, in 46 normal sera and 16 hyperamylasemic (but not macroamylasemic) sera, less than 52% of the amylase activity was precipitated by polyethylene glycol. This test provides a rapid, simple, and accurate means of determining if macroamylasemia is the cause of hyperamylasemia.

Marked hyperamylasemia associated with carcinoma of the lung.

We present a case of marked hyperamylasemia associated with undifferentiated small cell carcinoma of the lung. The serum alpha-amylase had an electrophoretic mobility similar to that of salivary gland enzyme (s-type), and that in tissue extracts from the lung tumor and metastatic skin nodules showed similar migration. No evidence of a salivary or pancreatic cause of hyperamylasemia was found at autopsy, and macroamylasemia was excluded. We suggest that the strikingly increased serum alpha-amylase activity was a result of ectopic production of this enzyme by tumor. We compare results for this case to other published reports.