Serum amylase and lipase levels are typically elevated in persons with acute pancreatitis. However, these elevations may only indicate pancreastasis. In research studies, amylase or lipase levels at least 3 times above the reference range are generally considered diagnostic of acute pancreatitis. Serum amylase determinations are routinely available, but they are not specific for pancreatitis. Preferably, the amylase P level should be measured, which is somewhat more specific to pancreatic pathology. Elevations can occur in patients with small intestinal obstruction, mesenteric ischemia, tubo-ovarian disease, renal insufficiency, or macroamylasemia. Rarely, elevations may reflect parotitis. The serum half-life of amylase is short, and elevations generally return to the reference ranges within a few days. Lipase has a slightly longer half-life and its abnormalities may support the diagnosis if a delay occurs between the pain episode and the time the patient seeks medical attention. Elevated lipase levels are more specific to the pancreas than elevated amylase levels. Lipase levels remain high for 12 days. In patients with chronic pancreatitis (usually caused by alcohol abuse), lipase levels may be elevated in the presence of a normal serum amylase level. The level of serum amylase or lipase does not indicate whether the disease is mild, moderate, or severe, and monitoring levels serially during the course of hospitalization does not offer insight into the prognosis. Determine alkaline phosphatase, total bilirubin, aspartate aminotransferase (AST), and alanine aminotransferase (ALT) levels to search for evidence of gallstone pancreatitis. An ALT level higher than 150 U/L suggests gallstone pancreatitis and a more fulminant disease course. Obtain measurements for blood urea nitrogen (BUN), creatinine, and electrolytes; a great disturbance in the electrolyte balance is usually found, secondary to third spacing of fluids. Measure blood glucose level because it may be elevated from B-cell injury in the pancreas. Measure calcium, cholesterol, and triglyceride levels to search for an etiology of pancreatitis (eg, hypercalcemia or hyperlipidemia) or complications of pancreatitis (eg, hypocalcemia resulting from saponification of fats in the retroperitoneum). However, be aware that baseline serum triglyceride levels can be falsely lowered during an episode of acute pancreatitis. A complete blood count (CBC) demonstrates leukocytosis (white blood cell [WBC] count higher than 12,000/µL) with the differential being shifted toward the segmented polymorphonuclear (PMN) cells. Leukocytosis may represent inflammation or infection. Hemoconcentration at admission (an admission hematocrit value greater than 47%) has been proposed as a sensitive measure of more severe disease. However, this has subsequently been shown to have value only as a negative predictor—that is, a lack of hemoconcentration effectively rules out severe disease. If blood transfusion is necessary, as in cases of hemorrhagic pancreatitis, obtain type and cross-match. A C-reactive protein (CRP) value can be obtained 24-48 hours after presentation to provide some indication of prognosis. Higher levels have been shown to correlate with a propensity toward organ failure. A CRP value in double figures (ie, ≥ 10 mg/dL) strongly indicates severe pancreatitis. CRP is an acute-phase reactant that is not specific for pancreatitis. Evaluate arterial blood gases if a patient is dyspneic. Whether tachypnea is due to acute respiratory distress syndrome (ARDS) or diaphragmatic irritation must be determined. Lactic dehydrogenase (LDH), BUN, and bicarbonate levels should be measured both at admission and at 48 hours in order to help determine the Ranson criteria for survival. Immunoglobulin G4 (IgG4) levels can be checked to evaluate for autoimmune pancreatitis, especially in recurrent acute pancreatitis that is not explained by an obvious etiology. However, this test is not specific, because IgG4 levels can be elevated in as many as 10% of patients with acute pancreatitis who do not have autoimmune pancreatitis. Trypsin and its precursor trypsinogen-2 in both the urine and the peritoneal fluid have been evaluated as possible markers for acute pancreatitis (especially post-ERCP pancreatitis) but are not widely used. Trypsinogen activation peptide (TAP) is formed when trypsinogen is cleaved to form trypsin and can be measured commercially in the urine to diagnose acute pancreatitis and to help determine the severity. Although not currently in use clinically, polymorphisms in the chemokine monocyte chemotactic protein 1 (MCP-1) gene may also predict severity. This is the first gene identified that plays a role strictly in predicting the severity of disease.
A.D.A.M. Medical Encyclopedia. Chronic pancreatitis. Updated October 15, 2019. Accessed November 30, 2021. https://medlineplus.gov/ency/article/000221.htm A.D.A.M. Medical Encyclopedia. Acute pancreatitis. Updated October 17, 2019. Accessed November 30, 2021. https://medlineplus.gov/ency/article/000287.htm A.D.A.M. Medical Encyclopedia. Enzyme. Updated January 16, 2021. Accessed December 4, 2021. https://medlineplus.gov/ency/article/002353.htm A.D.A.M. Medical Encyclopedia. Lipase test. Updated January 24, 2021. Accessed November 30, 2021. https://medlineplus.gov/ency/article/003465.htm A.D.A.M. Medical Encyclopedia. Venipuncture. Updated April 24, 2021. Accessed November 30, 2021. https://medlineplus.gov/ency/article/003423.htm American Board of Internal Medicine. ABIM laboratory reference ranges. Updated July 2021. Accessed November 30, 2021. https://www.abim.org/Media/bfijryql/laboratory-reference-ranges.pdf ARUP Consult. Acute pancreatitis. Updated November 2021. Accessed November 30, 2021. https://arupconsult.com/content/pancreatitis-acute ARUP Consult. Chronic pancreatitis. Updated November 2021. Accessed November 30, 2021. https://arupconsult.com/content/pancreatitis-chronic Bartel M. Acute pancreatitis. Merck Manuals Consumer Edition. Updated September 2020. Accessed November 30, 2021. https://www.merckmanuals.com/home/digestive-disorders/pancreatitis/acute-pancreatitis Bartel M. Acute pancreatitis. Merck Manuals Professional Edition. Updated September 2020. Accessed November 30, 2021. https://www.merckmanuals.com/professional/gastrointestinal-disorders/pancreatitis/acute-pancreatitis Bartel M. Chronic pancreatitis. Merck Manuals Consumer Edition. Updated September 2020. Accessed November 30, 2021. https://www.merckmanuals.com/home/digestive-disorders/pancreatitis/chronic-pancreatitis Bartel M. Chronic pancreatitis. Merck Manuals Professional Edition. Updated September 2020. Accessed November 30, 2021. https://www.merckmanuals.com/professional/gastrointestinal-disorders/pancreatitis/chronic-pancreatitis Devkota BP. Lipase. In: Staros EB, ed. Medscape. Updated November 18, 2019. Accessed November 30, 2021. https://emedicine.medscape.com/article/2088094-overview Freedman SD, Forsmark CE. Chronic pancreatitis: Clinical manifestations and diagnosis in adults. In: Whitcomb DC, ed. UpToDate. Updated June 1, 2020. Accessed November 30, 2021. https://www.uptodate.com/contents/chronic-pancreatitis-clinical-manifestations-and-diagnosis-in-adults MedlinePlus: National Library of Medicine. Lipase tests. Updated November 30, 2020. Accessed November 30, 2021. https://medlineplus.gov/lab-tests/lipase-tests/ MedlinePlus: National Library of Medicine. Fasting for a blood test. Updated March 3, 2021. Accessed November 30, 2021. https://medlineplus.gov/lab-tests/fasting-for-a-blood-test/ National Heart, Lung, and Blood Institute. Blood tests. Date unknown. Accessed November 30, 2021. https://www.nhlbi.nih.gov/health-topics/blood-tests National Cancer Institute. Introduction to the digestive system. Date unknown. Accessed December 4, 2021. https://training.seer.cancer.gov/anatomy/digestive/ National Institute of Diabetes and Digestive and Kidney Diseases. Pancreatitis. Updated November 2017. Accessed November 30, 2021. https://www.niddk.nih.gov/health-information/digestive-diseases/pancreatitis/all-content Penner RM, Fishman MB. Evaluation of the adult with abdominal pain. In: Auerbach AD, Aronson MD, eds. UpToDate. Updated May 10, 2021. Accessed November 30, 2021. https://www.uptodate.com/contents/evaluation-of-the-adult-with-abdominal-pain Pirahanchi Y, Sharma.S. Biochemistry, lipase. In: StatPearls. Updated July 22, 2021. Accessed November 30, 2021. https://www.ncbi.nlm.nih.gov/books/NBK537346/ Vege SS. Approach to the patient with elevated serum amylase or lipase. In: Whitcomb DC, ed. UpToDate. Updated May 20, 2020. Accessed November 30, 2021. https://www.uptodate.com/contents/approach-to-the-patient-with-elevated-serum-amylase-or-lipase Vege SS. Clinical manifestations and diagnosis of acute pancreatitis. In: Whitcomb DC, ed. UpToDate. Updated October 28, 2021. Accessed November 30, 2021. https://www.uptodate.com/contents/clinical-manifestations-and-diagnosis-of-acute-pancreatitis Vege SS. Management of acute pancreatitis. In: Whitcomb DC, ed. UpToDate. Updated November 8, 2021. Accessed November 30, 2021. https://www.uptodate.com/contents/management-of-acute-pancreatitis
Acute pancreatitis is a reversible inflammatory process of the pancreas caused by auto digestion that generally presents with epigastric abdominal pain that may radiate to the back and is worsened by the ingestion of food. Acute pancreatitis is often mild, but severe disease can have a mortality rate of up to 30%. The most common causes are gallbladder disease, alcohol use, and hypertriglyceridemia. In addition to abdominal pain, patients may present with nausea and vomiting, which are nonspecific in most cases, so imaging and laboratory testing are important for definitive diagnosis. Lipase is the preferred laboratory test for diagnosing acute pancreatitis, as it is the most sensitive and specific marker for pancreatic cell damage. Additional laboratory testing, such as complete blood count (CBC) and lactate dehydrogenase (LDH) tests, are useful to obtain prognostic information.
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