|Year : 2015 | Volume
| Issue : 1 | Page : 13-15
Increased levels of pancreatic enzymes in sickle cell anemia and the effect of proteinuria
Mathias Abiodun Emokpae, Idahosa Ehioghae
Department of Medical Laboratory Science, School of Basic Medical Sciences, College of Medical Sciences, University of Benin, Benin City, Nigeria
|Date of Web Publication||4-Nov-2015|
Dr. Mathias Abiodun Emokpae
Department of Medical Laboratory Science, School of Basic Medical Sciences, College of Medical Sciences, University of Benin, Benin City
Source of Support: None, Conflict of Interest: None
Background/Objective: Sickle cell disease (SCD) is the most common hemoglobinopathy in Nigeria, and the condition can affect any part of the body including the pancreas. The study seeks to evaluate the levels of pancreatic enzymes in blood and urine of SCD patients in steady clinical state, and the effect of proteinuria on the enzyme levels as proteinuria was previously reported in SCD subjects. Materials and Methods: Urine and plasma amylase, serum lipase, and proteinuria were determined in 150 subjects comprising 100 SCD patients and 50 age/sex matched apparently healthy subjects with normal hemoglobin using commercially available reagent test kits. Results: Urine amylase (P = 0.029), serum amylase (P < 0.001), lipase (P = 0.008), and proteinuria (P < 0.001) were significantly higher in steady state SCD patients compared with controls. Significant decreases were observed in urine amylase (P = 0.022), serum amylase (P < 0.001), lipase (P < 0.001), and proteinuria (P < 0.001) in SCD patients without proteinuria compared with SCD patients with proteinuria. Conclusion: Pancreatic enzymes levels were increased in SCD patients which indicate that these patients may be predisposed to pancreatitis and the levels of these enzymes were further increased in those with proteinuria.
Keywords: Lipase and proteinuria, serum amylase, sickle cell disease
|How to cite this article:|
Emokpae MA, Ehioghae I. Increased levels of pancreatic enzymes in sickle cell anemia and the effect of proteinuria. J Med Investig Pract 2015;10:13-5
|How to cite this URL:|
Emokpae MA, Ehioghae I. Increased levels of pancreatic enzymes in sickle cell anemia and the effect of proteinuria. J Med Investig Pract [serial online] 2015 [cited 2018 Oct 17];10:13-5. Available from: http://www.jomip.org/text.asp?2015/10/1/13/169054
| Introduction|| |
Sickle cell disease (SCD) also known as drepanocytosis is an autosomal recessive genetic disorder characterized by chronic anemia and vaso-occlusive painful crisis. SCD is caused by a single nucleotide substitution of thymidine for adenine (GAG−>GTG) of the β-chain that results in the amino acid valine instead of glutamic acid. This basically is responsible for all the changes in the properties of the hemoglobin (Hb) molecule, with tendencies to polymerize in the deoxygenated state, in which the red cells assumed an abnormal rigid, elongated, and crescent cell shaped which obstruct normal blood flow through microvessels. This impedes blood flow to organs and tissues causing infarctions and ischemic necrosis., Most organs of the body are affected thus leading to acute or chronic multisystem dysfunction.
In our previous studies,, we reported the involvement of kidney pathology in SCD. Functional changes occur in the kidney with increasing age, proteinuria, severe anemia, and hematuria were observed to be reliable markers and predictors of chronic renal disease in SCD disease. Oral glucose intolerance was also reported in a group of patients, indicating that insulin secretion from the pancreas may be compromised in a steady state SCD. Abdominal pain was observed to be common in SCD and may present a diagnostic challenge since pancreatitis is uncommon in SCD patients., Some cases of acute pancreatitis were, however, reported in African-Americans who had no evidence of drug- or toxin-induced injury or obstruction etiology. This study was therefore designed to evaluate pancreatic enzymes and the effect of proteinuria in steady state SCD patients.
| Materials and Methods|| |
The study was conducted at the Department of Medical Laboratory Science, College of Medical Sciences, University of Benin, Benin City. The SCD patients were recruited from among patients on a routine visit to the Sickle Cell Centre, Benin City. Those subjects with edema, severe jaundice, abnormal chest and abdominal findings, and those with other hemoglobinopathies were excluded from the study. The study protocol was approved by the Edo State Ethical Clearance Committee before the commencement of the study. While control subjects were apparently healthy Hb AA selected from among students of the University. Informed consent was given by all participants.
Five milliliters of blood were collected ascetically and dispensed into a plain container. A urine sample was also collected into a sterile universal container and was used for amylase and protein. The blood sample was allowed to clot at room temperature and was centrifuged at 1500 rpm for 10 min; the serum was separated into a separate tube. The serum was stored at −20°C for 2 weeks prior to analysis for serum amylase and lipase. Serum amylase and lipase, as well as urine amylase, were determined using reagents supplied by AGAPE diagnostics. The changes in absorbance were monitored spectrophotometrically every minute for 3 min at 405 nm. The urine protein was initially evaluated using urinalysis test strip and the urine samples showing positive were re-assayed by the quantitative sulfosalicylic acid colorimetric method. Control sera were included in all assays to ensure accuracy and precision of the analytes.
The data obtained were statistically evaluated using Statistical Package for Social Science (SPSS) version 16.0 (Chicago IL, USA). The values are presented as mean ± standard error of the mean for both tests and controls. Student's t-test was used to compare data at 95% confidence intervals (P < 0.05). One-way analysis of variance was used to compare mean values between SCD patients with and without proteinuria as well as the controls.
| Results|| |
A total of 150 subjects (100 SCD patients and 50 apparently healthy Hb AA subjects) were evaluated in the study. The age ranged from 15 to 24 years with the mean of 23.1 ± 1.0 years for the SCD patients while the controls range from 17 to 25 years with the mean of 24.3 ± 0.9 years. Urine amylase (P = 0.029), serum amylase (P < 0.001), lipase (P = 0.008), and proteinuria (P < 0.001) were significantly higher in steady state SCD patients compared with controls [Table 1].
|Table 1: Comparison of urine and serum amylase, serum lipase levels in SCD patients and normal hemoglobin AA controls|
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[Table 2] shows the measured variables in SCD patients with and without proteinuria. Significant decreases were observed in urine amylase (P = 0.022), serum amylase (P < 0.001), lipase (P < 0.001), and proteinuria (P < 0.001) in SCD patients without proteinuria compared with SCD patients with proteinuria. However, SCD patients with or without proteinuria had higher levels of measured parameters compared with control subjects.
|Table 2: One-way ANOVA of urine and serum amylase, serum lipase in SCD patients with and without proteinuria|
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| Discussion|| |
The data presented indicate that SCD patients on steady clinical state had significantly higher levels of urine amylase (P = 0.029), serum amylase (P < 0.001), lipase (P = 0.008), and proteinuria (P < 0.001) than subjects with normal Hb. The SCD Patients with proteinuria had higher levels of urine amylase, serum amylase and lipase, and proteinuria compared with those SCD patients without proteinuria. The finding of increased serum amylase in SCD patients compared with controls is consistent with that reported by Adekile and Akinseye-Akintujoye. Urine amylase and serum lipase were observed to be higher in SCD patients than controls. This may indicate a predisposition of SCD patients to chronic pancreatitis. The study by Adekile and Akinseye-Akintujoye  was conducted on 26 SCD patients, and we have revisited the issue with a larger population size and assayed serum lipase and urine amylase as well as the effect of proteinuria on pancreatic enzymes in SCD patients. Even though acute pancreatitis was reported to be uncommon in SCD patients, some cases have been reported,, and ischemic bowel secondary to SCD has been reported with increasing frequency., The etiology of abdominal pain in SCD was ascribed to mesenteric and retroperitoneal adenopathy, infarction in vertebral bodies, hepatobiliary disease, and splenic infarction. The conditions mentioned above are the natural history of SCD which are contributing factors to abdominal pain. It may be that chronic intermittent ischemia that occurred due to occasional obstruction of normal blood flow as a result of sickle red blood cell polymerization in reduced oxygen tension may have led to increased levels of pancreatic enzymes. Abadin et al. observed that the bowel injury seen in SCD patients with bowel ischemia may be due to an extreme manifestation of a spectrum of pathology that ranges from minor abdominal pain secondary to SCD, transient ischemia to transmural bowel infarction.
In a report of hepatobiliary manifestations of SCD, it was observed that pancreas may be affected directly from red cell sickling process or as a result of chronic hemolysis and multiple transfusions.
Pancreatic enzymes in SCD patients with proteinuria were higher than those without proteinuria. With improved medical care, the life expectancy of SCD patients has increased, and chronic complications such as renal insufficiency also occur with increasing frequency. It was reported that 18% of all SCD patients with proteinuria may develop glomerular pathology with time. The increased levels of pancreatic enzymes observed in SCD patients with proteinuria compared to those without proteinuria may be as a result of glomerular involvement. It is suggested that the increased levels of the pancreatic enzyme may be due to increased hepatic secretions due to loss of protein. The altered glomerular permselectivity causing proteinuria may have caused increased secretion of the enzymes. The proposed mechanisms that established a relationship between proteinuria and increased pancreatic enzymes may be similar to that involved between proteinuria and lipid metabolism. The reduced plasma oncotic pressure occasioned by the loss of protein in urine may directly stimulate the synthesis of pancreatic enzymes by the liver.,
| Conclusion|| |
Pancreatic enzyme levels are increased in SCD patients in steady clinical state and thus indicate that these patients may be predisposed to pancreatitis. The levels of these enzymes were further increased in those with proteinuria. In SCD patients with abdominal pain, clinicians should maintain high levels of suspicion of pancreatitis.
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Conflicts of interest
There are no conflicts of interest.
| References|| |
Ballas SK. Sickle cell anaemia: Progress in pathogenesis and treatment. Drugs 2002;62:1143-72.
Bunn HF. Pathogenesis and treatment of sickle cell disease. N Engl J Med 1997;337:762-9.
Ahmed S, Siddiqui AK, Siddiqui RK, Kimpo M, Russo L, Mattana J. Acute pancreatitis during sickle cell vaso-occlusive painful crisis. Am J Hematol 2003;73:190-3.
Emokpae MA, Uadia PO, Gadzama AA. Correlation of oxidative stress and inflammatory markers with the severity of sickle cell nephropathy. Ann Afr Med 2010;9:141-6.
Abdu A, Emokpae MA, Uadia PO, Kuliya-Gwarzo A. Proteinuria among adult sickle cell anemia patients in Nigeria. Ann Afr Med 2011;10:34-7.
Adekile AD, Akinseye-Akintujoye O. Serum amylase levels in homozygous sickle cell patients. J Natl Med Assoc 1991;83:459-60.
Kumar A, Posner G, Marsh F, Bellvue R, Dosik H. Acute pancreatitis in sickle cell crisis. J Natl Med Assoc 1989;81:91-2.
Sheehan AG, Machida H, Butzner JD. Acute pancreatitis in a child with sickle cell anemia. J Natl Med Assoc 1993;85:70-2.
Engelhardt T, Pulitzer DR, Etheredge EE. Ischemic intestinal necrosis as a cause of atypical abdominal pain in a sickle cell patient. J Natl Med Assoc 1989;81:1077, 1080-4, 1087-8.
Abadin SS, Salazar MR, Zhu RY, Connolly MM, Podbielski FJ. Small bowel ischemia in a sickle cell patient. Case Rep Gastroenterol 2009;3:26-29.
Issa H, Al-Salem AH. Hepatobilliary Manifestations of sickle cell anemia. Gastroenterol Res 2010;3:1-8.
Arogundade AF, Hassan MD, Sanusi AA, Salawu L, Durosinmi MA, Akinsola A. Kidney Dysfunction in Patients with Sickle Cell Disease: A Retrospective Review. African Association Nephrology Conference; 2009. p. 29-30. [book of abstract].
Thomas AN, Pattison C, Serjeant GR. Causes of death in sickle-cell disease in Jamaica. Br Med J (Clin Res Ed) 1982;285:633-5.
Kaysen GA. Lipid metabolism in the nephritic syndrome. In: Keane WF, Stein JH, editors. Lipids and Renal Disease. Contemporary Issues in Nephrology. New York: Churchill Livingstone; 1991. p. 63-84.
Marsh JB, Drabkin DL. Experimental reconstruction of metabolic pattern of lipid nephrosis: Key role of hepatic protein synthesis in hyperlipemia. Metabolism 1960;9:946-55
[Table 1], [Table 2]