Title: Evaluation of tumor necrosis factor-α (TNF-α) and C-reactive protein over lipase amylase ratio for acute pancreatitis in north Indian population

Authors: Sweta Kumari, Amod Kumar, Musarrat Parveen, Amitesh Kumar, S.S.Haque, Md.Tanweeruddin

 DOI:  https://dx.doi.org/10.18535/jmscr/v5i7.68

Abstract

Acute pancreatitis is an acute inflammatory disease of pancreas. Pancreatitis is due to premature, intra-pancreatic activation of pancreatic proenzymes. Increased levels of serum amylase and lipase establish the diagnosis of acute pancreatitis. Aim of the study was to determine the ratio of serum lipase to serum amylase (L/A) along with TNF-α and CRP in acute pancreatitis patients in north Indian population. The mean lipase/ amylase ratio (4.17±1.27 U/L) levels are significantly higher in severe acute pancreatitis. The study showed no significant age difference between group A (N=60; mean age 40.25±12.31 years) and control group B (N=60; mean age 37.92±9.69 years). Out of 60 patients of acute pancreatitis, 32 were having severe disease with CRP level between 96-192 mg/l while in mild disease 18 patients were having severe disease with CRP level between 24-48 mg/L and only10 patient were having normal CRP level i.e. below 8 mg/L, and TNF-α in case of acute pancreatitis 12.20±3.32 compared to control(9.86±4.57) pg/ml The lipase/ amylase ratio is a good predictor factor and is useful in distinguishing acute episode of alcoholic from non-alcoholic acute pancreatitis. It may useful in predicting the severity of acute pancreatitis.

Keywords: Acute pancreatitis; lipase; amylase; lipase/ amylase ratio (L/A).

References

1.      Cherry IS, Crandal Al. Specific of pancreatic lipase: its appearance in blood after pancreatic injury. Am J Physiol 1932; 100: 266-73

2.      Maes B, Hastier P, Buckley JM, et al. Extensive aetiological investigations in acute pancreatitis: results of a 1-year prospective study. Eur J Gastroenterol Hepatol 1999; 11: 891-6.

3.      Renner IG, Savage WT 3rd, Pantoja JL, et al: Death due to acute pancreatitis. A retrospective analysis of 405 autopsy cases. Dig Dis Sci 1985; 30: 1005-18.

4.      Halvorsen FA, Ritland S. Acute pancreatitis in Buskerud County, Norway. Incidence and etiology. Scand J Gastroenterol 1996; 31: 411-4.

5.      Uhl W, Isenmann R, Curti G, et al. Influence of etiology on the course and outcome of acute pancreatitis. Pancreas 1996; 13: 335-43.

6.      Appelros S, Borgstrom A. Incidence, aetiology and mortality rate of acute pancreatitis over 10 years in a defined urban population in Sweden. Br J Surg 1999; 86: 465-70.

7.      Greenberger NJ, Tokes PP. Approach to the patients with pancreatitic disease. In: Braunwald E, Isselbacher KJ, Petersdorf RG, Wilson JD, Martin JB, Fauci AS, eds. Harrison's Principle of Internal Medicine. 12th ed. New York: McGraw Hill; 1987:1368-72.

8.      Winn Deen ES, David H, Siglet E and Chavzer R. Clin Chem 2005;34(10):2005-2008.

9.      Junge W et al. Biochem 1989; 22:109.

10.  Moss DW, Henderson AR. Clinical Enzymology. In Burtis CA, Ashwood ER (eds):Tietz Text book of Clinical Chemistry,3rdedition,pp 617-721.Philadelphia,WB Saunders 1999.

11.  Wu JS, Chen YF. Clinical Observation of acute pancreatitis. Taiwan Yi Xue Hui Za Zhi 1969; 68: 672-7.

12.  Imrie CW, Benjamin IS, Ferguson JC, et al. A single-centre double-blind trial of Trasylol therapy in primary acute pancreatitis. Br J Surg 1978; 65: 337-41.

13.  Moossa AR. Diagnostic tests and procedures in acute pancreatitis. N Engl J Med 1984; 311: 639-43.

14.  Cherry IS, Crandal Al. Specific of pancreatic lipase: its appearance in blood after pancreatic injury. Am J Physiol 1932; 100: 266-73

15.  Maes B, Hastier P, Buckley JM, et al. Extensive aetiological investigations in acute pancreatitis: results of a 1-year prospective study. Eur J Gastroenterol Hepatol 1999; 11: 891-6.

16.  Renner IG, Savage WT 3rd, Pantoja JL, et al: Death due to acute pancreatitis. A retrospective analysis of 405 autopsy cases. Dig Dis Sci 1985; 30: 1005-18.

17.  Halvorsen FA, Ritland S. Acute pancreatitis in Buskerud County, Norway. Incidence and etiology. Scand J Gastroenterol 1996; 31: 411-4.

18.  Uhl W, Isenmann R, Curti G, et al. Influence of etiology on the course and outcome of acute pancreatitis. Pancreas 1996; 13: 335-

19.  Appelros S, Borgstrom A. Incidence, aetiology and mortality rate of acute pancreatitis over 10 years in a defined urban population in Sweden. Br J Surg 1999; 86: 465-70.

20.  Greenberger NJ, Tokes PP. Approach to the patients with pancreatitic disease. In: Braunwald E, Isselbacher KJ, Petersdorf RG, Wilson JD, Martin JB, Fauci AS, eds. Harrison's Principle of Internal Medicine. 12th ed. New York: McGraw Hill; 1987: 1368-72.

21.  Fan ST, Choi TK, Lai CS, Wong J. Influence of age on the mortality from acute pancreatitis. Br J Surg 1988; 75: 463-66.

22.  Murthy Naga Venkatesha PJ, Benegal Vivek and Murthy Prathima. Alcohol dependence in Indian Women: A clinical perspective

23.  Kuo-Chin Chang, Chi-Sin Changchien, Chung-Mou Kuo,k Yi-Chun Chiu, SEng-Kee Chuah, King-Wah Chiu, Chung-Huang Kuo. Clinical analysis of the efficacy in Lipase/Amylase ratio for acute pancreatitis.  Intern Med Taiwan 2005; 15: 113-20

24.  Tenner SM, Steinber WM. The admission serum lipase/ amylase ratio differentiates alcoholic from nonalcoholic acute pancreatitis. Am J Gastroenterol 1992; 87: 1755-58.

25.  Pacheco RC, Oliveira LC, Lipase/amylase ratio in biliary acute pancreatitis and alcoholic acute/acutized chronic pancreatitis. Arq Gastroenterol 2007; 44 (1): 35-8.

26.  Kazmierczak SC, Catrou PG, Van Lente F. Enzymatic markers of gallstone induced pancreatitis identified by ROC curve analysis, discriminant analysis, logistic regression, likelihood ratios, and information theory. Clin Chem 1995; 41: 523-31.

Corresponding Author

Dr S.S.Haque

Department of Biochemistry, Indira Gandhi Institute of Medical Sciences, Patna-14