Lviv clinical bulletin 2019, 2(26)-3(27): 16-23

Peculiarities of Clinical Indices, Duration and Complication of Acute Pancreatitis in Patients With Comorbid Obesity

A. Kebkalo, O. Tkachuk, A. Reiti

Shupyk National Medical Academy of Postgraduate Education

Introduction. Obesity is considered a global problem of humanity of the third millennium. According to the World Health Organization, obesity is an epidemic non-infectious disease. About 30.0 % of the planet’s population is overweight or obese. This indicator is progressively increasing, because there is no country in the world where this disease is not registered. Obesity can cause a lot of concomitant diseases. It is not surprising that in patients with obesity the risk of developing acute pancreatitis increases.

It is known that acute pancreatitis is an inflammatory disease of the pancreas. People with obesity have a potentially worse prognosis for the course of the disease and the development of complications. Available studies indicate a direct correlation between enlargement of parapancreatic tissue in patients with acute pancreatitis and body mass index (BMI) increase.

 The aim of the study is to find out the features of clinical indicators, course and complications of acute pancreatitis in patients with comorbid obesity.

Materials and methods. In our work, we used a retrospective analysis. We have analyzed medical documentation of 567 patients, diagnosed with acute pancreatitis and treated at the “Kyiv Regional Clinical Hospital” from January 1, 2011 to February 2, 2019. The acute pancreatitis was diagnosed based on the criteria: pain in the epigastrium, nausea or vomiting within 48 hours prior to ingestion and increase in blood amylase more than triple. The study included patients who originally contacted the hospital. Patients with repeated cases of acute pancreatitis or exacerbation of chronic pancreatitis have been excluded from the study. Diagnosis of acute pancreatitis was confirmed by additional instrumental tests: ultrasound and computer tomography. Patients under the age of 18 years, those who were not examined fully and patients with oncological pathology were also excluded from the study. 85 patients were excluded from the study by matching exclusion criteria and 482 patients were analyzed in this study. Anthropometric examination was performed for all parameters, including sex, age, weight (kg), height (m), abdominal circumference (cm). Next concomitant diseases noted in analyzed patients medical records: diabetes type II (CD), arterial hypertension, dyslipidemia, chronic kidney disease, cardiovascular system diseases. Initially, for admitted patients a general blood test, a biochemical assay, the bacterioscopy of liquids, and a measurement of blood pressure were performed.

Biliary etiology of acute pancreatitis was confirmed by the presence of concretions according to the results of ultrasound, computer tomography, or magnetic resonance cholangiopancreatography, as well as increased cholestatic enzymes (alkaline phosphatase, gamma-glutamyl trespeptidase). Alcohol genesis of the disease was concluded by the presence of alcohol and the absence of concretions, metabolic disorders (hypertriglyceridemia, hypercalcemia) or other causes that could cause acute pancreatitis (trauma, medicines, etc.).

The initial assessment of the prognostic severity of the disease was calculated according to APACHEІI. The scale of assessment included 12 physiological indicators, age and health scores that were translated and summed up. The score ​​equal to or greater than 8 predicted a more severe course of the disease. The CT severity index was also calculated on the basis of computed tomography of the abdominal cavity with intravenous contrast after 7 days of hospitalization. The severity index of CT is the sum of pancreatic inflammation points (Baltаzar scale from 0 to 4) and pancreatic necrosis (from 0 to 6). The total score ranges from 0 to 10, respectively: up to 3 points – mild course, 4-6 points – moderate flow, 7 or more – severe course of acute pancreatitis. The obtained data were statistically processed in Exel 2010 using a descriptive method with relative, absolute numbers, mean square deviations and their errors. A correlation relationship between variables was studied using Pearson’s criterion (R2). The significance differences between the two independent groups were calculated using Students t-criterion.

Results. In our study we had 482 patients, 260 patients (54.0 %) had obesity (the study group), for comparison, a control group of patients with normal body weight was chosen, the total number of which was 222 (46.0 %) patients. Obesity patients had a higher average age (55.4 ± 9.4 years, p = 0.01), also they had statistically greater percentage of severe cases of acute pancreatitis (85 (32.7 %) vs 16 (7.2 %); p = 0.01). We note the increase in the percentage of the course of severe pancreatitis in patients with weight gain from 10.20 % to 53.93 % (p = 0.03). Obesity patients had the longer bed-days in the hospital than in patients with normal body weight. In addition, they observed an increase of twice the bed in the reanimation and intensive care unit (5.8 ± 0.8 vs 2.7 ± 0.5 days, p = 0.01). When investigating the mortality rate, it should be noted that the main cause of death was the progression of organ failure of 30 (6.3 %), pulmonary embolism (TB) – 15 (3.1 %) and DIC 18 (3.7 %).

Conclusions. The presence of obesity in patients involves a high risk of severe acute pancreatitis, this risk increases with an increase in the body mass index. In addition, obese patients are provided with a higher bed-day in-patient and in-patient-care settings, which increases the total cost of treatment and requires a cost-effective algorithm in the future. A high mortality rate in obese patients requires improved treatment algorithm.


  1. Krasilnikov DM, Mavrin MI, Minnegaliev MM, Salimzyanov ShS. Results of Surgical Treatment of Patients with Pancreatic Necrosis and Its Complications. Materials of the IX All-Russian Congress of Surgeons (Volgograd, September 20–22, 2000). Volgograd, 2000, p. 55-56. (Russian).
  2. Acharya C, Cline RA, Jaligama D et al. Fibrosis reduces severity of acute-onchronic pancreatitis in humans. Gastroenterology. 2013;145:466-475.
  3. Banks PA, Bollen TL, Dervenis C et al. Classification of acute pancreatitis 2012: revision of the Atlanta classification and definitions by international consensus. Gut. 2013;62:102-111.
  4. Brisinda G, Maria G, Ferrante A, Civello I. Evaluation of prognostic factors in patients with acute pancreatitis. Hepato-Gastroenterol. 1999;46:1990-1997.
  5. Chen CH, Dai CY, Hou NJ et al. Etiology, severity and recurrence of acute pancreatitis in southern Taiwan. J Formos Med Assoc. 2006;105:550-555.
  6. Connor S, Alexakis N, Raraty MG, Ghaneh P, Evans J, Hughes M et al. Early and late complications after pancreatic necrosectomy. Surgery. 2005;137(5):499-505.
  7. De Waele B, Vanmierlo B, Van Nieuwenhove Y, Delvaux G. Impact of body overweight and class I, II and III obesity on the outcome of acute biliary Pancreas. 2006;32:343-345.
  8. Funnell IC, Bornman PC, Weakley SP, Terblanche J, Marks IN. Obesity: an important prognostic factor in acute pancreatitis. Br J Surg. 1993;80:484-486.
  9. Gloor B, Mіller CA, Worni M, Martignoni ME, Uhl W, Bіchler MW. Late mortality in patients with severe acute pancreatitis. Br J 2011;88:975-979.
  10. Halonen KI, Leppaniemi AK, Puolakkainen PA, Lundin JE, Kemppainen EA, Hietaranta AJ, Haapiainen RK et al. Severe acute pancreatitis: prognostic factors in 270 consecutive patients. 2000;21:266-271.
  11. Johnson CD, Toh SKC, Campbell MJ. Combination of APACHE-II score and an obesity score (APACHE-O) for the prediction of severe acute pancreatitis. Pancreatology. 2004;4:1-6.
  12. Karimgani I, Porter KA, Langevin RE, Banks Prognostic factors in sterile pancreatic necrosis. Gastroenterology. 1992;103:1636-1640.
  13. Khatua B, El-Kurdi B, Singh VP. Obesity and pancreatitis. Curr Opin Gastroenterol. 2017;33(5):374-382.
  14. Lankisch PG, Schirren CA. Increased body weight as a prognostic parameter for complications in the course of acute pancreatitis. Pancreas. 1990;5:626-629.
  15. Larvin M, McMahon MJ. APACHE-II score for assessment and monitoring of acute pancreatitis. Lancet. 1989;11:201-205.
  16. Martinez J, Sanchez-Paya J, Palazon JM, Aparicio JR, Pico A, Perez Mateo Obesity: a prognostic factor of severity in acute pancreatitis. Pancreas. 1999;19:15-20.
  17. Martіnez J, Sanchez-Paya J, Palazon JM, Suazo-Barahona J, Robles-Dnaz G, Perez-Mateo Is obesity a risk factor in acute pancreatitis? A meta-analysis. Pancreatology. 2004;4:42-46.
  18. Mery CM, Rubio V, Duarte-Rojo A, Suazo-Barahona J, Pellez-Luna M, Milke P, Robles-Diaz G. Android fat distribution as predictor of severity in acute pancreatitis. Pancreatology. 2012;2:543-549.
  19. Mortele KJ, Wiesner W, Intriere L, Shankar S, Zou KH, Kalantari BN et al. A Modified CT Severity Index for Evaluating Acute Pancreatitis:Improved Correlation with Patient Outcome. AJR Am J Roentgenol. 2004;183(5):1261-1265.
  20. Navina S, Acharya C, DeLany JP et al. Lipotoxicity causes multisystem organ failure and exacerbates acute pancreatitis in obesity. Sci Transl Med. 2011;3:107-110.
  21. Obesity: preventing and managing the global epidemic. Report of a WHO World Health Organ Tech Rep Ser. 2000;894:i–xii, 1–253.
  22. Papachristou GI, Papachristou DJ, Avula H, Slivka A, Whitcomb DC. Obesity increases the severity of acute pancreatitis: performance of APACHE-O score and correlation with the inflammatory response. Pancreatology 2006;6:279-285.
  23. Pitha J, Kovar J, Blahova T. Fasting and nonfasting triglycerides in cardiovascular and other diseases. Physiol Res. 2015;64(3 Suppl):323-330.
  24. Porter KA, Banks PA. Obesity as a predictor of severity in acute pancreatitis. Int J Pancreatol. 2001;10:247-252.
  25. Saisho Y, Butler AE, Meier JJ et al. Pancreas volumes in humans from birth to age one hundred taking into account sex, obesity, and presence of type-2 Clin Anat. 2007;20:933-942.
  26. Schaffler A, Hamer O, Dickopf J. Admission resistin levels predict peripancreatic necrosis and clinical severity in acute pancreatitis. Am J Gastroenterol. 2010;105:2474-2484.
  27. Sekimoto M, Takada T, Kawarada Y et al. JPN Guidelines for the management of acute pancreatitis: epidemiology, etiology, natural history, and outcome predictors in acute pancreatitis. J Hepatobiliary Pancreat Surg. 2006;13:10-24.
  28. Sharma A, Muddana V, Lamb J, Greer J, Papachristou GI, Whitcomb DC. Low serum adiponectin levels are associated with systemic organ failure in acute pancreatitis. Pancreas. 2009;38:907-912.
  29. Smeets XJNM, Knoester I, Grooteman KV, Singh VK, Banks PA, Papachristou GI et al. Dutch Pancreatitis Study Group. Eur J Gastroenterol Hepatol. 2019;31(3):316-322.
  30. Suazo-Barahona J, Carmona-Sanchez R, Robles-Diaz G et al. Obesity: a risk factor for severe acute biliary and alcoholic pancreatitis. Am J Gastroenterol. 2008;93:1324-1328.
  31. Suazo-Barahona J, Carmona-Sanchez R, Robles-Diaz G, Milke-Garcia P,Vargas-Vorackova F, Uscanga-Dominguez L et al. Obesity: a risk factor for severe acute biliary and alcoholic pancreatitis. Am J Gastroenterol. 1998;93:1324-1328.
  32. Talamini G, Bassi C, Falconi M, Sartori N, Frulloni L, Di Francesco V, Vesentini S, Pederzoli P, Cavallini G: Risk of death from acute pancreatitis. Role of early, simple ‘routine’ Int J Pancreatol. 2006;19:15-24.
  33. Toh SK, Walters CD, Johnson CD. APACHEO a new predictor of severity in acute pancreatitis. 2006;110:A437.
  34. Tsai CJ. Is obesity a significant prognostic factor in acute pancreatitis? Di Dis Sci. 1998;43:2251-2254.
  35. Vidarsdottir H, Moller PH, Thorarinsdottir H, Bjornsson ES. Acute pancreatitis: a prospective study on incidence, etiology, and outcome. Eur J Gastroenterol Hepatol. 2013;25:1068-1075.
  36. Vipperla K, Somerville C, Furlan A et al. Clinical profile and natural course in a large cohort of patients with hypertriglyceridemia and pancreatitis. J Clin. Gastroenterol. 2017;51:77-85.
  37. Xin MJ, Chen H, Luo B, Sun JB. Severe acute pancreatitis in the elderly: etiology and clinical characteristics. World J Gastroenterol. 2008;14:2517- 2521.