Dietary habits as risk factor of gallstone disease in Benghazi, Libya: a case control study
DOI:
https://doi.org/10.18203/2349-2902.isj20243980Keywords:
Gall bladder stone, Dietary risk factors, Al-Jala hospital, Case-control studyAbstract
Background: Gallstone disease is one of the most common diseases in developed and developing countries; recent studies have expressed evidence in the context of the role of nutrition in the gallstone disease etiology. The most common risk factors for gallstones formations are old age, female gender, obesity and diabetes mellitus. The dietary risk factors, includes consumption of carbohydrates, fats, proteins and dietary products, Moreover, healthy dietary pattern, coffee, rich sources of vitamins as fruits and vegetables do have protection role of gallstones. Our aim is to determine the dietary habits as a risk factor of gallstone diseases admitted in Al-Jala Hospital.
Methods: An analytic case control study the data collected from documents of gall bladder stone (GBS) cases that have presented in surgical department and controls from other departments at Al Jala Hospital of Benghazi-Libya between January 2023 and December 2023.
Results: The results of the study showed that cases diagnosed with GBS had high dietary intake of carbohydrates, fat, dairy products and meats and whereas had low dietary intake of vegetables and fruits which highly containing fibers, vitamins and minerals in contrast controls had low intake of carbohydrates, fat, dairy products and meats and whereas had high dietary intake of vegetables and fruit (vitamins and minerals) and caffeine.
Conclusions: The study concluded that dietary risk factors that contributing to the high prevalence of gall stone formation were because of high intake of high carbohydrates, proteins and fatty diets and low intake of dietary fiber vitamins and minerals as well as caffeine also cases ender and high body mass index (BMI) play important role in gall stone formation.
Metrics
References
Hundt M, Wu CY, Young M. Anatomy, Abdomen and Pelvis: Biliary Ducts. StatPearls. StatPearls Publishing; Treasure Island (FL). 2022.
Salazar MC, Brownson KE, Nadzam GS, Duffy A, Roberts KE. Gallbladder Agenesis: A Case Report. Yale J Biol Med. 2018;91(3):237-41.
Rehfeld JF, Knop FK, Asmar A, Madsbad S, Holst JJ, Asmar M. Cholecystokinin secretion is suppressed by glucagon-like peptide-1: clue to the mechanism of the adverse gallbladder events of GLP-1-derived drugs. Scand J Gastroenterol. 2018;53(12):1429-32. DOI: https://doi.org/10.1080/00365521.2018.1530297
Tsai TJ, Chan HH, Lai KH, Shih CA, Kao SS, Sun WC, et al. Gallbladder function predicts subsequent biliary complications in patients with common bile duct stones after endoscopic treatment? BMC Gastroenterol. 2018;18(1):32. DOI: https://doi.org/10.1186/s12876-018-0762-6
Rebholz C, Krawczyk M, Lammert F. Genetics of gallstone disease. Eur J Clin Invest. 2018;48(7):e12935. DOI: https://doi.org/10.1111/eci.12935
Shabanzadeh DM. New determinants for gallstone disease? Dan Med J. 2018;65.
Del Pozo R, Mardones L, Villagrán M, Muñoz K, Roa S, Rozas F, et al. Effect of a high-fat diet on cholesterol gallstone formation. Rev Med Chil. 2017;145(9):1099-105. DOI: https://doi.org/10.4067/s0034-98872017000901099
Shiffman ML; Kaplan GD; Brinkman-Kaplan V; Vickers FF Prophylaxis against gallstone formation with ursodeoxycholic acid in patients participating in a very-lowcalorie diet program. Ann Intern Med. 1995;122:899-905. DOI: https://doi.org/10.7326/0003-4819-122-12-199506150-00002
Wang DQ, Cohen DE, Carey MC. Biliary lipids and cholesterol gallstone disease. J Lip Res. 2009;50:S406-11. DOI: https://doi.org/10.1194/jlr.R800075-JLR200
Katsika D, Grjibovski A, Einarsson C, Lammert F, Lichtenstein P, Marschall HU. Genetic and environmental influences on symptomatic gallstone disease: A Swedish study of 43,141 twin pairs. Hepatology. 2005;41:1138-43. DOI: https://doi.org/10.1002/hep.20654
Lammert F, Miquel JF. Gallstone disease: from genes to evidence-based therapy. J Hepatol. 2008;48(1):S124-35. DOI: https://doi.org/10.1016/j.jhep.2008.01.012
Diehl AK. Epidemiology and natural history of gallstone disease. Gastroenterol Clin North Am. 1991;20:1-19. DOI: https://doi.org/10.1016/S0889-8553(21)00531-8
Grundy SM Cholesterol gallstones: a fellow traveler with metabolic syndrome? Am J Clin Nutr. 2004;80:1-2. DOI: https://doi.org/10.1093/ajcn/80.1.1
Banim PJ, Luben RN, Bulluck H, Sharp SJ, Wareham NJ, Khaw KT, et al. The aetiology of symptomatic gallstones quantification of the effects of obesity, alcohol and serum lipids on risk. Epidemiological and biomarker data from a UK prospective cohort study (EPIC-Norfolk). Eur J Gastroenterol Hepatol. 2011;23:733-40. DOI: https://doi.org/10.1097/MEG.0b013e3283477cc9
Friedman GD, Kannel WB, Dawber TR. The epidemiology of gallbladder disease: observations in the Framingham Study. J Chronic Dis. 1966;19:273-92. DOI: https://doi.org/10.1016/0021-9681(66)90132-9
Cuevas A, Miquel JF, Reyes MS, Zanlungo S, Nervi F. Diet as a risk factor for cholesterol gallstone disease. J Am Coll Nutr. 2004;23:187-96. DOI: https://doi.org/10.1080/07315724.2004.10719360
Hofmann AF. Primary and secondary prevention of gallstone disease: implications for patient management and research priorities. Am J Surg. 1993;165:541-8. DOI: https://doi.org/10.1016/S0002-9610(05)80958-4
Dowling RH. Review: pathogenesis of gallstones. Alim Pharmacol Ther. 2000;14:39-47. DOI: https://doi.org/10.1046/j.1365-2036.2000.014s2039.x
Amigo L, Zanlungo S, Mendoza H, Miquel JF, Nervi F. Risk factors and pathogenesis of cholesterol gallstones: state of the art. Eur Rev Med Pharmacol Sci. 1999;3:241-6.
Paumgartner G, Sauerbruch T. Gallstones: pathogenesis. Lancet. 1991;338:1117-21. DOI: https://doi.org/10.1016/0140-6736(91)91972-W
Miyasaka K, Takata Y, Funakoshi A. Association of cholecystokinin-A receptor gene polymorphism with cholelithiasis and the molecular mechanisms of this polymorphism. J Gastroenterol. 2002;37(S14):102-6. DOI: https://doi.org/10.1007/BF03326426
Carey MC, Paigen B. Epidemiology of the American Indians’burden and its likely genetic origins. Hepatology. 2002;36:781-91. DOI: https://doi.org/10.1053/jhep.2002.36545