Альманах клинической медицины. 2017; 45: 384-391
Влияние холецистэктомии в молодом возрасте на течение метаболического синдрома у женщин
https://doi.org/10.18786/2072-0505-2017-45-5-384-391Аннотация
Актуальность. Сегодня в фокусе внимания исследователей находятся такие проблемы, как метаболический синдром и процессы формирования неалкогольной жировой болезни печени, выявление факторов, влияющих на скорость развития дистрофических и фибротических изменений в ткани печени. Настоящее исследование демонстрирует попытку более детального изучения метаболических нарушений и состояния ткани печени в постхолецистэктомическом периоде у пациентов с изначально регистрируемым метаболическим синдромом.
Цель – изучить влияние холецистэктомии в молодом возрасте на течение метаболического синдрома у женщин.
Материал и методы. Проведено ретроспективное аналитическое исследование. В выборку включены 57 пациенток с признаками метаболического синдрома (критерии IDF 2005 г.) в возрасте от 18 до 44 лет (молодой возраст согласно определению Всемирной организации здравоохранения). Из них 27 пациенток, страдающих желчнокаменной болезнью, составили основную группу, 30 пациенток, перенесших холецистэктомию в этот возрастной промежуток, вошли в группу сравнения. Проанализированы данные анамнеза, клинического обследования, лабораторные показатели, данные ультразвукового исследования органов брюшной полости, эзофагогастродуоденоскопии, водородного дыхательного теста с лактулозой, а также результаты пункционной биопсии печени.
Результаты. Неалкогольный стеатогепатит в постхолецистэктомическом периоде ассоциирован с избыточным бактериальным ростом в тонкой кишке (р = 0,026), ультразвуковыми признаками холангита (р = 0,041), синдромом диареи (р = 0,027). Фиброз статистически значимо чаще регистрировался в сочетании с хронической диареей (р = 0,034) и клиническими проявлениями постхолецистэктомического синдрома в анамнезе (р = 0,044). Выявлена сильная прямая корреляционная связь между степенью фиброза и длительностью постхолецистэктомического периода (r = 0,77; р = 0,047).
Заключение. Холецистэктомия в молодом возрасте является предиктором прогрессирования метаболических расстройств у женщин с метаболическим синдромом.
Список литературы
1. Shen C, Wu X, Xu C, Yu C, Chen P, Li Y. Association of cholecystectomy with metabolic syndrome in a Chinese population. PLoS One. 2014;9(2):e88189. doi: 10.1371/journal.pone.0088189.
2. Kwak MS, Kim D, Chung GE, Kim W, Kim YJ, Yoon JH. Cholecystectomy is independently associated with nonalcoholic fatty liver disease in an Asian population. World J Gastroenterol. 2015;21(20):6287–95. doi: 10.3748/wjg.v21.i20.6287.
3. Wang HG, Wang LZ, Fu HJ, Shen P, Huang XD, Zhang FM, Xie R, Yang XZ, Ji GZ. Cholecystectomy does not significantly increase the risk of fatty liver disease. World J Gastroenterol. 2015;21(12):3614–8. doi: 10.3748/wjg.v21.i12.3614.
4. Ahmed F, Baloch Q, Memon ZA, Ali I. An observational study on the association of nonalcoholic fatty liver disease and metabolic syndrome with gall stone disease requiring cholecystectomy. Ann Med Surg (Lond). 2017;17:7–13. doi: 10.1016/j.amsu.2017.03.015.
5. Cortés V, Quezada N, Uribe S, Arrese M, Nervi F. Effect of cholecystectomy on hepatic fat accumulation and insulin resistance in non-obese Hispanic patients: a pilot study. Lipids Health Dis. 2017;16(1):129. doi: 10.1186/s12944-017-0525-3.
6. Ramos-De la Medina A, Remes-Troche JM, Roesch-Dietlen FB, Pérez-Morales AG, Martinez S, Cid-Juarez S. Routine liver biopsy to screen for nonalcoholic fatty liver disease (NAFLD) during cholecystectomy for gallstone disease: is it justified? J Gastrointest Surg. 2008;12(12):2097–102. doi: 10.1007/s11605-008-0704-7.
7. Loria P, Lonardo A, Lombardini S, Carulli L, Verrone A, Ganazzi D, Rudilosso A, D'Amico R, Bertolotti M, Carulli N. Gallstone disease in non-alcoholic fatty liver: prevalence and associated factors. J Gastroenterol Hepatol. 2005;20(8):1176–84. doi: 10.1111/j.1440-1746.2005.03924.x.
8. Turnbaugh PJ, Hamady M, Yatsunenko T, Cantarel BL, Duncan A, Ley RE, Sogin ML, Jones WJ, Roe BA, Affourtit JP, Egholm M, Henrissat B, Heath AC, Knight R, Gordon JI. A core gut microbiome in obese and lean twins. Nature. 2009;457(7228):480–4. doi: 10.1038/nature07540.
9. Pattni SS, Brydon WG, Dew T, Walters JR. Fibroblast growth factor 19 and 7α-hydroxy-4-cholesten-3-one in the diagnosis of patients with possible bile acid diarrhea. Clin Transl Gastroenterol. 2012;3:e18. doi: 10.1038/ctg.2012.10.
10. Julio-Pieper M, Bravo JA, Aliaga E, Gotteland M. Review article: intestinal barrier dysfunction and central nervous system disorders – a controversial association. Aliment Pharmacol Ther. 2014;40(10):1187–201. doi: 10.1111/apt.12950
11. Teixeira TF, Souza NC, Chiarello PG, Franceschini SC, Bressan J, Ferreira CL, Peluzio Mdo C. Intestinal permeability parameters in obese patients are correlated with metabolic syndrome risk factors. Clin Nutr. 2012;31(5):735–40. doi: 10.1016/j.clnu.2012.02.009.
12. Berr F, Kullak-Ublick GA, Paumgartner G, Münzing W, Hylemon PB. 7 alpha-dehydroxylating bacteria enhance deoxycholic acid input and cholesterol saturation of bile in patients with gallstones. Gastroenterology. 1996;111(6):1611–20.
13. Guo C, Chen WD, Wang YD. TGR5, not only a metabolic regulator. Front Physiol. 2016;7:646. doi: 10.3389/fphys.2016.00646.
14. Trabelsi MS, Daoudi M, Prawitt J, Ducastel S, Touche V, Sayin SI, Perino A, Brighton CA, Sebti Y, Kluza J, Briand O, Dehondt H, Vallez E, Dorchies E, Baud G, Spinelli V, Hennuyer N, Caron S, Bantubungi K, Caiazzo R, Reimann F, Marchetti P, Lefebvre P, Bäckhed F, Gribble FM, Schoonjans K, Pattou F, Tailleux A, Staels B, Lestavel S. Farnesoid X receptor inhibits glucagon-likepeptide-1 production by enteroendocrine L cells. Nat Commun. 2015;6:7629. doi: 10.1038/ncomms8629.
15. Cani PD, Amar J, Iglesias MA, Poggi M, Knauf C, Bastelica D, Neyrinck AM, Fava F, Tuohy KM, Chabo C, Waget A, Delmée E, Cousin B, Sulpice T, Chamontin B, Ferrières J, Tanti JF, Gibson GR, Casteilla L, Delzenne NM, Alessi MC, Burcelin R. Metabolic endotoxemia initiates obesity and insulin resistance. Diabetes. 2007;56(7):1761–72. doi: 10.2337/db06-1491.
Almanac of Clinical Medicine. 2017; 45: 384-391
The influence of cholecystectomy at young age on the course of metabolic syndrome in women
https://doi.org/10.18786/2072-0505-2017-45-5-384-391Abstract
Rationale: At present, the metabolic syndrome and pathophysiology of non-alcoholic fatty liver disease, as well as identification of factors that may influence the rate of development of dystrophy and fibrosis in the liver are in the focus of investigators' attention. This study represents an attempt to detail metabolic derangements and liver tissue abnormalities after cholecystectomy in patients with metabolic syndrome at baseline.
Aim: To study the influence of cholecystectomy performed at younger age on the course of metabolic syndrome in women.
Materials and methods: This was a retrospective analytical study in a sample of 57 female patients with metabolic syndrome (International Diabetes Federation criteria 2005) aged from 18 to 44 years (young age according to the World Health Organization definition). From those, 30 patients with cholelithiasis were included into the control group and 27 patients who had undergone cholecystectomy in this age range were included into the comparison group. We analyzed their past history, results of clinical examination, laboratory tests, abdominal ultrasound examination, esophagogastroduodenoscopy, hydrogen respiration test with lactulose, as well as the results of needle liver biopsy.
Results: Non-alcoholic steatohepatitis after cholecystectomy was associated with the excessive bacterial growth in the small intestine (р = 0.026), ultrasound signs of cholangitis (р = 0.041), and diarrhea syndrome (р = 0.027). Liver fibrosis was significantly more frequent in association with chronic diarrhea (р = 0.034) and past clinical signs of post-cholecystectomy syndrome (р = 0.044). There was a strong direct correlation between the grade of fibrosis and the time since cholecystectomy (r = 0.77; р = 0.047).
Conclusion: Cholecystectomy performed at young age predicts progression of metabolic abnormalities in women with metabolic syndrome.
References
1. Shen C, Wu X, Xu C, Yu C, Chen P, Li Y. Association of cholecystectomy with metabolic syndrome in a Chinese population. PLoS One. 2014;9(2):e88189. doi: 10.1371/journal.pone.0088189.
2. Kwak MS, Kim D, Chung GE, Kim W, Kim YJ, Yoon JH. Cholecystectomy is independently associated with nonalcoholic fatty liver disease in an Asian population. World J Gastroenterol. 2015;21(20):6287–95. doi: 10.3748/wjg.v21.i20.6287.
3. Wang HG, Wang LZ, Fu HJ, Shen P, Huang XD, Zhang FM, Xie R, Yang XZ, Ji GZ. Cholecystectomy does not significantly increase the risk of fatty liver disease. World J Gastroenterol. 2015;21(12):3614–8. doi: 10.3748/wjg.v21.i12.3614.
4. Ahmed F, Baloch Q, Memon ZA, Ali I. An observational study on the association of nonalcoholic fatty liver disease and metabolic syndrome with gall stone disease requiring cholecystectomy. Ann Med Surg (Lond). 2017;17:7–13. doi: 10.1016/j.amsu.2017.03.015.
5. Cortés V, Quezada N, Uribe S, Arrese M, Nervi F. Effect of cholecystectomy on hepatic fat accumulation and insulin resistance in non-obese Hispanic patients: a pilot study. Lipids Health Dis. 2017;16(1):129. doi: 10.1186/s12944-017-0525-3.
6. Ramos-De la Medina A, Remes-Troche JM, Roesch-Dietlen FB, Pérez-Morales AG, Martinez S, Cid-Juarez S. Routine liver biopsy to screen for nonalcoholic fatty liver disease (NAFLD) during cholecystectomy for gallstone disease: is it justified? J Gastrointest Surg. 2008;12(12):2097–102. doi: 10.1007/s11605-008-0704-7.
7. Loria P, Lonardo A, Lombardini S, Carulli L, Verrone A, Ganazzi D, Rudilosso A, D'Amico R, Bertolotti M, Carulli N. Gallstone disease in non-alcoholic fatty liver: prevalence and associated factors. J Gastroenterol Hepatol. 2005;20(8):1176–84. doi: 10.1111/j.1440-1746.2005.03924.x.
8. Turnbaugh PJ, Hamady M, Yatsunenko T, Cantarel BL, Duncan A, Ley RE, Sogin ML, Jones WJ, Roe BA, Affourtit JP, Egholm M, Henrissat B, Heath AC, Knight R, Gordon JI. A core gut microbiome in obese and lean twins. Nature. 2009;457(7228):480–4. doi: 10.1038/nature07540.
9. Pattni SS, Brydon WG, Dew T, Walters JR. Fibroblast growth factor 19 and 7α-hydroxy-4-cholesten-3-one in the diagnosis of patients with possible bile acid diarrhea. Clin Transl Gastroenterol. 2012;3:e18. doi: 10.1038/ctg.2012.10.
10. Julio-Pieper M, Bravo JA, Aliaga E, Gotteland M. Review article: intestinal barrier dysfunction and central nervous system disorders – a controversial association. Aliment Pharmacol Ther. 2014;40(10):1187–201. doi: 10.1111/apt.12950
11. Teixeira TF, Souza NC, Chiarello PG, Franceschini SC, Bressan J, Ferreira CL, Peluzio Mdo C. Intestinal permeability parameters in obese patients are correlated with metabolic syndrome risk factors. Clin Nutr. 2012;31(5):735–40. doi: 10.1016/j.clnu.2012.02.009.
12. Berr F, Kullak-Ublick GA, Paumgartner G, Münzing W, Hylemon PB. 7 alpha-dehydroxylating bacteria enhance deoxycholic acid input and cholesterol saturation of bile in patients with gallstones. Gastroenterology. 1996;111(6):1611–20.
13. Guo C, Chen WD, Wang YD. TGR5, not only a metabolic regulator. Front Physiol. 2016;7:646. doi: 10.3389/fphys.2016.00646.
14. Trabelsi MS, Daoudi M, Prawitt J, Ducastel S, Touche V, Sayin SI, Perino A, Brighton CA, Sebti Y, Kluza J, Briand O, Dehondt H, Vallez E, Dorchies E, Baud G, Spinelli V, Hennuyer N, Caron S, Bantubungi K, Caiazzo R, Reimann F, Marchetti P, Lefebvre P, Bäckhed F, Gribble FM, Schoonjans K, Pattou F, Tailleux A, Staels B, Lestavel S. Farnesoid X receptor inhibits glucagon-likepeptide-1 production by enteroendocrine L cells. Nat Commun. 2015;6:7629. doi: 10.1038/ncomms8629.
15. Cani PD, Amar J, Iglesias MA, Poggi M, Knauf C, Bastelica D, Neyrinck AM, Fava F, Tuohy KM, Chabo C, Waget A, Delmée E, Cousin B, Sulpice T, Chamontin B, Ferrières J, Tanti JF, Gibson GR, Casteilla L, Delzenne NM, Alessi MC, Burcelin R. Metabolic endotoxemia initiates obesity and insulin resistance. Diabetes. 2007;56(7):1761–72. doi: 10.2337/db06-1491.
