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A New Paradigm in Gallstones Diseases and Marked Elevation of Transaminases

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A New Paradigm in Gallstones Diseases and Marked Elevation of Transaminases A New Paradigm in Gallstones Diseases and Marked Elevation of Transaminases. , 2017; 16 (2): 285-290 285 ORIGINAL ARTICLE March-April, Vol. 16 No. 2, 2017: 285-290 The Official Journal of the Mexican Association of Hepatology, the Latin-American Association for Study of the Liver and the Canadian Association for the Study of the Liver A New Paradigm in Gallstones Diseases and Marked Elevation of Transaminases: An Observational Study Sara Campos,* Nuno Silva,** Armando Carvalho** * Gastroenterology department, Centro Hospitalar e Universitário de Coimbra (CHUC). ** Internal Medicine department, Centro Hospitalar e Universitário de Coimbra (CHUC). ABSTRACT Background. In clinical practice, it is assumed that a severe rise in transaminases is caused by ischemic, viral or toxic hepatitis. Nevertheless, cases of biliary obstruction have increasingly been associated with significant hypertransaminemia. With this study, we sought to determine the true etiology of marked rise in transaminases levels, in the context of an emergency department. Mate- rial and methods. We retrospectively identified all patients admitted to the emergency unit at Centro Hospitalar e Universitário de Coimbra between 1st January 2010 and 31st December 2010, displaying an increase of at least one of the transaminases by more than 15 times. All patient records were analyzed in order to determine the cause of hypertransaminemia. Results. We analyzed 273 patients – 146 males, mean age 65.1 ± 19.4 years. The most frequently etiology found for marked hypertransaminemia was pancreaticobiliary acute disease (n = 142;39.4%), mostly lithiasic (n = 113;79.6%), followed by malignancy (n = 74;20.6%), ischemic hepatitis (n = 61;17.0%), acute primary hepatocellular disease (n = 50;13.9%) and muscle damage (n = 23;6.4%). We were not able to determine a diagnosis for 10 cases. There were 27 cases of recurrence in the lithiasic pancreaticobiliary pathology group. Recur- rence was more frequent in the group of patients who had not been submitted to early cholecystectomy after the first episode of bil- iary obstruction (p = 0.014). The etiology of hypertransaminemia varied according to age, cholestasis and glutamic-pyruvic transaminase values. Conclusion. Pancreaticobiliary lithiasis is the main cause of marked hypertransaminemia. Hence, it must be considered when dealing with such situations. Not performing cholecystectomy early on, after the first episode of biliary obstruction, may lead to recurrence. Key words. Transaminases. Biliary obstruction. Ischemic hepatitis. Viral hepatitis. Toxic hepatitis. INTRODUCTION integrity of the hepatocyte membrane, transaminases plas- ma levels increase. Levels up to 300 IU/L are nonspecific Liver enzymes, routinely used in the evaluation of pa- and can be observed in various situations. Conversely, a tients, tend to be elevated in about 7-12%.1 of the Portu- marked increase of aminotransferases (greater than 15 guese population. These changes are classically divided times the upper limit of normal5) arises in a number of into “cholestatic” or “hepatocellular” patterns, according more restricted situations. In the scarce published litera- to abnormal parameters: while in cholestatic disorders an ture, it is argued that these large increases generally point increase in alkaline phosphatase and gamma glutamyl to a viral, toxic or ischemic hepatocellular damage.5-8 transferase prevails,2,3 in hepatocellular disorders the in- However, in our clinical practice, we have often en- creasing value of aminotransferases is the most predomi- countered cases of marked hypertransaminemia associated nant. In fact, aminotransferases are considered sensitive with biliary obstruction without showing this typical indicators of liver injury,4 since increased levels are found cholestatic pattern. In fact, such kind of situations has in- on hepatocytes and only small concentrations (up to 40 creasingly been documented in the literature.9-12 IU/L) are present in blood circulation in normal situa- Bearing these predicaments in mind, we undertook this tions. When there is a hepatocellular injury with loss of study, with the purpose of determining the actual rate and Manuscript received: May 10, 2016. Manuscript accepted: July 18, 2016. DOI:10.5604/16652681.1231588. 286 , 2017; 16 (2): 285-290 etiology of severely elevated liver aminotransferases in a We defined abusive alcohol consumption as an intake Hospital emergency department. greater than 40 g/day in males and 20 g/day in females.14 Ischemic hepatitis was considered whenever a marked MATERIAL AND METHODS increase of aminotransferases occurred in a patient with clinical cardiac, circulatory or respiratory failure.15 Type of the study The elevation of aminotransferases was considered cryptogenic when no cause was found, despite the per- Observational. formed work-up (no alcohol or intravenous drug use or history of ischemic hepatitis, negative abdominal ultra- Time horizon, Setting and Participants sound, serology and autoimmunity, with or without histo- logical examination). All patients admitted to the emergency department at Centro Hospitalar e Universitário de Coimbra (CHUC) Ethical approval between 1st January 2010 and 31st December 2010, dis- playing an increase of at least one of the transaminases by All procedures performed in this study that concerned more than 15 times, were retrospectively evaluated. These human participants were in accordance with ethical stand- patients were identified through computer records pro- ards of the institution and with the 1964 Helsinki declara- vided by the Department of Biochemistry of CHUC. We tion and its later amendments. followed these patients until July 2012. Exceptionally, and given the public health interest of this retrospective study and the observational design of the Study perspective and variables protocol, it was decided not to send a consent form to the patients. Nonetheless, the authors are able to certify that Descriptive study. We characterized the sample ac- the data collection by the physician was subject to profes- cording to the following variables: age, gender, risk factors sional confidentiality and ethical code and that the ano- for liver disease (metabolic syndrome - hypertension, dia- nymity of all the participants was guaranteed by the betes mellitus and dyslipidemia; alcoholism; hepatotoxic assignment of a unique identification number that was medications), prior cholecystectomy, cancer, thyroid dis- only accessible to the researchers involved with this study. ease, heart failure, symptoms, results of complementary All collected data was treated, published and presented in tests (blood tests, abdominal ultrasonography, endoscopic a grouped manner, in order to prevent the identification of retrograde cholangiopancreatography, histology), follow- the participants. Only the researchers were granted access up and final diagnosis. to the collected data, and its storage was assured for a 5- year period counting from the last publication until its Definitions subsequent destruction. The researchers take full respon- sibility for the confidentiality of the collected data. A marked increase of aminotransferases (hyper- transaminemia) was considered when at least one ami- Statistical analysis notransferase (glutamic pyruvic transaminase - GPT or glutamic oxalacetic transaminase - GOT) exceeded 15 We performed a descriptive analysis of patients who pre- times5 the reference upper limit established by the labo- sented marked liver aminotransferases elevation in the ratory of the Hospital (45 IU/L), that is, greater than 700 emergency department [frequency, mean, standard devia- IU/L. tion and median]. We described the episode, causes and fol- Cholestasis was defined when alkaline phosphatase low-up. We evaluated the influence of cholecystectomy in and/or gamma-glutamyl transferase exceeded the upper the recurrence of hypertransaminemia using the χ2 test. We normal limit, which is 120U/L and 55U/L, respectively. analyzed the influence of some characteristics (age, pres- We considered the following drugs with potential ence of cholestasis, the average value of GPT) in the differ- hepatotoxicity: acetaminophen, amiodarone, amoxicillin- ential diagnosis of altered aminotransferases, through: clavulanic acid, carbamazepine, fluconazole, glyburide, heparin, isoniazid, ketoconazole, labetalol, nitrofurantoin, • χ2 test for comparison of dichotomous qualitative vari- non-steroidal anti-inflammatory drug, phenytoin, proton ables, if necessary with continuity correction. pump inhibitors, sulfonylureas, trazodone, allopurinol, • The Kruskal-Wallis test for the qualitative or quantita- azathioprine, captopril, anti-oral contraceptives, corticos- tive analysis ordinal variables. Significant differences teroids, hydralazine, methotrexate, methyldopa, quinidine were considered whenever p < 0.05. Statistical analysis and erythromycin.13 was performed using SPSS, version 20. A New Paradigm in Gallstones Diseases and Marked Elevation of Transaminases. , 2017; 16 (2): 285-290 287 RESULTS Table 1. Primary etiology of marked hypertransaminemia. Defining the population Groups of primary Subdivision of etiologies (N) diagnosis (N) During the period of study, 152,718 patients were ob- Pancreaticobiliary Lithiasic (113): served in the emergency department of our Hospital. diseases (136) Cholelithiasis + biliary colic (31) Three hundred and twenty four patients (0.2%) displayed a Cholelithiasis + acute pancreatitis (28) Cholelithiasis + acute cholecystitis (12) marked
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