Serum Transaminases In Patients Research Articles

Elevated serum transaminases in patients with acute coronary syndromes: Do we need a revision of exclusion criteria for clinical trials?

Elevations of hepatic transaminase (serum alanine transaminase [ALT] and serum aspartate aminotransferase [AST]) levels in patients with acute coronary syndrome (ACS), although transient, may result in exclusions from clinical efficacy trials due to suspected liver disease. The aim of this study was to evaluate the concentrations of serum transaminases in ACS and relate these to currently accepted AST/ALT exclusion criteria from clinical trials. One hundred consecutive patients with ACS were prospectively examined. Blood samples for AST, ALT, total bilirubin and troponin I concentration were obtained at the time of admission and after 6, 12 and 24 hours. Eighty percent of patients had elevated AST, and 47% ALT; 43% of patients characterized AST concentration > 3 × upper limit of normal (ULN) in at least one measurement, while 8% of patients presented ALT concentration > 3 × ULN. AST presented higher concentrations when compared to ALT, resulting in a high De-Ritis ratio at every time point. No significant or high correlations were found between the concentrations of serum transaminases, De-Ritis ratio and troponin I. Two different cut-off values of troponin I were adopted to define the amount of infarcted myocardium that distinguished 28-31% of individuals with "large infarction". Among these patients, approximately 93% presented AST concentrations > 3 × ULN. Hepatic transaminases are often elevated in ACS, with the majority of patients with more extensive myocardial injury presenting high concentrations of AST. In the setting of ACS, current transaminase thresholds for liver dysfunction used in clinical trials may lead to excessive and inadequate exclusions of patients with larger infarcts from such trials.

Dipeptidyl peptidase-4 inhibitor (teneligliptin) significantly reduces liver fat content and delays progression of non-alcoholic steatohepatitis in type 2 diabetes mellitus patients

Background: Dipeptidyl peptidase (DPP)-4 inhibitors, anti-diabetic agents, are expected to be effective for treatment of non-alcoholic fatty liver disease (NAFLD). Several studies have shown that some DPP-4 inhibitors alleviate hepatic steatosis or steatohepatitis in type 2 diabetic mice or rats. Teneligliptin is DPP4 inhibitor whose efficacy to control blood sugar is well established but its effect on liver is not studied well. In present study we investigated effect of teneligliptin, a DPP-4 inhibitor on patients of type 2 diabetes with non-alcoholic steatohepatitis (NASH). Methods: This was a randomized, double-blind study in which 64 patients between ages of 18 to 80 years were selected for study. Participants were identified as type 2 diabetes with biopsy confirmed NASH. We excluded the patients with glucocorticoid use, hepatitis B or C, and other diseases that might affect liver function. Results: The mean HbA1c change after 48 weeks of therapy in group A was-1.06 % and in group B was-0.77% and this was statistically insignificant (p>0.06). The mean AST change after 48 weeks of therapy in group A was-45.4% and in group B was-33.3% and this was statistically significant (p<0.001). The mean ALT change after 48 weeks of therapy in group A was-41.6% and in group B was-22.7% and this was statistically significant (p<0.001). The change in liver fat content (LFC) after 48 weeks of therapy in group A was-15.4% and group B was-7.14% and this was also statistically significant (p<0.001).Conclusions: Result of our study revealed that teneligliptin significantly reduce serum transaminases in patients of NASH with type 2 DM. Teneligliptin significantly reduce LFC and delay progression of NASH independent of diabetes control in type 2 diabetes mellitus (DM) patients. These data show significant antisteatotic and anti-inflammatory effect of teneligliptin in type 2 diabetes patients.

5. Correlation of carotid atherosclerosis and serum transaminases in patients with non-alcoholic fatty liver disease

5. Correlation of carotid atherosclerosis and serum transaminases in patients with non-alcoholic fatty liver disease

Profile of serum transaminases in patients with dengue infection in a tertiary care hospital

Background: Although dengue virus is a non hepatotropic virus, liver injury due to dengue infection is not uncommon. Atypical manifestations with liver involvement have frequently been reported, ranging from mild elevations of aminotransferase levels to fulminant hepatitis. The aim of the present study is to study the serum transaminases level in various forms of dengue infection and correlate with severity.Methods: An analysis of 151 serologically confirmed cases (0-14 yrs) of dengue from June 2017 to July 2017 at a tertiary care hospital, Dharwad was made to assess the frequency and degree of hepatic dysfunction in children with dengue infection by analyzing serum transaminase levels. Patients were classified according to WHO as dengue without warning signs, with warning signs and severe dengue. Patients were divided into primary and secondary dengue based on serology and serum transaminases levels were assessed in each of the above groups. Patients with normal aminotransferase levels were categorized into Grade A, those with atleast one of the enzymes raised to less than 3 times the reference range as Grade B, those with atleast one of the enzymes elevated more than 3 times but less than 10 times as Grade C and those with elevations more than 10 times as Grade D. χ2 test was applied to check statistical significance.Results: During the study period, the total number of serologically confirmed cases of dengue were 151 among which dengue fever without warning signs were 38, with warning signs were 91 and severe dengue were 22. Serum transaminase levels were significantly raised in severe dengue (χ2=14.228, df=6, p=0.027).It was also found that transaminases were significantly higher in secondary dengue infection than primary dengue ( χ2=10.155, df=3, p=0.017). Transaminases were significantly elevated in non-survivors (χ2=16.958, df=3, p<0.001).Conclusions: Hepatic dysfunction was common in all forms of dengue infection, with AST rising significantly more than ALT. Transaminases were significantly elevated in severe dengue and secondary dengue infections. Patients with significantly high transaminases had a poor outcome.

Investigation of the relation between thrombocyte counts and serum transaminases in patients with Crimean Congo hemorrhagic fever

Abstract Objective Fever, thrombocytopenia and transaminase elevation are consistent features of Crimean-Congo hemorrhagic fever (CCHF). This study which was done in a hyperendemic region for CCHF, was carried out to find the frequencies of elevated transaminases among CCHF patients with thrombocytopenia. Methods Thrombocyte counts, aspartate aminotransferase (AST), alanine aminotransferase (ALT) test results on admission and follow-up of hospitalized CCHF patients were collected retrospectively. Results When we assessed data on admission, all patients with thrombocyte ≤50,000/μL had elevated AST as well as all but one (98.1%) had elevated ALT levels. When the lowest thrombocyte count was taken into account, concordant AST, ALT levels of all patients with thrombocyte ≤50,000/μL were above normal. Conclusion Conclusively, acute CCHF patients with thrombocyte <50,000/μL should necessarily have elevated ASTs, ALTs.

Association of serum transaminases with short- and long-term outcomes in patients with ST-elevation myocardial infarction undergoing primary percutaneous coronary intervention

BackgroundAlanine transaminase (ALT) and aspartate aminotransferase (AST) are referred to as liver transaminases. Although used routinely in clinical practice for decades, their role as predictors of mortality has not been examined until recently. We studied the predictive value of these serum transaminases in patients with ST-segment elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (PCI).MethodsWe analyzed records of 2417 consecutive STEMI patients with no preexisting liver disease who were treated with primary PCI at the Cardiovascular Center in the First Hospital of Jilin University. The outcomes measured were all-cause mortality at the first month and at 2 years. The relationship between the baseline serum transaminase levels and primary outcome was determined.ResultsWe found a significant correlation between elevated liver transaminases and the Killip classification (P < 0.001 for ALT; P < 0.001 for AST), cardiac troponin I (P = 0.002 for ALT; P < 0.001 for AST), infarct-related coronary artery (P = 0.036 for ALT; P = 0.011 for AST), and pre-thrombolysis-in-myocardial-infarction (pre-TIMI) flow (P < 0.001 for ALT and AST). The serum level of ALT and AST were high along with the increasing of the grade of Killip classification. The primary infarct-related coronary artery in patients with ALT ≥95th percentage was left anterior descending artery (56%), followed by right coronary artery (36%). The OR for all-cause mortality at 2 years for participants with ALT ≥95th percentage was 5.370 (95% CI: 2.899–9.948), 7.034 (95% CI: 3.718–13.307) after adjustment for age and gender and 1.051 (95% CI: 0.302–3.652) after adjustment for all covariables. The OR for all-cause mortality at 2 years for participants with AST ≥95th percentage was 5.370 (95% CI 2.899–9.948) and 5.699 (95% CI 3.030–10.718) after adjustment for age and gender and 1.796 (95% CI: 0.588–5.481) after adjustment for all covariables. ALT (HR 1.004, 95% CI 1.001–1.006, P = 0.010) and AST (HR 0.999, 95% CI 0.998–1.000, P = 0.030) were associated with early all-cause mortality in patients with STEMI treated with PCI but not at 2 years post-procedure, unless for AST and ALT levels ≥95th percentage. Moreover, short- and long-term outcomes were significantly worse when both AST and ALT levels ≥95th percentage (P < 0.001).ConclusionsSerum transaminases ≥95th percentage were associated with a significantly increased incidence of short- and long-term all-cause mortality.Trial registrationRegistration number: ChiCTR-EPC-16008199, 31 March 2016.

Characterization of agomelatine-induced liver injury, incidence and risk factors: A pooled analysis of 7605 treated patients

Introduction/objectiveThe hepatic safety of agomelatine was assessed in 49 phase II and III studies. The aim was to analyze the characteristics of patients who developed an increase in transaminases whilst taking agomelatine.MethodA retrospective pooled analysis of changes in serum transaminase in 7605 patients treated with agomelatine (25 mg or 50 mg/day) from 49 completed studies was undertaken. A significant increase in serum transaminase was defined as &gt; 3-fold the upper limit of normal (&gt; 3 ULN). Final causality was determined in a case-by-case review by five academic experts.ResultsTransaminase increased to &gt; 3 ULN in 1.3% and 2.5% of patients treated with 25 mg and 50 mg of agomelatine respectively, compared to 0.5% for placebo. The onset of increased transaminases occurred at &lt; 12 weeks in 64% of patients. The median time to recovery (to ≤ 2ULN) was 14 days following treatment withdrawal. Liver function tests recovered in 36.1% patients despite the continuation of agomelatine, suggesting the presence of a liver adaptive mechanism. Patients with elevated transaminases at baseline, secondary to obesity and fatty liver disease (NAFLD), had an equally increased risk of developing further elevations of transaminases with agomelatine and placebo. This reflects the widespread fluctuations of serum transaminases in patients with NAFLD.ConclusionsThe overall incidence of abnormal transaminases was low and dose dependent. No specific population was identified regarding potential risk factors. Withdrawal of agomelatine led to rapid recovery, and some patients exhibited an adaptive phenomenon. The liver profile of agomelatine seems safe when serum transaminases are monitored.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Significance of hepatitis B virus genotypes A to E in a cohort of patients with chronic hepatitis B in the Seine Saint Denis District of Paris (France)

The aim of this study was to examine the genetic variability of the hepatitis B virus (HBV) and its significance. HBV genotypes, core promoter and precore mutants were characterized in 109 consecutive patients with biopsy-proven HBV chronic hepatitis. Genotypes A (26.6%), B (12.8%), C (18.3%), D (18.3%), and E (14.7%) indicate a wide genotypic distribution. Patients were from Asia (30.3%), Europe (28.4%), Sub Saharan Africa (23.9%), the Caribbean (10.1%), North Africa (5.5%), and Madagascar (1.8%). HBV genotypes A and D (HBV/A and /D) infected all subgroups except Asian patients. HBV/B or /C were found in 97% of Asian patients, whereas HBV/E only infected sub-Saharan African and Caribbean patients. Differences according to genotypes were: an increased prevalence of anti-HBe antibodies in patients infected with HBV/D (P = 0.003), higher serum transaminases in patients infected with HBV/A and/D (P = 0.043), more severe liver fibrosis in patients infected with HBV/A, /C and/D (P = 0.02). Precore and core promoter mutants were found in 87% of anti-HBe positive patients, and were associated with HBV/D (P = 0.04) and severe liver fibrosis (P = 0.002). It is concluded that HBV genotypes A, B, C, D, and E circulate in the Seine Saint Denis District, reflecting the geographical origin of patients. HBV/A, /C and/D seem to be associated with more severe hepatic disease.

Silymarin treatment of viral hepatitis: a systematic review

Silymarin from the milk thistle herb (Silybum marianum) is used by many patients with chronic viral hepatitis, but its efficacy remains unknown. We performed a systematic review of silymarin for the treatment of chronic viral hepatitis B and C. An exhaustive search strategy identified 148 papers that studied silymarin compounds in liver disease. Of these, four trials included patients with hepatitis C, one included hepatitis B patients, and two, unspecified chronic viral hepatitis. However, only one trial exclusively studied patients with hepatitis C, and none involved patients with only hepatitis B. Silymarin treatment resulted in a decrease in serum transaminases compared with baseline in four studies, and compared with placebo in only one study. There is no evidence that silymarin affects viral load or improves liver histology in hepatitis B or C. No studies were found that investigated the use of silymarin concomitantly with interferon, nucleoside analogues, or other conventional treatments for hepatitis B or C. In conclusion, silymarin compounds likely decrease serum transaminases in patients with chronic viral hepatitis, but do not appear to affect viral load or liver histology. Nevertheless it may be worthwhile to determine its effects in conjunction with standard antiviral treatment.

Etiology and Pathogenesis of Marked Elevation of Serum Transaminase in Patients With Acute Gallstone Disease

From 1980 through 1988, biliary surgery was performed in 197 patients with acute gallstone disease and concomitant elevation of serum glutamic oxalacetic transaminase (SGOT) or serum glutamic pyruvic transaminase (SGPT) of over 300 Karmen units. In 137 patients, anatomic inspection and liver biopsy were performed during the acute stage of the disease. Impacted and floating bile duct stones were found in 69 (50%) and in 43 (32%) of the 137 patients, respectively. The main liver histology was necrosis of liver cells. After surgery, high serum transaminase fell rapidly with immediate recovery in 99% of the patients. In the remaining 60 patients, their signs and symptoms settled soon after initial conservative treatment and surgery was performed after an average time of 21 days. At laparotomy, impacted bile duct stones were found in 2 (3%) and liver histology revealed regeneration of liver cells. These findings suggest that marked elevation of serum transaminase in patients with acute gallstone disease might be due to an acute inflammatory liver cell injury caused by impacted bile duct stones or migrating stones, which would be transient and reversible after early resolution of the bile duct obstruction.

Sulfation of lithocholate as a possible modifier of chenodeoxycholic acid-induced elevations of serum transaminase in patients with gallstones.

Chenodeoxycholic acid (CDC), through its metabolite, lithocholic acid (LC), is hepatotoxic in certain species. The cause of elevations of serum transaminase in 25% of humans ingesting CDC, however, is unknown, but also may be due to LC. Because efficient hepatic sulfation of LC may protect against hepatic injury, the aim of this study was to determine if sulfation of LC might modify CDC-induced elevations of transaminase. Pretreatment sulfation fraction (SF) was estimated in 63 randomly selected patients with gallstones in a double-blind randomized trial of CDC, 750 mg/d, 375 mg/d, or placebo; in 27 of these, SF was repeated at 1 or 2 yr. In four other patients, the SF was measured at 2 yr only. Serum glutamic oxaloacetic transaminase and serum glutamic pyruvic transaminase were determined monthly for 3 mo and then every 3 or 4 mo; an elevation of transaminase was defined as > 150% of the normal upper limit in asymptomatic patients. 10 muCi of (3)H-glyco-LC (sp act 84 mCi/mol) was ingested 10-12 h before fasting duodenal biliary drainage. Bile acids in bile were separated by thin-layer chromatography. The SF was estimated as a percentage of total radioactivity (scintillation counting) in sulfated glyco-LC. The standard deviation for replicate SF determinations (n = 311) was 2.1% The pretreatment SF (mean 60.7+/-1.7 SEM) correlated inversely with age (r = 0.336, P < 0.005) and directly with the obesity index (r = 0.495, P > 0.001), but was independent of sex. The SF, remeasured at 1 or 2 yr, did not change significantly with time or CDC. Among CDC-treated patients, elevations of transaminase occurred in 75% of patients with a SF < 45% vs. 11% with a SF > 45% (P < 0.001). In conclusion, a SF < 45% occurred in patients with gallstones who had a high probability of developing elevated serum transaminase when treated with CDC. Thus, sulfation of lithocholate may modify CDC-induced elevations of serum transaminase.

Changes in the serum transaminases in patients with syphilis.

Changes in the serum transaminases in patients with syphilis.

An evaluation of serum transaminase in the jaundice states.

13 that the serum glutamic oxalacetic transaminase (SGOT) became elevated after myocardial infarction, a large number of reports have been published dealing with abnormal elevation of this enzyme in diseases of the heart and other organ systems. Generally, elevated SGOT has been observed in 6 chief groups of ill­ nesses. These include injury to skeletal muscle, hepatobiliary disease, extensive damage to the brain, hemolytic anemia, certain chemical and drug intoxications, and, in some instances, pulmonary infarction. 1-8 • 10-12, 14-19, 21 , 22, 24, 26-34 Apart from the characteristically transient elevation of SGOT after myocardial infarc­ tion, there have been no established unified criteria for the evaluation of abnormal levels of SGOT in these other pathologic condi­ tions. This paper deals with a study of the lev el of serum transaminase in patients with jaundice of varying etiology. These cases, for the most part, were followed by serial determinations of SGOT and, to a limited extent, by analyses of serum glutamic pyruvic transaminase (SGPT). METHODS AND MATERIALS