Elevated alt virus




















Hepatitis delta virus HDV was collected at study entry only. Patients in the US and Australia accrued up to four years of follow-up and those from Thailand up to 18 months. HIV RNA was quantified by the approved, standard test used at each site, which were performed according to manufacturer's instructions. This longitudinal study included data from up to 9 visits for each participant. Standard descriptive statistics e. The prevalence and cumulative incidence of grade 2 or higher ALT elevation and the change in median ALT over time were displayed graphically.

Multiple logistic regression with robust variance estimation was used to determine characteristics associated with ALT elevations of grade 2 or higher while accounting for within-subject correlation [18]. To account for the prospective study design and the fundamental differences between the cohorts, we forced covariates for study visit, study site and gender into all multivariate models.

Observations with missing data were included in the multiple regression analyses using multiple imputation [19]. All statistical analyses were performed using SAS 9. The majority of the cohort was male About half the cohort was HBeAg positive Across the person-visits, the median ALT was 36 IQR 26—50 and notably, it remained relatively stable throughout follow-up Figure 1.

Only 74 person-visits In contrast the cumulative incidence of grade 3 or higher elevation was low at 8. The majority of the ALT elevations Three of these patients had elevated ALT for at least 2 years 5 consecutive study visits. We were unable to determine if these persistent elevations of ALT were associated with adverse outcomes. Anti-HBe seroconversion was observed in a total of 10 patients but elevated ALT was observed prior to anti-HBe seroconversion in only one patient.

In this patient, ALT elevation continued following seroconversion. In the other 9 patients, there was no change in ALT either prior to or following anti HBe seroconversion. Elevated ALT is generally regarded as a marker of hepatic necrosis and inflammation, although liver damage may be present with normal ALT [5] , [20]. Only three patients had elevated ALT for a prolonged period at least 2 years. In addition, most published observational cohort studies of patients with hepatitis co-infection have included both HCV and HBV co-infection with a higher percentage of patients co-infected with HCV than HBV [7] — [8] , [17] , [21] — [31].

Follow up in these studies ranged from 6 months to 4. In contrast, in our study One previously published observational cohort describing liver disease included only HIV-HBV co-infected patients and reported that patients with mean transaminases above the ULN were significantly more likely to develop advanced liver disease [29]. A significant association between lower CD4 count and elevated ALT has not been consistently reported in previous studies.

In one study of patients with HIV-HBV co-infection there was no significant association between mean CD4 count during follow up and the development of advanced liver disease [29] , while Sulkowski et al. In studies of HIV mono-infected patients that exclude viral hepatitis, one study has reported an increased risk of ALT with lower CD4 while another study reported the opposite findings [33] — [34].

However, elevated ALT can occur secondary to both the adaptive and innate immune responses summarised in [36]. HBeAg could also be a surrogate for duration of infection with HBV, a variable we were unable to collect in this cohort. In general, patients who are HBeAg positive are infected for a shorter duration of time than those who are HBeAg negative [47] and are therefore more likely to enter an immunoactive phase which may contribute to an elevated ALT.

There are several limitations to this study. First, it is possible we may have underestimated the prevalence of an elevated ALT in our cohort as patients only had ALT collected every 6 months. There were person-visits excluded from the analysis due to missing ALT data. However, we think this was unlikely to have had an effect on the final results because of the large overall sample size.

Second, our use of the revised more stringent guidelines for defining normal ALT may have increased the prevalence of an elevated ALT; however, we considered that this definition was appropriate given that previous studies showed ALT levels are lower in co-infection even in the setting of liver disease [6] and that they are the currently accepted normal levels of ALT in patients with HBV mono-infection [AASLD guidelines [48] ]. Fourth, we recruited patients from three geographically different sites; therefore the HBV genotype distribution and ethnicity were different; however, recruitment site was not a significant factor in any of the analyses.

Finally, we did not directly assess liver disease severity, other than the Childs-Pugh scores. The Childs-Pugh scores for the cohort ranged from 5—7 throughout follow-up, which is indicative of relatively mild liver disease in the cohort, and therefore our results might not be applicable to cohorts with more advanced liver disease. Competing Interests: The authors have declared that no competing interests exist.

Some patients in the study were recruited from this clinic, and they attended TSPC for their study visits. Margolick, Lisa P. Phair, Steven M. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. National Center for Biotechnology Information , U.

PLoS One. Published online Nov 1. The NAFLD fibrosis score Table 3 uses clinical data to predict risk of liver-related complications and death from advanced disease.

However, its use may be limited by operator experience and in patients with elevated body mass index. Age, ALT level, AST level, body mass index, diabetes mellitus or glucose intolerance, platelet count, serum albumin level. Alcoholic Liver Disease. Excessive alcohol intake is the primary cause of liver-related mortality in western countries. This index differentiates the conditions based on ALT level, AST level, height, mean corpuscular volume, sex, and weight.

Drug-Induced Liver Injury. The true incidence of drug-induced liver injury is unknown and likely underreported, although it has been estimated at Information from references 25 and Statin-induced liver injuries are rare. Food and Drug Administration now recommends only baseline measurement of ALT and AST before initiation of statins, and does not recommend routine liver monitoring for patients taking statins.

Viral Hepatitis. Hepatitis B and C are common causes of elevated transaminase levels. Preventive Services Task Force recommends screening high-risk patients with hepatitis B surface antigen and hepatitis C virus antibody testing.

Hereditary Hemochromatosis. Hereditary hemochromatosis is an autosomal recessive disease causing increased iron absorption in the intestines and release by tissue macrophages. Mild, asymptomatic elevations in liver enzymes can occur because iron itself does not elicit a significant inflammatory response in the liver. Transferrin saturation and serum ferritin level should be measured to rule out hereditary hemochromatosis in patients with elevated transaminase levels.

Alpha 1 -Antitrypsin Deficiency. Alpha 1 -antitrypsin deficiency is a genetic condition that primarily causes chronic lung and liver disease. Diagnosis begins with testing for serum alpha 1 -antitrypsin deficiency. If levels are very low, protein phenotyping or genotyping to look for the PiZZ variant should follow. Autoimmune Hepatitis. The prevalence of autoimmune hepatitis is 11 to 17 per , persons.

Hypergammaglobulinemia is common in patients with autoimmune hepatitis, with total immunoglobulin G levels generally 1. Although antinuclear antibody testing is commonly ordered, it has lower sensitivity and specificity. Wilson Disease. Wilson disease is a rare autosomal recessive disorder, occurring in approximately one in 30, persons, and is related to ineffective copper metabolism. It usually occurs in Eastern Europeans younger than 35 years.

A serum ceruloplasmin measurement is the initial test. Extrahepatic Causes. A number of extrahepatic sources of asymptomatic transaminase elevations may be considered based on the clinical picture. A large prospective study performed in the United Kingdom evaluated nearly 1, primary care patients with abnormal transaminase levels or liver function testing for two years to determine the cause of the abnormalities.

Only 17 1. This study, along with guidelines, informs the evaluation of mildly elevated transaminase levels in primary care Figure 1. Algorithm for the management of mildly elevated liver transaminase levels. Information from references 3 through 6 , and This article updates previous articles on this topic by Oh and Hustead , 9 by Giboney , 44 and by Johnston. Data Sources : A PubMed search was completed using the key terms elevated, liver function tests, transaminases, and aminotransferases.

In addition, we used the key words nonalcoholic fatty liver disease, alcoholic liver disease, viral hepatitis, hemochromatosis, alpha 1 -antitrypsin deficiency, autoimmune hepatitis, and Wilson's disease alone or in combination with aminotransferases. Search dates: May 1, , to April 8, The views expressed in this manuscript are those of the authors and do not reflect the official policy or position of the Department of the Army, the Department of Defense, or the U.

Already a member or subscriber? Log in. Interested in AAFP membership? Learn more. Community Hospital. Address correspondence to Robert C. Reprints are not available from the authors. A systematic review of the prevalence of mildly abnormal liver function tests and associated health outcomes. Eur J Gastroenterol Hepatol. The prevalence and predictors of elevated serum aminotransferase activity in the United States in — Am J Gastroenterol.

Changes in the prevalence of the most common causes of chronic liver diseases in the United States from to Clin Gastroenterol Hepatol. Consensus recommendations for managing asymptomatic persistent non-virus non-alcohol related elevation of aminotransferase levels: suggestions for diagnostic procedures and monitoring.

Dig Liver Dis. Investigating mildly abnormal serum aminotransferase values. ACG clinical guideline: evaluation of abnormal liver chemistries. Muscular exercise can cause highly pathological liver function tests in healthy men.

Br J Clin Pharmacol. The ratio of aspartate aminotransferase to alanine aminotransferase: potential value in differentiating nonalcoholic steatohepatitis from alcoholic liver disease. The diagnosis and management of non-alcoholic fatty liver disease: practice guideline by the American Gastroenterological Association, American Association for the Study of Liver Diseases, and American College of Gastroenterology [published correction appears in Gastroenterology. J Hepatol. Physical activity recommendations, exercise intensity, and histological severity of nonalcoholic fatty liver disease.

Lifestyle changes for the treatment of nonalcoholic fatty liver disease: a review of observational studies and intervention trials. Therap Adv Gastroenterol. Dietary fructose in nonalcoholic fatty liver disease.

Epidemiology of nonalcoholic fatty liver disease and nonalcoholic steatohepatitis in the United States and the rest of the world. Clin Liver Dis. Department of Health and Human Services, U. Department of Agriculture. Yellowish or greenish colour of the sputum has marginally raised probability of bacterial infection than colourless sputum Starting antibiotic based on sputum colour is not justifiable. National Center for Biotechnology Information , U. Journal List Malays Fam Physician v.

Malays Fam Physician. Author information Copyright and License information Disclaimer. Corresponding author. Tel: , Fax: , Email: ym. This article has been cited by other articles in PMC. Abstract Abnormal liver function test with raised alanine aminotransferase ALT and raised aspartate aminotransferase AST are commonly seen in primary care setting.

In the primary care setting, what will be your plan of management? Progress of Mr TA His viral hepatitis screenings were all normal. References 1. Liver enzyme alteration: a guide for clinicians. Giboney PT. Mildly elevated liver transaminase levels in the asymptomatic patient. Am Fam Physician. Green RM, Flamm S. AGA technical review on the evaluation of liver chemistry tests.



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