World Rural Health Conference
Home Print this page Email this page Small font size Default font size Increase font size
Users Online: 638
Home About us Editorial board Search Ahead of print Current issue Archives Submit article Instructions Subscribe Contacts Login 


 
 Table of Contents 
CASE REPORT
Year : 2019  |  Volume : 8  |  Issue : 7  |  Page : 2542-2544  

A case of idiopathic GGT elevation with acute hepatitis A


Health Unit, American Embassy, New Delhi, India

Date of Submission26-Apr-2019
Date of Decision26-Apr-2019
Date of Acceptance28-May-2019
Date of Web Publication31-Jul-2019

Correspondence Address:
Dr. Jaspreet Singh
Physician, Health Unit, American Embassy, New Delhi
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jfmpc.jfmpc_342_19

Rights and Permissions
  Abstract 


Ursodeoxycholic acid modifies the bile acid pool and its effect on lowering liver enzymes is well documented in certain cases like chronic hepatitis but on the other hand it is known to worsen when given in advanced stages of liver disease. Also, it's effects are still unknown for variety of liver insults. We hereby report a case of Idiopathic Gamma Glutaryl Transferase (GGT) elevation which responded well to Ursodeoxycholic acid.

Keywords: Ursodeoxycholic acid, GGT elevation, Hepatitis A


How to cite this article:
Singh J, Jones G, Mahan D. A case of idiopathic GGT elevation with acute hepatitis A. J Family Med Prim Care 2019;8:2542-4

How to cite this URL:
Singh J, Jones G, Mahan D. A case of idiopathic GGT elevation with acute hepatitis A. J Family Med Prim Care [serial online] 2019 [cited 2019 Aug 20];8:2542-4. Available from: http://www.jfmpc.com/text.asp?2019/8/7/2542/263778




  Background Top


Gamma-glutamyltranspeptidase (GGT) catalyzes the transfer of the gamma-glutamyl group from gamma-glutamyl peptides such as glutathione to other peptides and to L-amino acids. GGT is present in cell membranes in many tissues, including the kidneys, pancreas, liver, spleen, heart, brain, and seminal vesicles. GGT is highly non-specific and may be elevated in diseases of the above mentioned organs along with use of alcohol and some drugs.[1]

Hepatitis A is an acute viral hepatitis caused by the Hepatitis A virus (HAV), which is one of the most common causes of acute hepatitis in the world.[2] HAV is predominantly spread through the fecal–oral route through contaminated food or water.[3] About 1.5 million new cases occur every year worldwide.[4] China and India—the world's most populous countries with rapid socio-economic development—are high endemic areas for HAV infection.[5] Hepatitis A infection leads to lifelong immunity and more than 90% of infections are asymptomatic [6], but most of them will have elevated liver enzymes.[7]

Hepatitis A vaccination provides good seroconversion of about 95% after about 2 weeks in all international inactivated vaccines except Chinese vaccines, which take a little longer time to come into effect.[8]


  Case Review Top


A 54-year-old post-menopausal expat female living in New Delhi, India, presented with one day of loose bowel movements (7-8 episodes), along with fever, chills, nausea and one episode of vomiting. She reported that she had eaten at a local restaurant before her symptoms began, and felt that to be the cause of her illness. She also gave a history of travel to Punjab 15 days ago. Having initially treated her symptoms at home with over-the-counter medications, she now complained of weakness due to the suspected food poisoning. Her chronic medications include vitamin D and an over-the-counter antacid when needed. She also had a sulfa allergy. She was a non-smoker and her alcohol consumption presently was negligible for the last 5 years. Prior to that, she used to drink one beer per week for 20 years. Past surgical history included appendectomy and cesarean sections. She had Hepatitis A infection during her childhood and never received the Hepatitis A vaccine thereafter. She reported an episode of persistent itching with rash in 2005 (as depicted in [Figure 1] and [Figure 2]), and was found to have abnormally elevated liver enzymes. She continued to travel extensively throughout the world serving in the United States Foreign Service. Her GGT levels remained persistently elevated with AST and ALT levels that were intermittently elevated to 2-3 times normal. Her ALT has always been higher than the AST when elevated. Serological testing for autoimmune, viral and metabolic etiologies was reportedly normal. She did had a positive ANA with low titers, which was not deemed clinically significant. She was also evaluated for celiac disease which was negative. Iron studies, pancreatic and thyroid function were normal. Serum copper levels were low but ceruloplasmin levels were normal. Alpha 1 antitrypsin phenotype was negative. Hepatobiliary scintigraphy was done in 2015, which showed mild cholestasis. She was advised in May 2017 to have an Echocardiography done to evaluate the palpitations. It was suggestive of trace TR, but was otherwise normal. A sleep study was suggested, in light of her complaint of disturbed sleep. There is no history of Type II Diabetes Mellitus or dyslipidemia. Ultrasound guided biopsy done of right breast showed micro calcifications of right breast in 2015, suggestive of fibrocystic dysplasia. There was no history of blood transfusions or high risk sexual behaviors.
Figure 1: Initial rash in 2005.

Click here to view
Figure 2: Initial rash in 2005.

Click here to view


On presentation, she appeared clinically dehydrated with an otherwise unremarkable physical examination. She was given intravenous fluid resuscitation and blood samples were sent for analysis. Her liver function tests were again abnormal. Total bilirubin was 2.2 mg/dl, ALT was elevated at 2.5 times normal (135 U/L), AST was elevated at 2 times normal (91 U/L) and GGT was elevated at six times normal (388 U/L), She met pre-diabetes criteria with a hemoglobin A1c of 6.2. The rest of her blood, urine and stool tests were normal. Further work-up was ordered, and Hepatitis A IgM was positive. She was also tested for Hepatitis B and C which were negative. Abdominal ultrasound showed hepatomegaly with biliary sludge in her gallbladder. She responded to symptomatic management and repeat liver function tests done 2 weeks later showed a declining trend. A routine test done in April 2017 had a normal total bilirubin, ALT and AST, but GGT remained elevated at 5 times normal (322 U/L). Evaluation for autoimmune hepatitis was conducted which was negative.

She was started on ursodeoxycholic acid, (UDCA) as it is a 7beta-epimer of chenodeoxycholic acid, which has multiple hepatoprotective activities. UDCA modifies the bile acid pool, decreasing levels of endogenous, hydrophobic bile acids while increasing the proportion of nontoxic hydrophilic bile acids. UDCA has a choleretic effect, increasing hepatocellular bile acid excretion, as well as cytoprotective, antiapoptotic, and immunomodulatory properties.[9] Her repeat liver functions after 6 months were normal except total bilirubin which was borderline high at 1.3 mg/dl.

A plan was made to repeat the liver functions 6 monthly and consider liver biopsy if the liver enzymes become elevated again without any obvious new liver issues.[10]


  Recommendations Top


Each case of Hepatitis A with positive antibody titers should be reviewed carefully, and patients should still be vaccinated as infection may not provide lifelong immunity.

In addition, ursodeoxycholic acid may play a useful role in the treatment of idiopathic GGT elevation, Significant improvement of abnormal liver tests may be achieved during UDCA therapy in patients with numerous liver diseases.[9] However, the long term effects of UDCA in disease progression and survival are still unknown. In order to recommend UDCA for long term in liver diseases, further trials possibly multi-centric trials would be needed.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Koenig G, Seneff S. Gamma-Glutamyltransferase: A predictive biomarker of cellular antioxidant inadequacy and disease risk. Dis Markers 2015;2015:818570.  Back to cited text no. 1
    
2.
Centers for Disease Control Prevention. Prevention of hepatitis A through active or passive immunization: Recommendation of the Advisory Committee on Immunization Practices (ACIP). MMWR Recomm Rep 1999;48:1-37.  Back to cited text no. 2
    
3.
Franco E, Meleleo C, Serino L, Sorbara D, Zaratti L. Hepatitis A: Epidemiology and prevention in developing countries. World J Hepatol 2012;4:68-73.  Back to cited text no. 3
    
4.
World Health Organization. The Global Prevalence of Hepatitis A Virus Infection and Susceptibility: A Systematic Review. Geneva: WHO; 2010. [updated 2015 Jan]; Available from: http://apps.who.int/iris/bitstream/10665/70180/1/WHO_IVB_10.01_eng.pdf.  Back to cited text no. 4
    
5.
Barzaga BN. Hepatitis A shifting epidemiology in South-East Asia and China. Vaccine 2000;18:S61-4.  Back to cited text no. 5
    
6.
Jacobsen KH, Wiersma ST. Hepatitis A virus seroprevalence by age and world region, 1990 and 2005. Vaccine 2010;28:6653-7.  Back to cited text no. 6
    
7.
Agrawal S, Dhiman RK, Limdi JK. Evaluation of abnormal liver function tests. Postgrad Med J 2016;92:223-34.  Back to cited text no. 7
    
8.
Cui F, Liang X, Wang F, Zheng H, Hutin YJ, Yang W. Development, production, and postmarketing surveillance of hepatitis A vaccines in China. J Epidemiol 2014;24:169-77.  Back to cited text no. 8
    
9.
Angulo P. Use of ursodeoxycholic acid in patients with liver disease. Curr Gastroenterol Rep 2002;4:37-44.  Back to cited text no. 9
    
10.
Kwo PY, Cohen SM, Lim JK. ACG clinical guideline: Evaluation of abnormal liver chemistries. Am J Gastroenterol 2017;112:18-35.  Back to cited text no. 10
    


    Figures

  [Figure 1], [Figure 2]



 

Top
   
 
  Search
 
Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

 
  In this article
   Abstract
  Background
  Case Review
  Recommendations
   References
   Article Figures

 Article Access Statistics
    Viewed34    
    Printed0    
    Emailed0    
    PDF Downloaded11    
    Comments [Add]    

Recommend this journal