Journal Reading

Rare cause of acute hepatitis: a common energy

drink
Jennifer Nicole Harb, Zachary A Taylor, Vikas Khullar, Maryam Sattari
Pembimbing : dr. Arif Gunawan, Sp.PD, MARS

Heike Esfandari
(030.13.091)

K E PA N I T E R A A N K L I N I K I L M U P E N YA K I T D A L A M
R S U D K A R AWA N G
FK TRISAKTI
Abstract

Acute hepatic injury is confirmed by a raised

serum alanine transaminase activity
Nearly 50% of cases of acute liver failure in
the USA are due to drug-induced liver injury
(DILI)
Vitamins and nutrients, such as niacin, are
present in quantities that greatly exceed the
recommended daily intake, lending to their
high risk for harmful accumulation and toxicity
 Leukopeni (3.000
Drinking 4-5 /uL)
energy drinks Trombositopeni
daily for 3 weeks (6.000 /uL)
Hiperbilirubinemia
Man hemoglobin (5 g /
aged dl)
Malaise 50 Antibodi
Anorexia years antinuclear +
Abdominal Antibodi DNA
pain anti-double-
Nausea stranded +
Vomiting Lupus
Generalised antikoagulan +
jaundice Penurunan kadar
Scleral icterus komplemen (C3 =
Dark urine 26 mg/dl, C4 = 5
mg/dl)
LDH (529 IU / L)
 Physical
Physical Lab
Anorexia
Abdominal pain Leucocytes:
Nausea 17800/mm3

Vomiting
Generalised
Neutrophils
jaundice 9.900/mm3
Scleral icterus TGP, TGO, Glycemia
Dark urine within normal ranges
Specific tumor
markers-negative
 Screening Result
Hepatitis A Negative
Hepatitis B Negative
Hepatitis C Positive
CMV Negative
EBV Negative
Herpes simplex Negative

RUQ Ultrasound: echogenic liver without cirrhosis, common bile

duct obstruction or gallstones
Liver biopsy: Severe Acute hepatitis
Investigation on DD

Though the patient was found to have HCV infection, it was not
responsible for his acute infection because HCV has a window
period of antibody production until 10 weeks while the patients
symptoms only began 2 weeks prior
Ischaemic hepatic injury is less likely because it is accompanied by
end-organ hypoperfusion such as renal acute tubular necrosis which
is not present in the patient
 Excessive consumption of energy drinks

Contains vitamin B3 (niacin) with high hepatotoxicity level

(dose dependent)

Intrinsic toxic reaction related to high serum levels of niacin

that high affinity, low nicotinic acid receptors

Elevated aminotransferases and direct hyperbilirubi-naemia

Total bilirubin :
AST : 1802 U/L ALT : 1203 U/L
10.3 mg/dL
 Niacin hepatotoxicity is believed to be a dose-
dependent, direct toxic with doses above 500
mg daily. reported energy drink-associated
acute hepatitis (around 300 mg of niacin daily).
Our patient presented having elevated
transaminases and significantly elevated direct
hyperbilirubinaemia. Interestingly, his AST was
elevated, disproportionately greater than the
ALT (AST 4051 U/L, ALT 2073) and he denied
any acute or chronic alcohol use. This abnormal
AST>ALT ratio was similarly present in the
previously reported case of energy-drink-related
hepatitis
 Liver injury secondary to the consumption of
dietary and herbal supplements remains a
diagnostic challenge for clinicians due to the
lack of clearly defined diagnostic criteria. The
primary treatment for toxin-mediated liver injury
is discontinuation of the offending hepatotoxin
and monitoring to ensure the liver tests
normalise. Recovery will occur in the majority of
patients following withdrawal of the offending
agent.
 Drug-induced and toxin-induced liver injury is a
diagnosis exclusion, and relies on chronological
and clinical criteria
Herbal and dietary supplements, including
energy drinks should be considered in the
differential diagnosis in patients presenting with
acute liver injury of unknown case
Patients should be educated with the
overconsumption of niacin-rich energy drinks