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Paper text:
hepatitis e virus ( hev ) is an important cause of acute viral hepatitis in the developing world .
glucose-6 phosphate dehydrogenase ( g6pd ) deficiency reportedly affects 2.214% of the general population in north india.1 though hev usually presents as a mild self - limiting illness , its association with g6pd deficiency may lead to exaggerated intravascular hemolysis , severe hyperbilirubinemia and acute renal failure .
a 48-year - old man presented to emergency services with complaint of a two - week period of yellowish discoloration of the eyes and urine . for four days
one day prior to presentation , the patient developed slurring of speech with altered sleep - wake pattern .
the patient had history of fever , which subsided with onset of jaundice ; the fever was reportedly intermittent and not associated with chills or rigors , and which subsided by antipyretic .
there was no history of any alcohol or drug intake , or of any previous neurological symptoms or family history of wilson s disease . on examination
, the patient was conscious but disoriented , and in appearance was pale and deeply icteric .
abdominal examination revealed hepatomegaly at 3 cm below the right costal margin , with no splenomegaly .
laboratory investigations revealed hemoglobin of 5.8 g / dl , total leucocyte count of 5700/l , platelet count of 320000/l , total bilirubin of 53.39 mg / dl ( conjugated fraction of 20.25 mg / dl ) , aspartate transaminase of 4553 u / l , alanine aminotransferase of 3907 u / l , lactate dehydrogenase ( ldh ) of 6230 u /
l , serum creatinine of 3.4 , prothrombin time of 44 s ( control : 12 s ) and international normalized ratio of 3.03 .
the workup for jaundice showed positivity for igm anti - hev ( eiagen hev igm kit ; adaltis , spain ) and negativity for hepatitis a antibody igm ( igm anti - hav kit ; adaltis ) , hepatitis b surface antigen ( hbsag ) ( monalisa hbsag plus kit ; bio - rad , usa ) and hepatitis c virus antibody ( innotest hcv ab iv kit ; innogenetics , belgium ) .
serum ceruloplasmin levels were normal and autoimmune markers ( antinuclear antibody , smooth muscle antibody , liver - kidney microsomal antibody ) were negative .
there was no kayser - fleischer ( kf ) ring . in view of the markedly increased bilirubin and low hemoglobin ,
the patient was found to be deficient for g6pd , with raised plasma hemoglobin levels .
the patient s renal functions worsened , and creatinine gradually increased to 8.1 mg / dl .
considering the coagulopathy , encephalopathy and intravascular hemolysis , a diagnosis of hev - related acute liver failure with hemolysis with acute kidney injury was made .
the patient was managed with hemodialysis , transfusion of packed red cells , intravenous antibiotics and other supportive measures , and a gradual improvement in the patient s status occurred over the next four weeks .
hemoglobin levels increased to 7.9 g / dl and liver and renal functions normalized ( fig .
the patient was discharged in stable condition and remains well one month after the discharge . at the three - month follow - up ,
hev is one of the most common causes of acute viral hepatitis in northern india and is usually a self - limiting illness.2 however , in rare cases , it has been associated with severe life - threatening complications such as acute hemolytic crisis leading to acute renal failure on the background of g6pd deficiency .
g6pd deficiency reportedly affects 2.214% of the north indian population , and co - existence of both illnesses , though rare , has been documented.2,3 acute viral hepatitis and hev per se can lead to mild hemolysis ; however , cases of severe hemolysis with markedly raised bilirubin with acute kidney injury , as in our patient , are very rare.3,4 our patient had severe intravascular hemolysis , as evidenced by the rapid fall in hemoglobin , marked elevation in mixed hyperbilirubinemia , hemoglobinuria , and markedly raised plasma ldh .
abid et al.3 were the first to describe this rare life - threatening association in a series of five cases , four of which experienced renal failure leading to a long , protracted course of illness .
occasional reports have also suggested that hev can cause massive hemolysis and renal injury in patients with g6pd deficiency.4,5 the mechanism of hemolysis in g6pd deficient patients is oxidative stress , which may be precipitated by drugs or infection .
acute viral hepatitis leads to hepatic dysfunction , further leading to accumulation of harmful oxidants that result in reduced glutathione levels .
glutathione levels are already low in red blood cells of g6pd deficient subjects , however , and the further reduction due to viral hepatitis precipitates severe hemolysis.6,7 a recent review of all such cases reported to date suggested that renal failure occurs in the setting of high bilirubin levels , but the exact cause remained undetermined.8 it has been proposed that acute tubular necrosis and mechanical tubular obstruction due to hematin and bilirubin may contribute.7 wilson s disease can also present as an acute hemolytic crisis , however , it was excluded in our case according to the ceruloplasmin levels being normal and the kf ring being absent .
our patient developed acute renal failure , requiring three sessions of hemodialysis . during subsequent outpatient visits , testing of the viral markers ( hbs antigen , igm anti - hbc , hcv rna and anti - hcv ) was repeated and negative results obtained .
we again repeated testing for ceruloplasmin levels and 24-hour urine copper level , and both were found to be normal .
the possibility of wilson s disease was very low , as wilsonian acute liver failure does nt improve short of liver transplant . in light of the case
presented herein , we suggest that physicians consider the possibility of hemolysis for patients with acute viral hepatitis and very high bilirubin levels .
testing of g6pd levels , even when results are normal , should ( ideally ) be repeated at 68 weeks , as levels can be falsely normal due to the presence of fresh red blood cells in the circulation following a hemolytic episode . a patient with hemolysis who develops renal failure
should be managed carefully , with optimal correction of fluid and electrolyte imbalance , and avoidance of nephrotoxic and hemolysis - producing drugs .
abstractacute viral hepatitis is usually a self - limiting illness . 
 however , it can lead to complications that can be life - threatening , such as acute liver failure . 
 glucose 6 phosphate dehydrogenase ( g6pd ) deficiency in the setting of acute viral hepatitis can lead to a massive hemolysis , manifesting as acute kidney injury and markedly raised bilirubin levels ; although cases are rare . here , we report such a case . the patient had a viral hepatitis e infection and presented with kidney injury requiring dialysis . 
 examination showed very high mixed hyperbilirubinemia due to massive intravascular hemolysis . 
 the patient experienced a long , protracted course of illness , requiring renal replacement therapy with other supportive management , which led to improvement over a period of four weeks . 
 this case highlights the importance of recognizing associated hemolysis in a patient with viral hepatitis who presents with very high bilirubin levels or associated kidney injury 
 . such patients will require aggressive supportive care with prompt fluid and electrolyte management .