Journal of Cancer Research and Therapeutics

: 2014  |  Volume : 10  |  Issue : 2  |  Page : 401--403

An acute unusual presentation of hepatocellular carcinoma

Zubin Dev Sharma, Vijayashree Shrirang Gokhale, Neha Chaudhari, Arjun Lal Kakrani 
 Department of Medicine, Padmashree Dr. D.Y. Patil Medical College and Research Hospital, Pimpri, Pune, Maharashtra, India

Correspondence Address:
Zubin Dev Sharma
Department of Medicine, Padmashree Dr. D.Y. Patil Medical College and Research Hospital, Pimpri, Pune - 411 018, Maharashtra


Hepatocellular Carcinoma (HCC) is a growing cause of mortality world over. The common risk factors include cirrhosis, viral infections, aflatoxin amongst others. Alpha Fetoprotein (AFP) levels and Ultrasonography (USG) are the preferred surveillance tools in early diagnosis of HCC. Here we present an unusual case of a young female with no known risk factors, no cirrhosis, no viral markers, and normal AFP levels who had a Acute hepatic failure eventually diagnosed as Primary Hepatocellular carcinoma.

How to cite this article:
Sharma ZD, Gokhale VS, Chaudhari N, Kakrani AL. An acute unusual presentation of hepatocellular carcinoma.J Can Res Ther 2014;10:401-403

How to cite this URL:
Sharma ZD, Gokhale VS, Chaudhari N, Kakrani AL. An acute unusual presentation of hepatocellular carcinoma. J Can Res Ther [serial online] 2014 [cited 2020 Jul 14 ];10:401-403
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Hepatocellular Carcinoma is potential complication of various conditions like alcoholic cirrhosis, Hepatitis B, C and even NASH. Raised alfa-feto protein levels are one of the hallmarks of hepatocellular carcinoma. It mostly develops in a cirrhotic patient and may present with jaundice, bloating from ascites, easy bruising from blood clotting abnormalities or as loss of appetite, unintentional weight loss, abdominal pain, especially in the right upper quadrant, nausea, emesis, or fatigue. Here we present an unusual case, where HCC developed in a female with no risk factors, negative AFP levels and presented as acute hepatic failure.


A 40-year-old female presented with complaints of nausea and vomiting since a month. The vomiting was non projectile, bilious, non-blood stained and often contained food particles. There was also history of high grade fever associated with chills intermittently; since a month. Patient had yellow discoloration of eyes, skin and swelling all over the body since past fifteen days. There were complaints of breathlessness, initially on exertion and progressing to breathlessness at rest since last fifteen days. There was associated abdominal pain and weight loss of around 8 kgs in last 1 month. Patient had decreased appetite as well.

There was no history of altered bowel habits, clay coloured stools, hematemesis, malena, pruritus or alcohol consumption. There was history of menorrhagia since 5-6 years and multiple blood transfusions in last 2 years for anaemia.

Patient had multiple foetal losses in the past. There was no history of jaundice. No history of recurrent respiratory illnesses. There was no family history of similar illness.

On examination, the patient was conscious, had pulse-120b/m, BP-94/60 mm Hg, severe pallor, deep icterus, anasarca. There was no lymphadenopathy, clubbing or cyanosis. On abdominal examination, there was abdominal wall oedema, hepatomegaly 5 cms. below the costal margins in mid-clavicular line, firm in consistency with a smooth surface and was slightly tender. Spleen was also palpable 4 cms below costal margin. There was no clinically detectable ascites. There was a short systolic murmur at the base of heart. Other systems were unremarkable.

On investigations, patient had severe anaemia with Hb-2gm%, total leucocyte count- 10,900 with 70% polymorphs, 27% lymphocytes, 2% eosinophils and 1% monocytes. The ESR was raised at 85mm in 1 st hour. The platelet count was at 1.65 lakhs/cumm. The reticulocyte count was 0.2% and peripheral picture showed microcytic, hypochromic cells with tear drop cells. Premature cells and malarial parasites were not seen.

In liver function tests, total bilirubin was 34.8 gm%, direct-17.4 gm%. S. ALT-36 IU/L, S. AST-95 IU/L, S. ALP-134 IU/L, total proteins 4.6 gm%, S. Albumin-2.4 gm%, S. Globulin-2.2 gm% with A:G ratio of 1.09. The Prothrombin time/INR was increased to 1.7. renal function tests were also deranged with blood urea- 86 mg% and S. Creatinine-2.3 mg%. S. Sodium-125 mg%, S. Potassium- 4.7 mg%. The patient was negative for viral markers in the form of HBsAg, Anti HCV, HAV IgM, HEV IgM and HIV.

Ultrasonography of abdomen showed hepatomegaly (15.9cms), hypoechoeic with no focal lesions. Common bile duct and portal vein seem to be normal on examination. Spleen was enlarged with dilated splenic vein (13 mms). There was minimal ascites. The portal vein doppler was normal. A 2D echo cardiography revealed mild tricuspid regurgitation with right ventricular systolic pressure of 30mmhg. Ejection fraction was 60%. Total CPK levels and CPK MB fraction were normal.

The patient was negative for dengue IgM/IgG, widal, leptospira IgM, APLA. Auto-antibody panel was negative. A contrast CT abdomen couldn't be done in view of deranged renal function tests.

In hospital, by day 5, the patient's condition deteriorated and consciousness level worsened. She developed large ecchymotic patches over limbs. The urine output decreased to less than 200 ml in last 24 hours. S. Ammonia increased to 113 IU, Prothrombin time/INR increased to 2.5. A non contrast CT Brain was negative for any intracranial bleed. A liver biopsy was not performed because of deranged coagulation profile.

The sickling test with sodium metabisulfite was negative and a repeat PBS was negative for schistocytes. S. LDH levels were increased to 1640. S.G6PD was 35. Hb Electrophoresis showed normal pattern. S. Ceruloplasmin levels were normal at 34.4 mg/dl. S. AFP was also negative (10 ng/ml) and S.TIBC, S. Ferritin were normal.

By day 8, patient developed hypotension and despite all supportive care, she succumbed to her illness.

A necropsy of liver was obtained [Figure 1]. On low power section of this tissue, lobular architecture of liver was not well appreciated [Figure 2] and [Figure 3]. On high power sections, many thick hepatic cords were arranged in a trabecular pattern. Cells were larger than normal Hepatocytes and were in deranged arrangement, retained polygonal shape with abundant eosinophilic cytoplasm. Nuclei showed variation in size and shape with prominent nucleoli. Occasional giant cell and pseudo glandular structure were also seen. Hyperchromasia and irregular nuclear chromatin were seen. A final impression of well differentiated hepatocellular carcinoma was made.{Figure 1}{Figure 2}{Figure 3}


The hepatocellular carcinoma (HCC) in this case was unusual in its presentation, both in the patient as well as a disease.The case represents primary hepatocellular carcinoma presenting as an acute hepatic failure in a young female with no known risk factors for HCC, no cirrhosis, no focal lesions on imaging, negative viral markers, no iron overload state, and negative AFP levels. This unusual presentation of HCC presenting as an acute hepatic failure is a rare occurrence.

Hepatocellular carcinoma in adults is largely a disease of age more than 40 years with a strong male preponderance. Increasing age and male sex are independent risk factors for HCC. [1] Men have a higher prevalence of hepatocellular carcinoma than women; the ratio of affected men to affected women varies between 2:1 and 4:1, depending on the geographic region. [2] There is variant which occurs in younger age group with female predominance called as the Fibrolamellar variant, but the clinical course and histopathological characteristics in our patient did not match this type. In fibrolamellar variant, a visible central scar, representing fibrosis rather than a vascular entity as in focal nodular hyperplasia, is noted in 20-60% of cases.

Another interesting feature in our case was a fulminant course and severe hyperbilirubinemia. Jaundice is rarely deep in patients of HCC. The fulminant course in the form of acute liver failure is more common with lymphomas of the liver as compared to hepatocellular carcinoma. HCC has a more indolent course with more constitutional symptoms and long history of chronic liver disease.

Ultrasonography (USG) is the surveillance test of choice for HCC. [3] Ultrasonography has a sensitivity of approximately 65% and a specificity of more than 90% for early detection. [4] In this case, we could not identify any dysplastic nodules or focal mass on USG. A contrast CT of the abdomen could not be done in view of the deranged renal function test.

Further on, normal serum alpha fetoprotein levels are also unusual in this case. In a cochrane systematic review on screening for HCC in Hepatitis B patients published in 2003 and updated in 2004 showed sensitivity of 64.3% and specificity of 93.8% of AFP as a screening tool for HCC in patients with Hepatitis B. [5] Further, raised AFP levels are more suggestive of advanced stage of HCC. Also, very high bilirubin levels correlate with high AFP levels. So, in this patient normal AFP levels with such a fulminant presentation are certainly unusual.

Thus, this case report illustrates the fact that hepatocellular carcinoma can present as acute liver failure in a young patient with no cirrhosis, no viral markers, no risk factors, normal AFP levels, no focal lesions on imaging and severe hyperbilirubinemia. The possibility of HCC should be kept in every unexplained acute hepatic failure, even in young patients as in our case.


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