Case Report: Diagnosis of Liver Cancer in a 42-Year-Old Male

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This case report discusses the diagnosis of liver cancer in a 42-year-old male with risk factors like smoking and alcohol consumption. It covers the symptoms, diagnosis, epidemiology, aetiology and risk factors of liver cancer.

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Introduction:
In this case report, case of Mr. A is being discussed. He was admitted to XYZ hospital after
referral from his general practitioner. Past history, presenting signs and symptoms of Mr. A
will be discussed to make diagnosis of his liver cancer. Other aspects of liver cancer like
epidemiology, aetiology and risk factors also will be discussed.
Family, Social and Past history:
Mr. A is a 42 years male staying with his wife and 10 years son. He stays in the small town of
South-west Queensland. He was associated with smoking and alcohol consumption since last
20 years. Grandfather and mother of Mr. A died due to liver cancer. His mother also was
associated with colorectal cancer. Hence, he was aware of the cancer related aspects. His past
medical history indicates asthma, high blood pressure and diabetes. He was diagnosed with
liver cancer six months back. Prior to diagnosis, he was associated with pain like upper
abdominal pain, loss of appetite and nausea and vomiting. Abdominal pain was being treated
by his GP with pain killers; however, there was no improvement in his condition.
Presenting Signs and Symptoms:
Mr. A was exhibiting persistent symptoms of abdominal pain and loss of appetite. Hence, he
was accessed to Dr. X. During this presentation, fluid in the abdomen was observed.
Moreover, Dr. X observed yellow discoloration of Mr. A’s skin. Mr. A also complained that
he was experiencing general weakness and fatigue. Other symptoms of liver cancer were also
evident in Mr. A like weight loss, abdominal swelling and chalky stools. Mr. A also
mentioned that he was feeling full after small meal. Dr. X also reported enlarged liver and
spleen of Mr. A (Mareng et al., 2016).
Diagnosis:
In the initial phase, blood analysis was performed for Mr. A to comprehend health status of
him. Dr. X ordered blood analysis for him. During blood analysis, his haemoglobin was 12.2
g/Dl and haematocrit was 32.2 %. These values indicate no variation from the normal health
condition. It was also observed that his leucocytes and platelets were raised upto 17,
500/mm3 and 562,200/ mm3 respectively. Blood cell count values indicate probable infection
in Mr. A. Since, Mr. A was associated with persistent abdominal pain; liver function tests
were ordered for him. Following were the blood biochemical results for Mr. A : total
bilirubin 4.0 mg/Dl, albumin 3.3 g/Dl and AST/ALT 56/68 IU/L. Liver function tests values
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indicate damaged liver. Mr. A was associated with alcohol consumption and smoking since
long duration; hence, there was possibility of liver cirrhosis and liver cancer in him.
Henceforth, serum tests for the tumor markers were ordered for Mr. A. Tumor markers like
alpha-fetoprotein (α-FP), serum carcinoembryonic antigen (CEA) and CA 19-9 increased
upto 558 ng/Ml, 5.8 ng/Ml, and 45 U/Ml respectably. α-FP less than 10 ng/Ml is considered
as the normal level in the adults while increase in the α-FP levels above 500 ng/Ml is
considered as diagnostic feature of liver cancer. Normal range of CEA is less than 5.0 ng/Ml
in smokers. Normal range of CA 19-9 is 0- 37 /Ml (Redondo-Muñoz et al., 2019).
Consequently, abdominal sonography was ordered for Mr. A. Abdominal ultrasonography
demonstrated that 7.2 cm mass in the left medial segment of the liver. Left hepatic duct was
enclosed by this mass and intrahepatic bile duct get dilated in the left lobe. Increased mass
was observed in the right posteroinferior segment. Moreover, intrahepatic bile ducts of left
lobe expanded. However, it was not evident in the endoscopic retrograde cholangiography. It
indicates that tumor obstructed bile duct branches. Hypervascularity of periphery of tumor
was evident during hepatic angiography. Hepatic angiography also demonstrated
hypovascular mass in the left lobe and dot-like lesions around the left lobe.
Autopsy studies indicated that both hepatocellular carcinoma and cholangiocarcinoma co-
exist in Mr. A. Dual cancers like hepatocellular carcinoma and cholangiocarcinoma can exists
either as separate tumors or adjoining but autonomous tumors or combination of both types.
In case of Mr. A, separate tumors of hepatocellular carcinoma and cholangiocarcinoma were
observed. Both the tumors were observed in the same lobe in Mr. A. Usually, hepatocellular
carcinoma is evident during the evaluation of the cholangiocarcinoma. It is evident from the
literature that hepatocellular carcinoma is usually occur in patients with liver cirrhosis or
chronic hepatitis infection (Wang et al., 2019; Sammon et al., 2018). However, Mr. A was
not associated with liver cirrhosis or chronic hepatitis infection in the past. Hence, analysis of
viral markers was ordered for Mr. A. Viral markers observed in Mr. A were HBsAg (−), anti-
HBs (+), and anti-HCV (−). Persons like Mr. A are usually associated with liver cirrhosis
(Lin et al., 2019). Augmented levels of bilirubin in Mr. A is the diagnostic feature of liver
cirrhosis. Magnetic resonance elastography (MRE) is also useful for the diagnosis of liver
cirrhosis (Xiao et al.,2017; Loomba et al., 2017). MRE demonstrated liver stiffness which
indicates liver cirrhosis in case of Mr. A. Molecular testing needs to be carried out for the
identification of the specific genes involved in the cancer. However, molecular testing was
not performed in case of Mr. A for the identification genes responsible for the DNA damage
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response, cell cycle control, apoptosis and signal transduction (Banaudha and Verma, 2015).
Identification of these genes would have been helpful in ordering targeted therapy for Mr. A.
Liver biopsy was ordered for Mr. A. Variation was observed in clinical guideline/pathway for
the diagnosis of liver cancer in Mr. A. Liver biopsy is usually ordered, in cases of doubtful
liver cancer diagnosis. However, in case of Mr. A elevated levels of α-FP and radiographic
techniques indicated diagnosis of liver cancer. Hence, liver biopsy was not warranted for Mr.
A. However, liver biopsy was performed in Mr. A, despite risks associated with liver biopsy
like pain, bleeding, infection and accidental injury to nearby organ (CCA, 2016; Labgaa and
Villanueva, 2015). Pathobiology of liver cancer initiate with genomic DNA damage post
HBV/HCV infection, alcohol consumption and metabolic disorders (Aleksandrova et al.,
2016). It results in the liver injury and inflammation like cirrhosis. In the promotion stage,
there is loss of cellular growth control which results in the adenomatous hyperplasia or
dysplasia (Li and Zhang, 2017; Li and Ye, 2017). Finally, it results in the hepatocellular
carcinoma. All these clinicopathologic features of liver cancer in Mr A were identified using
serum markers like α-FP, CEA and CA 19-9 and radiographic techniques.
Epidemiology:
Incidence of liver cancer is more in sub-Saharan and Southeast Asia. Worldwide,
approximately 700,000 people diagnosed with liver cancer and approximately 600,000 people
die due to liver cancer every year. According to the Australian Institute of Health and
Welfare, liver cancer stood at 16th place among most common diagnosed cancers. Liver
cancer was the 7th cause of cancer death in Australia (AIHW, 2018). In 2018, 2000 people
death occurred due to liver cancer. It was evident that incidence rate of liver cancer was
expected to rise with increase in the age of the person and it peaks after the age of 55 years.
Survival rate was approximately 18 % for the period of 5 years in comparison to the general
Australian population. However, survival rate was more in young people and metropolitan
residents (AIHW, 2018). Australian Cancer Research Foundation estimated 67.2 years as the
median age for the diagnosis of liver cancer. Age standardised incidence of liver cancer in
males and females are 2.06 and 0.99 % respectively in Australia (ACRF, 2018). Death rate
due to liver cancer is 2.5 % more in males in comparison to females in Australia. It has been
observed that age standardised liver cancer is more in overseas born population (AIHW,
2018).
Aetiology and Risk factors:
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Different risk factors responsible for the occurrence of liver cancer are tobacco screening (21
%), Hepatitis C virus infection (19 %), Hepatitis B virus infection (16 %), alcohol (15 %) and
obesity (25 %) (Rawla et l., 2018). Non-alcoholic fatty liver disease (NAFLD) and non-
alcoholic steatohepatitis (NASH) also results in the cirrhosis (Massoud et al., 2018; Oda et
al., 2015). Agents like aflatoxins, vinyl chloride and thorium dioxide, anabolic steroids and
arsenic are responsible for the liver cancer. Hemochromatosis, a genetic disease is also a
prominent risk factor for liver cancer. Hemochromatosis is a condition associated with body’s
augmented capacity to absorb and store iron specifically in the liver. It results in the cirrhosis
and liver failure. Risk of liver cancer is 20 times more in people with hemochromatosis as
compared to normal people.
Conclusion:
Mr. A was diagnosed with liver cancer at the age of 42; although, he was associated with risk
factors of liver cancer in the past 20 years. He was associated with abdominal pain since last
six months without improvement despite consumption of pain killers. It indicates, he was
associated with liver cancer since last six months without treatment. Stepwise pathway was
followed for the diagnosis of liver cancer. Abdominal pain lead to carry out liver function
test. Liver function test confirmed liver damage followed by liver cirrhosis and liver cancer.
Liver cancer was confirmed by liver biomarkers and abdominal ultrasonography. Liver
biopsy was also performed. Since, liver biopsy was not required because liver cancer was
conformed through liver biomarkers and abdominal ultrasonography. It reflects, clinical
diagnosis pathway was not followed in case of Mr. A. In future, clinical diagnostic pathway
would be accurately followed by avoiding liver biopsy.
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References:
Aleksandrova, K., Stelmach-Mardas, M., and Schlesinger, S. (2016) Obesity and Liver
Cancer. Recent Results in Cancer Research. 208, pp. 177-198.
Australian Institute of Health and Welfare, (AIHW) 2018 Cancer in Aboriginal & Torres
Strait Islander people of Australia, Cancer series no. 109. AIHW, Canberra.
https://www.aihw.gov.au/reports/cancer/cancer-in-indigenous-australians/contents/cancer-
type/liver-cancer-c22. Accessed on 06 March 2019.
Australian Institute of Health and Welfare, (AIHW) 2018 Mortality rates.
https://www.aihw.gov.au/getmedia/ce1fd0a9-049a-4325-bd74.../liver-cancer.xlsx.aspx.
Accessed on 06 March 2019.
Australian Institute of Health and Welfare, (AIHW) 2018 Cancer data in Australia, Cancer
series no. 122. https://www.aihw.gov.au/reports/cancer/cancer-data-in-australia/contents/
summary. Accessed on 06 March 2019.
Australian Cancer Research Foundation. (ACRF) 2018. Liver Cancer.
https://www.acrf.com.au/support-cancer-research/types-of-cancer/liver-cancer/ Accessed on
06 March 2019.
Banaudha, K.K., and Verma, M. (2015) Epigenetic biomarkers in liver cancer. Methods in
Molecular Biology. 1238, pp. 65-76.
Cancer Council Australia, (CCA) (2016). Optimal cancer care pathway for people with
hepatocellular carcinoma. https://www.cancer.org.au/content/ocp/health/optimal-cancer-
care-pathway-for-people-with-hepatocellular-carcinoma-june-2016.pdf. Accessed on 06
March 2019.
Labgaa, I., and Villanueva, A. (2015) Liquid biopsy in liver cancer. Discovery Medicine.
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Li, H.M., and Ye, Z.H. (2017). Microenvironment of liver regeneration in liver cancer.
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Noninvasive Diagnosis of Advanced Fibrosis in NAFLD: A Prospective Study. American
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Marengo, A., Rosso, C., and Bugianesi E. (2016) Liver Cancer: Connections with Obesity,
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Massoud, O., and Charlton, M. (2018). Nonalcoholic Fatty Liver Disease/Nonalcoholic
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Oda, K., Uto, H., Mawatari, S., and Ido, A. (2015) Clinical features of hepatocellular
carcinoma associated with nonalcoholic fatty liver disease: a review of human studies.
Clinical Journal of Gastroenterology. 8(1), pp. 1-9.
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