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).
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 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 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.
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:
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.
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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