Recently an oncologist asked me to see a sprite 70 year old, a hepatitis-C-virus carrier, with an unfortunate diagnosis of liver cancer. He had been diagnosed a few months earlier and was treated elsewhere with chemoembolization but the tumour had started to grow again. The scan showed the tumour was still operable with a chance to cure. The patient and oncologist were informed of my views. A few days later I was left speechless by what the oncologist conveyed to me about the same patient. When the oncologist informed the referring physician that he agreed with the suggestion of surgery, the physician replied “I am not comfortable with this suggestion. Surgery is not a good treatment for patients with hepatitis-C-induced liver cancer because they do not do as well as patients with hepatitis-B-induced liver cancer.”

Chronic carriers of hepatitis B (HBV) and C virus (HCV) are at increased risk of developing liver cancer [also known as hepatocellular carcinoma (HCC) or hepatoma]. At the present moment, the only chance to cure a patient with HCC is surgical removal of the tumour or to perform a liver transplant. Other methods such as systemic chemotherapy, chemoembolization, local destruction with heat (called radio-frequency ablation) or freezing (called cryotherapy) and alcohol injection are palliative or control methods. While there are some recent studies showing that radio-frequency destruction of a tumour less than 3 cm in diameter may give equivalent results to surgical removal, the medical community is still waiting for confirmation by other bigger and more stringent studies yet to be performed.

A recent study from Osaka, Japan looked at the different risk of recurrence after liver operation between patients with HBV and HCV related HCC (Ann Surg 2006; 244: 771 -780). A total of 417 patients with HCC had the tumour surgically removed. Sixty six patients had HBV-induced HCC (B-HCC) while 351 patients had HCV-induced HCC (C-HCC). These patients were monitored for a median follow-up period of over 10 years. The 3-, 5- and 10-year disease-free survival rates for C-HCC vs B-HCC were 40 vs 57 %, 24 vs 54 % and 12 vs 28 %, respectively. The study showed that patients with HCV-induced HCC have poorer disease free survival than those with HBV-induced HCC. While no doctors can promise any patients a 100% cure rate, at least they can tell him, or her, what the chance of cure is with each form of treatment modality. Chemoembolization can temporize the life of a patient with HCC but the chance of chemoembolization giving a patient a 5-year disease-free survival is, if not zero, near zero.

Every patient has the right to be fully informed of the facts about their condition and treatment options. As doctors, we have the duty to inform and to educate the patient about the condition. I have often heard the statement ‘The patient cannot appreciate the information given to make the right decision’. I beg to defer. If you say to a patient ‘Method A can give you a 24% chance to see the year 2011 while Method B is unlikely to keep you alive till 2011’, what do you think the patient’s answer will be? The doctor’s duty is to assess the patient’s fitness to withstand any form of treatment. It is also the doctor’s duty to assess what the best forms of treatment are, based on facts, and to present them in the order of best choice, second choice and third choice. If the patient is fit to undergo surgery and the risk from the operation is small, then the doctor is duty bound to inform without bias. The final decision on which form of treatment the patient wants rests squarely with the patient and no one else.

Hippocrates said “The physician must be able to tell the antecedents, know the present, and foretell the future – must mediate these things, and have two special objects in view with regard to diseases, mainly, to do good or to do no harm”. Does the act of ruling out a form of treatment because ‘I am not comfortable with it’ constitute causing harm? You tell me. You are the patient.

On 28th December 1895, Wilhelm Conrad Röntgen, a German scientist, published a report titled “On a new kind of ray: A preliminary communication”. In this report he referred to the radiation as ‘X’ to indicate that it was an unknown type of radiation. Since then the term X-ray has been used to describe all forms of imaging by the lay public. Nowadays, medical imaging includes ultrasound scanning, computed tomography (more commonly called CT scan or CAT scan), magnetic resonance imaging (commonly called MRI) and positron emission tomography (more commonly known as PET imaging or PET scan) on top of the original standard X-ray imaging.

Not infrequently I am bombarded with the question “Why was this not seen on the scan?” by patients or relatives who sought another medical opinion from me on their cancers. For example, a CT scan of the abdomen performed prior to an operation for colon cancer showed no evidence of spread within the abdomen. However, at the time of surgery, the surgeon discovered that the colon cancer had spread beyond the colon and multiple tumour deposits were found on the surface of the intestines and internal surface of the abdomen. (This is called carcinomatosis peritonei.) The reason why this was not detected prior to surgery is because CT scan resolution has a limitation. Any lesion or structure bigger than 1 cm in diameter can be seen and characterized with confidence on CT scanning. Consequently, the radiologist can comment on its significance and relevance. However, lesions or structures smaller than 1 cm in size may not be seen and therefore missed. Even though it might have been seen, the radiologist will not be able to comment on its significance with confidence.

Since the advent of PET scanning, it is not unusual to have a patient coming into my clinic to say “I want a PET scan because my friend says it will definitely show me where the cancer is in my body”. Well, the answer to that is “Yes and No, actually”. The first thing to say is that a PET scan is not suitable for all types of cancer. Before the PET scan is performed, the patient is injected with a radioactive tagged molecule, usually glucose. When the tumour cells take in the glucose molecule, it will show up as a bright spot on the PET scan. When no bright spots are seen on the scan, it could mean one of the following: (1) no cancer deposit is present in the body; (2) there is a cancer deposit in the body but the cancer cells did not take up the glucose molecule so it is not seen; or (3) cancer cells which initially took up the radioactive tagged glucose molecule can lose the ability to take up the molecule following chemotherapy. As a result when a PET scan is performed, the scan becomes negative but in truth the cancer is still present in the body.

Another question I often face is “I already have had a PET scan performed, why do I need another CT scan before the surgery?”  Good question. A PET scan is like a light house. It gives you a road map of the total body as to where the trouble spot is in your body. Once you have located the problematic area, you need to have a detailed picture of the area. A CT scan provides the surgeon with a detailed image of the relevant area. It gives the surgeon information about the surrounding blood vessels, adjacent organs and structures in relation to the cancer deposits. This information allows the surgeon to plan his surgical approach before the actual surgery.

No imaging techniques can be 100% accurate. When a scan fails to detect an underlying cancer in the body, this occurrence is called a false negative. When a scan ‘detects’ a cancer that is not really there, this occurrence is called a false positive. At this present moment, it is not possible to find an imaging method that has 0% false negative and 0% false positive.

People who are chronic carriers of the hepatitis B (HBV) or hepatitis C (HCV) virus have an increased risk of developing chronic liver disease (CLD). Liver cirrhosis and liver cancer [ also called hepatoma or hepatocellular carcinoma (HCC) ] are the two most dreaded complications of chronic HBV / HCV infection. Since there isn’t a single blood test or one genetic test that can accurately predict who is at risk of developing liver cancer, all HBV and HCV carriers are advised to undergo regular screening for life. This usually involves having a blood test for alfa-fetoprotein (AFP) level and an ultrasound scan of the liver at 6 monthly intervals. The screening programme is an attempt to detect any potential liver cancer at an early stage so that curative surgery can be undertaken. However, many carriers tend to overlook the necessity of having regular screening because they may have had normal screening results for years on end. After a while of being told nothing is amiss, one becomes complacent and thinks “Ah, it’s probably alright to skip the screening this time. I will go next time”. That omission may well have robbed you of the chance of detecting an early cancer in your liver. But, ‘Where is the evidence?’ you might ask.

There have been many studies from the Japanese medical community showing the benefit of a regular screening programme for early detection of liver cancer in chronic HBV / HCV carriers. The most recent study came from Kurume University in Fukuoka, Japan (2006; 40: 942 – 948). The study involved 574 patients with HCC. In group A, 91 patients with HCC had been on regular screening for HCC at a specialized department for liver disease. In group B, 301 patients with HCC had been on periodic screening at other institutions and in group C, 182 patients with HCC had not received any form of screening and had the HCC diagnosed incidentally or when symptoms occurred. Those in group A had significantly smaller tumours at the time of diagnosis when compared to those in groups B and C (20.4 mm vs 27.1mm vs 57.8mm). Consequently, the percentage of patients able to receive treatment (either surgery or local ablation therapy) was higher in group A (73%) than those in group B (52%) and group C (26%). This higher proportion of patients who were able to receive treatment also translated into a better 5-year survival rate for group A patients (52%) than group B (40%) or C (23%) patients. Another study from Ogaki, Japan, also showed that many more carriers who received regular surveillance from a hospital or primary care physician had HCC diagnosed at an earlier stage than those not in any surveillance programme. Correspondingly, the patients who were on surveillance had better survival rates (Clin Gastroenterol Hepato; 2006; 4: 1170-1176).

If the earlier detection figures only applied to Japanese in Japan then such screening practices would be of limited value. A recent study from Victoria, Australia looked at the characteristics of the HCC tumour and patient outcome in patients who had regular surveillance compared to those who had none. Screened patients had smaller tumours, more likely to be involving one side of the liver only, discovered at an earlier stage and before the tumour had invaded the vessels. The overall median survival in screened patients was 882 days compared to only 99 days in those who had no regular surveillance (J Gastroenterol Hepatol 2005; 20: 873 – 881).

Until we can predict which HBV / HCV carrier is more likely to develop HCC, we can only advise all carriers to undergo regular screening. This does not prevent them from developing HCC but it helps us doctors to detect the tumour at an earlier stage. Sadly, I still see patients with HCC who do not participate in regular screening. As a result, I find myself having fewer treatment options to offer and the patients having poorer survival outcome. If you think 6 monthly follow up is a nuisance or inconvenience, you should see what some Japanese doctors practice. They screen their patients every 3 months!