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home - Liver - Miscellaneous - Hepatocellular Carcinoma Written by Dr Sebastian Zeki

Recognises the importance of sepsis as a complication
Aware of the differential diagnosis and management of sepsis and its
possible sequelae

Knows the appropriate use of the appropriate antibiotics and their
complications Aware of prevention of nosocomial infection

Understands the principles and practice of diagnosis and treatment of

Prepared to involve and liaise with specialist sepsis support



Knows the importance of clinical nutrition and its disturbances in
patients with acute and chronic liver disease

Appreciates indications for enteral or parenteral support and
understanding of limitations of these interventions

Shows ability to make careful nutritional assessment
Can liaise with nutritional support team where appropriate


Understands prognostic scoring systems including Child - Pugh
MELD UKELD Maddrey and disease-specific scoring systems where
they exist

Builds the use of accredited quantitative scoring systems into routine
clinical liver practice clinical colleagues and junior staff

Shows consistent application of evidence-based in the
evaluation of liver disease and the determination of prognosis

Hepatocellular Carcinoma

Choice of staging systemPrimary staging for all patients with HCC should be clinical staging, and the CLIP system was preferred.They also recommended secondary staging with the AJCC/UICC (TNM) staging system for patients undergoing surgery (liver transplan-tation, resection). Other Factors Influencing Survival:High versus low-incidence regions: Survival shorter in high-incidence regions.Tumor histology: Well-differentiated, clear cell and fibrolamellar tumors and the presence of tumor encapsulation have been associated with a better prognosis.Serum AFP level: Correlates with tumor size and extent.Increase when mass > 3 cm; Rise to 1000 -10,000 ng/mL as tumour >5 cm diam.Serum AFP level is independent predictor of survival; High AFP levels assoc. with poorly differentiated tumors.Variant estrogen receptors: Some aggressive HCC have variant oestrogen receptor with constitutive transcriptional activity.Hepatitis C- Prognosis worse if compared to Hep B Okuda system (Tumor size + Severity of cirrhosis )Does not stratify patients by vascular invasion or nodal metsBecause most patients staged according to this system are not candidates for resection, it is a purely clinical scoring system. The Cancer of the Liver Italian Program score (CLIP)Combines tumor-related features (macroscopic tumor morphology, serum AFP, and the presence of PV thrombosis) +Severity of cirrhosis Prognostic score ranges from 0-6.CLIP better at predicting survival compared to the TNM, Okuda, or Child-Pugh systems, esp with nonsurgical therapy (eg, transarterial chemoemboli-zation, TACE). The French prognostic classification5 prognostic factors:-Karnofsky performance status-Serum bilirubin >50 micromol/L (>2.9 mg/dL)-Serum alkaline phosphatase a>2x ULN.-Serum AFP >35 ng/mL-Ultrasonographic portal obstructionPatient put in 3 groups with 1yr survival of 72, 34, and 7 %, respectively. The Barcelona staging classificationBased on extent of primary lesion, performance status, the presence of constitutional symptoms, vascular invasion and extrahepatic spread, and Okuda stage.Early stage (A) - Asymptomatic with tumors suitable for radical therapies; Intermediate stage (B-) Asymptomatic with multinodular HCCAdvanced stage (C)- Symptomatic, vascular invasion and/or extrahepatic spread.Stage D - Either Okuda stage III tumors or ECOG performance 3/4. Stage B and C patients candidates for palliative/ clinical trialsStage D - symptom control only Tumor, node, metastasis (TNM) staging5yr survival: Stage I – 55 %; Stage II – 37 %; Stage III – 16 %If have cirrhosis, liver function dominates prognosis so Okuda and CLIP more useful. Prognostic Scoring Systems Median survival following diagnosis ranges from 6 to 20 months. EpidemiologyThe M:F ratio is 4:1.The mean age of onset is 50-60 years.It’s most common in SEAsia (35/100,000). Hepatitis B0.47 % per year get HCC.Higher in Asians.Much higher if HBeAg +ve/with higher HBV DNA levels/ co-infected with HCVEnvironmental toxinsAflatoxin-mycotoxin in corn/soybeans/peanuts p53 gene mutatorThe blue-green algal toxin Microcystin (pond-water contaminant).Betel nut chewing also for oesophageal and head/neck SCCHepatitis C- HCC in HCV only if advanced fibrosisRisk factors with HCV:Genotype 1b;Concomitant heavy alcohol use, DM, and obesity; Cirrhosis; HBV coinfectionCirrhosisCompensated cirrhotics-4 % annual incidence of HCCChronic hepatitis-1% annual risk . Higher if AFP (<20 µg/L).Chronic hepatitis/cirrhosis who have hepatitis B, hepatitis C, or hereditary hemochromatosis (HH) have the highest HCC risk-HCC in HH with cirrhosis onlyTobacco and alcohol abuse-Both are a risk factorNAFLD and DM- DM risk x2.5 tho may be because of NAFLD, also a HCC risk factor. + Risk reducers:Coffee Consumption(>2 cups/day - 43 % risk reduc-tion).Statins-possible but unproven as yet. - HCC growth patterns:Large solitary mass.Multi-focal ACC with dominant mass and satellite lesions.Diffuse infiltration.Fibrolamellar HCC (non-cirrhotic). Forms: 1) Nodule 2) Solitary 3) Diffuse HCC manifestations: Hepatomegaly. Hepatic impairment. Bloody ascites. Fever. Increased ALP. Polycythaemia/Leukocytosis. Hypoglycaemia/hypercalcaemia. RadiologyUSS shows- HCC<3 cm - hypoechoic.Vascular invasion is common (PV>HV). CT shows hypodensity on non-contrast in PV imaging.CT can also show a central necrotic area.On MRI-T1:hypodense;T2:Hyperintensive. MRI angiography can be useful.PET can be useful. Risk Factors Written by Dr Sebastian Zeki