Hepatitis B surface antigen prevalence High 8% Intermediate 2 7% Low <2% Plate 2.1 Global distribution of hepatitis B prevalence. (Reproduced by permission of WHO. Available from: http://www.who.int/csr/disease/hepatitis/ HepatitisB_whocdscsrlyo2002_2.pdf. Accessed 20 October, 2010.)
Change in SDR since 1970 (%) 600 500 400 300 200 100 UK under 65 standard death rate for various diseases (1970 = 100%) UK circulation UK IHD UK stroke UK cancer UK chest UK liver UK luminal GI UK diabetes UK blood 0 1984 1982 1980 1978 1976 1974 1972 1970 2006 2004 2002 2000 1998 1996 1994 1992 1990 1988 1986 Year Plate 4.1 UK death rates for those under 65 from major diseases compared with 1970.
Incidence rate/100,000 population (log scale) Incidence rate/100,000 population (log scale) 100.00 10.00 1.00 0.10 0.01 1978 1980 1982 1984 1986 1988 1990 1992 1994 1996 1998 2000 2002 2004 Year 100.00 10.00 1.00 0.10 0.01 1978 1980 1982 1984 1986 1988 1990 1992 1994 1996 1998 2000 2002 2004 Year MaligLT PLT IHBD Liver NOS GB EHBD BTUS PancT MaligLT PLT IHBD Liver NOS GB EHBT BTUS PancT Plate 4.2 Age-standardised incidence rates per 100,000 population of England and Wales for selected hepatobiliary tumours in males and females, 1979 2004. MaligLT, all malignant liver tumours; PLT, primary liver tumours; IHBD, intrahepatic bile duct tumours; Liver NOS, unspecified liver tumours; GB, gall bladder tumours; EHBD, extrahepatic bile duct tumours; BTUS; PancT, pancreatic tumours.
Plate 8.1 Combined HCC-CC. Cholangiocellular component with desmoplastic stroma (left) are separated from HCC nodules by a thin pseudocapsule (right). Plate 8.2 Fibrolamellar HCC. Gross appearance with central scarring resembling focal nodular hyperplasia. Histology shows large eosinophilic cells separated by bands of lamellar collagen. Plate 8.3 Large HCA associated with long exposure to danazol. Note a marked cellular atypia raising the differential diagnosis of well-differentiated HCC. A second nodule with similar histology on biopsy disappeared 6 months after drug withdrawal.
Plate 8.4 Endocrine neoplasm misdiagnosed as macrotrabecular, small-cell HCC. Strong immunostaining for synaptophysin confirm the endocrine nature of the tumour. Plate 8.5 Liver angiomyolipoma. Predominantly myomatous tumour consists of large discohesive cells exhibiting with oncocytic cytoplasmic transformation. Positive HMB-45 immunostaining confirms the diagnosis of AML.
Plate 16.1 A CEUS image of a non-specific rounded hypoechoic lesion in a cirrhotic liver (left-hand image, arrow). The microbubble specific image in chrome is on the right and the arrow demonstrates that the lesion is hypervascular in the arterial phase (note timer at the bottom left-hand corner) with haphazard angiogenic vessels in a basket-weave like pattern. Plate 16.2 The same lesion demonstrating washout in the late phase at 3 minutes post-injection. This feature has a high sensitivity for detecting malignancy with CEUS. The overall enhancement characteristics would be compatible with a HCC.
Intravascular Intracellular F-18 FDG G LU T F-18 FDG Hexokinase X G-6-phosphatase F-18 FDG-6-P X Glycolysis Plate 17.1 The metabolic pathway of F-18 FDG. F-18 FDG is actively transported into cells via GLUT membrane transporters and is phosphorylated by hexokinase to FDG glucose-6- phosphate (FDG-6-P). FDG-6-P is not a substrate for the next enzyme in the glycolysis pathway and also has a much slower rate of dephosphorylation, compared with glucose-6-phosphate and thus is progressively trapped within metabolically active cells. (C) (D) Plate 17.2 C-11 acetate and F-18 FDG PET/CT studies in a patient with metastatic HCC. Coronal C11-acetate PET only image demonstrates bony metastases in the upper and lower thoracic spine (arrows) not clearly seen on the FDG-PET coronal image. (C) Fused C11-acetate image demonstrating the avid lytic metastasis (arrow) in the vertebral body, which is FDG negative on image (D). (Image courtesy of Professor S. Fanti.)