Porphyria cutanea tarda (PCT) is the most common form of porphyria across the world. Unlike other forms of porphyria, which are inborn errors of metabolism, PCT is usually an acquired liver disease caused by exogenous factors, chief among which are excess alcohol intake, iron overload, chronic hepatitis C, estrogen therapy, and cigarette smoking. The pathogenesis of PCT is complex and varied, but hereditary or acquired factors that lead to hepatic iron loading and increased oxidative stress are of central importance. Iron loading is usually only mild or moderate in degree (less than that associated with full-blown hemochromatosis) and is usually acquired and/or due to mutations in HFE. Among acquired factors are excessive alcohol intake and chronic hepatitis C infection, which, like mutations in HFE, decrease hepcidin production by hepatocytes. The decrease in hepcidin leads to increased iron absorption from the gut. In the liver, iron-loading and increased oxidative stress leads to the formation of non-porphyrin inhibitor(s) of uroporphyrinogen decarboxylase and to oxidation of porphyrinogens to porphyrins. The treatment of choice of active PCT is iron reduction by phlebotomy and maintenance of a mildly iron-reduced state without anemia. Low-dose anti-malarials (cinchona alkaloids) are also useful as additional therapy or as alternative therapy for active PCT in those without hemochromatosis or chronic hepatitis C. In this review, we provide an update of PCT with special emphasis upon the important role often played by the hepatitis C virus.

Metastasis is still poorly understood and thus further research must be conducted to provide insight into the driving factors. Novel research has revealed the significance of the microenvironment in the delegation of metastasis, expanding the field of cancer metastasis to cells and cell environments surrounding the migrated tumor cells. Research on hepatic metastasis is an ever-growing domain of this field, as several primary tumors can metastasize to the liver. The two features within the liver that promote metastasis—cellular and acellular—are found in the current interpretation of liver microenvironment. Novel findings of both are included in this review. Different hypotheses detailing the methods by which metastasis can occur must be included to understand the significance of the microenvironment, as well as a brief overview of the methods that can be used during research. This review aims to highlight the importance of liver microenvironment on the development or potential regression of hepatic metastasis through discussing both acellular and cellular components of liver microenvironment and their interaction with metastasis.

To investigate the role of pre-core and basal core promoter (BCP) mutants in hepatitis B e antigen (HBeAg)-negative chronic hepatitis B (e-CHB) in Iran, Hepatitis B virus strains from 30 patients and 42 anti-HBe-positive asymptomatic carriers (ASCs) were characterized. G 1896 A pre-core stop mutants, detected in 77 % of e-CHB patients and 85 % of ASCs, showed no association with virus load or aminotransferase levels. Twenty per cent of e-CHB patients and 31 % of ASCs harboured T 1762 A 1764 mutants. When this double mutation was associated with G 1757 , it was linked to a higher virus load in patients than when it was associated with A 1757 (10 5?2±1?8 vs 10 3?2±0?8 copies ml "1 ; P=0?004). Interestingly, the most common BCP mutations were T 1764 and G 1766 , which were present in 33 % of e-CHB patients and 29 % of ASCs. These were associated with higher virus load and aminotransferase levels compared with patients lacking core promoter mutations, although this was not significant. The T 1764 G 1766 double mutation was only present in strains with A 1757 (P<0?001), which is more frequent in strains of genotype D than in those belonging to other genotypes. On the other hand, the T 1762 A 1764 double mutation was found more frequently in association with G 1757 than with A 1757. The T 1762 A 1764 double mutation forms a binding site for hepatocyte nuclear factor 1 (HNF1), which is constrained by A 1757. However, the T 1764 G 1766 double mutant may form a binding site for HNF3. Thus, position 1757 affects the emergence of promoter double mutants and would predict a relative genotypic restriction of both the T 1762 A 1764 and the T 1764 G 1766 double mutants.

Background-Recent studies have suggested that Cytotoxic T lymphocytes (CTL) play a key role in eliminating hepatitis B virus (HBV).