It is noteworthy that the S ORF is overlapped

with polymerase ORF in the HBV genome.3 Assuming the deletion of sW74* from nucleotide 1284-1744 (W64 to the end of S ORF), this deletion mutant also destroys amino acids 429-581 of polymerase, an important part of the reverse-transcriptase domain. This viral strain is therefore supposed to not replicate by itself. Virologically, other viral strains with competent replication must become the major strain. However, the results derived from the cloning and pyrosequencing check details failed to confirm this inference. In other words, if the pyrosequencing results are correct, the viral strain is supposed to not replicate profoundly, and this patient is unlikely to have such a high viral load. On the contrary, if the pyrosequencing results are not valid, the authors need to document the existence of other competent viral strains and prove that the HBsAg produced by this viral strain could Pifithrin-�� chemical structure not be detected by common HBsAg antibody. Taken together, these observations suggest that the peginterferon-related HBsAg loss reported by Hsu and Yeh may not be attributed to these viral mutants, but may instead be caused by certain epigenetic

or genetic modifications in hepatocytes that are driven by host immunity. These mutant strains are merely the products selected by host immune pressure. In conclusion, HBsAg loss after peginterferon therapy cannot be convincingly explained by these viral mutants. Further studies are required to examine the underlying mechanisms involved in peginterferon-induced HBsAg loss. Tai-Chung Tseng M.D.* ‡, Jia-Horng Kao Ph.D.† ‡, * Division of Hepatogastroenterology, Department of Internal Medicine, Buddhist Tzu Chi General Hospital Taipei Branch, Taipei, Taiwan, † Division of Gastroenterology, Department of Internal Medicine, ‡ Graduate Institute of Clinical Medicine, National Taiwan University College

of Medicine and National Taiwan University Hospital, Taipei, Taiwan. “
“This chapter discusses the background, prevention, Dimethyl sulfoxide diagnosis, treatment and prognosis of Budd-Chiari syndrome (BCS). The most common causes of BCS are myeloproliferative disorders leading to a hypercoagulable predisposition. The key to prevention of the progression of disease is early identification and intervention with decompression/thrombolysis when the presentation is acute, and the initiation of anticoagulation in the subacute/chronic forms before the development of complications of portal hypertension. The diagnosis and clinical presentation will vary depending upon whether the thrombosis is acute or chronic. The medical management of BCS depends upon early diagnosis and treatment. If the patient already has end-stage cirrhosis with multiple complications of portal hypertension, the disease may be too advanced for anti-coagulation/decompression to change prognosis, and referral for liver transplantation is preferred.