ABSTRACT
BACKGROUND/AIM: Hepatic steatosis is considered to be mostly associated with viral factors in genotype 3 and metabolic factors in genotype 1 chronic hepatitis C, while there are rather few data for genotype 4. We determined the parameters associated with steatosis in 350 chronic hepatitis C patients, focusing on genotype 4. METHODS: Histological lesions were evaluated according to Ishak's classification and steatosis was semiquantitatively graded. Several patient characteristics on the biopsy day were also evaluated. RESULTS: Steatosis was present in 73% of patients without significant differences among genotypes. Moderate/severe steatosis was more frequent in genotype 3 than 4 (44% vs 26%, P= 0.025) and similar between genotype 4 and 1 patients. Moderate/severe steatosis was associated with body mass index (BMI) in genotype 4 (P= 0.023) and gamma-glutamyl-transpeptidase in genotype 3 patients (P= 0.044). In 150 nondiabetic patients with BMI < or =25 kg/m(2), moderate/severe steatosis was present in 15, 40, and 11% of genotype 1, 3, and 4 patients, respectively, (P= 0.005) and was independently associated only with genotype 3. In multivariate analysis, steatosis grade or moderate/severe steatosis was independently associated with higher BMI, genotype 3, and lower cholesterol. CONCLUSIONS: Moderate or severe steatosis is significantly less frequent in genotype 4 than 3 chronic hepatitis C patients and similar between genotype 4 and 1. In nondiabetic, nonoverweight patients, moderate or severe steatosis is present in only 10-15% of genotype 4 or 1 compared with 40% of genotype 3 patients. Thus, hepatic steatosis in genotype 4 is mostly associated with metabolic factors, similar to those in genotype 1.
Subject(s)
Fatty Liver/etiology , Hepatitis C, Chronic/genetics , Adult , Biopsy , Body Mass Index , Cholesterol/blood , Fatty Liver/metabolism , Fatty Liver/pathology , Female , Follow-Up Studies , Genotype , Hepacivirus/genetics , Hepacivirus/immunology , Hepatitis C Antibodies/analysis , Hepatitis C, Chronic/complications , Hepatitis C, Chronic/metabolism , Humans , Male , Middle Aged , Prognosis , Prospective Studies , RNA, Viral/analysis , Risk Factors , Severity of Illness IndexABSTRACT
Fludarabine is used widely for the treatment of chronic lymphocytic leukaemia, but not as yet implicated in the emergence of hepatitis B surface antigen (HBsAg) variants following hepatitis B virus (HBV) reactivation. Such a variant was detected in a 78-year-old female who was HBsAg(-)/anti-HBc(+)/anti-HBs(+)/anti-HBe(+), and with normal ALT levels, who developed HBV reactivation after fludarabine treatment. She had high HBV-DNA levels, and became positive for HBeAg, in the absence of detectable HBsAg. HBV-DNA was extracted from serum and the HBsAg encoding region of the genome was amplified by PCR, followed by cloning and sequencing. The HBV strain appeared to be subtype adw, but had higher nucleotide homology with ayw than adw isolates, supported further by phylogenetic tree analysis. Amino-acid sequence comparisons over the alpha determinant region revealed the following substitutions: C124N, G130R, and N146S. There were also unique substitutions outside the alpha determinant. All these mutations appeared to have a profound effect on the antigenicity of this region, which resulted in failure to detect HBsAg by commercially available diagnostic assays. It is concluded that a surface variant emerged in an HBsAg(-)/anti-HBs(+) patient with chronic lymphocytic leukaemia following fludarabine treatment, with an unprecedented number of amino-acid substitutions in the alpha determinant region of HBsAg, including a subtype switch.
Subject(s)
Antineoplastic Agents/therapeutic use , Hepatitis B Surface Antigens/genetics , Hepatitis B Surface Antigens/isolation & purification , Hepatitis B/complications , Hepatitis B/virology , Leukemia, Lymphocytic, Chronic, B-Cell/complications , Leukemia, Lymphocytic, Chronic, B-Cell/drug therapy , Vidarabine/analogs & derivatives , Aged , Amino Acid Sequence , Female , Humans , Mutation , Phylogeny , Vidarabine/therapeutic useABSTRACT
Most individuals acquire Epstein-Barr virus (EBV) infection in young age. Because of uncommon presentation and misdiagnosis, clinical manifestations are less well described in older age. We present two cases of elderly patients with predominant symptoms attributed to cold agglutinin haemolytic anaemia due to acute EBV infection without fever, lymphadenopathy, pharyngitis or splenomegaly. We conclude that misleading clinical manifestations are frequent in older individuals and may lead to inappropriate diagnostic invasive procedures.
