Can type C hepatitis infection be complicated by malignant lymphoma?
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Hepatitis virus infection, especially type C (hepatitis C virus [HCV]), has been suggested to be one of the important pathogenetic factors for low- and high-grade B-cell lymphoma, including splenic marginal zone lymphoma (SMZL), in southern Europe. Here, we analyzed the incidences of HCV and hepatitis B virus (HBV) infections, and the clinicopathologic features in 29 cases of splenic diffuse large B-cell lymphoma (DLBCL), 10 SMZL, 3 splenic mantle cell lymphoma, 1 hairy cell leukemia, 13 B-chronic lymphocytic leukemia, and 12 hepatosplenic T-cell and natural killer cell lymphoma. Fifteen (51.7%) splenic DLBCL cases were HCV antibody-positive, and another 6 (20.7%) had the HBsAg. The incidence of each was significantly (P < .01) higher than those of HCV (9.3%) and HBV (1.9%) infections in 54 node-based DLBCL cases. Four examined HCV-positive DLBCL cases showed no type II cryoglobulinemia. HCV RNA was detected in fresh tumor tissues from 6 of 7 examined DLBCL cases, and HBV DNA was present in another 2, as evaluated by real-time polymerase chain reaction. Immunohistologically, tumor cells in 5 of 7 examined DLBCL cases showed intracytoplasmic reactions for HCV NS3 and E2 proteins and the viral receptor CD81. Of 6 cases, 2 showed an intranuclear reaction for the HBV surface protein. By Southern blot analysis, no rearrangement of the Bcl2 gene was detected in the tumor tissue of 7 HCV-positive DLBCL cases. For the other types of malignant lymphoma, 1 case each of SMZL (10%) and hepatosplenic T-cell and natural killer cell lymphoma (8.3%) showed HCV infection. In conclusion, persistent human hepatitis virus infections, especially HCV, may play an important role in the tumorigenesis of splenic DLBCL in Japan.
The mechanism by which hepatitis C virus (HCV) causes chronic, progressive liver damage is unknown. Factors other than the virus itself have been implicated. The role of liver steatosis has been recently studied. Hepatic steatosis is a common histologic finding occurring in >50% of patients with chronic hepatitis C. Both host and viral factors have been demonstrated to play an important role in its development. In patients infected with genotype 1, steatosis appears due to co-existence of Non-alchoholic steatohepatitis (NASH) with HCV and associated with increased body mass index (BMI). Some recent observations suggest that steatosis may be of viral origin and related to genotype 3. This fact raises the possibility of a direct effect of specific viral sequences on the pathogenesis of lipid accumulation. Furthermore, hepatic steatosis attributed to genotype 3 correlates directly with serum and intrahepatic titers of HCV RNA. Resolution of steatosis after successful antiviral therapy as well as steatosis being a sign of recurrent HCV infection in patients with genotype 3 add convincing evidence that steatosis is viral-related. The pathogenic mechanism induced by genotype 3 is speculative. Correlation between steatosis, intrahepatic HCV RNA, and core protein expression suggest a direct effect. Further support is provided by the finding that HCV core protein induces steatosis in transgenic mice. Another possibility relates to interaction with hepatic triglyceride turnover. In conclusion, for patients infected with genotype 1 BMI plays a role in the pathogenesis of steatosis, while in those infected with genotype 3 steatosis may be due to a virus-specific cytopathic effect. Regardless of etiology, the contribution of both to liver fibrosis progression appears to be accepted.
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Progressive partial lipodystrophy is a clinical syndrome characterized by progressive loss of subcutaneous fat. A 27-year-old female developed progressive loss of fat from the face and upper part of the torso associated with increased bulkiness of the body below the pelvis following an attack of hepatitis. She had been persistently hepatitis B surface antigen positive and her serum was positive for IgG antibodies to hepatitis B core antigen. Although the woman had hypocomplementaemia of the C3 component of complement, there was no evidence of renal involvement.
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The distribution of hepatitis C virus (HCV) genotypes was studied in 202 anti-HCV-positive liver transplant candidates with end-stage liver disease. HCV sequences were successfully amplified from 185 patients: In the first 100, the genotype was determined by direct sequencing in the NS5 region, and in the remaining 85, type-specific primers were used for genotyping. Eighty-five patients (46.0%) were infected with type 1a HCV strains, 52 (28.1%) with type 1b, 14 (7.6%) with type 2b, 13 (7.0%) with type 4, 5 (2.7%) with type 3a, 2 (1.1%) with type 2a, and 1 (0.5%) with type 2c. Thirteen HCV-positive patients (7.0%) could not be genotyped. The relatively low prevalence of genotype 1b in this population of end-stage liver disease patients speaks against postulated higher pathogenicity of this genotype.
We report on two women (one 52-year-old who underwent kidney transplantation 15 months ago and the other, 71-year-old, undergoing hemodialysis) both with adult polycystic kidney disease who had to be hospitalized because of recurrent fever attacks up to 40 degrees C without any remarkable abdominal symptoms. Staphylococcus hominis and E. coli were recovered respectively from blood cultures of both patients. Evidence for the presence of a solitary infected cyst in the liver could only be obtained by computed tomography (CT) with i.v. administration of a contrast medium. In both cases the infected liver cyst was non-operatively drained with a CT-guided percutaneous catheter and therefore the necessity of laparotomy was avoided.
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M. mulatta monkeys were inoculated faeco-orally by enteric non-A, non-B virus to study the development of clinical, biochemical, histopathological and serological changes in the blood and liver. Pooled stool samples positive for putative non-A, non-B viral antigen by micro-ELISA and aggregated viral particles by immune electron microscopy, were administered in two M. mulatta monkeys. Biochemical, histopathological and serological changes were seen in the blood and liver and excretion of 27 nm virus like particles around 27 days of inoculation in the experimental monkey but not in the control animal.
The frequency of the seromarkers of HIV, HCV, and HBV in the donor population from all donor centers in Germany became available from the multicenter study of the transfusion services. From these data the risk of virus transmission by blood products can be estimated at 1:1 million for HIV and 1:50,000 for HBV. For HCV, preliminary data indicate the risk for Germany in less than 1:20,000. The risk is even lower, with less than 1:200,000 when calculated from seroconversion data of a rural donor population. The safety of blood products has been very much improved due to the continuous donor selection over the last years and by the epidemiologic situation in Germany.
OBJECTIVES: To compare the influence of hepatitis E virus (HEV) infection on the replication of hepatitis B virus (HBV) by observing clinical features, the relationship between the number of HBV DNA copies in serum, the degree of hepatic function impairments and prognosis of chronic hepatitis B patients with hepatitis E superinfection. METHODS: One hundred and fifteen chronic hepatitis B (CHB) patients and 115 CHB patients with hepatitis E (HE) superinfection were studied and compared. 74 liver tissue biopsy samples of the CHB and 51 of the CHB-HE sufferers were obtained. HBsAg, anti-HBs, HBeAg, anti-HBe, anti-HBc, anti-HBc-IgG, anti-HBc-IgM, HBV DNA and anti-HEVIgM were detected respectively by enzyme linked immunosorbent assay and polymerase chain reaction. RESULTS: The number of HBV DNA copies in sera in the CHB-HE group and the severity of the clinical features were significantly higher than those in the CHB group. The former group had a poorer prognosis with a 49.6% occurrence rate of severe hepatitis and a 25.2% death rate while in the latter group the corresponding rates were just 4.4% and 1.7%. CONCLUSION: Re-infection with HEV, in those CHB patients, severely damaged their hepatic functions and increased their mortality; the older the patient and the higher the level of HBV DNA, the poorer the prognosis.
The mechanism of shock in patients with dengue hemorrhagic fever (DHF) has not yet been fully understood. In this study, we investigated the possibility of splanchnic venous pooling as a contributor for circulatory dysfunction in these patients. Ultrasonographic studies of portal vein and inferior vena cava were done in 45 patients with serologically or PCR-confirmed diagnosis of dengue virus infection. The size of portal vein and inferior vena cava, mean blood flow velocity in the right portal vein, and modified portal vein congestion index were compared between patients with dengue fever (DF, n = 20), DHF without shock (n = 14), and dengue shock syndrome (DSS, n = 11) during the toxic stage, convalescent stage, and at follow-up. The portal vein was significantly more dilated in patients with shock (DSS) than DHF without shock and than DF during the toxic and convalescent stages (P < 0.05), but not at follow-up. The change in the size of inferior vena cava followed the opposite trend (not statistically significant). Portal vein blood flow velocity was lower and congestion index was higher in shock cases (DSS) than DHF without shock and than DF at toxic and convalescent stages (P < 0.01). The differences disappeared at follow-up. Hepatosplanchnic venous pooling and/or dysfunction occur and correlate with the severity of circulatory derangement and shock in patients with DHF. The cause(s) and significance of hepatosplanchnic circulatory dysfunction in DHF and possibly other viral hepatic diseases deserve further study.
INTRODUCTION: Cystic echinococcosis (CE) is a world-wide zoonosis but is relatively rare in Western industrial countries. Surgery is the treatment of choice. However, the technical procedure varies and evidence-based knowledge is fragmentary. Cystectomy and partial resection of the liver (pericystectomy, segmental resection, hemihepatectomy) are the procedures under debate. OBJECTIVE: We present a descriptive analysis of the patients suffering from CE (anamnesis, cyst location, procedures, morbidity, lethality, hospital stay, and long-term follow-up). METHODS: A retrospective analysis was made of the medical records and questionnaires of patients surgically treated within a period of 16 years at a German university hospital. RESULTS: Sixty-four patients had 101 parasitic cysts which were treated by 67 operations. The average volume of the cysts was about 400 ml (range 10 - 2200 ml). Eighty-six cysts were located within the liver and 15 in extrahepatic sites. The parasitic lesions were removed by hemihepatectomy (n = 4), segmental liver resection (n = 9), pericystectomy (n = 24), cystectomy (n = 34), and cysto-jejunostomy (n = 1). During the first half of the observation period resective procedures were preferred (81 %) whereas during the second half cystectomy predominated (82 %). Lethality was 0 %. Postoperative morbidity after resective procedures and cystectomy was 47 % and 17 %, respectively. Relapses were not observed after cystectomy, but occurred in four cases following resective procedures (twice after hemihepatectomy, 4 and 7 years later, respectively; once after segmental liver resection and once following cysto-jejunostomy, both 2 years after the respective procedure). The more extensive the surgical procedure the longer was the hospital stay. CONCLUSION: Cystectomy should be performed as the procedure of choice because it proved to be safe, simple, effective, and meets all criteria of the surgical treatment for hydatid disease, i. e., complete elimination of the parasite, no intra-operative spillage especially by the use of Aaron's cone, and saving healthy tissue. Pericystectomy should be used for peripheral liver cysts only partially surrounded by liver tissue.