Quantification of intrahepatic hepatitis B virus (HBV) DNA in patients with chronic HBV infection.

No data are available about the amount of hepatitis B virus (HBV) genomes in liver of patients with chronic HBV infection. The aim of this study was to quantify the intrahepatic HBV DNA in hepatitis B surface antigen (HBsAg)-positive patients with either active or suppressed viral replication and in HBsAg-negative subjects with occult HBV infection. We optimized the Roche "Amplicor HBV Monitor" kit for quantifying liver HBV DNA and analyzed hepatic DNA extracts and serum samples from 19 HBs-Ag-positive and 43 HBsAg-negative individuals. Eight of the HBsAg carriers had active HBV replication, and for 3 of them we analyzed samples obtained before and at the end of 1 year of lamivudine treatment. Five hepatitis Delta virus (HDV) coinfected patients and 6 healthy HBsAg carriers had inhibited HBV activity. Among the HBsAg-negative subjects 21 had occult HBV infection and 22 had no evidence of HBV infection. The median of HBV genomes per microgram of liver DNA milliliter of serum was 34,500 to 2,620,000 in patients with active viral replication, 20,000 to 3,900, 000 before and 10,000 to 2,800 at the end of therapy in lamivudine-treated individuals, 9,800 to 600 in HDV-infected individuals, and 7,450 to 17,400 in healthy HBsAg carriers. These data indicate that cases with suppressed HBV activity, despite the very low levels of viremia, maintain a relatively high amount of intrahepatic viral genomes. This virus reservoir is likely involved in HBV reactivation, which is usually observed after stopping lamivudine treatment. Finally, the analysis of cases with occult HBV infection showed that the assay we used was able to specifically detect and quantify as few as 100 copies of viral genomes per microgram of liver DNA.

Occult hepatitis B virus infection in patients with chronic hepatitis C liver disease.

BACKGROUND: Hepatitis B virus (HBV) infections in patients who lack detectable hepatitis B surface antigen (HBsAg) are called occult infections. Although such infections have been identified in patients with chronic hepatitis C liver disease, their prevalence and clinical significance are not known. METHODS: With the polymerase chain reaction, we searched for HBV DNA in liver and serum samples from 200 HBsAg-negative patients with hepatitis C virus (HCV)-related liver disease (147 with chronic hepatitis, 48 with cirrhosis, and 5 with minimal histologic changes). One hundred of the patients had detectable antibodies to the HBV core antigen (anti-HBc); 100 were negative for all HBV markers. Eighty-three were treated with interferon alfa. We also studied 50 patients with liver disease who were negative both for HBsAg and for HCV markers. In six patients found to have occult HBV infection, we evaluated possible genomic rearrangements through cloning or direct sequencing procedures. RESULTS: Sixty-six of the 200 patients with chronic hepatitis C liver disease (33 percent) had HBV sequences, as did 7 of the 50 patients with liver disease unrelated to hepatitis C (14 percent, P=0.01). Among the 66 patients, 46 were anti-HBc-positive and 20 were negative for all HBV markers (P<0.001). Twenty-two of these 66 patients (33 percent) had cirrhosis, as compared with 26 of the 134 patients with hepatitis C infection but no HBV sequences (19 percent, P=0.04). HBV sequences were detected in 26 of the 55 patients in whom interferon therapy was ineffective and 7 of the 28 patients in whom interferon therapy was effective (P=0.06). None of the sequenced HBV genomes had changes known to interfere with viral activity and gene expression. CONCLUSIONS: Occult hepatitis B infection occurs frequently in patients with chronic hepatitis C liver disease and may have clinical significance.

[Preterm premature rupture of membranes in the 19th week of pregnancy. A clinical case]. / Rottura pretermine prematura delle membrane (pPROM) alla 19a settimana di gravidanza. Caso clinico.

A case of premature rupture of membranes occurred at 19 weeks of pregnancy is reported. The patient underwent a genetic amniocentesis at 16 weeks of gestational age. During the hospitalization period, she presented amniotic fluid leakage responsible of olygohidramnios. She was treated with antibiotic, spasmolytic, tocolytic and cortisone therapy. All subsequent parameters were evaluated: blood cell count, heart rate frequency, body temperature. Ultrasound examinations were performed every two weeks. Cervical smears to detect infections were normal. Labour started at 28 weeks and the patient delivered spontaneously a 1010 g male baby, Apgar 4/8. The heaviest complication was a cerebral hemorrhage and the subsequent frontoparietal hematoma which progressively reduced. To date the neurological prognosis is good.

[Congenital factor XIII deficiency in pregnancy. A case report]. / Deficit congenito del fattore XIII in gravidanza. Esposizione di un caso clinico.

Congenital factor XIII deficiency is a rare hemorrhagic syndrome with an altered fibrin stability, hemorrhagic diathesis and habitual abortions. After a short introduction, a case report is described and the clinical differences between plasmatic and platelet deficiency pointed out.

[Current orientation about congenital Cytomegalovirus infection]. / Attuali orientamenti in tema di infezione congenita da Cytomegalovirus.

The CMV infection in pregnancy make serious problems about the diagnosis and the fetal prognosis. Infact primary infection by CMV is loaded by an high risk of congenital infection and the presence of antibodies IgG do not prevent a possible reinfection. Furthermore, the latent presence in the host of CMV induces his reactivation when the immunosorveillance decreases during pregnancy. The consequences of primary infection are well shown during pregnancy and they are very grave, but also the reactivations induce especially neurological consequences, that however are shown only after some months from delivery. Therefore in consideration of the prognosis and the poor therapeutics, the management in these cases is essentially to give minute details to the mother about all the consequences for the fetus without to exclude, because of serious sequels, so that just she can to decide the future of her pregnancy.

[Myelodysplasia in triplet pregnancy]. / Mielodisplasia in gravidanza trigemina.

INTRODUCTION: The myelodysplastic syndromes (MSD) are a group of hematologic disorders that manifest dysplastic hematopoiesis and usually a hypercellular bone marrow. Ineffective hematopoiesis leads to haematologic failure in these syndromes. The MDS are a rare event during pregnancy although the exact incidence is unknown it is likely to be less than that for leukaemia. CLINICAL REPORT: The case, a 29 year old woman, presented during 23rd week of her first, triplet, pregnancy with symptoms of anemia and thrombocytopenia is described. DISCUSSION: The pathogenetic aspect and diagnostic management is discussed, underlined especially under the point of view of the triplet pregnancy. It is suggested that the association of myelodysplastic syndromes during pregnancy is coincidental and that acute leukemia evolves in a majority of these cases. Furthermore, refractory macrocytic anemias in pregnancy need to be carefully evaluated for a primary myelodysplastic state.