Objective To evaluate the clinical aspects of hepatitis C virus (HCV) liver disease in anti‐HCV + ve mothers, both during pregnancy and six months after delivery, and to assess the outcome of pregnancy. Setting Obstetric department for high risk pregnancies of the University of Padova, Italy. Participants Seventeen hundred consecutive pregnant women were studied. Methods Each woman underwent the following: 1. serological screening for hepatitis surface antigen (HBsAg), antibodies to HCV (anti‐HCV), antibodies to human immunodeficiency virus type 1 (HIVI) within the first trimester of pregnancy; and 2. clinico‐biochemical assessment in order to ascertain previous or active liver disease and risk factors for viral infections. Results Twenty‐nine (1.7%) of the 1700 women were found anti‐HCV positive. Eight of them had an associated positivity for HIV infection. HCV‐RNA was positive in 64.2% of anti‐HCV positive women. Liver function tests (included transaminases) were within the normal range in 27 mothers (both during and six months after delivery). Only 2/29 women had a slight increase in AST/ALT; liver biopsy in these cases was compatible with mild chronic active hepatitis. In all women the outcome of pregnancy was favourable (12/29 anti‐HCV positive mothers underwent caesarean delivery for causes independent from HCV infection). Conclusions A substantial proportion of anti‐HCV positive pregnant mothers, even if asymptomatic, have circulating HCV‐RNA. The pregnancy does not induce a deterioration of liver disease, and vice versa, HCV infection does not increase the risk of obstetric complications.

We carried out a 3-year pilot study of 59 consecutive women with osteoporosis of primary biliary cirrhosis (PBC), allocating them to two groups according to the severity of bone demineralization assessed by means of dual-photon absorptiometry (DPA) of the lumbar spine, Group A (36 patients; bone mineral density [BMD] > 0.800 g/cm2) received no treatment; group B (23 patients; BMD < 0.800 g/cm2) was treated as follows: oral 1,25-dihydroxyvitamin D (0.5 microgram twice a day for 5 days) followed by a 1-month course with oral calcium carbonate (1,500 mg/day) +carbocalcitonin (40 UMRC intramuscularly three times weekly). This treatment was repeated every 3 months. The following parameters were assessed at baseline and every 12 months: DPA, serum and urinary minerals, serum parathyroid hormone (PTH), osteocalcin (BGP), 25-hydroxyvitamin D, and 1,25-dihydroxyvitamin D. During follow-up, 11 initially untreated patients whose BMD dropped below 0.800 g/cm2 were switched to the treatment group (8 after 12 months and 3 after 24 months). No significant changes were observed in either group for PTH, BGP, or vitamin D metabolites. Comparing patients who were always treated, those who were never treated, and those who switched to the treatment group (ever treated) in this 36-month period, the percentage of annual bone loss in the never-treated patients was significantly less (p < 0.002) than in the ever-treated patients, suggesting the presence of two subgroups in PBC patients; one with rapid bone loss and the other with slow bone loss. Moreover, in the ever-treated patients, ADFR (activate, depress, free, repeat) therapy resulted in an improvement in BMD (p < 0.05 compared with the value before therapy). We conclude that ADFR therapy is effective in the treatment of patients with PBC with severe osteodystrophy, despite no change in osteoblastic activity, although controlled, randomized studies are in order to confirm our data.

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