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Osteoporosis is a complication of chronic liver disease, with impact on morbidity, quality of life, and survival. The progress of medicine and the new therapies stretched the disease's natural history and improved the survival of patients with liver disease. So, it is fundamental to make better the quality of life and to prevent complications. Metabolic bone disorders are common complications of chronic liver disease (CLD). Patients with CLD have an increased risk of bone fractures, with significant impact on morbidity, quality of life, and even on survival. Bone diseases, including osteomalacia, osteoporosis, and osteopenia, are frequently observed in many types of liver disease. The pathogenesis of damage and the mechanisms of bone loss are different in relation to the specific liver disease. The relevance of these conditions induced many authors to create a new nosographic entity known as "hepatic osteodystrophy", although this term is rarely used anymore and it is now commonly referred to as osteopenia or osteoporosis associated with chronic liver disease. This review is based on the personal experiences of the authors and upon research done of the available literature on this subject matter. The authors searched the PubMed database for publications containing the term "liver disease" in combination with "bone disease", "hepatic osteodistrophy", "osteoporosis", "osteopenia", "osteomalacia", and "fractures". They selected publications from the past 10 years but did not exclude older seminal publications, especially for colestatic liver diseases. This review of literature shows that osteoporosis crosses all CLD. It is important to underline that the progress of medicine and the new therapies stretched the disease's natural history and improved the survival of patients with CLD. It is fundamental to make better the quality of life and it is mandatory to prevent complications and in particular the osteoporotic ones, especially fractures.

OBJECTIVE: The present study aimed to develop a food for special medical purposes (FSMP) and to assess its efficacy as adjuvant therapy in patients with chronic hepatitis C virus (HCV). DESIGN: Open randomized clinical trials with a tomato-based FSMP used as adjuvant treatment to the pharmacological therapy with pegilated interferon and ribavirin. SUBJECTS: Eight healthy volunteers and 39 HCV patients. INTERVENTIONS: For the bioavailability study, healthy subjects consumed 100 g/die FSMP for a week and their serum carotenoid profile at baseline, after the week of administration and 7 days later was determined. The same quantity of FSMP for 6 months by 20 of the 39 HCV patients was consumed in the clinical trial. Serum transaminase, haemoglobin (Hb) and hydroperoxide concentrations during the therapy were monitored in all patients. RESULTS: FSMP consumption caused a fourfold increase of lycopene serum concentration in healthy subjects. A significant increase of carotenoids after 1 month of consumption also in patients with HCV was recorded. Transaminase and Hb serum levels, as well as therapeutic response, were not influenced by FSMP. The decrease in serum hydroperoxides was independent from FSMP consumption in long-term responder patients, whereas nonresponder (NR) patients of FSMP group showed higher reductions than NR patients of Control group. CONCLUSIONS: The FSMP was effective in improving carotenoid status in healthy subjects. In HCV patients, it did not influence the therapeutic response, but it prevented carotenoid serum depletion and it was effective in improving the oxidative status during antiviral therapy in NR patients

We studied serological and tissue markers of Hepatitis B virus (HBV) infection in seven healthy carriers of HBsAg and in 58 patients with chronic active hepatitis (CAH), of whom 20 were HBsAg positive and 38 HBsAg negative. Surface antigen was found as the only marker of HBV infection in the liver tissue of all healthy carriers and HBsAg positive in 40% of the CAH patients. Core antigen was detected only in CAH patients: 7/20 HBsAg positive (in two alone and in five together with HBsAg) and 5/38 HBsAg negative (four with circulating anti-HBs and anti-HBc and one with only anti-HBc). All the healthy carriers of the surface antigen presented HBsAg in the liver as the only marker of HBV. Furthermore, all healthy carriers were found to be anti-HBe positive, whereas in the 16 HBsAg positive CAH patients examined for the e system, HBeAg and anti-HBe were found with the same frequency (43.7%). Of the 33 HBsAg negative CAH patients examined, anti-HBe was present in four who also had circulating anti-HBc and anti-HBs. In HBsAg positive CAH patients core antigen was found in the liver tissue of 4/7 HBeAg positive cases and in 2/7 anti-HBe positive, while surface antigen was detected in 3/7 HBeAg positive, 5/7 anti-HBe positive and in the two HBeAg/anti-HBe negative individuals. In HBsAg negative CAH patients, surface antigen was never found in the liver tissue; core antigen was detected, however, in five who had circulating anti-HBc (one in the presence and four in the absence of anti-HBe). In conclusion, from these data it would appear that the various serological patterns of HBV infection, particularly as concerns the presence of antibodies and presence or absence of HBsAg, are not invariably able to predict whether or not HBV antigens are present in liver tissue or, in other words, if active replication does occur.

The morphologic characterization of portal and lobular infiltrates of chronic active hepatitis (CAH) was performed on liver biopsy sections from 18 patients: 6 HBsAg-positive/anti-delta-negative with tissue signs of hepatitis B virus (HBV) replication, 6 HBsAg-positive/anti-delta-positive with tissue signs of hepatitis delta virus (HDV) replication, and 6 HBsAg-negative without clinical or serologic evidence of autoimmune disease. No statistically significant differences were found among all the three groups of patients studied. Results from the 6 HBsAg-negative cases with T4/T8 ratio greater than 1 confirm the differences reported between this type and autoimmune forms of CAH. The lack of statistically significant differences among patients with CAH of different etiology suggests that etiologic factors play a minor role in determining the characteristics of the inflammatory liver infiltrates.

α1fetoproteina (AFP) e stata da vari AA. riscontrata con notevole frequenza nel siero di soggetti con carcinoma primitivo del fegato, solo sporadicamente in altre epatopatie acute o croniche, specie dell’infanzia, ed in tumori metastatici epatici. Vari AA. hanno inoltre recentemente segnalato frequente associazione tra antigene Australia (Au) e carcinoma epatocellulare. Nel siero di 57 epatopazienti acuti o cronici Au-positivi e di 17 soggetti con neoplasie epatiche primitive o secondarie e stata ricercata AFP mediante elettrosineresi. Con la fissazione del complemento e stata valutata la presenza di Au nel siero dei pazienti con tumore epatico. AFP e stata ritrovata nel 55,5 % dei tumori primitivi del fegato ed in nessuno degli altri casi; Au era presente nel 22,2 % dei casi di carcinoma epatocellulare ed in nessuno dei tumori secondari. Tali dati, unitamente alla frequente associazione di epatoma con cirrosi post-necrotica e con dati anamnestici di pregressa epatite acuta, inducono a prospettare possibili correlazioni patogenetiche tra infezione epatitica ed epatoma. L’esistenza inoltre, sia nella nostra casistica sia in quelle di altri AA., di non trascurabile incidenza di epatopatie croniche e di carcinomi epatocellulari in nuclei familiari, rende suggestiva 1’ipotesi di fattori predisponenti su base genetica, capaci di condizionare le modalite evolutive dell’infezione epatitica.