[HAV infection in patients with chronic hepatitis C]. / Infezione da HAV in pazienti con epatite cronica HCV-correlata.

AIM: In most cases, hepatitis A virus (HAV) infection causes a self-limiting benign acute hepatitis which confers permanent acquired immunity. However, in patients with pre-existing chronic hepatitis, HAV superinfection can cause acute hepatitis with severe progression leading to a fulminant form or linked to the risk of a rapid deterioration of hepatic function. For such a reason, some Authors recommend anti-HAV vaccination for subjects with HCV-correlated chronic hepatitis before the initiation of peg-Interferon and Ribavirin treatment. Subsequently, the real prevalence of IgG anti-HAV antibodies in patients with HC HCV-related and in healthy subjects from Eastern Sicily has been verified. PATIENTS AND METHODS: In 254 subjects affected by HC HCV-related it has been carried out the research of antibodies IgG and IgM anti HAV. The control group was formed by 685 non hepatopathic subjects, subdivided in range of ages. RESULTS: 97.64% out of the patients affected by HC HCV related exhibit antibodies IgG anti HAV, while only 2.36% of them was negative. The prevalence of infection in the control group has been stratified in relation to different ranges of age of the people taken into consideration. CONCLUSIONS: The results obtained in this study performed in our geographical area, let us to suggest that it is not necessary the anti HAV vaccination during the phase of pre-treatment for HC HCV-related.

Ibuprofen blocks changes in Na v 1.7 and 1.8 sodium channels associated with complete Freund's adjuvant-induced inflammation in rat.

UNLABELLED: Although nerve growth factor plays a role in augmenting sodium channel expression in small dorsal root ganglion (DRG) cells, the cytochemical mediators responsible for enhanced expression in large DRG neurons are unknown. To narrow the search for mediators involved in the increased production of sodium channels in large DRG neurons, we examined the effect of cyclooxygenase inhibition on sodium channel production during inflammation. Thirty minutes before the subcutaneous injection of complete Freund's adjuvant (CFA), rats received ibuprofen (nonselective, cyclooxygenase inhibitor), NS-398 (selective, cyclooxygenase inhibitor), or vehicle. Withdrawal thresholds from thermal and mechanical stimulation were measured before and immediately after CFA injection and at selected hourly intervals after injection for the next 24 hours. Sodium channel up-regulation was then examined in DRG by using site-specific, anti-sodium channel antibodies, Na(v) 1.7 and 1.8. Both ibuprofen and NS-398 provided analgesia during the second phase of inflammatory hyperalgesia that begins 3 hours after CFA injection. The up-regulation, predominantly of Na(v) 1.7 and minimally of Na(v) 1.8 channels, seen in vehicle-treated rats was suppressed by both drugs at 24 hours after injection. By 72 hours after injection, no difference in labeling between the drug- and vehicle-treated animals was observed. Sodium channel labeling in large DRG neurons returned to baseline between 1 and 2 weeks after CFA injection, whereas small cell labeling persisted. The cytochemical signal for sodium channel up-regulation in the large DRG cells that most closely correlates with inflammatory hyperalgesia is mediated at least in part through products of the cyclooxygenase pathway. PERSPECTIVE: Expression of sodium channels in dorsal root ganglia increases dramatically during inflammation. The increase in sodium channels is thought to enhance neuronal excitability and to play a role in hyperalgesia and wound vigilance during healing. We provide evidence that prostaglandins play a role in signaling channel augmentation.