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Infection with Helicobacterspp. is increasingly linked with hepatobiliary inflammation and neoplasia in people and in a variety of animals. We sought to determine if Helicobacterspecies infection is associated with Cholangiohepatitis in cats. Deoxyribonucleic acid was extracted from tissue blocks from cats with Cholangiohepatitis (32), noninflammatory liver disease (13), and cats with normal liver histology (4). Deoxyribonucleic acid was polymerase chain reaction‐amplified with 2 sets of Helicobactergenus‐specific primers, gel purified, and sequenced. Polymerase chain reaction‐positive hepatic tissue was further examined with Steiner's stain, immunocytochemistry for Helicobacterspecies, and eubacterial fluorescent in situ hybridization. Gastric tissues of cats with known Helicobacterinfection status served as controls for deoxyribonucleic acid extraction and sequence comparison. Helicobacterspecies were detected in 2/32 cats with Cholangiohepatitis, and 1/17 controls. Sequences had 100% identity with Helicobacterspecies liver, Helicobacter pylori, and Helicobacter fenelliaelcinaediiin a cat with suppurative cholangitis, Helicobacterspecies liver, Helicobacter pylori, and Helicobacter nemistrineaein a cat with mild lymphocytic portal hepatitis, and Helicobacter billsin a cat with portosystemic vascular anomaly. In contrast, sequences from gastric biopsies showed highest homology (99–100%) to “Helicobacter heilmannii,” Helicobacter bizzozeronii, Helicobacter felis, and Helicobacter salomonis.Fluorescent in situ hybridization revealed a semicurved bacterium, with Helicobacter‐like morphology, in an intrahepatic bile duct of the cat with suppurative cholangitis. This study has identified Helicobacterdeoxyribonucleic acid in 2/32 cats with Cholangiohepatitis and 1/13 cats with noninflammatory liver disease. Deoxyribonucleic acid sequences of hepatic Helicobacterspecies were distinct from those found in the stomach and are broadly consistent with those identified in cat intestine and bile, and hepatobiliary disease in people and rodents.

In this study, thirty-nine patients were examined. All of them suffered from hip joint prostheses loosening and underwent revision surgery. Bioptic samples were collected at the interface between bone and implant either at the stem or cotyle level. Immunohistochemistry was performed to detect IL-1α, IL-1β, IL-6 and TNF, cytokines that directly cause bone resorption and indirectly induce synthesis of other bone resorbing cytokines. Quantitative analysis of the positive cells and correlation with clinical data was performed. It resulted that there is a great variability in positive cells for cytokines according to the harvest site; anyway, cytokines tend to be higher in patients carrying a joint prosthesis with polyethylene acetabular component and it is associated with plastic wear particles, even though there is no direct correlation between wear amount and cytokine levels. There is a statistically significant negative correlation between metal wear and a cytokine (IL-6); cytokines levels do not depend on the implant time to failure and do not correlate with pain score. As expected, cytokines levels tend to be lower in subjects being treated with non-steroidal antiinflammatory drugs. It can be concluded that plastic wear is the factor inducing the highest cytokine levels in the tissues around the prosthesis at the interface; cytokines that are an indicator of osteolysis risk.