Up to 20% of all infective endocarditis are blood culture-negative and therefore a diagnostic challenge. Here we present the case of an infective endocarditis due to Helicobacter cinaedi finally diagnosed using different molecular methods. This highly fastidious gram-negative spiral rod is increasingly recognized as a human pathogen, above all in immunocompromised patients. So far H. cinaedi has been associated with bacteremia, cellulitis, arthritis and meningitis. A 71-year-old man presented with fever and progressive dyspnea for weeks. He was immunocompromised by long-term steroid therapy. As one major and two minor Duke’s criteria (vegetation, fever and aortic valve stenosis as predisposition) were present, an infective endocarditis was suspected and an empiric therapy with amoxicillin/clavulanic acid and gentamicin was established. The persistent severe aortic regurgitation resulted in a valve replacement. Histological evaluation of the aortic valve showed a polypous-ulcerative endocarditis. Gram stain and culture remained negative. Broad-range bacterial PCR targeting the 16S rRNA gene on the biopsy of the aortic valve identified H. cinaedi as the causative agent. The antibiotic therapy was simplified accordingly to ceftriaxone and gentamicin with a recommended duration of 6 weeks. Ten days after valve replacement the patient was discharged. To complete our molecular finding, we sequenced nearly the complete 16S rRNA gene (accession number KF914917) resulting in 99.9% identity with H. cinaedi reference sequences. Based on this result, 2 species-specific PCR tests amplifying part of the ctd gene were established and applied to the valve specimen. The 2 PCRs confirmed H. cinaedi. In addition, we analyzed stool, urine and saliva from the patient using H. cinaedi PCR. The fecal and urine specimen showed a positive signal, saliva was PCR-negative. We identified H. cinaedi as causative agent of a culture-negative endocarditis in an immunocompromised patient using broad-range and specific PCR. In addition to 2 cases from Japan presented on international meetings in 2010 and 2013, our case report shows that H. cinaedi should be recognized as additional causative organism of infective endocarditis. The use of molecular diagnostic techniques proved to be a powerful complement for the detection of blood culture-negative infective endocarditis.

Background: 25 to 50% of patients suffering from colorectal cancer develop liver metastases. The incidence of regional lymph node (LN) metastases within the liver is up to 14%. The need for perihilar lymph node dissection (LND) is still a controversial topic in patients with colorectal liver metastases (CRLM). This study investigates the role of perihilar LND in patients with CRLM. Methods: For this retrospective study, patients undergoing surgery for CRLM at the University Hospital Basel between May 2009 and December 2021 were included. In patients with perihilar LND, LN were stained for CK22 and examined for single tumour cells (2 mm). Results: 112 patients undergoing surgery for CRLM were included. 54 patients underwent LND, 58/112 underwent liver resection only (LR). 3/54 (5.6%) showed perihilar LN metastases in preoperative imaging, and in 10/54 (18.5%), micro-metastases could be proven after CK22 staining. Overall complications were similar in both groups (LND: 46, 85.2%; LR: 48, 79.3%; p = 0.800). The rate of major complications was higher in the LND group (LND: 22, 40.7%; LR: 18, 31%, p = 0.002). Median recurrence-free survival (RFS) (LND: 10 months; LR: 15 months, p = 0.076) and overall survival (OS) were similar (LND: 49 months; LR: 60 months, p = 0.959). Conclusion: Preoperative imaging is not sensitive enough to detect perihilar LN metastases. Perihilar LND enables precise tumour staging by detecting more lymph node metastases, especially through CK22 staining. However, perihilar LND does not influence oncologic outcomes in patients with CRLM.

Recurrence poses a notable challenge after hepatocellular carcinoma (HCC) treatment, impacting more than 70% of patients who undergo surgical resection. Recurrence stems from undetected micro-metastasis or de novo cancer, potentially triggered by postsurgical liver regeneration. Prior research employed HCC cell lines in orthotopic models to study the impact of liver regeneration, but their limited validity prompted the need for a more representative model. Here, we introduce a novel approach utilizing patient-derived HCC organoids to investigate the influence of liver regeneration on HCC. Patient tumor tissues are processed to create tumor organoids, embedded in a three-dimensional basement membrane matrix, and cultured in a liver-specific medium. One million organoids are injected into the right superior lobe (RSL) of immunodeficient mice, confirming macroscopic tumor growth through sonography. The intervention group undergoes resection of the left lateral lobe (LLL) (30% of total liver volume) or additionally, the middle lobe (ML) (65% of total liver volume) to induce liver regeneration within the tumor site. The control group experiences re-laparotomy without liver tissue resection. After 2 weeks, both groups undergo tumor and normal tissue explantation. In conclusion, this patient-derived HCC organoid model offers a robust platform to investigate the impact of liver regeneration post-cancer resection. Its multi-cellular composition, genetic diversity, and prolonged culture capabilities make it an invaluable tool for studying HCC recurrence mechanisms and potential interventions.