Postoperative Bleeding Complications Associated With Novel Oral Anticoagulants in Mohs Micrographic Surgery.

BACKGROUND: Novel oral anticoagulants (NOACs) are commonly prescribed, recently developed anticoagulants, but limited data exist on NOAC-related bleeding complications in Mohs micrographic surgery (MMS). OBJECTIVE: To assess the risk of postoperative bleeding in patients taking NOACs compared with patients taking no antithrombotic medications. METHODS/MATERIALS: A 5-year retrospective chart review of all MMS cases performed by a single surgeon was conducted. Patient and surgery characteristics, anticoagulant use, and bleeding complications were recorded. RESULTS: Two thousand one hundred eighty-one MMS cases in 1,545 patients were included. There were 696/2,181 cases in which patients were taking at least 1 antithrombotic medication, with 149 on NOAC monotherapy and 15 on NOAC and aspirin combination therapy. Bleeding complications occurred in 22/2,181 cases. Patients on NOAC monotherapy did not have an increased risk of bleeding complications compared with patients on no antithrombotic medications (odds ratio [OR]:1.70, 95% confidence interval [CI]: 0.36-7.97, p = .50). In contrast, patients on NOAC and aspirin combination therapy exhibited an increased bleeding risk (OR: 20.5, 95% CI: 3.99-105.7, p < .001). CONCLUSION: Novel oral anticoagulant use alone during MMS was not associated with an increased postoperative bleeding risk, supporting the safety of continuing NOAC therapy during MMS. However, NOAC and aspirin combination therapy was associated with a high postoperative bleeding risk. Nonetheless, these bleeding events did not lead to adverse long-term outcomes.

Rescuing chemotaxis of the anticancer agent Salmonella enterica serovar Typhimurium VNP20009.

The role of chemotaxis and motility in Salmonella enterica serovar Typhimurium tumor colonization remains unclear. We determined through swim plate assays that the well-established anticancer agent S. Typhimurium VNP20009 is deficient in chemotaxis, and that this phenotype is suppressible. Through genome sequencing, we revealed that VNP20009 and four selected suppressor mutants had a single nucleotide polymorphism (SNP) in cheY causing a mutation in the conserved proline residue at position 110. CheY is the response regulator that interacts with the flagellar motor-switch complex and modulates rotational bias. The four suppressor mutants additionally carried non-synonymous SNPs in fliM encoding a flagellar switch protein. The CheY-P110S mutation in VNP20009 likely rendered the protein unable to interact with FliM, a phenotype that could be suppressed by mutations in FliM. We replaced the mutated cheY in VNP20009 with the wild-type copy and chemotaxis was partially restored. The swim ring of the rescued strain, VNP20009 cheY(+), was 46% the size of the parental strain 14028 swim ring. When tested in capillary assays, VNP20009 cheY(+) was 69% efficient in chemotaxis towards the attractant aspartate as compared to 14028. Potential reasons for the lack of complete restoration and implications for bacterial tumor colonization will be discussed.