Extracorporeal shock wave lithotripsy of biliary and pancreatic stones

The aim of the study was to answer the following questions: Is extracorporeal shock wave lithotripsy for gallbladder stones a safe and effective therapy? (Chapter 2) Is simultaneous treatment with extracorporeal shock wave lithotripsy and the solvent methyl te.rt-butyl ether feasible, safe. and more effective than either treatment alone? (Chapter 3) Is ultrasonography reliable for the evaluation of ESWL-results? (Chapter 4) What proportion of patients, with symptomatic gallbladder stones, is suitable for the current operative and non-operative treatment modalities? (Chapter 5) Is stone recurrence inevitable after gallbladder saving therapies? (Chapter 6) Is extracorporeal shock wave lithotripsy a safe and effective therapy for common bile duct stones? (Chapter 7) Is extracorporeal shock wave lithotripsy a safe and effective therapy for pancreatic duct stones? (Chapter 8

Liver fibrosis after extracorporeal shock-wave lithotripsy of gallbladder stones - A case report

We encountered significant liver fibrosis in a healthy young patient undergoing laparoscopic cholecystectomy for symptomatic gallstone disease. Twelve months prior to cholecystectomy the patient underwent multiple extracorporeal shock-wave lithotripsy (ESWL) sessions with adjuvant oral bile-acid therapy. Since the site of fibrosis corresponded clearly to the shock-wave transmission path, which was in accordance with animal studies, it was concluded that this liver fibrosis was a side effect of biliary ESWL. Based on these findings and the literature, we conclude that further assessment of the long-term safety of ESWL is still warranted, especially in patients undergoing multiple ESWL sessions

Paracetamol modulates biofilm formation in Staphylococcus aureus clonal complex 8 strains

Staphylococcus aureus biofilms are a major problem in modern healthcare due to their resistance to immune system defenses and antibiotic treatments. Certain analgesic agents are able to modulate S. aureus biofilm formation, but currently no evidence exists if paracetamol, often combined with antibiotic treatment, also has this effect. Therefore, we aimed to investigate if paracetamol can modulate S. aureus biofilm formation. Considering that certain regulatory pathways for biofilm formation and virulence factor production by S. aureus are linked, we further investigated the effect of paracetamol on immune modulator production. The in vitro biofilm mass of 21 S. aureus strains from 9 genetic backgrounds was measured in the presence of paracetamol. Based on biofilm mass quantity, we further investigated paracetamol-induced biofilm alterations using a bacterial viability assay combined with N-Acetylglucosamine staining. Isothermal microcalorimetry was used to monitor the effect of paracetamol on bacterial metabolism within biofilms and green fluorescent protein (GFP) promoter fusion technology for transcription of staphylococcal complement inhibitor (SCIN). Clinically relevant concentrations of paracetamol enhanced biofilm formation particularly among strains belonging to clonal complex 8 (CC8), but had minimal effect on S. aureus planktonic growth. The increase of biofilm mass can be attributed to the marked increase of N-Acetylglucosamine containing components of the extracellular matrix, presumably polysaccharide intercellular adhesion. Biofilms of RN6390A (CC8) showed a significant increase in the immune modulator SCIN transcription during co-incubation with low concentrations of paracetamol. Our data indicate that paracetamol can enhance biofilm formation. The clinical relevance needs to be further investigated.</p