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Cardiovascular disease is an important contributor to morbidity and mortality in people living with HIV . The immature platelet fraction (IPF) is increased in HIV-negative patients with cardiovascular disease and evidence suggests that an enlarged IPF is associated with adverse cardiovascular events. In this multi-center observational study, we aimed to investigate how the IPF in people living with HIV is influenced by antiretroviral therapy and cardiovascular disease. Subjects without cardiovascular disease that received antiretroviral therapy showed a smaller IPF accompanied by lower D-dimer and C-reactive protein (CRP) levels compared to therapy-naïve subjects (mean IPF: 2.9% vs. 3.9%, p = .016; median D-dimer: 252 µg/L vs. 623 µg/L, p

One of the most challenging complications of total knee arthroplasty (TKA) is periprosthetic joint infection (PJI). There is growing evidence of a good anti-infective effect of intrawound vancomycin powder in total joint arthroplasty. At the same time, various different locally applied substances have become popular in total joint arthroplasty. The objective of this study was therefore to investigate a possible inhibition of the bactericidal effect of vancomycin by tranexamic acid, adrenalin, lidocaine, or dexamethasone. The bactericidal effect of vancomycin was quantified using the established method of the agar diffusion test. The plates were incubated with Staphylococcus aureus or Staphylococcus epidermidis and four wells were stamped out. The wells were filled with vancomycin alone, the tested substance alone or a mixture of the two. The fourth well remained empty as a control. The plates were incubated overnight at 37 °C and the zone of inhibition in each field was measured on the next day. All tests were run three times for each pathogen and mean values and standard deviations of the measurements were calculated. Differences between the substances were tested using the t-test at a level of significance of 0.05. The bacterial growth was homogeneous on all plates. The baseline value for the zone of inhibition of vancomycin was on average 6.2 ± 0.4 mm for Staphylococcus aureus and 12 ± 0.3 mm for Staphylococcus epidermidis. In all other substances, no inhibition was detected around the well. The combination of vancomycin and each other substance did not show any different result compared to vancomycin alone. The bactericidal effect of vancomycin on staphylococci is not altered by tranexamic acid, adrenalin, dexamethasone, or lidocaine in vitro.

Purpose: Flexion deformity after total knee arthroplasty (TKA) is associated with poor function and dissatisfaction and should, therefore, be avoided. In the case of preoperative flexion deformity, an increased distal resection of the femur may be necessary. The degree of resection required has only been determined for cruciate-retaining (CR) prostheses to date and varies considerably from study to study. Although, for many surgeons, the algorithm for the treatment of a flexion deformity includes the resection of the posterior cruciate ligament (PCL) before additional distal resection, the degree of resection necessary for posterior-stabilized (PS)-type prostheses is not known., Methods: Fifty consecutive patients (50 knees) who were due to undergo navigated TKA were included in this prospective study. At the end of the operation, the flexion deformity resulting from different sizes of distal femoral augmentations on the trial implants (0-8.5 mm) was determined using the navigation system., Results: A linear relationship of 2.2° ± 0.3° flexion deformity per mm distal femoral augmentation was found. This was not dependent on age, sex, the preoperative coronal alignment, or the preoperative flexion deformity., Conclusions: In conclusion, after the removal of posterior osteophytes and posterior capsule release, around 5 mm of the distal femur must be further resected in the case of 10° flexion deformity and 9 mm in the case of 20° flexion deformity., Level of Evidence: II (Prospective cohort study).

Objective: In orthopedic joint injection, the most frequently used local anesthetics are ropivacaine, bupivacaine, and 1% or 2% lidocaine. The aim of this study was to examine effects of these various anesthetics on the viability of human chondrocytes. Our hypothesis was that all local anesthetics tested damage human chondrocytes in vitro ., Methods: Primary human chondrocytes were isolated and cultured from 6 donated human knee joints (mean age of donors 61.2 years). Local anesthetics were added to these cultures. Toxicity analysis was performed by visualization of cell structure using light microscopy. Determination of vital chondrocytes was performed by use of a Casy cell counter. Chondrocytes' cell death was examined by fluorescence microscopy and an XTT ELISA assay., Results: Light microscope and fluorescence microscope data revealed a defect cell structure and increased number of dead cells after addition of 1% or 2% lidocaine and bupivacaine but not ropivacaine. We were able to show an increased level of XTT activity after treatment with bupivacaine, 2% lidocaine or ropivacaine. The count of vital chondrocytes was significantly decreased after treatment with bupivacaine, 1% or 2% lidocaine, and ropivacaine., Conclusions: The data show that treatment with local anesthetics induces cell damage of human chondrocytes in vitro . Ropivacaine seems to be a local anesthetic with the lowest toxic potential on human chondrocytes, a feature that may favor its preference for use in joint injection.

Dysregulated intestinal epithelial apoptosis initiates gut injury, alters the intestinal barrier, and can facilitate bacterial translocation leading to a systemic inflammatory response syndrome (SIRS) and/or multi-organ dysfunction syndrome (MODS). A variety of gastrointestinal disorders, including inflammatory bowel disease, have been linked to intestinal apoptosis. Similarly, intestinal hyperpermeability and gut failure occur in critically ill patients, putting the gut at the center of SIRS pathology. Regulation of apoptosis and immune-modulatory functions have been ascribed to Thirty-eight-negative kinase 1 (TNK1), whose activity is regulated merely by expression. We investigated the effect of TNK1 on intestinal integrity and its role in MODS. TNK1 expression induced crypt-specific apoptosis, leading to bacterial translocation, subsequent septic shock, and early death. Mechanistically, TNK1 expression in vivo resulted in STAT3 phosphorylation, nuclear translocation of p65, and release of IL-6 and TNF-α. A TNF-α neutralizing antibody partially blocked development of intestinal damage. Conversely, gut-specific deletion of TNK1 protected the intestinal mucosa from experimental colitis and prevented cytokine release in the gut. Finally, TNK1 was found to be deregulated in the gut in murine and porcine trauma models and human inflammatory bowel disease. Thus, TNK1 might be a target during MODS to prevent damage in several organs, notably the gut.

The case presented here describes the fatal outcome of a right heart catheterization of a female patient with scleroderma. At autopsy, a massive fibrosis of the cardial muscle, the atrioventricular, and the sinoatrial node was described. Patients with scleroderma are prone to cardiac involvement and have an increased risk of sudden cardiac death. The discussion of this case reflects on identifiable risk factors for cardiac complications in scleroderma. These are the parallel affection of the skeletal musculature, the presence of ventricular ectopies and a dilated right atrium and pericardial effusions. Physicians should be aware of the fact that patients with advanced cardiac fibrosis may be at higher risk of complications in relation with invasive procedures.

Introduction: Patients with chronic headache are seen in an interdisciplinary pain clinic after many years of treatment. Compared with other pain syndromes, the standards for diagnosis and treatment are widely accepted according to the guidelines of the International Headache Society. Nevertheless, many patients continue to suffer. Analysis of their special clinical features may help to clarify what kind of conditions potentially cause chronicity., Patients and Methods: A total of 193 patients were seen in 1992-1993 in our pain clinic. Epidemiological, medical and psychological data were analyzed retrospectively. Classification of headache syndromes and pain behavior was based on the criteria of the International Headache Society, taxonomy of the Multiaxial Pain Classification System for Somatic Dimensions (MASK-S) and "Stages of Chronicity". Important psychodynamic factors were taken from standardized psychological interviews., Results: The patients had a mean age of 46 years; 67 % of them were female. Fifty-three percent of the patients suffered from chronic tension headache; a high percentage was suspected to be caused by analgesic intake. Because of their pain behavior, 68 % were classified as being in an advanced chronic stage with a poor prognosis. The most important findings of the psychological diagnosis was that 40 % of patients had a depressive style of conflict solving., Conclusions: The results are discussed with respect to their relevance in explaining development of chronic pain, as seen in selected headache patients in an interdisciplinary pain clinic.