Glioblastoma multiforme (GBM) is the most aggressive and most common type of cancer originating in the brain. In this publication we discuss our approach to support the GBM standard therapy (surgery, chemotherapy and radiation) by the administration of donkey milk (200 ml per os and day) as well as by the application of the neuroleptic drug quetiapine. Our therapeutic strategy can easily be tested in a clinical context because quetiapine is often routinely applied during tumor therapy in order to suppress depressions. Donkey milk is known to stabilize the immune system which is strongly compromised in the case of GBM patients under a standard therapy. Since it is discussed in the literature that donkey milk and quetiapine have anti-tumor properties, especially, in the case of GBM, we focus on certain compounds in donkey milk and their potential interference with quetiapine. These compounds are proteins with a carbohydrate specificity, e. g. lectins which are able to bind galactose residues in a specific way, such as human galectin-3. Such lectins and their ligands are related to crucial tumor migration pathways. This can be achieved by a multimodal strategy combining molecular modeling with histological and radiological examinations. In addition, Atomic Force Microscopy (AFM) and X-ray nanotomography with synchrotron beams are extremely helpful because they enable a high-resolution three-dimensional imaging of cell- and tissue-probes. In combination with molecular modelling

Background: Alcoholic hepatitis (AH) is a severe inflammatory liver disorder with mortality rates of 20–50% at 90 days. Ferritin is an acute-phase reactant elevated in AH due to hepatocellular injury, systemic inflammation, and altered iron homeostasis. Its prognostic significance in AH has not been fully elucidated. To evaluate the association between serum ferritin levels and short-term clinical outcomes in patients with alcoholic hepatitis.

Methods: This retrospective cohort study utilized the TriNetX US Collaborative Network. Patients with AH (ICD-10: K70.1, K70.10, K70.11) and documented serum ferritin were included. Patients with autoimmune hepatitis, viral hepatitis, hemochromatosis, Wilson disease, and primary biliary or sclerosing cholangitis were excluded. Patients were stratified into low-ferritin (1,000 ng/mL) and high-ferritin (≥1,000 ng/mL) cohorts. The primary outcome was all-cause mortality within 90 days. Secondary outcomes included hepatic failure, sepsis, shock, ascites, spontaneous bacterial peritonitis (SBP), esophageal variceal bleeding, and hepatic encephalopathy.

Results: Of 73,476 patients, 58,815 had ferritin 1,000 ng/mL, and 14,661 had ferritin ≥1,000 ng/mL. Patients with elevated ferritin had significantly higher 90-day mortality (20.0% vs. 8.7%; HR 2.66, p 0.001). Elevated ferritin was also associated with increased risks of hepatic failure (HR 1.55), sepsis (HR 1.85), shock (HR 1.94), ascites (HR 1.17), SBP (HR 1.52), and hepatic encephalopathy (HR 1.32) (all p 0.001). Esophageal variceal bleeding was less frequent in the high-ferritin cohort (HR 0.73, p 0.001).

Conclusion: Serum ferritin ≥1,000 ng/mL is associated with significantly worse 90-day outcomes in AH. Ferritin represents a simple, inexpensive biomarker that may aid in prognostic assessment and risk stratification. Prospective studies with multivariable adjustment are warranted.

Background: Patients with cirrhosis are at increased risk of sepsis due to cirrhosis-associated immune dysfunction, bacterial translocation, and hemodynamic derangements. However, large-scale propensity matched data comparing outcomes between cirrhotic and non-cirrhotic patients with septic shock remain limited. This study aimed to evaluate the impact of cirrhosis on mortality, renal, hemorrhagic, thromboembolic, and respiratory outcomes in patients with septic shock.

Methods: We conducted a retrospective propensity score-matched cohort study using the US Collaborative Network from 43 healthcare organizations in the TriNetX research network. Patients with septic shock were identified using ICD-10 CM codes and stratified by the presence or absence of cirrhosis. Propensity score matching (1:1) was performed for age, sex, race, BMI, diabetes, and baseline laboratory values, yielding 96,986 patients per cohort. Outcomes included mortality, acute kidney injury (AKI), continuous renal replacement therapy (CRRT), disseminated intravascular coagulation (DIC), gastrointestinal bleeding (GIB), intracranial hemorrhage (ICH), pulmonary embolism (PE), hospital-acquired pneumonia (HAP), and mechanical ventilation. Cross-sectional risk analysis and Kaplan-Meier survival analysis with hazard ratios (HR) were performed.

Results: Patients with cirrhosis and septic shock had significantly higher mortality compared to non-cirrhotic patients (32.8% vs 27.3%; HR 1.23, 95% CI 1.21–1.25, p = 0.001). Cirrhosis was associated with significantly increased risks of AKI (39.0% vs 34.1%; HR 1.18, 95% CI 1.16–1.20, p = 0.001), CRRT (8.2% vs 6.0%; HR 1.39, 95% CI 1.34–1.44, p = 0.001), DIC (2.3% vs 1.4%; HR 1.68, 95% CI 1.57–1.80, p = 0.001), GIB (7.6% vs 4.6%; HR 1.67, 95% CI 1.61–1.73, p = 0.001), and mechanical ventilation (22.5% vs 19.3%; HR 1.18, 95% CI 1.16–1.21, p = 0.001). There was no significant difference in ICH (HR 1.01, p = 0.906) or HAP (HR 0.96, p = 0.371). PE risk was marginally lower in cirrhotic patients on cross-sectional analysis (RR 0.95, p = 0.025) but did not reach significance on survival analysis (HR 0.96, p = 0.054).

Conclusions: In this large propensity score-matched cohort, cirrhosis was independently associated with significantly higher rates of mortality, AKI, CRRT, DIC, GIB, and mechanical ventilation in patients with septic shock. These findings highlight the need for early aggressive management and close monitoring of hemorrhagic, renal, and coagulation complications in cirrhotic patients presenting with septic shock.