Notes

Occurrence of Respiratory Syncytial Computer virus Infection between Hospitalized Grown ups, 2017-2020.
(CTEPH). Fortschr Röntgenstr 2021; DOI 10.1055/a-1502-7541.
· Schüßler A, Richter M, Tello K et al. Evaluation der diagnostischen Genauigkeit und der Strahlendosis der Dual-Energy-Computertomografie (DECT) bei chronisch thromboembolischer pulmonaler Hypertonie (CTEPH). Fortschr Röntgenstr 2021; DOI 10.1055/a-1502-7541.Smoking worsens the prognosis of patients with HNSCC. Furthermore, smoking is associated with the prevalence of co- and multimorbidity, so that it is assumed that not smoking per se, but co-/multimorbidity worsens the prognosis due to lack of compliance to therapy, e. g. by reducing the dose of the planned radio(chemo)therapy (RCT). However, data on this topic are currently sparse and contradictory, especially for HNSCC.Patient records and tumor documentation of 643 consecutive cases of the Head and Neck Tumor Center of the University Hospital Kiel were retrospectively evaluated. Patient characteristics and smoking habits were recorded and correlated with co-/multimorbidity and treatment course.The 643 patient files examined show that 113 (17.6 %) patients did not smoke, 349 (54.3 %) were active and 180 (28 %) patients had previously smoked. 315 (49 %) are treated exclusively by surgery; 121 (18.8 %) by surgery + adjuvant RCT and 72 (11.2 %) by surgery + adjuvant RT. 111 (17.3 %) receive a primary RCT and 24 (3.7 %) a primary RT. 131 (20.4 %) show co-/multimorbidity and 512 (79.6 %) do not. Smoking (> 10 py) is significantly associated with comorbidity (p = 0.002). However, smoking and comorbidity, neither alone nor in combination, are correlated with the achievement of the target dose of RCT (p > 0.05).As expected, smoking is significantly linked to co-/multimorbidity. Dose reduction of R(C)T is just as frequent in active smokers and patients with co-/multimorbidity as in non-smokers and patients without co-/multimorbidity. Thus, smoking and co-/multimorbidity influence the prognosis in other ways than by interfering with planned therapy regimens.
The influence of smoking on survival in patients with HNSCC is well documented in the literature. There is little data on changes in smoking habits after diagnosis. Here, the effect on survival of the reduction of smoking compared to full smoking cessation is investigated.

Patient records and tumor documentation of 643 consecutive HNSCC cases of the Head and Neck Tumor Center of the University Hospital Kiel are evaluated retrospectively smoking habits before and after treatment and survival are evaluated.

Change in smoking behavior at the initial diagnosis of HNSCC leads to a significant positive effect on the prognosis compared to continued smoking. There is no difference between smoke reduction and weaning. Masitinib This effect is based solely on those patients who are treated exclusively by surgery. Lifelong non-smokers have a significant survival advantage over active and ex-smokers, with no difference between the latter two groups.

The positive influence of changed smoking habits on the prognosis runs parvival estimates and therapy planning.
 Thrombin-activatable fibrinolysis inhibitor (TAFI) inhibits fibrinolysis and high levels may have an association with thrombosis. The aim of the current study was to investigate the association of TAFI antigen levels with pulmonary thromboembolism (PTE).

 A case-control study was conducted with 29 patients with PTE and 17 age- and gender-matched control individuals. Plasma levels of TAFI were measured at the time of diagnosis, then at 3 and 6 months after the event.

 Initial TAFI levels (%) were higher in patients with PTE than in the control group Initial TAFI levels (%) were higher in patients with PTE than in the control group (190,0 [65,0-250,0] vs 133,0 [83,0-153,0];
 = 0.003). TAFI levels significantly decreased at the third and sixth months after initial diagnosis (
 < 0.05). The percentage reductions in TAFI levels were 12 and 36.8% at 3 and 6 months, respectively. The Odss ratio (OR) of TAFI level for PTE was found to be 1.024 (95% CI 1.007-1.040;
 = 0.005). There was no significant correlation of initial TAFI levels with age, gender, smoking status, history of thrombosis, pulmonary artery pressure, and D-dimer levels (
 > 0.05). In the sixth month of treatment, patients with residual thrombosis were seen to have similar baseline levels and reductions of TAFI as patients without residual thrombosis (
 > 0.05).

 The result of this study suggests that high TAFI levels may have a role in the occurrence of PTE without impact on treatment outcome.
 The result of this study suggests that high TAFI levels may have a role in the occurrence of PTE without impact on treatment outcome.
 The way by which 1-deamino-8-D-arginine vasopressin (DDAVP) acts on platelets remains unclear. Data from the literature tend to show that there is no definite effect on platelet activation, but recent work has suggested that a subtype of platelets, activated by the combined action of collagen and thrombin, was triggered by DDAVP. Moreover, platelet microparticles (PMPs), which have been shown to be procoagulant, have rarely been studied in this context. The goal of this study was to analyze the effects of DDAVP on PMPs' release through platelet activation.

 Fifteen out of 18 consecutive patients undergoing a therapeutic test with DDAVP were included. They were suffering from factor VIII deficiency or from von Willebrand disease. The expression of P-selectin and PAC-1 binding on platelets and the numbers of circulating PMPs were evaluated ex vivo before and after DDAVP infusion. Peripheral blood was collected on CTAD to limit artifactual platelet activation.

 DDAVP induced a significant decrease of platelet counts and volume. Only small changes of P-selectin expression and PAC-1 binding were observed. Considering PMPs, two populations of patients could be defined, respectively, with (120%,
 = 6) or without (21%,
 = 7) an increase of PMPs after DDAVP. The decrease in platelet counts and volume remained significant in the group of responders.

 This study shows that DDAVP induces the generation/release of PMPs in some patients with factor VIII deficiency and von Willebrand disease 1 hour after DDAVP infusion.
 This study shows that DDAVP induces the generation/release of PMPs in some patients with factor VIII deficiency and von Willebrand disease 1 hour after DDAVP infusion.
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