The inventory of problems-29 is a cross‑culturally valid symptom validity test: Initial validation in a Turkish community sample

Because the actuarial evidence base for symptom validity tests (SVTs) is developed in a specific population, it is unclear whether their clinical utility is transferable to a population with different demographic characteristics. To address this, we report here the validation study of a recently developed free-standing SVT, the Inventory of Problems-29 (IOP-29), in a Turkish community sample. We employed a mixed design with a simulation paradigm: The Turkish IOP–29 was presented to the same participants (N = 125; 53.6% female; age range: 19–53) three times in an online format, with instructions to respond honestly (HON), randomly (RND), and attempt to feign a psychiatric disorder (SIM) based on different vignettes. In the SIM condition, participants were presented with one of three scripts instructing them to feign either schizophrenia (SIM-SCZ), depression (SIM-DEP), or posttraumatic stress disorder (SIM-PTSD). As predicted, the Turkish IOP–29 is effective in discriminating between credible and noncredible presentations and equally sensitive to feigning of different psychiatric disorders: The standard cutoff (FDS ≥ .50) is uniformly sensitive (90.2% to 92.9%) and yields a specificity of 88%. Random responding produces FDS scores more similar to those of noncredible presentations, and the random responding score (RRS) has incremental validity in distinguishing random responding from feigned and honest responding. Our findings reveal that the classification accuracy of the IOP–29 is stable across administration languages, feigned clinical constructs, and geographic regions. Validation of the Turkish IOP–29 will be a valuable addition to the limited availability of SVTs in Turkish. We discuss limitations and future directions

Systemic versus localized coagulation activation contributing to organ failure in critically ill patients

In the pathogenesis of sepsis, inflammation and coagulation play a pivotal role. Increasing evidence points to an extensive cross-talk between these two systems, whereby inflammation not only leads to activation of coagulation but coagulation also considerably affects inflammatory activity. The intricate relationship between inflammation and coagulation may not only be relevant for vascular atherothrombotic disease in general but has in certain clinical settings considerable consequences, for example in the pathogenesis of microvascular failure and subsequent multiple organ failure, as a result of severe infection and the associated systemic inflammatory response. Molecular pathways that contribute to inflammation-induced activation of coagulation have been precisely identified. Pro-inflammatory cytokines and other mediators are capable of activating the coagulation system and downregulating important physiological anticoagulant pathways. Activation of the coagulation system and ensuing thrombin generation is dependent on an interleukin-6-induced expression of tissue factor on activated mononuclear cells and endothelial cells and is insufficiently counteracted by physiological anticoagulant mechanisms and endogenous fibrinolysis. Interestingly, apart from the overall systemic responses, a differential local response in various vascular beds related to specific organs may occur