Pulmonary Embolism and Acute Psychosis, a Case Report of an Outpatient with a Mild Course of COVID-19.

The increased risk for thromboembolism in hospitalized COVID-19 patients has been communicated extensively. The fact that home quarantined patients can develop pulmonary embolism, however, has so far not been reported. Furthermore, attention should be brought to psychotic developments in COVID-19 patients. We report a 46-year-old previously healthy patient with a mild course of COVID-19, who developed a massive pulmonary embolism with right heart strain while being home quarantined. He was hospitalized and anticoagulant therapy was started. Nine days after admission, the patient appeared increasingly psychotic and suffered from hallucinations as well as paranoid thoughts. After treatment with risperidone and valproate, the patient's condition improved. At a follow-up 1 month after discharge, he was completely recovered regarding the respiratory, cardiac, and psychic situation. SARS-CoV-2 infection can not only increase the prevalence of thromboembolism in hospitalized patients but also in outpatients. COVID-19 also increases the risk of developing psychiatric reactions.

Reversible myocardial oedema due to acute myocardial infarction as differential diagnosis of cardiac transthyretin amyloidosis.

Using bone-avid radiotracers, cardiac transthyretin (TTR) amyloidosis can be diagnosed by scintigraphy, thus obviating endomyocardial biopsy. Radiotracer accumulation, however, may also be due to other causes. A 68-year-old male with acute myocardial infarction underwent recanalization of the left anterior descending coronary artery (LAD). Postinterventionally, transthoracic echocardiography showed hypokinesia of the septum and anterior wall and a thickened myocardium with granular sparkling appearance. Cardiac amyloidosis was suspected. A 99mTc-3,3-diphosphono-1,2-propanodicarboxylic acid whole-body scan 4 days after LAD recanalization showed Perugini 2 myocardial tracer uptake. Monoclonal gammopathy was excluded, and cardiac TTR amyloidosis was diagnosed. Three months later, 99m-Tc-hydroxydiphosphate scan showed no myocardial tracer uptake. Cardiac magnetic resonance imaging revealed late gadolinium enhancement within the LAD supply area. No mutation of the TTR gene was found. Suspicion of amyloidosis should consider not only echocardiography but also history and clinical findings. Myocardial oedema due to reperfusion should be acknowledged as a differential diagnosis for cardiac uptake of bone-avid radiotracers.

PI3K activity in dendritic cells exerts paradoxical effects during autoimmune inflammation.

The peripheral activation of autoreactive T cells and subsequent central nervous system (CNS) immune cell infiltration are key events relevant for experimental autoimmune encephalomyelitis (EAE), a commonly employed multiple sclerosis (MS) model, influenced by TH1 and TH17 mediated immunity. The phosphoinositide-3-kinase (PI3K)-AKT kinase pathway modulates outcome during EAE, with direct actions of PI3K on adaptive immunity implicated in deleterious and effects on antigen presenting cells involved in beneficial responses during EAE. Here, by genetically deleting the regulatory subunit of Class Ia PI3K, p85α, in selective myeloid cells, we aimed to resolve the impact of PI3K in EAE. While genetically deleting PI3K in LysM expressing cells exerted unremarkable effects, attenuating PI3K function in CD11c+ dendritic cells (DCs), promoted secretion of pathogenic EAE promoting cytokines, particularly skewing TH1 and TH17 immunity, while notably, improving health in EAE. Neutralizing IFN-γ activity using blocking antibodies revealed a prolonged TH1 response was critical for the decreased disease of these animals. Thus, PI3K-AKT signaling in DCs acts in a paradoxical manner. While attenuating EAE associated TH1 and TH17 responses, it impairs health during autoimmune inflammation.