No abstract

Generalized lymphadenopathy is a common cause of concern for both patients and clinicians. Possible etiologies include infections, malignancies and autoimmune diseases. Kikuchi Fujimoto disease (KFD) is a hyperergic condition that presents with fever, lymphadenopathy and can include systemic involvement, thus being easily mistaken for the above-mentioned entities. We report the case of a previously healthy 18- year old male who presented with a selflimiting generalized lymphadenopathy, high fevers, skin vasculitis and polyserositis. The lymph-node biopsy revealed a histiocytotic necrotizing lymphadenitis, suggestive of Kikuchi’s disease. This case emphasizes the importance of KFD in the differential diagnosis of lymphadenopathy, especially in young adults.

Because Th17-polarized airway inflammation correlates with poor control in bronchial asthma and is a feature of numerous other difficult-to-treat inflammatory lung diseases, new therapeutic approaches for this type of airway inflammation are necessary. We assessed different licensed anti-inflammatory agents with known or expected efficacy against Th17-polarization in mouse models of Th17-dependent airway inflammation. Upon intravenous transfer of in vitro derived Th17 cells and intranasal challenge with the corresponding antigen, we established acute and chronic murine models of Th17-polarised airway inflammation. Consecutively, we assessed the efficacy of methylprednisolone, roflumilast, azithromycin, AM80 and rapamycin against acute or chronic Th17-dependent airway inflammation. Quantifiers for Th17-associated inflammation comprised: bronchoalveolar lavage (BAL) differential cell counts, allergen-specific cytokine and immunoglobulin secretion, as well as flow cytometric phenotyping of pulmonary inflammatory cells. Only rapamycin proved effective against acute Th17-dependent airway inflammation, accompanied by increased plasmacytoid dendritic cells (pDCs) and reduced neutrophils as well as reduced CXCL-1 levels in BAL. Chronic Th17-dependent airway inflammation was unaltered by rapamycin treatment. None of the other agents showed efficacy in our models. Our results demonstrate that Th17-dependent airway inflammation is difficult to treat with known agents. However, we identify rapamycin as an agent with inhibitory potential against acute Th17-polarized airway inflammation.

Despite advances in lung transplantation (LTx), morbidity, and mortality are high. We hypothesized that pleural effusions requiring thoracocentesis lead to poor outcomes after LTx. We performed a single‐center retrospective analysis of thoracocenteses after initial hospital discharge in LTx patients between March 2008 and September 2020 to identify risk factors, etiologies, and outcomes. Of the 1223 patients included, 113 patients (9.2%) required a total of 195 thoracocenteses. The cumulative incidence of thoracocentesis was 10.6% at 1 year and 14.2% at 5 years after transplantation. We observed a bimodal distribution of pleural effusion onset with a threshold at 6 months. Late‐onset effusions were mostly of malignant or cardiac origin. We observed a high rate of nonspecific effusions (41.5%) irrespective of the timepoint post‐transplantation. Patients with late‐onset effusions had significantly lower survival compared to a matched controlled group (HR 2.43; 95% CI (1.27–4.62). All pulmonary function parameters were significantly decreased in patients requiring thoracocentesis compared to matched controls. Male sex and re‐transplantation were risk factors for pleural effusions. In conclusion, pleural effusions requiring thoracocentesis occur frequently in LTx patients and lead to a reduced long‐term allograft function. Late‐onset effusions are associated with a lower survival.