Increased FDG-PET/CT pericardial uptake identifies acute pericarditis patients at high risk for relapse.

OBJECTIVES: We aimed to evaluate the prognostic value of FDG pericardial uptake using FDG-PET/CT in patients admitted for acute pericarditis with pericardial effusion. METHODS: In this monocentric retrospective cohort study, all patients admitted for idiopathic acute pericarditis with pericardial effusion from January 2009 to December 2016 who underwent a FDG-PET/CT at diagnosis were considered. Pericardial FDG uptake was measured by generating a volume of interest to calculate the maximal standardized uptake value. The primary outcome was the pericarditis relapse rate during follow-up. RESULTS: FDG-PET/CT was performed 23 [7-99] days after diagnosis in 39 patients (52 [18-83] years, 43.6% of women) admitted for acute pericarditis with pericardial effusion. During a median follow-up period of 7.6 [2.4-77.2] months, 7 (17.9%) patients suffered pericarditis relapse that occurred 3.8 [1.6-14.6] months after FDG-PET CT. In the multivariable analysis, pericardial FDG uptake at diagnosis (OR: 16.6; 95% confidence interval [CI]: 1.25 to 220.8; p = 0.033) was independently associated with pericarditis relapse. Eventually, patients with pericardial FDG uptake at diagnosis had a higher recurrence rate during follow up (p = 0.047). CONCLUSIONS: In acute pericarditis with pericardial effusion, increased FDG-PET/CT pericardial uptake is associated with a higher risk for relapse.

Systemic inflammatory disorders in patients admitted for aseptic meningitis.

Acute meningitis can be the first manifestation of an underlying systemic inflammatory disorder (SID). In the current study, we aimed to identify clinical indicators for SIDs in patients admitted for acute aseptic meningitis. All patients hospitalised for acute aseptic meningitis over a 4-year period in a department of internal medicine were included retrospectively. Patients with neoplastic meningitis were excluded. Extraneurological signs were recorded using a systematic panel. Systemic inflammatory disorder diagnosis was made according to current international criteria. Forty-three (average age 46 years [range 19-82 years], 60% females) consecutive patients were analysed retrospectively. Of these, 23 patients had an SID (mostly sarcoidosis and Behçet's disease). -Multiple logistic regression analysis showed that the probability of an SID was 93.7% in patients with both neurological and extraneurological signs, but 14.9% in patients with neither neurological nor extraneurological signs. In conclusion, clinical sorting according to both neurological and extraneurological signs could help to identify patients with acute aseptic meningitis caused by an SID.

Prostaglandin D2 amplifies lupus disease through basophil accumulation in lymphoid organs.

In systemic lupus erythematosus (SLE), autoantibody production can lead to kidney damage and failure, known as lupus nephritis. Basophils amplify the synthesis of autoantibodies by accumulating in secondary lymphoid organs. Here, we show a role for prostaglandin D2 (PGD2) in the pathophysiology of SLE. Patients with SLE have increased expression of PGD2 receptors (PTGDR) on blood basophils and increased concentration of PGD2 metabolites in plasma. Through an autocrine mechanism dependent on both PTGDRs, PGD2 induces the externalization of CXCR4 on basophils, both in humans and mice, driving accumulation in secondary lymphoid organs. Although PGD2 can accelerate basophil-dependent disease, antagonizing PTGDRs in mice reduces lupus-like disease in spontaneous and induced mouse models. Our study identifies the PGD2/PTGDR axis as a ready-to-use therapeutic modality in SLE.

JC virus granule cell neuronopathy: A cause of infectious cerebellar degeneration.

JC virus (JCV) infection of glial cells can lead to progressive multifocal leukoencephalopathy (PML) in immunocompromised patients. A newly described phenotype of the infection is infection of neurons. This distinct clinical and radiological syndrome is named JCV granule cell neuronopathy, characterized by exclusive or predominant cerebellar atrophy. We report the clinical and radiological longitudinal findings of 5 HIV-infected patients referred to us between September 2004 and November 2011 who exhibited JCV granule cell neuronopathy (4 probable cases and 1 possible). The association of immunocompromised status, progressive cerebellar syndrome, MRI abnormalities with cortical cerebellar atrophy and cerebrospinal fluid positive for JCV on PCR allowed for a highly probable diagnosis. The reversal of the immunocompromised status is the only way to stop the disease evolution. Motor functioning can remain impaired, but the illness itself, unlike progressive multifocal leukoencephalopathy, does not seem to threaten life.