SARS-CoV-2 Seroprevalence among Healthcare Workers after the First and Second Pandemic Waves.

Background: The Grand Hôpital de Charleroi is a large non-academic Belgian hospital that treated a large number of COVID-19 inpatients. In the context of this pandemic, all professions-combined healthcare workers (HCWs), and not only direct caregivers, are a frontline workforce in contact with suspected and confirmed COVID-19 cases and seem to be a high-risk group for exposure. The aim of our study was to estimate the prevalence of anti-SARS-CoV-2 antibodies in HCWs in our hospital after the first and second pandemic waves and to characterize the distribution of this seroprevalence in relation to various criteria. Methods: At the end of the two recruitment periods, a total of 4008 serological tests were performed in this single-center cross-sectional study. After completing a questionnaire including demographic and personal data, possible previous COVID-19 diagnostic test results and/or the presence of symptoms potentially related to COVID-19, the study participants underwent blood sampling and serological testing using DiaSorin's LIAISON® SARS-CoV-2 S1/S2 IgG test for the first phase and LIAISON® SARS-CoV-2 TrimericS IgG test for the second phase of this study. Results: In total, 302 study participants (10.72%) in the first round of the study and 404 (33.92%) in the second round were positive for SARS-CoV-2-IgG antibodies. The prevalence of seropositivity observed after the second wave was 3.16 times higher than after the first wave. We confirmed that direct, prolonged, and repeated contact with patients or their environment was a predominant seroconversion factor, but more unexpectedly, that this was the case for all HCWs and not only caregivers. Finally, the notion of high-risk contact seemed more readily identifiable in one's workplace than in one's private life. Conclusions: Our study confirmed that HCWs are at a significantly higher risk of contracting COVID-19 than the general population, and suggests that repeated contacts with at-risk patients, regardless of the HCWs' professions, represents the most important risk factor for seroconversion (Clinicaltrials.gov number, NCT04723290).

Isolated ACTH deficiency in a patient with empty sella as revealed by severe hyponatremia.

Hyponatremia due to isolated adrenocorticotropic hormone (ACTH) deficiency is difficult to diagnose as it is usually indistinguishable from non-endocrine syndrome of inappropriate antidiuretic hormone secretion (SIADH). We present a case secondary to empty sella. Most patients with empty sella remain asymptomatic throughout life and require no treatment; however, in cases involving the development of isolated ACTH deficiency, corticosteroid treatment should be enforced to avoid fatal consequences.

PROLONGED FEVER WITHOUT OBVIOUS ETIOLOGY FINALLY DIAGNOSED AS HIGH-GRADE SOFT TISSUE SARCOMA.

Sarcomas represent a challenge t clinicians as they are rare and diagnosis is often delayed. Soft tissue sarcomas are relatively uncommon cancers, the incidence is estimated about 1% from all malignant tumors. Due to aggressive biological behavior of pleomorphic undifferentiated sarcoma diagnosis must hi made as quickly as possible. MRI is the standard imaging modality for investigating possibl3 malignant masses. Excisional biopsy appears to be necessary for differentiating soft tissus sarcoma from expanding hematoma. FDG PET scans may be helpful in specific circum. stances (as was the situation in our case, because the lesion is composed from two components: an area without precise edges and a necrotic-cystic area).

A novel splice-site mutation in angiotensin I-converting enzyme (ACE) gene, c.3691+1G>A (IVS25+1G>A), causes a dramatic increase in circulating ACE through deletion of the transmembrane anchor.

BACKGROUND: Angiotensin-converting enzyme (ACE) (EC 4.15.1) metabolizes many biologically active peptides and plays a key role in blood pressure regulation and vascular remodeling. Elevated ACE levels are associated with different cardiovascular and respiratory diseases. METHODS AND RESULTS: Two Belgian families with a 8-16-fold increase in blood ACE level were incidentally identified. A novel heterozygous splice site mutation of intron 25 - IVS25+1G>A (c.3691+1G>A) - cosegregating with elevated plasma ACE was identified in both pedigrees. Messenger RNA analysis revealed that the mutation led to the retention of intron 25 and Premature Termination Codon generation. Subjects harboring the mutation were mostly normotensive, had no left ventricular hypertrophy or cardiovascular disease. The levels of renin-angiotensin-aldosterone system components in the mutated cases and wild-type controls were similar, both at baseline and after 50 mg captopril. Compared with non-affected members, quantification of ACE surface expression and shedding using flow cytometry assay of dendritic cells derived from peripheral blood monocytes of affected members, demonstrated a 50% decrease and 3-fold increase, respectively. Together with a dramatic increase in circulating ACE levels, these findings argue in favor of deletion of transmembrane anchor, leading to direct secretion of ACE out of cells. CONCLUSIONS: We describe a novel mutation of the ACE gene associated with a major familial elevation of circulating ACE, without evidence of activation of the renin-angiotensin system, target organ damage or cardiovascular complications. These data are consistent with the hypothesis that membrane-bound ACE, rather than circulating ACE, is responsible for Angiotensin II generation and its cardiovascular consequences.