Anti–N-methyl-D-aspartate receptor (NMDAR) encephalitis is an auto-immune neurological disorder characterized by the presence in the cerebrospinal fluid (CSF) of antibodies against the GluN1 subunit of NMDA receptors in the brain. The etiology of the disease remains largely unknown. In this study, we aimed to investigate the possible existence of pharmacovigilance signals relating to a link between vaccination and the occurrence of anti-NMDAR encephalitis. We performed a case/non-case study using data from the World Health Organization pharmacovigilance database (VigiBase) up to 31 December 2021. All individual case study reports (ICSRs) linked to a vaccine and coded with the MedDRA Lower Level Term (LLT) “anti-NMDA receptor encephalitis” were analysed. We calculated the Reporting Odds Ratio (ROR) and 95% Confidence Interval (CI) for each type of vaccine. A total of 29,758,737 ICSRs were registered in VigiBase, of which 70 were coded under the selected LLT, and 29/70 (41.4%) involved a vaccine. Of these cases, 53.8% involved children aged younger than 15 years. The median time to onset of anti-NMDAR encephalitis after vaccination was 4 days (range 0–730). The highest RORs were observed for the diphtheria/polio/tetanus/pertussis vaccine [54.72 (95% CI 26.2–114.3)], yellow fever vaccine [50.02 (95% CI 15.7–159)] and human papillomavirus vaccine [32.89 (15.8–68.7)]. All cases were coded as serious; 13 patients did not recover, or were left with permanent sequelae. Nine patients recovered without sequelae or are on the path to recovery, and one patient died. In summary, pharmacovigilance signals were observed for anti-NMDAR encephalitis and vaccination. Clinicians need to be aware of this potential risk, and encourage to report any case of anti-NMDAR encephalitis occurring after vaccination.

No abstract

Larger turbine shroud will result in lower tip leakage losses but will increase the rotor mechanical stresses; hence optimization is necessary, especially at the preliminary design of the engine. The improved process developed is as follows: from blade and shroud geometry, the algorithm performs several 3D mechanical analyses in finite element software, allowing the calculation of interpolations to finally extract the largest shroud size. The relative deviation on stress between the 3D new software analysis and the existing process does not exceed 4%, which is acceptable for the preliminary design. In addition, the time saved is considerable: 10 minutes for the existing process as opposed to 1 minute for the lighter simulations. This new optimization method shows that a local and targeted dimensioning, limiting the number of parameters and constraints, responds quickly and precisely to the problem. However, the choice of variable parameters is crucial, hence the importance of the influence of the parameters. This optimization method contributes to the preliminary design phase of the shroud to reduce the design time and gain in accuracy while ensuring the robustness of the process, therefore in the logic of the development of a full Preliminary Multidisciplinary Design Optimization (PMDO) system for the turbine design.

AimSweet’s syndrome is an acute febrile neutrophilic dermatosis first described in 1964 by Robert Douglas Sweet. The pathophysiological mechanism is not fully established, however several cases of Sweet’s syndrome have been reported following drug administration.MethodsTo investigate the existence of pharmacovigilance signals between drugs and the occurrence of Sweet’s syndrome, we performed a case/non‐case study on reports of “acute febrile neutrophilic dermatosis” registered in the French pharmacovigilance database. Reporting Odds Ratio (ROR) with its 95% confidence interval were calculated.ResultsAmong the 994,789 reports recorded in the database, 136 were Sweet’s syndrome. 50.7% of patients were men; median age was 59 years (range 15‐91). 224 drugs were mentioned as suspects: 21.0% were antibacterials, 19.2% were antineoplastics, 12.1% were immunosuppressants. Median time to onset from drug initiation to the development of Sweet’s syndrome was 15 days (range 1‐1095). Highest ROR were observed with bortezomib (74.04 [40.8‐134.2]), azacitidine (72.14 [29.4‐176.9]), perfilgrastim (67.05 [21.2‐211.6]), azathioprine (55.46 [34.8‐88.4]) and bendamustine (35.84 [11.4‐112.8]).ConclusionPharmacovigilance signals have been observed between the occurrence of Sweet’s syndrome and colony‐stimulating factors, immunosuppressants, antineoplastics and antibiotics. Clinicians should be aware of the potential associations with these drugs and encourage reporting any case of drug‐induced Sweet’s syndrome.