Introduction:Few clinical trials and cohort studies have evaluated the efficacy of bictegravir/emtricitabine/tenofovir alafenamide (B/F/TAF) in people with HIV (PWH) with preexisting M184V/I or other nucleos(t)ide reverse transcriptase inhibitor (NRTI) resistance-associated mutations (RAMs). Real-world data are also scarce.Methods:Retrospective review of treatment-experienced patients who started B/F/TAF in a cohort of PWH. HIV-RNA less than 50 copies/ml was analyzed at 48 weeks in an intention-to-treat (ITT) analysis (missing=failure) and per protocol analysis (patients with missing data or changes for reasons other than virological failure were excluded). Results were compared in patients with and without previous NRTI-RAMs.Results:Five hundred and six PWH were included (16.2% women). Median age and time with HIV infection were 52.3 and 18.9 years, respectively. At baseline, viral load was less than 50 copies/ml in 440 patients (86.6%). Overall, 69 (13.6%) participants had documented preexisting NRTI-RAMs: 57 (11.2%) M184V/I and 30 (5.9%) tenofovir RAMs. In the ITT analysis, 83% (420/506) had HIV-RNA less than 50 copies/ml [82.2% (359/437) and 88.4% (61/69) in persons without and with NRTI-RAMs, respectively (P = 0.2)]. In the per protocol analysis 94.2% (420/445) had HIV-RNA less than 50 copies/ml [94.4% (359/380) vs. 93.8% (61/65); P = 0.2]. A total of 61 participants were excluded from the per protocol analysis (23 missing data, 19 discontinued B/F/TAF because of toxicity, 13 for other reasons, and 6 died).Conclusion:Switching to B/F/TAF is well tolerated and effective in the real-world setting, even in patients with preexisting NRTI RAMs, such as M184V and RAMs conferring resistance to tenofovir. These results confirm the robustness of this combination.

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Ventriculitis are a complication of meningitis (community-acquired or nosocomial) or another central nervous system infections as brain abscess. They are associated to a different spectrum of microorganisms from resistant gram-negative bacilli to staphylococci that can lead serious illness with high mortality. Difficult-to-treat resistance Gram-negative bacilli may increase to 20% deaths respect susceptible isolates of the same bacteria. We present the first report of a clinical cured case of difficult-to-treat resistant Pseudomonas aeruginosa (DTR-P) ventriculitis in which cefiderocol penetration into the central nervous system (CNS) has been confirmed in blood and cerebrospinal fluid (CSF). Cefiderocol might be considered for difficult-to-treat CNS infections in view of the recent new cases published together our one.

Objective. To analyze the efficacy and tolerability of the strategy to change from rilpivirine (RPV) based regimens to bictegravir / emtricitabine / tenofovir alafenamide (B/F/TAF). Methods. Single-center, observational and retrospective study. Patients who made the change to B/F/TAF before February 2020 were selected, analyzing the results after 24 and 48 weeks. The percentage that remained with an undetectable viral load was determined, as well as the changes in CD4 + lymphocytes, metabolic parameters and renal function. Results. A total of 42 patients were included. Thirty-two of the 35 patients (91.4%) who completed the 48 weeks of follow-up had an undetectable viral load. The CD4 + lymphocyte count remained stable at 24 and 48 weeks. The response to B/F/TAF was not influenced by the two analogs previously received. Conclusion. Switching from triple therapy with RPV to B/F/TAF is a safe and effective strategy in real life.

The cure for chronic human immunodeficiency virus (HIV) infections has been a goal pursued since the antiretroviral therapy that improved the clinical conditions of patients became available. However, the exclusive use of these drugs is not enough to achieve a cure, since the viral load rebounds when the treatment is discontinued, leading to disease progression. There are several theories and hypotheses about the biological foundations that prevent a cure. The main obstacle appears to be the existence of a latent viral reservoir that cannot be eliminated pharmacologically. This concept is the basis of the new strategies that seek a cure, known as kick and kill. However, there are other lines of study that recognize mechanisms of persistent viral replication in patients under effective treatment, and that would modify the current lines of research on the cure of HIV. Given the importance of these concepts, in this work, we propose to review the most recent evidence on these hypotheses, covering both the evidence that is positioned in favor and against, trying to expose what are some of the challenges that remain to be resolved in this field of research.

The significant impact of COVID-19 worldwide has made it necessary to develop tools to identify patients at high risk of severe disease and death. This work aims to validate the RIM Score-COVID in the SEMI-COVID-19 Registry. The RIM Score-COVID is a simple nomogram with high predictive capacity for in-hospital death due to COVID-19 designed using clinical and analytical parameters of patients diagnosed in the first wave of the pandemic. The nomogram uses five variables measured on arrival to the emergency department (ED): age, sex, oxygen saturation, C-reactive protein level, and neutrophil-to-platelet ratio. Validation was performed in the Spanish SEMI-COVID-19 Registry, which included consecutive patients hospitalized with confirmed COVID-19 in Spain. The cohort was divided into three time periods: T1 from February 1 to June 10, 2020 (first wave), T2 from June 11 to December 31, 2020 (second wave, pre-vaccination period), and T3 from January 1 to December 5, 2021 (vaccination period). The model’s accuracy in predicting in-hospital COVID-19 mortality was assessed using the area under the receiver operating characteristics curve (AUROC). Clinical and laboratory data from 22,566 patients were analyzed: 15,976 (70.7%) from T1, 4,233 (18.7%) from T2, and 2,357 from T3 (10.4%). AUROC of the RIM Score-COVID in the entire SEMI-COVID-19 Registry was 0.823 (95%CI 0.819–0.827) and was 0.834 (95%CI 0.830–0.839) in T1, 0.792 (95%CI 0.781–0.803) in T2, and 0.799 (95%CI 0.785–0.813) in T3. The RIM Score-COVID is a simple, easy-to-use method for predicting in-hospital COVID-19 mortality that uses parameters measured in most EDs. This tool showed good predictive ability in successive disease waves. Supplementary Information The online version contains supplementary material available at 10.1007/s11739-023-03200-3.

Background:Antiphospholipid syndrome (APS) is a systemic autoimmune disease, associated with a hypercoagulable state and fetal loss and with other clinical manifestations including cardiac involvement. APS occurs as a primary disorder (PAPS) or secondary to another autoimmune disease (SAPS). Due to its vascular nature, various organs and tissues may be affected, including the cardiac system. Cardiac manifestations of APS are valve abnormalities (valve thickening and vegetations), occlusive arterial disease (atherosclerosis and myocardial infarction) and pulmonary hypertension (PH).Objectives:To assess the prevalence of non-myocardial involvement (valvulopathy and pulmonary hypertension) in a cohort of patients with antiphospholipid antibodies (aPLs).Methods:Retrospective observational study in a Spanish reference center for systemic autoimmune diseases. All patients with aPLs and performed transthoracic echocardiogram (TTE) were included in the study. Patients were divided between PAPS, SAPS and aPLs carriers. A cohort of 50 patients with systemic lupus erythematosus (SLE) without aPLs was used as a control. Anti-cardiolipin, anti-B2GP1 and lupus anticoagulant antibodies were determined by standard techniques.Results:A total of 220 patients were reviewed. 145 (65.9%) were female. The mean age was 42 years. Among all patients with aPLs, 102 were PAPS, 73 SAPS, and 45 asymptomatic carriers (silent APS). Patients with aPLs, unlike patients with SLE without aPLs, presented more often pathological TTE (114 patients, 52%) (p = 0.02), with more valvular involvement (87, 39%) (p = 0.005) and pulmonary hypertension (21, 9.5%, p = ns). Valve involvement was identified in 99 patients: 45 in PAPS, 27 in SAPS, 14 in aPLs carriers and 13 in the SLE without aPLs, these differences being statistically significant (p = 0.002). Valvulopathy was asymptomatic in the majority of patients but required valve replacement in two patients. Mitral valve was the most affected, especially in the form of insufficiency (57%), followed by aortic valve, combined mitral and aortic valve, and less frequently the pulmonary valve alone (3 cases).aPLs globalPAPSSAPSaPLs carriersSLE w/o aPLsTotal220 (100%)102 (46.4%)73 (33.2%)45 (20.4%)50 (100%)Men75 (34.1%)41 (40.2%)23 (31.5%)11 (24.4%)6 (12%)Women145 (65.9%)61 (59.8%)50 (68.5%)34 (75.6%)44 (88%)Conclusion:Subclinical valve involvement was very common in patients with APS. There was no correlation with other clinical manifestations of APS nor were other risk factors identified. PH was less frequent than valvular involvement in patients with APS. However, despite not being statistically significant, close to 10% of patients with APS had PH compared to 6% of patients without APS.aPLs globalPAPSSAPSaPLs carriersSLE w/o aPLsTTE performed220 (100%)102 (46.4%)73 (33.2%)45 (20.4%)50 (100%)Pathological TTE114 (52%)16 (32%)p=0.02Valvular involvement87 (39%)45 (20.4%)27 (12.3%)14 (6.3%)13 (26%)p=0.005Pulmonary hypertension21 (9.5%)3 (6%)p=nsEvery patient with APS should have an echocardiogram in the initial study protocol in order to rule out both valvulopathy and pulmonary hypertension. This could modify the patient’s management both in the short and long term, as well as the prognosis.References:[1]Radin M, Ugolini-Lopes MR, Sciascia S, Andrade D. Extra-criteria manifestations of antiphospholipid syndrome: Risk assessment and management.Semin Arthritis Rheum. 2018;48(1):117–120.[2]Tenedios F, Erkan D, Lockshin MD. Cardiac involvement in the antiphospholipid syndrome.Lupus. 2005;14(9):691–696.[3]Kolitz T, Shiber S, Sharabi I, Winder A, Zandman-Goddard G. Cardiac Manifestations of Antiphospholipid Syndrome With Focus on Its Primary Form.Front Immunol. 2019;10:941.Disclosure of Interests:None declared

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