Gestational infection with Toxoplasma gondii remains a significant concern for the adequate progression of pregnancy, fetal health, and neonatal well-being. The current status of toxoplasmosis screening in Spain is heterogeneous, with a growing trend toward abandoning universal screening for this infection during pregnancy. However, its incidence has only declined marginally, and based on the current scientific evidence, we consider it beneficial to support gestational screening for toxoplasmosis.
Esophageal cancer represents an aggressive disease positioned as the seventh-leading cause of death from cancer. Esophageal cancer comprises two different diseases that should be distinguished by histology, i.e., squamous cell carcinoma and adenocarcinoma. The epidemiology and molecular differences between these two entities explain their different responsiveness to novel treatments which should be treated independently. The improvement in outcomes of patients with esophageal cancer are obtained when a multidisciplinary therapeutic strategy is utilized. The introduction of targeted therapies including immunotherapy has markedly improved patient outcomes. We present an updated version of the Spanish esophageal cancer guidelines, summarizing the current evidence and available therapies for the treatment of esophageal cancer.
Abstract Introduction Heart failure (HF) is currently a major public health problem because its high morbidity and mortality add to a high consumption of health resources. The study of predictors of mortality helps to identify patients for whom care should be intensified. Purposes In this study we aim to assess the incidence and predictors of mortality at one-year follow-up. Methods We conducted a prospective observational study. Patients were included from 67 HF units in Spain (from the registry of the SEC-Excelente-IC quality accreditation program of the Spanish Society of Cardiology). Patients were consecutively enrolled in two one-month cohorts (March and October) between 2019 and 2023. Demographic, clinical, laboratory, echocardiographic, and treatment variables were collected. To study the independent association of each variable with mortality a Cox multivariate regression model was performed. Results A total of 2245 patients were included (59.6% previous chronic HF, 40.4 de novo HF). Mean age was 71,05±12,28 years, 64.3% were male, the most frequent etiology was ischemic heart disease (31%), median left ventricular ejection fraction was 38% (interquartile range -IR-, 29%-54%), and median NTproBNP was 2000 (IR, 878-4612) pg/ml. 72.8% had arterial hypertension, 44.2% diabetes mellitus, 52.4% atrial fibrillation, 37.8% chronic kidney disease (CKD), 32.5% anemia, and 16.3% chronic obstructive pulmonary disease. At one-year of follow-up, mortality was 15,1%. Table 1 shows the variables independently associated with mortality. Conclusions At one year of follow-up, all-cause mortality was 15,1%. Ischemic etiology, previous admission for HF, a worse functional class and some comorbidities such atrial fibrillation, CKD, dementia, cancer, anemia or malnutrition are variables independently associated with mortality.
Background:Primary amoebic meningoencephalitis (PAM) is a rapidly progressive and often fatal central nervous system infection caused by Naegleria fowleri. Despite widespread environmental exposure to this free-living amoeba, clinical disease is rare, suggesting that it requires not only exposure to the amoeba but also a host vulnerability. Yet, the immune mechanisms controlling protection vs. susceptibility to N. fowleri remain poorly understood. Methods:We conducted comprehensive clinical, immunological, and genetic investigations in one of the few survivors of PAM. We performed high-dimensional immune profiling using Cytometry by Time-Of-Flight (CyTOF) to assess immune cell composition and activation state. We employed whole-exome sequencing (WES) to identify rare genetic variants that affect host responses. Functional immune assays were used to assess serum-mediated amoebicidal activity in vitro and to characterize key host defense pathways. Results:A previously healthy pediatric patient was diagnosed with PAM. Contrary to other cases, her clinical course lasted for more than 2 months before she recovered with miltefosine treatment. Immunologic evaluation showed this patient had normal numbers and frequencies of major lymphoid and myeloid immune cells. WES revealed a homozygous deletion in the complement component 2 (C2) gene, resulting in a complete absence of circulating C2 protein and abolishing classical complement pathway activity. Normal human serum induced complement-mediated lysis of N. fowleri trophozoites in vitro, whereas complement-depleted normal human serum and serum from our patient both failed to deposit membrane attack complex (MAC) or kill N. fowleri. MAC deposition and amoebicidal activity were restored by supplementing the patient's serum with purified human C2 protein. Conclusion:Our study demonstrates that PAM can be caused by a monogenic inborn error of immunity (IEI) and that the complement system is critical for human immunity against Naegleria fowleri.
