Periodontitis periapical sintomática y agranulocitosis por analgésicos

Se presentó un caso de agranulocitosis en una paciente de 62 años, atribuible a ingesta continuada de analgésicos sin prescripción, para tratar el dolor debido a periodontitis periapical sintomática. Se realizó tratamiento de conductos radiculares. Dada la escasa incidencia de agranulocitosis por analgésicos a pesar de la frecuente utilización de los mismos, hemos creído de interés su publicación ya que este efecto indeseable puede ser grave o incluso mortal en algún caso. A pesar de conocerse los efectos indeseables de los analgésicos, la automedicación en los pacientes sigue siendo frecuente. Debido al diagnóstico y al tratamiento precoces de la enfermedad, este caso evolucionó favorablemente hasta la total recuperación de la paciente

Iatrogènies medicamentoses

Els processos patològics apareguts com a conseqüència d'un acte mèdic s'agrupen sota el terme 'iatrogènia'. En el cas que siguin deguts a l'acció d'un fàrmac, s'anomenen 'iatrogénies medicamentoses', efectes indesitjables o tam- bé reaccions adverses. ..

Liberación de noradrenalina por reserpina II. Interacción con bretilio en conducto deferente de rata

Desde hace ya algunos años estudiamos en nuestro Departamento la interacción de la reserpina con distintas sustancias que actúan en la presinapsis adrenérgica (simpaticomiméticos indirectos, inhibidores de la MAO, etc.). El bretilio es un bloqueante de la conducción del impulso nervioso que actúa también a nivel presináptico. ..

Liberación de noradrenalina por reserpina I. Interacción con anfetamina y con bretilio en bazo de gato

Continuando con experiencias anteriores ya presentadas en esta Asociación (PLANAS y cols., 1977) sobre la interacción de la reserpina con distintos fármacos, hemos estudiado en esta ocasión las posibles modificaciones del efecto de la reserpina cuando previamente se perfunde el bazo de gato in situ con anfetamina o bretilio. ..

Evidencias farmacológicas de la participación del sistema opioide endógeno en la respuesta inflamatoria local de la pata de la rata

Hemos investigado el papel del sistema opioide endógeno (SOE) en la respuesta inflamatoria inducida por la inyección subplantar (SP) de salino (SS) y carragenina (CA) en la pata trasera de la rata. Se usó naloxona intraperitoneal (IP) para desenmascarar los efectos de los opiáceos endógenos liberados durante la inflamación periférica. Tres grupos de ratas recibieron uno de los siguientes tratamientos SP: SS, CA o ninguna inyección (NI). En condiciones basales y 3 horas después del tratamiento fueron evaluados el umbral del dolor por presión (PPT), el volúmen de la pata (edema) y la temperatura local. En cada grupo fueron también investigados los efectos del vehículo IP, naloxona y (+)-naloxona (0,1 mg/kg). Los grupos SS y CA indujeron una significativa respuesta inflamatoria con hiperalgesia, edema e hiperemia local. La administración IP de naloxona pero no de (+)-naloxona, 15 minutos antes de la prueba, incrementó significativamente el edema en todos los grupos de tratamiento (p< 0,05) sin alterar el PPT o la temperatura local. El ANOVA de dos vías, reveló que el tratamiento y los fármacos, así como sus interacciones tenían un impacto significativo en el edema el cual estaba relacionado con los efectos de la CA y la naloxona. Nuestros hallazgos ilustran la implicación del sistema opioide endógeno a la respuesta fisiológica a la lesión local, regulando la fuga microvascular en los tejidos inflamados

SARS-CoV-2 susceptibility and COVID-19 disease severity are associated with genetic variants affecting gene expression in a variety of tissues

Variability in SARS-CoV-2 susceptibility and COVID-19 disease severity between individuals is partly due to genetic factors. Here, we identify 4 genomic loci with suggestive associations for SARS-CoV-2 susceptibility and 19 for COVID-19 disease severity. Four of these 23 loci likely have an ethnicity-specific component. Genome-wide association study (GWAS) signals in 11 loci colocalize with expression quantitative trait loci (eQTLs) associated with the expression of 20 genes in 62 tissues/cell types (range: 1:43 tissues/gene), including lung, brain, heart, muscle, and skin as well as the digestive system and immune system. We perform genetic fine mapping to compute 99% credible SNP sets, which identify 10 GWAS loci that have eight or fewer SNPs in the credible set, including three loci with one single likely causal SNP. Our study suggests that the diverse symptoms and disease severity of COVID-19 observed between individuals is associated with variants across the genome, affecting gene expression levels in a wide variety of tissue types

Epidemiological trends of HIV/HCV coinfection in Spain, 2015-2019

Altres ajuts: Spanish AIDS Research Network; European Funding for Regional Development (FEDER).Objectives: We assessed the prevalence of anti-hepatitis C virus (HCV) antibodies and active HCV infection (HCV-RNA-positive) in people living with HIV (PLWH) in Spain in 2019 and compared the results with those of four similar studies performed during 2015-2018. Methods: The study was performed in 41 centres. Sample size was estimated for an accuracy of 1%. Patients were selected by random sampling with proportional allocation. Results: The reference population comprised 41 973 PLWH, and the sample size was 1325. HCV serostatus was known in 1316 PLWH (99.3%), of whom 376 (28.6%) were HCV antibody (Ab)-positive (78.7% were prior injection drug users); 29 were HCV-RNA-positive (2.2%). Of the 29 HCV-RNA-positive PLWH, infection was chronic in 24, it was acute/recent in one, and it was of unknown duration in four. Cirrhosis was present in 71 (5.4%) PLWH overall, three (10.3%) HCV-RNA-positive patients and 68 (23.4%) of those who cleared HCV after anti-HCV therapy (p = 0.04). The prevalence of anti-HCV antibodies decreased steadily from 37.7% in 2015 to 28.6% in 2019 (p < 0.001); the prevalence of active HCV infection decreased from 22.1% in 2015 to 2.2% in 2019 (p < 0.001). Uptake of anti-HCV treatment increased from 53.9% in 2015 to 95.0% in 2019 (p < 0.001). Conclusions: In Spain, the prevalence of active HCV infection among PLWH at the end of 2019 was 2.2%, i.e. 90.0% lower than in 2015. Increased exposure to DAAs was probably the main reason for this sharp reduction. Despite the high coverage of treatment with direct-acting antiviral agents, HCV-related cirrhosis remains significant in this population

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

SARS-CoV-2 susceptibility and COVID-19 disease severity are associated with genetic variants affecting gene expression in a variety of tissues

Variability in SARS-CoV-2 susceptibility and COVID-19 disease severity between individuals is partly due to genetic factors. Here, we identify 4 genomic loci with suggestive associations for SARS-CoV-2 susceptibility and 19 for COVID-19 disease severity. Four of these 23 loci likely have an ethnicity-specific component. Genome-wide association study (GWAS) signals in 11 loci colocalize with expression quantitative trait loci (eQTLs) associated with the expression of 20 genes in 62 tissues/cell types (range: 1:43 tissues/gene), including lung, brain, heart, muscle, and skin as well as the digestive system and immune system. We perform genetic fine mapping to compute 99% credible SNP sets, which identify 10 GWAS loci that have eight or fewer SNPs in the credible set, including three loci with one single likely causal SNP. Our study suggests that the diverse symptoms and disease severity of COVID-19 observed between individuals is associated with variants across the genome, affecting gene expression levels in a wide variety of tissue types

Differential clinical characteristics and prognosis of intraventricular conduction defects in patients with chronic heart failure

Intraventricular conduction defects (IVCDs) can impair prognosis of heart failure (HF), but their specific impact is not well established. This study aimed to analyse the clinical profile and outcomes of HF patients with LBBB, right bundle branch block (RBBB), left anterior fascicular block (LAFB), and no IVCDs. Clinical variables and outcomes after a median follow-up of 21 months were analysed in 1762 patients with chronic HF and LBBB (n = 532), RBBB (n = 134), LAFB (n = 154), and no IVCDs (n = 942). LBBB was associated with more marked LV dilation, depressed LVEF, and mitral valve regurgitation. Patients with RBBB presented overt signs of congestive HF and depressed right ventricular motion. The LAFB group presented intermediate clinical characteristics, and patients with no IVCDs were more often women with less enlarged left ventricles and less depressed LVEF. Death occurred in 332 patients (interannual mortality = 10.8%): cardiovascular in 257, extravascular in 61, and of unknown origin in 14 patients. Cardiac death occurred in 230 (pump failure in 171 and sudden death in 59). An adjusted Cox model showed higher risk of cardiac death and pump failure death in the LBBB and RBBB than in the LAFB and the no IVCD groups. LBBB and RBBB are associated with different clinical profiles and both are independent predictors of increased risk of cardiac death in patients with HF. A more favourable prognosis was observed in patients with LAFB and in those free of IVCDs. Further research in HF patients with RBBB is warranted