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1.
Intern Emerg Med ; 17(6): 1803-1812, 2022 09.
Artículo en Inglés | MEDLINE | ID: mdl-35678940

RESUMEN

OBJECTIVE: Patients who are over 65 years old represent up to 24% of emergency department (ED) admissions. They are at increased risk of under-triage due to impaired physiological responses. The primary objective of this study was to assess the prevalence of elevated lactate by point of care testing (POCT) in this population. The secondary objective was to assess the additional value of lactate level in predicting an early poor outcome, as compared to and combined with common clinical scores and triage scales. METHODS: This monocentric prospective study recruited ED patients who were over 65 years old between July 19th 2019 and June 17th 2020. Patients consulting for seizures or needing immediate assessment were excluded. POCT lactates were considered elevated if ≥ 2.5 mmol/L. A poor outcome was defined based on certain complications or therapeutic decisions. RESULTS: In total, 602 patients were included; 163 (27.1%) had elevated lactate and 44 (7.3%) had a poor outcome. There was no association between poor outcome and lactate level. Modified Early Warning Score (MEWS) was significantly associated with poor outcome, alongside National Early Warning Score (NEWS). Logistic regression also associated lactate level combined with MEWS and poor outcome. CONCLUSION: The prevalence of elevated lactate was 27.1%. Lactate level alone or combined with different triage scales or clinical scores such as MEWS, NEWS and qSOFA was not associated with prediction of a poor outcome. MEWS alone performed best in predicting poor outcome. The usefulness of POCT lactate measurement at triage is questionable in the population of 65 and above.


Asunto(s)
Sistemas de Atención de Punto , Sepsis , Anciano , Servicio de Urgencia en Hospital , Mortalidad Hospitalaria , Humanos , Ácido Láctico , Prevalencia , Estudios Prospectivos , Curva ROC , Estudios Retrospectivos
2.
Clin Sci (Lond) ; 103 Suppl 48: 367S-370S, 2002 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-12193124

RESUMEN

Asthma is a chronic respiratory disease that is characterized by airway inflammation, bronchoconstriction and the influx of pro-inflammatory cells, mostly eosinophils in the lung tissue and bronchoalveolar space. Amongst the many physiopathological roles attributed to endothelins (ETs), one is to modulate pulmonary functions. It is established that Balb/c mice develop allergen-induced Th(2)-cytokine gene expression, airway inflammation and hyper-responsiveness whereas C57Bl/6 mice are much less reactive. In the present study, we investigated the roles of ETs in these two murine models of allergic asthma (AA). Mice were sensitized and challenged with either saline (S) and/or ovalbumin (O) over 6 weeks (groups S/S and O/O) and treated chronically with ABT-627 or its vehicle. Twenty-four hours after the last sensitization, challenged mice developed a marked airway inflammatory response characterized by the accumulation of total inflammatory cells (a 21-fold increase) in the bronchoalveolar space, similar in both mouse strains. The increase in eosinophils was marked in both groups, representing 98% of total cell count in O/O versus <1% in S/S. Macrophages were also increased 3-fold in both strains. ABT-627 did reduce the accumulation of macrophages in both stains (36 to 53%) whereas it blocked by 76% the influx of eosinophils in Balb/c but not in C57Bl/6 mice. These results show that ET(A)-receptor antagonism is more effective against O/O-induced AA in Balb/c mice, even though both strains were associated with the same increase in key pro-inflammatory cells in the bronchoalveolar space. It is unclear whether this is due to a lack or a disproportionate expression of ET(A) receptors in these two murine strains, or in post-receptor transduction modulation, or different regulation of ET receptors in various pulmonary cells, after sensitization and challenge.


Asunto(s)
Antineoplásicos/uso terapéutico , Asma/tratamiento farmacológico , Antagonistas de los Receptores de Endotelina , Pirrolidinas , Animales , Asma/inmunología , Atrasentán , Líquido del Lavado Bronquioalveolar/inmunología , Eosinófilos/inmunología , Recuento de Leucocitos , Recuento de Linfocitos , Masculino , Ratones , Ratones Endogámicos BALB C , Ratones Endogámicos C57BL , Modelos Animales , Receptor de Endotelina A , Especificidad de la Especie
3.
Clin Sci (Lond) ; 103 Suppl 48: 371S-375S, 2002 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-12193125

RESUMEN

Acute pulmonary air embolism (APAE) injures the vascular endothelium in the lung and results in pulmonary hypertension (PH). Endothelins (ETs), a family of potent vasoactive peptides, are known to be associated with PH of various aetiologies. We evaluated the effects of ABT-627, a selective ET(A) receptor (ET(A)-R) antagonist in a rat model of APAE over 3 h. APAE rats developed a higher right ventricular systolic pressure (RVSP), lower mean arterial blood pressure (MABP), and had lower PaO(2). At 3 h, arterial plasma levels of ET-1 were increased. ABT-627-treated controls showed no effects. However, ABT-627 significantly lowered RVSP during APAE, abolished the short recovery phase (within 10-25 min) of MABP without affecting the subsequent lowering of MABP, and improved oxygen saturation in APAE rats. These results show that ET(A)-R subtype is involved in the pathogenesis of APAE since a blockade of this receptor subtype attenuated the cardiopulmonary deterioration and improved blood gas exchanges in rats with this disease.


Asunto(s)
Antagonistas de los Receptores de Endotelina , Embolia Pulmonar/tratamiento farmacológico , Pirrolidinas/uso terapéutico , Enfermedad Aguda , Animales , Atrasentán , Embolia Aérea/tratamiento farmacológico , Embolia Aérea/metabolismo , Endotelina-1/sangre , Endotelina-3/genética , Expresión Génica , Pulmón/metabolismo , Masculino , Modelos Animales , Oxígeno/sangre , Embolia Pulmonar/metabolismo , Ratas , Ratas Sprague-Dawley , Receptor de Endotelina A , Receptor de Endotelina B , Receptores de Endotelina/genética , Receptores de Endotelina/metabolismo
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