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1.
Rev. cuba. med. trop ; 73(2): e551, 2021. tab, graf
Article in Spanish | LILACS, CUMED | ID: biblio-1347496

ABSTRACT

El dengue es la infección trasmitida por vectores con mayor impacto en carga de enfermedad, económica y social a nivel mundial, con más de 3,6 billones de personas en riesgo de infección. Sus manifestaciones son variables, caracterizadas en su mayoría por síndrome febril con riesgo de sangrado, choque y muerte. El compromiso pulmonar es infrecuente, siendo el síndrome de dificultad respiratoria aguda una complicación inesperada, aunque informada, asociada a un mal pronóstico. Se presenta un paciente sin antecedentes relevantes de importancia, con focalización pulmonar severa asociado a infección por el virus dengue. En el caso presentado se descartaron procesos infecciosos bacterianos u otros agentes causales de síndrome de dificultad respiratoria aguda, lo que sumado a las características clínicas de ingreso, zona de ocurrencia del caso considerada como endémica, curso clínico, paraclínico y la franca positividad de las pruebas para dengue así como la seroconversión de estas, a pesar de no haber sido realizadas pruebas moleculares, se consideró como el agente causal más probable el virus dengue. Todo esto lleva a recomendar siempre considerarlo como potencial agente causal, lo que permite así un diagnóstico y manejo óptimos(AU)


Dengue is the vector-borne infection with the greatest impact on disease, economic and social burden worldwide, with more than 3.6 billion people under risk of contagion. Its manifestations are varied, most of them characterized by febrile syndrome with a risk of bleeding, shock and death. Pulmonary involvement is infrequent, and acute respiratory distress syndrome is an unexpected complication, though it has been reported in association to a bad prognosis. A case is presented of a male patient without relevant antecedents of interest, with severe pulmonary focalization associated to dengue virus infection. Bacterial infectious processes and other causative agents of acute respiratory distress syndrome were ruled out. In view of the patient's clinical status at admission, the endemicity of the patient's area of residence, the clinical and paraclinical course, and the obvious positivity of the dengue tests performed and their seroconversion, despite not having conducted molecular tests, it was concluded that the most probable causative agent was dengue virus. Therefore, it is recommended that dengue infection always be considered as a potential causative agent of acute respiratory distress syndrome, thus contributing to optimal diagnosis and management(AU)


Subject(s)
Humans , Male , Adult , Respiratory Distress Syndrome, Newborn , Endemic Diseases , Molecular Diagnostic Techniques , Dengue Virus , Prognosis , Cost of Illness , Seroconversion
2.
Expert Opin Ther Pat ; 27(8): 877-886, 2017 Aug.
Article in English | MEDLINE | ID: mdl-28592162

ABSTRACT

INTRODUCTION: Inhalation injury is the leading cause of death in burn patients and is usually caused by the uninhibited absorption of smoke, which has an extremely toxic effect on the respiratory system. The physiopathology of inhalation injury covers multiple factors and the injured respiratory system may present deterioration in a few hours. Areas covered: In this present review, we analyzed patents based on both natural and synthetic products developed for the treatment of smoke inhalation. We found 14 patents in Espacenet, 25 in WIPO and none in the USPTO data search. Expert opinion: Several previous reports on treatments used for smoke inhalation are discussed. Although there are a number of research based products for this injury, there has been no review of the patents dealing with treatments for smoke inhalation. The development of novel natural or synthetic products are discussed in detail in the review.


Subject(s)
Biological Products/therapeutic use , Drug Design , Smoke Inhalation Injury/drug therapy , Animals , Burns/pathology , Humans , Patents as Topic , Respiratory System/physiopathology , Smoke Inhalation Injury/physiopathology
3.
Lung ; 194(4): 487-99, 2016 08.
Article in English | MEDLINE | ID: mdl-27113373

ABSTRACT

BACKGROUND: The inhalation injury is usually initiated by uninhibited absorption of smoke, favoring the release of cytokines and other lipid mediators from inflammatory cells in lung airways and parenchyma. OBJECTIVES: To systematically review, examine, and synthesize the main inflammatory mediators analyzed in published studies in animals subjected to smoke inhalation, as well as oxidative stress. SEARCH STRATEGY: A comprehensive literature search was conducted through MEDLINE-PubMed, Web of Science, and Scopus. SELECTION CRITERIA: Studies with animals subjected to lung damage from smoke inhalation that evaluated the presence and the action of inflammatory mediators and oxidative stress. RESULTS: A total of 1332 studies were initially identified, with only 31 meeting the inclusion criteria. The inflammatory mediators and oxidative stress markers studied and presented in the articles described herein were varied; however, the most cited ones were tumor necrosis factor-alpha (6), IL-8 and IL-6 (both studied in five articles), IL-1ß and nuclear factor kappa ß (both studied in 4 articles), malondialdehyde (11 studies), and myeloperoxidase (7). It is worth noting that most studies evaluated more than one inflammatory mediator and oxidative stress marker. CONCLUSION: Based on this review, we could observe that the main inflammatory mediators and oxidative stress markers analyzed were TNF-α, IL-8, IL-6, IL-1ß, nuclear factor kappa ß, MDA, and MPO. However, it is necessary to increase the rigor of study design and data, in order to have studies that are more homogeneous and with appropriate methodological quality.


Subject(s)
Cytokines/metabolism , Inflammation Mediators/metabolism , Inflammation/metabolism , Oxidative Stress , Smoke Inhalation Injury/metabolism , Animals , Biomarkers/metabolism , Interleukin-1beta/metabolism , Interleukin-6/metabolism , Interleukin-8/metabolism , Malondialdehyde/metabolism , NF-kappa B/metabolism , Peroxidase/metabolism , Tumor Necrosis Factor-alpha/metabolism
4.
Rev. AMRIGS ; 51(4): 275-279, out.-dez. 2007. ilus, tab
Article in Portuguese | LILACS | ID: biblio-859916

ABSTRACT

Objetivo: Estudar o papel do probucol na lesão pulmonar obtida pela administração de doxorrubicina em ratos. Método: foi realizado um estudo piloto experimental, onde o probucol foi testado como protetor da injúria pulmonar obtida pela administração de doxorrubicina em ratos. Resultados: Na análise comparativa dos grupos, estudados por microscopia óptica, não houve diferença significativa de critérios previamente definidos, exceto pelo edema pleural (p < 0,05). Já na microscopia eletrônica, a agressão da doxorrubicina foi identificada através da desorganização estrutural. No grupo que recebeu probucol e doxorrubicina, não foi observada a mesma desorganização (p < 0,05). Conclusões: os resultados deste estudo piloto sugerem que o probucol exerceu um efeito protetor no tecido pulmonar agredido pela doxorrubicina e que a microscopia eletrônica é mais sensível na identificação de critérios de injúria pulmonar decorrente da exposição à doxorrubicina (AU)


Objective: To study the role of probucol in the pulmonary injury caused by doxorubicin in rats. Methods: An experimental study was carried out to verify where the probucol was protective of the pulmonary injury caused by the administration of doxorubicin in rats. Results: In the comparative analysis of the groups studied by optic microscopy, it did not have significant difference in pre-definite criterions, except for pleural edema (p < 0,05). In eletronic microscopy, the aggression of the doxorubicin was indicated through the structural disorganization. In the group that received probucol and doxorubicin was not observed the same disorganization (p < 0,05). Conclusion: The results suggest that the probucol was effective in the protection of pulmonary injury caused by doxorubicin and that the eletronic microscopy is more sensitive for pre-definite criterions of pulmonary injury (AU)


Subject(s)
Animals , Male , Probucol/therapeutic use , Doxorubicin/toxicity , Lung Injury/chemically induced , Lung Injury/pathology , Sarcoma/secondary , Lipid Peroxidation/drug effects , Doxorubicin/antagonists & inhibitors , Lung/drug effects , Lung Neoplasms/secondary
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