Amlodipino y choque vasodilatado en una unidad de cuidados intensivos de un hospital general: Reporte de caso / Amlodipine and vasodilated shock in an intensive care unit of a general hospital: Case report

Los calcio antagonistas son fármacos usados para diferentes patologías médicas; sin embargo la intoxicación puede ser grave. Presentamos el caso de una mujer joven intoxicada por amlodipino quien cursó con choque vasodilatado y disfunción multiorgánica, en quien se usó vasopresores múltiples a dosis por encima de las habituales para estabilizarla. (AU)

Calcium antagonists are used in a number of medical conditions, but intoxication with these drugs may be lethal.We present the case of a young women intoxicated with amlodipine who presented with vasodilated shock and multi organ disfunction in whom multiple vasopressors at maximum allowed doses were used to estabilize the patient. (AU)

Fiebre amarilla y disfunción multiorgánica: Reporte de tres casos / Yellow fever and multi organ dysfunction: Report of three cases

Fiebre amarilla es una enfermedad viral aguda causada por un virus de la familia Flaviviridae transmitida por vectores, caracterizada por síndrome ictérico febril hemorrágica y que puede cursar con disfunción multiorgánica, con alta mortalidad. Se reportan tres casos de pacientes que viajaron a La Merced, Chanchamayo, que cursaron con síndrome ictérico febril hemorrágico con disfunción multiorgánica, con diagnóstico serológico de fiebre amarilla; uno sobrevivió y dos fallecieron. (AU)

Yellow fever is a vector-borne disease caused by a virus of the Flaviviridae family that is characterized by fever and jaundice that may progressed to multi organ failure with high associated mortality. We report three cases of patients who had travelled to La Merced, Chanchamayo who presented with multi organ failure with confirmed serology for yellow fever, one survived and the other two died. (AU)

Acidosis láctica y choque distributivo por sobredosis de metformina: Reporte de caso / Lactic acidosis and distributive shock due to metformin overdose: Case report

Metformina es una biguanida usada como agente antihiperglicemiante, que promueve la euglicemia; su principal toxicidad es acidosis láctica. Se reporta el caso de un varón, adulto mayor, diabético e hipertenso quien se automedicó con 10 tabletas de metformina 850 mg; presentando acidosis láctica severa y choque distributivo requiriendo soporte y manejo en la Unidad de Cuidados Intensivos. (AU)

Metformin is a biguanide drug used as an oral antidiabetic medication whose main toxicity is lactic acidosis. We report the case of an old adult male diabetic and hypertensive patient who self prescribed 10 tablets of metformin 850mg presenting lactic acidosis and distributive shock requiring treatment in the intensive care unit. (AU)

Morbilidad y mortalidad de los pacientes con síndrome de distress respiratorio agudo/injuria pulmonar aguda por Influenza A H1N1 que requirieron soporte cardiopulmonar en un hospital general / Morbidity and mortality of patients with acute respiratory distress syndrome/acute pulmonary injury due to influenza A H1N1 who required cardiopulmonary support in a general hospital

Objetivo: Determinar la morbilidad y mortalidad de los pacientes con síndrome de distress respiratorio agudo (SDRA)/injuria pulmonar aguda (IPA) por Influenza A H1N1 que requirieron soporte cardiopulmonar en un hospital general. Material y métodos: Estudio retrospectivo, descriptivo, tipo serie de casos. Se revisaron las historias clínicas, las hojas de monitoreo ventilatorio y hemodinámico de los pacientes con SDRA/IPA secundario a Influenza A H1N1 atendidos en el Servicio de Cuidados Intensivos Generales (SCIG) del Hospital Nacional Cayetano Heredia entre mayo y setiembre de 2009. El diagnóstico de Influenza A H1N1 se realizó por PCR-RT. Resultados: Se atendieron 99 pacientes con Influenza A H1N1, 9 ingresaron al SCIG por SDRA/IPA; cinco requirieron ventilación mecánica invasiva (VMI), tres ventilación mecánica no invasiva y uno no requirió soporte ventilatorio. La edad promedio fue 43,3 ± 18,3 años; el tiempo de enfermedad 8 ± 3 días. Al ingreso, el 100% tuvo fiebre y disnea, el score APACHE II fue 10,5 ± 4,1 y el SOFA 5,6 ± 3,2; el Pa02/Fi02 96,74 ± 28,6. En 4/5 pacientes en VMI el Pa02/Fi02 a las 12 h y al final de la ventilación mecánica fue < 200. La presión en cuña estimada fue 15,69 ± 3,6 y el índice cardiaco por doppler esofágico 2,4 ± 0,34. La TGO fue 160 ± 152,15, DHL 2366,33 ± 1862,13 y CPK 216 ± 298,25. Todos los pacientes recibieron Oseltamivir 150 mg cada 12 h por 10 días. Cuatro pacientes fallecieron. Conclusiones: Los pacientes con SDRA/IPA por Influenza A H1 N1, fueron adultos jóvenes, con tiempo de enfermedad prolongado; con fiebre, disnea y linfopenia; sin compromiso cardiovascular y con hipoxemia refractaria como causa de muerte.

Objective: To determine the morbidity and mortality patterns of patients with acute respiratory distress syndrome (ARDS)/acute pulmonary injury (API) due to influenza A H1N1 who required cardiopulmonary support in a general hospital. Methods: Retrospective case series. Clinical charts, mechanical ventilation and hemodynamic monitoring charts of patients with ARDS/API due to influenza A H1N1 admitted to the general intensive care unit (GICU) of Hospital Nacional Cayetano Heredia from May to September 2009 were reviewed. The diagnosis of influenza H1N1 was confirmed with RT-PCR. Results: 99 patients with influenza A H1N1 were attended; 9 were admitted in the GICU with ARDS/API; five patients required invasive mechanical ventilation (IMV); three non-invasive mechanical ventilation (NIMV) and one did not require ventilatory support. Mean age was 43.3 ± 18.3 years; mean duration of symptoms was 8 ± 3 days. On admission, 100% of patients had fever and dyspnea; mean APACHE II score was 10.5 ± 4.1 and mean SOFA score was 5.6 ± 3.2; the mean Pa02/Fi02 was 96.74 ± 28.6. In 4/5 of patients requiring IMV the Pa02/Fi02 at 12 hours and at the end of mechanical ventilation was < 200. Estimated pulmonary wedge pressure was 15.69 ± 3.6 and the cardiac index estimated by esophageal doppler ultrasound was 2.4 ± 0.34. AST was 160 ± 152.15, LDH was 2366.33 ± 1862.13 and CK was 216 ± 298.25. All patients received oseltamivir 150 mg every 12 hours per 10 days. Four patients died. Conclusions: Patients with ARDS/API due to influenza A H1N1 were young adults with protracted disease with fever and lymphopenia, without cardiovascular involvement and with refractory hypoxemia as the main cause of death.

CCR2 receptor antagonists: optimization of biaryl sulfonamides to increase activity in whole blood.

A series of biarylsulfonamides was identified as hCCR2 receptor antagonist but suffered from high plasma protein binding resulting in a >100 fold shift in activity in a functional GTPγS assay run in tandem in the presence and absence of human serum albumin. Introduction of an aryl amide with ethylenediamine linker led to compounds with reduced shifts and improved activity in whole blood.

Pharmacological inhibition of C-C chemokine receptor 2 decreases macrophage infiltration in the aortic root of the human C-C chemokine receptor 2/apolipoprotein E-/- mouse: magnetic resonance imaging assessment.

UNLABELLED: Purpose- This study assessed the pharmacological effect of a novel selective C-C chemokine receptor (CCR) 2 antagonist (GSK1344386B) on monocyte/macrophage infiltration into atherosclerotic plaque using magnetic resonance imaging (MRI) in an atherosclerotic mouse model. METHODS AND RESULTS: Apolipoprotein E(-/-) mice expressing human CCR2 were fed a Western diet (vehicle group) or a Western diet plus10 mg/kg per day of GSK1344386B (GSK1344386B group). After the baseline MRI, mice were implanted with osmotic pumps containing angiotensin II, 1000 ng/kg per minute, to accelerate lesion formation. After five weeks of angiotensin II administration, mice received ultrasmall superparamagnetic iron oxide, an MRI contrast agent for the assessment of monocyte/macrophage infiltration to the plaque, and underwent imaging. After imaging, mice were euthanized, and the heart and aorta were harvested for ex vivo MRI and histopathological examination. After 5 weeks of dietary dosing, there were no significant differences between groups in body or liver weight or plasma cholesterol concentrations. An in vivo MRI reflected a decrease in ultrasmall superparamagnetic iron oxide contrast agent uptake in the aortic arch of the GSK1344386B group (P<0.05). An ex vivo MRI of the aortic root also reflected decreased ultrasmall superparamagnetic iron oxide uptake in the GSK1344386B group and was verified by absolute iron analysis (P<0.05). Although there was no difference in aortic root lesion area between groups, there was a 30% reduction in macrophage area observed in the GSK1344386B group (P<0.05). CONCLUSIONS: An MRI was used to noninvasively assess the decreased macrophage content in the atherosclerotic plaque after selective CCR2 inhibition.

Mixed messages: transcription patterns in failing and recovering human myocardium.

In previous studies, mechanical support of medically refractory hearts with a left ventricular assist device (LVAD) has induced regression of many morphological and functional abnormalities characteristic of failing human hearts. To identify transcriptional adaptations in failing and LVAD-supported hearts, we performed a comprehensive transcription analysis using the Affymetrix microarray platform and 199 human myocardial samples from nonfailing, failing, and LVAD-supported human hearts. We also used a novel analytical strategy that defines patterns of interest based on multiple intergroup comparisons. Although over 3088 transcripts exhibited significantly altered abundance in heart failure, most of these did not exhibit a consistent response to LVAD support based on our analysis. Of those 238 with a consistent response to LVAD support, more than 75% exhibited persistence or exacerbation of HF-associated transcriptional abnormalities whereas only 11%, 5%, and 2% exhibited partial recovery, normalization, and overcorrection responses, respectively. Even among genes implicated by previous reports of LVAD-associated myocardial improvements, partial or complete normalization of transcription did not predominate. The magnitude of differences in transcript abundance between nonfailing and failing hearts, and between failing an LVAD-supported hearts, tended to be low with changes greater than or equal to 2-fold infrequently observed. Our results indicate that morphological or functional myocardial improvements may occur without widespread normalization of pathological transcriptional patterns. These observations also suggest that many failure-associated transcriptional changes have only a limited role in regulating cardiac structure and function and may represent epiphenomena and/or nonspecific myocardial plasticity responses. Differences in mRNA localization, translation efficiency, and posttranslational protein modifications or interactions may be more pivotal in regulating myocardial structure and function.