[Heptopulmonary syndrome]. / Síndrome hepatopulmonar.

Hepatopulmonary syndrome is characterized by the presence of liver disease, pulmonary vascular dilatations, and arterial hypoxemia. It is usually associated with cirrhosis of any origin, but has been described in other liver diseases, both acute and chronic, and not always associated with portal hypertension. The gold standard method to detect pulmonary vascular dilations is contrast enhancement echocardiography with saline and is essential for the diagnosis of hepatopulmonary syndrome. These dilatations reflect changes in the pulmonary microvasculature (vasodilatation, intravascular monocyte accumulation, and angiogenesis) and induce a ventilation/perfusion mismatch, or even true intrapulmonary shunts, which eventually trigger hypoxemia. This syndrome worsens patients' prognosis and impairs their quality of life and may lead to the need for liver transplantation, which is the only effective and definitive treatment. In this article, we review the etiological, pathophysiological, clinical and therapeutic features of this syndrome.

Increased soluble CD36 is linked to advanced steatosis in nonalcoholic fatty liver disease.

BACKGROUND: Soluble CD36 (sCD36) clusters with insulin resistance, but no evidence exists on its relationship with hepatic fat content. We determined sCD36 to assess its link to steatosis in nonalcoholic fatty liver disease (NAFLD) and chronic hepatitis C (CHC) patients. MATERIALS AND METHODS: Two hundred and twenty-seven NAFLD, eighty-seven CHC, and eighty-five patients with histologically normal liver (NL) were studied. Steatosis was graded by Kleiner's histological scoring system. Serum sCD36 and hepatic CD36 expression was assessed by immunoassay and immunohistochemistry, respectively. RESULTS: In NAFLD, serum sCD36 levels were significantly higher in simple steatosis than in NL (361.4 ± 286.4 vs. 173.9 ± 137.4 pg/mL, respectively; P < 0.001), but not in steatohepatitis (229.6 ± 202.5 pg/mL; P = 0.153). In CHC, serum sCD36 levels were similar regardless of the absence (428.7 ± 260.3 pg/mL) or presence of steatosis (387.2 ± 283.6 pg/mL; P = 0.173). A progressive increase in serum sCD36 values was found in NAFLD depending on the histological grade of steatosis (P < 0.001), but not in CHC (P = 0.151). Serum sCD36 concentrations were independently associated with advanced steatosis in NAFLD when adjusted by demographic and anthropometric features [odds ratio (OR), 1.001; 95% confidence interval (CI), 1.000 to 1.002; P = 0.021] and by metabolic variables (OR, 1.002; 95% CI, 1.000 to 1.003; P = 0.001). Interestingly, a significant correlation was observed between hepatic CD36 and serum sCD36 (ρ = 0.499, P < 0.001). CONCLUSIONS: Increased serum sCD36 is an independent factor associated with advanced steatosis in NAFLD.

Neumonía en pacientes con demencia avanzada: enfoque terapéutico adoptado en un servicio de medicina interna de un hospital de media y larga estancia / Pneumonia in patients with advanced dementia: therapeutic approach adopted in an internal medicine service at a medium-to-long stay hospital

Introducción: La demencia es una enfermedad prevalente en las sociedades desarrolladas. La neumonía es la principal causa de muerte de los pacientes con demencia avanzada (DA). Numerosos expertos son partidarios de la adopción de un enfoque paliativo en estos enfermos. Objetivo: Conocer el tratamiento dispensado a pacientes con DA ingresados por neumonía en el Servicio de Medicina Interna de nuestro hospital. Metodología: Estudio retrospectivo con análisis de historias clínicas de 149 pacientes con DA que ingresan en nuestro servicio con neumonía del 1 de marzo de 2013 al 1 de junio de 2018. Resultados: Se incluyeron 149 sujetos. 147 (98 %) recibieron antibióticos i.v. 137 (91 %) sueroterapia i.v. Se realizaron 2,95 extracciones de sangre venosa por persona. A 22 (14 %) se les realizó al menos una gasometría arterial. 116 (77,8 %) portaron sonda urinaria. Se registraron 1,6 cambios de vía por persona. Se realizaron 10 sondajes nasogástricos (6,7). 64 fallecieron durante el ingreso (42,9 %). 35 (53,5 %) de ellos lo hicieron mientras recibían tratamientos encaminados a su curación. En tres la actitud fue puramente paliativa desde el principio. En 26 (40,6 %) la media de días que pasaron desde el primer día hasta la adopción de una estrategia puramente paliativa fue 13,3. De los 29 que fallecieron habiéndose adoptado dicho enfoque, 24 fueron sedados y fallecieron al cabo de 37,7 horas de media. En las últimas 48 horas de vida, 52 (81,2 %) presentaron síntomas y se realizaron numerosas pruebas o intervenciones. Conclusión: El enfoque terapéutico adoptado en nuestro servicio fue predominantemente curativo, medicalizado y alejado de una atención centrada en el paciente. (AU)

Introduction: Dementia is a prevalent disease in developed societies. Pneumonia is the leading cause of death in patients with advanced dementia (AD). Numerous experts are in favor of adopting a palliative approach in these patients. Objective: To analyze the treatment given to patients with AD admitted for pneumonia in the Internal Medicine Service of our hospital. Methodology: A retrospective study of the medical records of 149 patients with AD admitted for pneumonia in our service between 1/3/2013 and 1/6/2018. Results: A total of 149 patients were included; 147 (98 %) patients received intravenous antibiotics, 137 (91 %) received intravenous hydratation; 2.95 venous blood collections per person were performed; 22 (14 %) patients underwent at least one arterial gasometry; 116 (77.8 %) carried a urinary catheter; 1.6 changes of peripheral venous catheter were recorded per person; 10 (6.7 %) nasogastric tubes were placed; 64 (42.9 %) died during hospital stay; 35 (53.5 %) of them died while receiving treatments with curative intent. In 3 a purely palliative approach was selected from the beginning. In the remaining 26 patients the average number of days elapsed until a totally palliative approach was adopted was 13.3. Of the 29 patients who died with the latter approach, 24 were sedated and died after 37 hours on average. In the last 48 hours of life, 52 (81.2) presented symptoms and numerous tests or interventions were performed. Conclusion: The therapeutic approach adopted in our patients was predominantly curative, and still far removed from patient-centered care. (AU)

Síndrome hepatopulmonar / Heptopulmonary síndrome

El síndrome hepatopulmonar está caracterizado por la existencia de enfermedad hepática, dilatación vascular pulmonar e hipoxemia arterial. Generalmente se asocia a una cirrosis hepática de cualquier origen aunque se ha descrito en otras enfermedades hepáticas, tanto agudas como crónicas, y no siempre asociada a la hipertensión portal. La ecocardiografía con contraste es el estándar de oro para el diagnóstico de las dilataciones vasculares pulmonares y fundamental por tanto para el diagnóstico del síndrome hepatopulmonar. Estas dilataciones reflejan cambios en la microvascularización pulmonar (vasodilatación, acúmulo intravascular de monocitos y angiogénesis) e inducen un desequilibrio en la relación ventilación/perfusión, o incluso verdaderos shunts, que finalmente desencadenan la hipoxemia. El síndrome hepatopulmonar empobrece el pronóstico y la calidad de vida de los pacientes y puede determinar la necesidad de un trasplante hepático que es el único tratamiento de eficacia demostrada. En el presente artículo se revisan los principales aspectos etiopatogénicos, fisiopatológicos, clínicos y terapéuticos de este síndrome

Hepatopulmonary syndrome is characterized by the presence of liver disease, pulmonary vascular dilatations, and arterial hypoxemia. It is usually associated with cirrhosis of any origin, but has been described in other liver diseases, both acute and chronic, and not always associated with portal hypertension. The gold standard method to detect pulmonary vascular dilations is contrast enhancement echocardiography with saline and is essential for the diagnosis of hepatopulmonary syndrome. These dilatations reflect changes in the pulmonary microvasculature (vasodilatation, intravascular monocyte accumulation, and angiogenesis) and induce a ventilation/perfusion mismatch, or even true intrapulmonary shunts, which eventually trigger hypoxemia. This syndrome worsens patients’ prognosis and impairs their quality of life and may lead to the need for liver transplantation, which is the only effective and definitive treatment. In this article, we review the etiological, pathophysiological, clinical and therapeutic features of this syndrome