Postoperative arterial hypotension: the unnoticed enemy.

Postoperative hypotension is a frequently underestimated health problem associated with high morbidity and mortality and increased use of health care resources. It also poses significant clinical, technological, and human challenges for healthcare. As it is a modifiable and avoidable risk factor, this document aims to increase its visibility, defining its clinical impact and the technological challenges involved in optimizing its management, taking clinical-technological, humanistic, and economic aspects into account.

Optimización del uso de Agentes estimulantes del Receptor de la Eritropoyetina (AREs) en pacientes con neoplasias hematológicas basado en el nivel de hemoglobina reticulocitaria / Optimizing the use of Erythropoietin-Receptor stimulating Agents (ERAs) in patients with hematopoietic malignancies based on the level of reticulocyte hemoglobin

Los agentes estimulantes del Receptor de la Eritropoyetina (AREs) se usan en el tratamiento de la anemia de hemopatías malignas (HM). Sin embargo, la tasa de respuestas es variable por diversos factores como el déficit funcional de hierro (DFF). El nivel de hemoglobina (Hb) reticulocitaria es un parámetro fácil de obtener que ha mostrado su utilidad en el diagnóstico del DFF. El objetivo de este estudio fue identificar qué pacientes con HM tratados con AREs presentan DFF y si la Hb reticulocitaria predice la respuesta hemoglobínica en estos enfermos. Se incluyeron 42 pacientes con diagnostico de Mieloma Múltiple (n=17), Linfoma no Hodgkin (n=14), Linfoma de Hodgkin (n=3), Leucemia Linfática Crónica (n=4), Síndrome Mielodisplásico (n=2), Leucemia Linfoblástica Aguda (n=1) y Leucemia Mieloblástica Aguda (n=1). Veinticinco fueron tratados con Epoetina-beta, diez y seis con Darbepoetina y uno con Epoetina alfa.La respuesta fue favorable en el 28%, 53% y 58% de lospacientes a las 3, 6 y 12 semanas de tratamiento, respectivamente. Se detectó DFF en el 17% de los pacientes. En cuanto a la respuesta, no hubo diferencias estadísticamente significativas entre los pacientes con y sin DFF, si bien, a mitad de tratamiento, fue ligeramente superior en el grupo sin DFF (57% vs 43%, p>0.05). El nivel basal de Hb reticulocitaria se correlacionó con el grado de respuesta global a las 12 semanas de finalizar el tratamiento. Así, el 79% de los pacientes respondedores tenían una Hb reticulocitaria inicial >36·5 pg, mientras que este porcentaje bajó al 30% en los no respondedores (p = 0.024)En resumen, la Hb reticulocitaria es un método sensible ypreciso para detectar DFF en pacientes con HM bajo tratamiento con AREs. Además, un nivel elevado de Hb reticulocitaria basal es un parámetro que se asocia con respuesta favorable al tratamiento

The Erythropoietin-Receptor stimulating Agents (ERAs) areindicated in the supportive treatment of the anemia in hematological malignancies (HM). However, the response rate is variable due to factors such as the functional iron deficiency (FID). The level of the reticulocyte hemoglobin (RHb) is an easy-to-obtain parameter very useful for the diagnostic of the FID.The purpose of this study was to evaluate which patientswith HM treated with ERAs present FID. In addition, wetried to asses if the level of RH predicts the response in these patients.We included 42 patients with the following diagnostics:Multiple Myeloma (n= 17), Non Hodgkin Lymphoma(n=14), Hodgkin Lymphoma (n=3), Chronic lymphocyticLeukemia (n=4), Myelodisplastic syndrome (n=2), Acutelymphoblastic Leukemia (n=1), and Acute mieloblasticLeuKemia (n=1). Twenty five of them were treated withEpoetin beta, sixteen with darbepoetin alfa and one withEpoetin alfa at standard doses. The response was favorable in 28%, 53% and 58% of patients at the third, sixth and twelfth week of the treatment, respectively. FID was detected in 17% of the patients. Theresponse rate was not statistical significant different between patients with and without FID, although it was slightly superior in the group without FID (57% vs. 43%, p>0.05). Seventy nine percent of patients with a favorable response at twelve weeks showed an initial RH >36·5 pg, while this percentage was only 30% in patients who did not respond (p=0.024).In conclusion, RH is a sensitive and specific method to detect FID in patients with HM who are treated with ERAs.Furthermore, the high level of RH at the baseline is a predictor of favorable response of treatment, in these patients

Mitochondrial phylogeography and demographic history of the vicuña: implications for conservation.

The vicuña (Vicugna vicugna; Miller, 1924) is a conservation success story, having recovered from near extinction in the 1960s to current population levels estimated at 275,000. However, lack of information about its demographic history and genetic diversity has limited both our understanding of its recovery and the development of science-based conservation measures. To examine the evolution and recent demographic history of the vicuña across its current range and to assess its genetic variation and population structure, we sequenced mitochondrial DNA from the control region (CR) for 261 individuals from 29 populations across Peru, Chile and Argentina. Our results suggest that populations currently designated as Vicugna vicugna vicugna and Vicugna vicugna mensalis comprise separate mitochondrial lineages. The current population distribution appears to be the result of a recent demographic expansion associated with the last major glacial event of the Pleistocene in the northern (18 to 22 degrees S) dry Andes 14-12,000 years ago and the establishment of an extremely arid belt known as the 'Dry Diagonal' to 29 degrees S. Within the Dry Diagonal, small populations of V. v. vicugna appear to have survived showing the genetic signature of demographic isolation, whereas to the north V. v. mensalis populations underwent a rapid demographic expansion before recent anthropogenic impacts.

[Abdominal tuberculosis in patients with acquired immunodeficiency syndrome]. / Tuberculosis abdominal en los pacientes con síndrome de inmunodeficiencia adquirida.

BACKGROUND: In individuals with HIV infection, extrapulmonary forms of tuberculosis are considered as opportunistic infections and are included in the diagnosis of AIDS. They often have atypical clinical features. Abdominal participation is uncommon and its diagnosis may be difficult. METHODS: The clinical, radiological and pathological features of patients with a diagnosis of AIDS with abdominal tuberculosis in a series of 254 AIDS cases in a general hospital from 1984 to October 1990 were reviewed. RESULTS: Tuberculosis developed in 104 (41%) of AIDS patients. In 25 (24%) the disease was exclusively pleuropulmonary and in 79 (76%) extrapulmonary tuberculosis was present, either alone or in association. Extrapulmonary tuberculosis was the first opportunistic infection in 66 AIDS cases (26%). The abdominal participation was demonstrated in 19 patients, with the following localizations: lymph nodes (9), liver (8), spleen (5), ileum (1) and peritoneum (1). Four patients with splenic tuberculosis also had multifocal nodular lesions. CONCLUSIONS: Abdominal participation was found in 19 of the 104 AIDS patients with tuberculosis (18%). Lymph node involvement was the most common type. Hepatosplenic tuberculosis had a miliary form or showed multifocal images in echography or computed tomography.

Effects of oral hydralazine on gas exchange in patients with cor pulmonale.

Vasodilators lower total pulmonary vascular resistance in some patients with pulmonary hypertension, but if vasodilators worsen arterial oxygenation in cor pulmonale, as they do in some patients with left ventricular failure, the benefits of a decrease in vascular resistance would be offset by a lack of change or a deterioration in systemic oxygen delivery. Measurement was made of arterial and mixed venous blood gases, minute ventilation, shunt fraction, alveolar-arterial oxygen difference, pulmonary arterial pressures, and cardiac output before and four hours after a single dose of hydralazine, 75 mg orally, in six patients (Group I) and before and after 48 hours of hydralazine, 50 to 75 mg orally, every six hours in 10 patients (Group II). Cardiac output increased 36 percent in Group I and 48 percent in Group II. In both groups total pulmonary vascular resistance decreased (8.0 +/- 2.8 to 6.1 +/- 2.6 units in Group I, p less than 0.01; 9.7 +/- 3.7 to 5.6 +/- 2.1 units in Group II, p less than 0.01). Arterial PO2 increased significantly both in Group I (61 +/- 8 to 67 +/- 10 torr, p less than 0.05) and Group II (50 +/- 13 to 54 +/- 13, p less than 0.05); however shunt fraction and alveolar-arterial oxygen difference were unchanged. The ratio of dead space to tidal volume decreased slightly in both groups, and minute ventilation increased significantly. Systemic oxygen delivery was increased by 39 and 51 percent in Groups I and II, respectively. Thus, gas exchange may be preserved or improved when hydralazine is used in the treatment of cor pulmonale.

Disordered breathing and hypoxia during sleep in coronary artery disease.

The occurrence of breathing disorders and hypoxia during sleep was studied in 17 male patients with coronary artery disease, demonstrated by coronary angiography, who did not have symptomatic pulmonary disease. Thirteen patients (76 percent) experienced disordered breathing during sleep; of these, 11 had obstructive apnea and the other two had Cheyne-Stokes breathing. There was an average of 20 episodes of disordered breathing per hour during sleep among the 13 patients, with a mean duration of 24 seconds per episode; significant oxygen desaturation occurred in ten of these 13 patients. There was no episode of angina pectoris, myocardial infarction or sudden death. Although cardiac arrhythmias occurred in 12 patients, disordered breathing with hypoxia was not proven to be causative. Therefore, obstructive disordered breathing and nocturnal oxygen desaturation commonly occurred during sleep in patients with coronary artery disease. Although no immediate ill effects were noted, the longterm effects remain to be determined.

Mixed venous oxygenation in fatal gram-negative septicemia.

Changes in mixed venous and arterial PO2 values were examined during the early, middle and late stages of fatal gram-negative septicemia in seven patients. The early stage of septicemia was characterized by tachycardia (mean rate 108/min), mild hypotension (mean arterial pressure (MAP) 83 mmHg), arterial hypoxemia requiring supplemental oxygen therapy, and high, low or normal mixed venous PO2 (mean 37 mmHg). During the middle stage, hypotension was severe (MAP 67 mmHg) and mixed venous PO2 invariably rose (mean 50 mmHg). Arterial PO2 increased in association with the rise in mixed venous PO2, despite constant FIO2 and expired ventilation. Severe metabolic acidosis developed in six of the seven patients. In the final stage, mixed venous PO2 was normal (mean 42 mmHg) in the presence of continuing metabolic acidosis. We postulate that the elevations of mixed venous PO2 seen result from systemic arterial-venous shunting, and that during septicemia, the mixed venous PO2 is an unreliable index of tissue oxygenation. A theoretical model of the relationship of tissue oxygenation and mixed venous oxygenation in septicemia, based upon the above study, is presented.

Evidence for abnormal regulation of circulating 1 alpha,25-dihydroxyvitamin D in patients with sarcoidosis and normal calcium metabolism.

The effects of vitamin D, 2.5 mg (100,000 U)/d for 4 d, on serum calcium, serum 25-hydroxyvitamin D (25-OHD), and serum 1 alpha,25-dihydroxyvitamin D [1 alpha,25(OH)2D] were compared in 17 normal subjects and 6 patients with sarcoidosis who had normocalcemia and no history of hypercalcemia. The diagnosis was confirmed histologically in each of them. Vitamin D increased mean serum 25-PHD from 30 +/- 4 to 99 +/- 15 ng/ml (P < 0.001) and did not change mean serum 1 alpha,25(OH)2D (32 +/- 3 vs. 29 +/- 3 pg/ml) or mean serum calcium (9.5 +/- 0.1 vs. 9.6 +/- 0.1 mg/dl) in the normal subjects. In contrast, vitamin D increased mean serum 25-OHD from 19 +/- 3 to 65 +/- 19 ng/ml (p < 0.05), increased mean serum 1 alpha,25(OH)2D threefold from 40 +/- 7 to 120 +/- 24 pg/ml, and increased mean serum calcium from 9.4 +/- 0.2 to 9.8 +/- 0.2 mg/dl (P < 0.01). There was a significant positive correlation between the serum 1 alpha,25(OH)2D and serum calcium in these individuals (r = 0.663, P < 0.01) but not in the normal subjects. The results (a) provide further evidence for abnormal regulation of circulating 1 alpha,25(OH)2D in sarcoidosis and (b) indicate that the abnormality may exist in patients with normal calcium metabolism. Thus, the defect in vitamin D metabolism in sarcoid apparently is more common than was previously recognized.