Estudio prospectivo aleatorizado comparativo entre colecistectomía laparoscópica versus colecistectomía por puerto único en régimen ambulatorio

IntroductionThe aim of this study is to compare laparoscopic cholecystectomy (LC) with that performed using single umbilical incision laparoscopic surgery (SILS) in a major outpatient surgery (MOS) unit.Material and methodsA total of 50 patients with symptomatic cholelithiasis were prospectively randomised between October 2009 and June 2011, with 26 of them subjected to SILS, and 24 to CL. The variables analysed were, postoperative pain, analgesia requirements, presence of nausea/vomiting, operation time, complications, outpatient success rate, and aesthetic results.ResultsThere were no differences as regards postoperative pain, analgesia rescue, nausea/vomiting, or operation time (SILS 54 ± 21 min, CL 48.5 ± 17 min, P = .29). There was one case of morbidity in the SILS group which required further surgery. The outpatient surgical procedure was completed in 77% of patients of the SILS group, and in 83% of the CL group. Six patients (23%) from the SILS group, and 4 (17%) from the CL group remained in the unit for more than 24 h (P = .58). The aesthetic results were subjectively assessed as “very good” in the SILS group, and “good” in the CL group.ConclusionSILS cholecystectomy is feasible and safe when comparing it with laparoscopic cholecystectomy in selected patients, and obtains similar results when performed in a MOS unit. Larger studies are needed to determine the real benefits of this approach before recommending it as a routine technique. With more experienced surgical teams and greater awareness of the patients could possibly increase the number of candidates for outpatient cholecystectomy.     

Autophagy-regulating TP53INP2 mediates muscle wasting and is repressed in diabetes

A precise balance between protein degradation and synthesis is essential to preserve skeletal muscle mass. Here, we found that TP53INP2, a homolog of the Drosophila melanogaster DOR protein that regulates autophagy in cellular models, has a direct impact on skeletal muscle mass in vivo. Using different transgenic mouse models, we demonstrated that muscle-specific overexpression of Tp53inp2 reduced muscle mass, while deletion of Tp53inp2 resulted in muscle hypertrophy. TP53INP2 activated basal autophagy in skeletal muscle and sustained p62-independent autophagic degradation of ubiquitinated proteins. Animals with muscle-specific overexpression of Tp53inp2 exhibited enhanced muscle wasting in streptozotocin-induced diabetes that was dependent on autophagy; however, TP53INP2 ablation mitigated experimental diabetes-associated muscle loss. The overexpression or absence of TP53INP2 did not affect muscle wasting in response to denervation, a condition in which autophagy is blocked, further indicating that TP53INP2 alters muscle mass by activating autophagy. Moreover, TP53INP2 expression was markedly repressed in muscle from patients with type 2 diabetes and in murine models of diabetes. Our results indicate that TP53INP2 negatively regulates skeletal muscle mass through activation of autophagy. Furthermore, we propose that TP53INP2 repression is part of an adaptive mechanism aimed at preserving muscle mass under conditions in which insulin action is deficient.     

Infectious discitis caused by Enterobacter cloacae.

The case is reported of a patient who developed a vertebral osteomyelitis caused by Enterobacter cloacae. The organism was isolated in cultures of blood and vertebral puncture biopsy samples. The patient was satisfactorily treated with trimethroprim and sulphamethoxazole. Enterobacter cloacae, a Gram negative organism, has been confirmed as the cause of bacteremia in patients with burns, urinary infections, in adults with pneumonia, and in children with joint infections. Spondylodiscitis caused by Enterobacter cloacae has not previously been described.     

Bone metastases

Bone metastases represent a devastating clinical problem in the most frequent neoplasies, especially in multiple myeloma, tumours breast, prostate and lung. The consequences include pain which is refractory to conventional analgesics, osteolysis often leading to bone-marrow compression and pathological fractures, and metabolic disorders. Recent advances in diagnosis using imaging techniques as well as different biochemical techniques have helped accurate diagnosis and follow-up. The increase in survival has improved through a multimodal approach combining, inhibition of osteolysis, with prophylactic orthopaedic surgery and radiation therapy. Recent advances in basic research have determined the molecular metastatic that can predict its proclivity to metastasize. Basic research will improve understanding of the basic mechanisms and lead to the clarification of molecular targets that will help in the development of medicines capable of preventing, decreasing or blocking the metastatic process.     

Relationship of C-reactive protein levels with angiographic findings and markers of necrosis in non-ST-segment elevation acute coronary syndrome

INTRODUCTION AND OBJECTIVES: The mechanism responsible for elevated C-reactive protein levels (inflammation of the ruptured atherosclerotic plaque or myocardial necrosis) in acute coronary syndromes is controversial. The aim of this study was to investigate the relationship between C-reactive protein levels and angiographic complexity of the culprit lesion and troponin elevation in patients with non-ST elevation acute coronary syndromes. PATIENTS AND METHOD: The study group consisted of 125 patients with single-vessel disease. Troponin-I and C-reactive protein were measured, and the complexity of the culprit lesion was analyzed (TIMI flow and thrombus). Information on age, sex, smoking habit, hypertension, hypercholesterolemia and diabetes was obtained from the medical record. RESULTS: The quartile distribution of C-reactive protein showed more patients with TIMI flow < 3 (31%, 28%, 18%, and 55%; P=.02), thrombus (3%, 6%, 7%, and 28%; P=.007) and troponin-I elevation (19%, 44%, 50%, and 66%; P=.003) in the fourth quartile. Multivariate analysis showed both thrombus (OR = 4.1; 95% CI, 1.2-14.3; P=.03) and troponin elevation (OR = 2.6; 95% CI, 1.1-6.3; P=.03) to be associated with C-reactive protein > 18 mg/L (fourth quartile cut-off). When treated as a continuous variable, higher levels of C-reactive protein were also associated with thrombus (P=.02) and troponin elevation (P=.003). No other clinical variables were related with C-reactive protein levels. CONCLUSIONS: Both angiographic complexity of the culprit lesion and elevated troponin level are related with increased C-reactive protein levels in non-ST elevation acute coronary syndromes.     

Evidence that deletion at FCGR3B is a risk factor for systemic sclerosis

There is increasing evidence that gene copy number (CN) variation influences clinical phenotype. The low-affinity Fc receptor 3B (FCGR3B) located in the FCGR gene cluster is a CN polymorphic gene involved in the recruitment of polymorphonuclear neutrophils to sites of inflammation and their activation. Given the genetic overlap between systemic lupus erythematosus and systemic sclerosis (SSc) and the strong evidence for FCGR3B CN in the pathology of SLE, we hypothesised that FCGR3B gene dosage influences susceptibility to SSc. We obtained FCGR3B deletion status in 777 European Caucasian cases and 1000 controls. There was an inverse relationship between FCGR3B CN and disease susceptibility. CN of 1 was a significant risk factor for SSc (OR=1.55 (1.13-2.14), P=0.007) relative to CN2. Although requiring replication, these results suggest that impaired immune complex clearance arising from FCGR3B deficiency contributes to the pathology of SSc, and FCGR3B CN variation is a common risk factor for systemic autoimmunity.     

Effectiveness of the relative lymphocyte count to predict one-year mortality in patients with acute heart failure

Several works have endorsed a significant role of the immune system and inflammation in the pathogenesis of heart failure. As indirect evidence, an association between a low relative lymphocyte count (RLC%) and worse outcomes found in this population has been suggested. Nevertheless, the role of RLC% for risk stratification in a large and nonselected population of patients with acute heart failure (AHF) has not yet been determined. Thus, the aim of this study was to determine the association between low RLC% and 1-year mortality in patients with AHF and consequently to define whether it has any role for early risk stratification. A total of 1,192 consecutive patients admitted for AHF were analyzed. Total white blood cell and differential counts were measured on admission. RLC% (calculated as absolute lymphocyte count/total white blood cell count) was categorized in quintiles and its association with all-cause mortality at 1 year assessed using Cox regression. At 1 year, 286 deaths (24%) were identified. A negative trend was observed between 1-year mortality rates and quintiles of RLC%: 31.5%, 27.2%, 23.1%, 23%, and 15.5% in quintiles 1 to 5, respectively (p for trend <0.001). After thorough covariate adjustment, only patients in the lowest quintile (<9.7%) showed an increased risk for mortality (hazard ratio 1.76, 95% confidence interval 1.17 to 2.65, p = 0.006). When RLC% was modeled with restricted cubic splines, a stepped increase in risk was observed patients in quintile 1: those with RLC% values <7.5% and <5% showed 1.95- and 2.66-fold increased risk for death compared to those in the top quintile. In conclusion, in patients with AHF, RLC% is a simple, widely available, and inexpensive biomarker, with potential for identifying patients at increased risk for 1-year mortality.