[Beyond acute SARS-CoV-2 infection: A new challenge for Internal Medicine]. / Más allá de la infección aguda por SARS-CoV-2: un nuevo desafío para la Medicina Interna.

Infection with the new SARS-CoV-2 coronavirus has reached pandemic proportions, with a very high death toll worldwide. Despite the scientific community's strenuous efforts to address this disease in its acute phase, as well as in prevention through the development of vaccines in record time, there remains another important workhorse: understanding and treating the persistence of symptoms beyond the acute phase, the so-called protracted COVID-19 syndrome or persistent COVID. These persistent manifestations affect several organs and systems and may depend on both the pathogenic mechanisms of the virus and the pathophysiological response of the patient. One year after the onset of this pandemic, there is an urgent need to address this situation from a comprehensive approach.

Renal function at admission as a prognostic marker for patients hospitalised for a first episode of heart failure. Results of the PREDICE study. / Función renal al ingreso como marcador pronóstico en pacientes hospitalizados por un primer episodio de insuficiencia cardíaca. Resultados del estudio PREDICE.

BACKGROUND AND OBJECTIVE: Heart failure (HF) is a frequent condition that deteriorates quality of life and results in high morbidity and mortality. A considerable number of studies have been implemented in recent years to determine the factors that affect the prognosis of HF; however, few studies have assessed the prognosis of patients hospitalised for their first episode of HF. The aim of our study was to analyse the prognostic impact of renal function on patients hospitalised for a first episode of HF. MATERIAL AND METHODS: We recruited 600 patients hospitalised for a first episode of HF in 3 tertiary Spanish hospitals. We analysed the mortality risk during the first year of follow-up according to renal function at the time of admission. RESULTS: The patients with the highest degree of kidney failure at admission were older (P<.001), were more often women (p=.01) and presented a higher degree of dependence (P<.05), as well as a higher prevalence of arterial hypertension (P<.001), chronic renal failure (P<.001) and anaemia (P<.001). In the multivariate analysis, the degree of kidney failure at admission remained an independent predictor of increased mortality risk during the first year of follow-up. CONCLUSIONS: The presence of kidney failure at admission was a marker of poor prognosis in our cohort of patients hospitalised for a first episode of HF.

Decreased lipid metabolism but increased FA biosynthesis are coupled with changes in liver microRNAs in obese subjects with NAFLD.

BACKGROUND/OBJECTIVE: Many controversies regarding the association of liver miRNAs with obesity and nonalcoholic fatty liver diseases (NAFLD) call for additional validations. This study sought to investigate variations in genes and hepatic miRNAs in a sample of obese patients with or without NAFLD and human hepatocytes (HH). SUBJECTS/METHODS: A total of 60 non-consecutive obese women following bariatric surgery were recruited. Subjects were classified as NAFLD (n=17), borderline (n=24) and controls (n=19) with normal enzymatic profile, liver histology and ultrasound assessments. Profiling of 744 miRNAs was performed in 8 obese women with no sign of hepatic disease and 11 NAFLD patients. Additional validation and expression of genes related to de novo fatty acid (FA) biosynthesis, uptake, transport and ß-oxidation; glucose metabolism, and inflammation was tested in the extended sample. Induction of NAFLD-related genes and miRNAs was examined in HepG2 cells and primary HH treated with palmitic acid (PA), a combination of palmitate and oleic acid, or high glucose, and insulin (HG) mimicking insulin resistance in NAFLD. RESULTS: In the discovery sample, 14 miRNAs were associated with NAFLD. Analyses in the extended sample confirmed decreased miR-139-5p, miR-30b-5p, miR-122-5p and miR-422a, and increased miR-146b-5p in obese subjects with NAFLD. Multiple linear regression analyses disclosed that NAFLD contributed independently to explain miR-139-5p (P=0.005), miR-30b-5p (P=0.005), miR-122-5p (P=0.021), miR-422a (P=0.007) and miR-146a (P=0.033) expression variance after controlling for confounders. Decreased miR-122-5p in liver was associated with impaired FA usage. Expression of inflammatory and macrophage-related genes was opposite to decreased miR-30b-5p, miR-139-5p and miR-422a, whereas increased miR-146b-5p was associated with FABP4 and decreased glucose metabolism and FA mobilization. In partial agreement, PA (but not HG) led to decreased miR-139-5p, miR-30b-5p, miR-422a and miR-146a in vitro, in parallel with increased lipogenesis and FA transport, decreased glucose metabolism and diminished FA oxidation. CONCLUSION: This study confirms decreased liver glucose and lipid metabolism but increased FA biosynthesis coupled with changes in five unique miRNAs in obese patients with NAFLD.

Inflammation and insulin resistance exert dual effects on adipose tissue tumor protein 53 expression.

OBJECTIVE: The purpose of this study was to investigate the expression of human adipose tissue protein 53 (p53) in subjects who varied widely in terms of obesity and insulin resistance. We also analyzed different in vivo and in vitro models to try to comprehend the associations found in humans. METHODS: p53 was analyzed in human adipose and isolated adipocytes, in high fat-fed and GLP-1R KO mice, during in vitro adipogenesis, and in adipocytes after high glucose, rosiglitazone and inflammatory conditions. The effects of surgery-induced weight loss and ex vivo metformin were also evaluated. RESULTS: Omental (OM) p53 gene expression (+27%, P=0.001) and protein (+11%, P=0.04) were increased in obese subjects and high fat diet-induced obese mice (+86%, P=0.018). Although the obesity-associated inflammatory milieu was associated with increased OM p53, this was negatively related to insulin resistance and glycated hemoglobin, and positively with biomarkers for insulin sensitivity. Multiple linear regression analyses revealed that glycated hemoglobin (P<0.0001) and body mass index (P=0.048) contributed independently to explain 13.7% (P<0.0001) of the OM p53 variance. Accordingly, the improvement of insulin sensitivity with surgery-induced weight loss (+51%, P=0.01) and metformin (+42%, P=0.02) led to increased adipose p53. While the glucose-intolerant GLP-1R KO mice showed decreased mesenteric p53 (-45.4%, P=0.017), high glucose led to decreased p53 in pre-adipocytes (-27%, P<0.0001). Inflammatory treatments led to increased p53 (+35%, P<0.0001), while Rs downregulated this expression (-40%, P=0.005) in mature adipocytes. CONCLUSION: Inflammation and insulin resistance exert dual effects on adipose p53, which seems to be the final result of these opposing forces.

The lung innate immune gene surfactant protein-D is expressed in adipose tissue and linked to obesity status.

BACKGROUND: Surfactant protein-D (SFTPD) is a component of the lung innate immunity that enhances clearance of pathogens and modulates inflammatory responses. An inverse association of putative, lung-derived circulating SFTPD with obesity has been reported but no information is available concerning possible SFTPD gene expression in human adipose tissue. METHODS: SFTPD gene expression was analyzed in human omental (OM; n=156) and subcutaneous (SC; n=106) adipose tissue, and in isolated fat cells (n=12) in association with measures of obesity and glucose tolerance. RESULTS: SFTPD gene was expressed in human adipose tissue and adipocytes. This expression was decreased in OM and SC adipose tissue from obese subjects with (-47%, P<0.0001; and -37%, P=0.048) and without (-34%, P=0.001; and -22%, P=0.08; respectively) type 2 diabetes when compared with the control group. Indeed, OM SFTPD was inversely associated with body mass index (r=-0.33, P<0.0001), percent fat mass (r=-0.36, P<0.0001), waist perimeter (r=-0.26, P=0.002), diastolic blood pressure (r=-0.21, P=0.018) and fasting glucose (r=-0.21, P=0.012); and positively linked to the expression of insulin receptor substrate 1 (IRS1; r=0.25, P=0.004), perilipin A (PLIN; r=0.38, P=0.007) and fatty acid synthase (FASN; r=0.36, P<0.0001). Accordingly, increased SFTPD (4.5-fold, P=0.02) was detected in isolated adipocytes when compared with the stromal-vascular cell fraction, in parallel to IRS1, FASN and PLIN. CONCLUSIONS: Both OM and SC adipose tissue (mainly mature adipocytes) express SFTPD. This expression decreases with obesity and impaired glucose tolerance.

Inflammation in adipose tissue and fatty acid anabolism: when enough is enough!

Recent findings in adipose tissue (AT) have uncovered negative interactions among obesity, lipogenesis, and fatty acid (FA) storage, perhaps in response to the increased production of proinflammatory cytokines and transcription factors. Emerging evidence highlights that local hypoxia, generation of reactive oxygen and nitrogen species, increased immune cells infiltration and activation, senescence, inflammation, energy consumption, and decreased lipogenesis in the AT are interrelated and may lead to impaired cytokine and hormonal secretion by adipocytes, and ectopic fat deposition in obesity that strengths the increased risk of suffering metabolic disorders in obese subjects. The information summarized in this review attempts to defend the interdependent relationship of these proofs of concept, supporting the idea that "inflamed" and "dysfunctional" AT are synonymous when referring to obesity. This may happen in severe obese subjects with a large and long-lasting fat excess, when fat depots have reached the point in which excessive fat storage, cell density, and diminished oxygen availability promote decreased lipo/adipogenesis and increased lipolysis and FA release. This response may be induced by an important inflammatory component that promotes angiogenesis and insulin resistance, but also by leptin and the increase of T3 in hyperplastic AT.

Type I iodothyronine 5'-deiodinase mRNA and activity is increased in adipose tissue of obese subjects.

Differentiation and metabolism of adipose tissue are modulated by thyroid hormones (THs), but relatively little is known about the metabolism of THs in this tissue. Expression of the genes for type I iodothyronine 5'-deiodinase (D1), leptin (LEP) and stearoyl-CoA desaturase 1 (SCD-1) was evaluated in omental (OM) and subcutaneous (SC) fat using a cohort of 70 humans. Activities of iodothyronine deiodinases (D1, D2 and D3) were assessed in a randomly selected subpopulation of 19 subjects. D1 expression was upregulated in both OM (P=0.011) and SC (P=0.003) fat of obese subjects. Concomitantly, OM (P=0.002) and SC (P=0.028) LEP expression were increased in obesity, associated with both D1 mRNA (r=0.315, P=0.014) and activity (r=0.647, P=0.023) and inversely related to SCD-1 (r=-0.266, P=0.034) expression in SC fat. Also D1 (but not D2 and D3) activity was increased in OM (∼fourfold, P=0.010) and SC (∼eightfold, P=0.004) fat of obese when compared with non-obese subjects and correlated in both OM (r=0.528, P=0.036) and SC (r=0.749, P=0.005) fat with body mass index. Our results document increased D1 gene expression and activity in adipose tissue of obese humans and suggest a role of 3,5,3'-triiodo-L-thyronine formed by D1 in response to leptin in the modulation of adipose tissue metabolism.

Sensorimotor effects of plasticity-inducing percutaneous peripheral nerve stimulation protocols: a blinded, randomized clinical trial.

BACKGROUND: Electrical stimulation of skin afferents can induce somatosensory plasticity in humans. Nevertheless, it is unknown if this is possible to do through percutaneous stimulation of a peripheral nerve, which will allow for regional anaesthesia interventions. Furthermore, potentiation protocols applied over mainly non-nociceptive fibres inhibit nociception in rodents, but this has not been tested in humans. OBJECTIVE: To determine whether a protocol aiming to depress the nociceptive circuit and another aiming to potentiate non-nociceptive circuits produce regional hypoalgesia and changes in motor function, applied through percutaneous peripheral nerve stimulation (pPNS), and to assess which of them is more promising for pain relief, immediately and 24 h after the intervention. METHODS: PT-cLF protocol aims to depress the nociceptive pathway through Pain Threshold, continuous Low Frequency stimulation and ST-bHF aims to produce potentiation of the non-nociceptive pathway, through Sensory Threshold burst stimulation at High Frequency. All subjects (n = 29) went through both protocols and a control condition in a randomized and blinded crossover design. RESULTS: Compared to control, ST-bHF induced distal hypoalgesia, towards electrical (p = 0.04) and mechanical stimuli (p = 0.02) and produced mechanical hypoesthesia (p = 0.02). Contrarily, hypoalgesia was not observed after PT-cLF (p > 0.05) but increased electrical motor threshold (p = 0.04), reduced motor recruitment (p = 0.03), and the subjects reported feeling reduced strength (p < 0.01). CONCLUSION: This works provides evidence that is possible to induce antinociceptive plasticity in a wide territory using pPNS. Moreover, it demonstrates for the first time in humans that a protocol aiming to produce long-term potentiation applied predominantly over non-nociceptive afferents induces hypoesthesia and hypoalgesia.

Beyond acute SARS-CoV-2 infection: A new challenge for Internal Medicine.

Infection with the new SARS-CoV-2 coronavirus has reached pandemic proportions, with a very high death toll worldwide. Despite the scientific community's strenuous efforts to address this disease in its acute phase, as well as in prevention through the development of vaccines in record time, there remains another important workhorse: understanding and treating the persistence of symptoms beyond the acute phase, the so-called protracted COVID-19 syndrome or persistent COVID. These persistent manifestations affect several organs and systems and may depend on both the pathogenic mechanisms of the virus and the pathophysiological response of the patient. One year after the onset of this pandemic, there is an urgent need to address this situation from a comprehensive approach.

Thyroid hormone responsive Spot 14 increases during differentiation of human adipocytes and its expression is down-regulated in obese subjects.

CONTEXT: Very limited information is available regarding the function of human thyroid hormone responsive Spot 14 (human S14, hS14) in adipogenesis and human adiposity. OBJECTIVE: To evaluate hS14 levels during differentiation of human pre-adipocytes, in human fat depots and isolated fat cells. DESIGN: This was a cross-sectional study. SUBJECTS: A total of 161 omental (OM) and 87 subcutaneous (SC) adipose tissue samples obtained during elective surgical procedures from a population who varied widely in terms of obesity. MEASUREMENTS: hS14 gene expression and protein levels during adipogenesis were assessed by RT-PCR, western blot, and using an automated confocal imaging approach. RESULTS: hS14 gene expression levels were decreased in OM adipose tissue from overweight (-42.0%) and obese subjects (-56.5%) compared with lean subjects (P<0.05 and P<0.0001, respectively). hS14 mRNA (but not hS14-related) was inversely associated with obesity measures such as body mass index (P=0.001), percent fat mass (P=0.001), waist-to-hip ratio (P=0.020), and systolic blood pressure (P=0.031). hS14 gene expression and protein levels were up-regulated at the early stages of differentiation of human pre-adipocytes as well as for 3T3-L1 cells. That observation was most prominent in those individual cells exhibiting the more marked differentiation features. hS14 gene expression levels increased by approximately 45 000-fold in mature adipocytes. Increased hS14 levels were also found in stromal-vascular cells/pre-adipocytes (3.8-fold, P<0.05) and in adipose tissue samples (1.9-fold, P<0.0001) from SC compared with OM fat depots. CONCLUSIONS: These results suggest that hS14 is involved in human adipogenesis, but inversely related to obesity and OM fat accumulation.

Lactoferrin increases (172Thr)AMPK phosphorylation and insulin-induced (p473Ser)AKT while impairing adipocyte differentiation.

OBJECTIVE: Lactoferrin is a pleiotropic glycoprotein of the innate immune system with known effects on immunomodulation and cell differentiation. To gain an insight into the interaction among obesity, inflammation and insulin action, we aimed to examine the effects of lactoferrin on adipogenesis and the response to insulin in human hepatocarcinoma (HepG2) and 3T3-L1 cell lines. DESIGN: The cells were cultured with increasing lactoferrin concentration under non-inflammatory, inflammatory and standard conditions. The response to insulin was evaluated through (473Ser)AKT phosphorylation. The effects of lactoferrin on adipogenesis were studied through the expression of different lipogenic markers, AMP-activated protein kinase (AMPK) activation, retinoblastoma (Rb) activity and Oil Red O staining in 3T3-L1 cells. RESULTS: Lactoferrin increased dose-dependent insulin-induced (473Ser)AKT phosphorylation in both cell lines. Inflammation-induced decreased (473Ser)AKT phosphorylation was also rescued by lactoferrin. In addition, lactoferrin led to increased (p172Thr)AMPK during 3T3-L1 differentiation and to decreased adipogenesis (as shown by decreased expression of fatty acid synthase, acetyl-coenzyme A carboxylase-alpha and peroxisome proliferator-activated receptor-gamma in parallel with decreased formation of lipid droplets). Lactoferrin also increased dose-dependent Rb activity (expression and hypophosphorylation) during 3T3-L1 differentiation. CONCLUSION: Lactoferrin administration increased insulin-induced (473Ser)AKT phosphorylation, even in those conditions wherein the response to insulin was downregulated, and led to blunted adipogenesis in the context of increased (p172Thr)AMPK and Rb activity.

Early markers of acute respiratory distress syndrome development in severe trauma patients.

PURPOSE: The aim of the study was to identify early risk factors for development of acute respiratory distress syndrome (ARDS) in severe trauma patients. MATERIALS AND METHODS: This was a prospective observational study of 693 severe trauma patients (Injury Severity Score >or=16 and/or Revised Trauma Score or=2) of long bone fractures, and with chest injuries (rib/sternal fracture [ICD-9 code 807] and hemo/pneumothorax [ICD-9 code 860/861]). Patients with ARDS required more colloids (P = .005) and red blood cell units (P = .02) than patients without ARDS during the first 24 hours. Multivariate analysis showed that ARDS was related to chest trauma diagnosis (ICD-9 code 807) (odds ratio [OR], 3.85), femoral fracture (OR, 3.16), APACHE II score (OR, 1.05), and blood transfusion during resuscitation (OR, 1.32). CONCLUSIONS: Risk of ARDS development is related to the first 24-hour admission variables, including severe physiologic derangements and specific ICD-9-classified injuries. Blood transfusion may play an independent role.

[Treatment of syringomyelia in patients with Chiari malformation and craniosynostosis. A case report and review of the literature]. / Tratamiento de la siringomielia en pacientes con malformacion de Chiari y craneosinostosis. Caso clinico y revision de la bibliografia.

INTRODUCTION: Patients with multisutural or single craniosynostosis, often suffer from Chiari malformation and syringomyelia. The surgical management of syringomyelia in these patients is controversial. CASE REPORT: A 3-year-old girl was referred with complex craniosynostosis that had not been corrected surgically. She was asymptomatic despite the cranial MRI showed a Chiari malformation and one year later she developed a cervico-dorso-lumbar syringomyelia. She underwent a decompressive suboccipital craniectomy but subsequently suffered a worsening of syringomyelia. The intracranial pressure monitoring was pathological so it was decided to perform a decompressive bilateral fronto-parieto-temporal craniotomy and remodeling of the cranial vault, achieving a significant reduction of syringomyelia. CONCLUSIONS: After reviewing the literature, it is noted that there is currently no consensus on the treatment of syringomyelia in patients with craniosynostosis and Chiari malformation. Some authors recommend the simultaneous surgical suboccipital and cranial vault decompression, others only decompression of the cranial vault and other enlargement of the posterior fossa with distractors. In cases where the suboccipital decompression was performed first, the syringomyelia was not improved or stabilized. We conclude that the most effective treatment for patients with syringomyelia and craniosynostosis is decompressive remodeling of the cranial vault, as the main cause of syringomyelia is the raised intracranial pressure and lack of skull compliance.

TITLE: Tratamiento de la siringomielia en pacientes con malformacion de Chiari y craneosinostosis. Caso clinico y revision de la bibliografia.Introduccion. Los pacientes con craneosinostosis complejas o unisuturales presentan frecuentemente malformacion de Chiari y siringomielia. El tratamiento quirurgico de la siringomielia en estos pacientes es controvertido. Caso clinico. Niña de 3 años con craneosinostosis compleja no corregida quirurgicamente. Permanecio asintomatica a pesar de que en la resonancia magnetica craneal se evidencio una malformacion de Chiari y un año despues desarrollo una siringomielia cervicodorsolumbar. Se le realizo una craniectomia suboccipital descompresiva, pero posteriormente sufrio un empeoramiento de la siringomielia. El registro de presion intracraneal resulto patologico, por lo que se decidio realizar una craneotomia descompresiva frontoparietotemporal bilateral y remodelacion de la boveda craneal, con lo que se consiguio una disminucion significativa de la siringomielia. Conclusiones. Tras la revision de la bibliografia, se observa que actualmente no existe un consenso sobre el tratamiento de la siringomielia en los pacientes con craneosinostosis y malformacion de Chiari. Algunos autores recomiendan la simultanea descompresion quirurgica suboccipital y de la boveda craneal, otros solo la descompresion de la boveda craneal, y otros la ampliacion de la fosa posterior con distractores. En los casos en los que se realizo primero la descompresion suboccipital no se consiguio resolver ni estabilizar la siringomielia. Concluimos que el tratamiento mas eficaz para los pacientes con siringomielia y craneosinostosis es la remodelacion descompresiva de la boveda craneal, ya que el principal factor causante de la siringomielia es la hipertension intracraneal y la falta de distensibilidad del craneo.

Diazoxide enhances excitotoxicity-induced neurogenesis and attenuates neurodegeneration in the rat non-neurogenic hippocampus.

Diazoxide, a well-known mitochondrial KATP channel opener with neuroprotective effects, has been proposed for the effective and safe treatment of neuroinflammation. To test whether diazoxide affects the neurogenesis associated with excitotoxicity in brain injury, we induced lesions by injecting excitotoxic N-methyl-d-aspartate (NMDA) into the rat hippocampus and analyzed the effects of a daily oral administration of diazoxide on the induced lesion. Specific glial and neuronal staining showed that NMDA elicited a strong glial reaction associated with progressive neuronal loss in the whole hippocampal formation. Doublecortin immunohistochemistry and bromo-deoxyuridine (BrdU)-NeuN double immunohistochemistry revealed that NMDA also induced cell proliferation and neurogenesis in the lesioned non-neurogenic hippocampus. Furthermore, glial fibrillary acidic protein (GFAP)-positive cells in the injured hippocampus expressed transcription factor Sp8 indicating that the excitotoxic lesion elicited the migration of progenitors from the subventricular zone and/or the reprograming of reactive astrocytes. Diazoxide treatment attenuated the NMDA-induced hippocampal injury in rats, as demonstrated by decreases in the size of the lesion, neuronal loss and microglial reaction. Diazoxide also increased the number of BrdU/NeuN double-stained cells and elevated the number of Sp8-positive cells in the lesioned hippocampus. These results indicate a role for KATP channel activation in regulating excitotoxicity-induced neurogenesis in brain injury.

[Spinal epidural abscess caused by Acinetobacter baumannii mimicking a herniated lumbar disc]. / Absceso epidural vertebral por Acinetobacter baumanii que simula hernia discal lumbar.

INTRODUCTION: A vertebral epidural abscess usually offers a very varied clinical picture of systemic involvement with signs of infection, general malaise and neurological focus. It is diagnosed by means of magnetic resonance imaging, which reveals large lesions with frequent involvement of soft tissues and peripheral contrast enhancement. CASE REPORT: A 35-year-old male with lumbar-radicular pain in the right S1 with Lasègue's sign at 20 degrees on the right side and abolition of the Achilles' reflex. Magnetic resonance imaging showed an extradural lesion in L5-S1, dependent on the disc space, which suggested a herniated disc. The rest of the anamnesis, explorations and analyses were normal except for a slightly high erythrocyte sedimentation rate. The patient was submitted to surgery and an epidural abscess was observed from which an Acinetobacter baumanii was recovered. Treatment was established with antibiotics and a rigid lumbosacral orthosis. At three months clear signs of discitis were observed in magnetic resonance images; these were completely resolved at eight months, when the patient was asymptomatic. CONCLUSIONS: Epidural abscess must be included in the differential diagnosis of a herniated disc because in the early phases it can give rise to symptoms of lumbar-radicular pain that are identical to those caused by a herniated lumbar disc. This is the first case of an epidural abscess produced by A. baumanii.

[Surgical treatment of symptomatic arachnoid cysts in children]. / Tratamiento quirúrgico de los quistes aracnoideos sintomáticos en niños.

INTRODUCTION: When symptomatic, arachnoid cysts (AC) must be treated surgically. The best surgical technique, however, is at the present time still subject to controversy -implantation of a cyst-peritoneal shunt (CPS) or fenestration of the cyst, either by means of a craniotomy or by using endoscopic techniques. PATIENTS AND METHODS: This paper reports the findings from a series of 18 patients under 10 years of age who were treated for symptomatic ACs. An increase in the cranial perimeter was observed in 12 patients, 4 had headaches and 2 children suffered convulsive crises. In 11 cases the location was supratentorial and in 7 it was found to be infratentorial. RESULTS: Treatment involved a cyst-peritoneal or ventriculoperitoneal shunt in 12 cases. Endoscopic treatment of the cyst was carried out in 5 of the patients and in 1 case craniotomy debridement was performed. Seven of the 18 children required a second intervention to resolve the clinical condition, either due to poor valve functioning or because the endoscopic treatment was insufficient. Complications included 2 subdural haematomas, which required surgical treatment. No mortality or morbidity occurred. CONCLUSIONS: The progress being accomplished in endoscopic techniques can make them the ideal form of treatment rather than craniotomy debridement techniques, although the high percentage of no-resolution in children below the age of 15 months must be taken into account. CPS solves the problem of these cysts with a lower degree of surgical risk, but it has a high rate of reintervention, as well as the dependence on the shunt. In the review of the literature we carried out it was seen that reports are still published concerning series treated by both cyst fenestration and by means of shunts.

Assessment of thromboprophylaxis in medical patients hospitalized in Andalusia. A multicenter study. / Adecuación de tromboprofilaxis en pacientes médicos hospitalizados en Andalucía. Estudio multicéntrico.

BACKGROUND AND OBJECTIVES: Hospitalized patients are a population at risk for venous thromboembolism (VTE). The PRETEMED-2007 clinical practice guidelines help identify high-risk medical patients who are suited to thromboprophylaxis. These guidelines therefore provide a standard for prophylaxis in such patients. We evaluated the risk of VTE and the adjustment of thromboprophylaxis to the standards of the PRETEMED-2007 guidelines in patients hospitalized in internal medicine departments. PATIENTS AND METHODS: An observational, cross-sectional multicenter study was performed in 2010 in 16 hospitals in Andalusia and included 20 consecutive patients per center. The study variables were age, sex, risk factors for VTE and hemorrhage, the risk-adjusted PRETEMED of VTE, adjustment of thromboembolic prophylaxis at admission and at discharge and hospital mortality. RESULTS: The study included 293 patients (57.8% men) with a mean age of 69 (±15) years. The most common triggers for VTE were acute severe infection (27.3%) and neoplasia (16.4%). Some 43.4% of the patients presented a risk of hemorrhage. The risk of VTE at admission and discharge was high in 47.8% and 31% and moderate in 8.2% and 10.6%, respectively. A total of 91.7% and 17.3% of the patients underwent prophylaxis with low-molecular-weight heparin on admission and at discharge, respectively. The prescription was appropriate for 59.9% of the patients at admission (overutilization 38.4%, underutilization 1.7%) and for 74.7% at discharge (overutilization 5.4%, underutilization 19.9%). The adjustment was greater in patients older than 60 years and with greater hemorrhagic risk. CONCLUSIONS: For 60% of the patients admitted to the departments of internal medicine in Andalusia, the thromboprophylaxis was appropriate. The inadequacy of thromboprophylaxis (40%) is mostly due to overutilization. These results suggest significant space for improvement.

Epidermoid carcinoma of the lung in stage I: factors of prognostic interest.

Factors affecting stage I epidermoid cancer of the lung were studied in a series of 29 patients treated only by surgery and followed up for ten years. A set of 13 variables with a possible influence on prognosis were investigated. The application of the Cox Univariate Analysis to the different variables showed the grade of cell differentiation and the mitotic index to be predictors. In the Cox Multivariate Analysis, the proportional regression equation revealed two independently significant variables (p < 0.01), which were the Mitotic Index and Nuclear Area. Grouping patients on the basis of the prognostic variables indicated allows a better prediction for survival to be made for this series of patients.

Use of epsilon aminocaproic acid (EACA) in the preoperative management of ruptured intracranial aneurysms.

The authors report their experience with the use of epsilon aminocaproic acid (EACA) in the preoperative management of a series of patients with ruptured intracranial aneurysms. A similar series of patients was taken as control. They found that EACA is of definite value in preventing recurrent hemorrhage in the preoperative period. The significance of antifibrinolytic therapy in ruptured intracranial aneurysms is discussed.