ABSTRACT
AIMS: Covid-19 caused changes on the delivery of diabetes care. This study aimed to explore perceptions of healthcare providers across Europe concerning 1) the impact of covid-19 on delivery of diabetes care; 2) impact of changes in diabetes care on experienced workload; 3) experiences with video consultation in diabetes care. METHODS: Cross-sectional survey among healthcare providers in the Netherlands, United Kingdom, Turkey, Ukraine and Sweden, with a focus on primary care. RESULTS: The survey was completed by 180 healthcare providers. During the COVID-19 pandemic 57.1% of respondents provided less diabetes care and 72.8% observed a negative impact on people with diabetes. More than half of respondents (61.9%) expressed worries to some extent about getting overloaded by work. Although the vast majority considered their work meaningful (85.6%). Almost half of healthcare providers (49.4%) thought that after the pandemic video-consultation could be blended with face-to-face contact. CONCLUSIONS: Less diabetes care was delivered and a negative impact on people with diabetes was observed by healthcare providers. Despite healthcare providers' feeling overloaded, mental wellbeing seemed unaffected. Video consultations were seen as having potential. Given the remaining covid-19 risks and from the interest of proactive management of people with diabetes, these findings urge for further exploration of incorporating video consultation in diabetes care.
Subject(s)
COVID-19 , Diabetes Mellitus , Humans , COVID-19/epidemiology , Pandemics , Cross-Sectional Studies , Health Personnel , Europe/epidemiology , Diabetes Mellitus/diagnosis , Diabetes Mellitus/epidemiology , Diabetes Mellitus/therapySubject(s)
Bone Neoplasms/secondary , Carcinoma, Hepatocellular/pathology , Clavicle , Liver Neoplasms/pathology , Adult , Biopsy , Bone Neoplasms/diagnostic imaging , Carcinoma, Hepatocellular/diagnostic imaging , Carcinoma, Hepatocellular/genetics , Humans , Liver/surgery , Liver Neoplasms/diagnostic imaging , Liver Neoplasms/genetics , Liver Transplantation , Magnetic Resonance Imaging , Male , UltrasonographyABSTRACT
Large bowel adenocarcinoma is one of the most frequent human neoplasms and despite recent insights into the pathophysiology and molecular basis of this disease, mortality remains high in advanced and metastatic cases. Most guidelines recommend adjuvant chemotherapy for tumours involving lymph nodes, but not for patients with localized stage I or II disease. However, it is well known that approximately 20% of stage II colorectal carcinoma patients eventually recur, mainly with distant or peritoneal involvement and show bad prognosis. It would be important to predict which patients are at increased risk of recurrence to guide potential adjuvant therapy use in this controversial setting. In this sense, only microsatellite stability has been proposed as a predictive tool in some guidelines. The tripartite motif family protein 72 (TRIM72) is a ubiquitin ligase, involved in the cell membrane repair machinery and known to be associated to insulin resistance. Its potential role in colon cancer has recently been proposed. The aim of this study is to determine the potential predictive value of TRIM72 immunohistochemical expression in stage II colon carcinoma. We have retrospectively reviewed a series of 95 patients with stage II colon microsatellite stable carcinomas operated with a curative intent at a single large tertiary hospital in Madrid (Spain) between 2006 and 2012. None of the patients received adjuvant chemotherapy. We reviewed the histopathological slides and constructed a tissue microarray (TMA) of three representative areas to perform immunohistochemical staining for TRIM72. In our series 30 patients (31.7%) recurred after a median follow-up of 17.5 months. Lack of immunohistochemical expression of TRIM72 in the tumor was significantly and independently associated to recurrence. A recent report by Chen et al. has shown that TRIM72 can be measured in plasma for colon carcinoma detection as an alternative to CEA or CA19.9, with lower levels in patients with carcinoma. Our report is the first one to show that lower immunohistochemical expression of TRIM72 predicts recurrence in colon stage II carcinoma. We feel this predictive influence can be related to its crucial role as a central regulator in many signaling pathways (PI3K-AKT, ERK). As an ubiquitin ligase, the lack of TRIM72 could increase the levels of several potential oncogenic molecules and therefore lead to a more aggressive phenotype. It remains to be shown whether chemotherapy could change the clinical behaviour of this bad prognosis group. We propose TRIM72 immunohistochemical analysis as a potential tool to predict recurrence risk in stage II colon carcinoma patients. Our results should be confirmed in larger series, but could open the way to management strategies refinement in this early stage group of patients.
Subject(s)
Adenocarcinoma/pathology , Biomarkers, Tumor/analysis , Colorectal Neoplasms/pathology , Neoplasm Recurrence, Local/metabolism , Tripartite Motif Proteins/metabolism , Aged , Aged, 80 and over , Female , Humans , Immunohistochemistry , Male , Middle Aged , Neoplasm Recurrence, Local/pathology , Prognosis , Retrospective StudiesABSTRACT
A correction to this article has been published and is linked from the HTML and PDF versions of this paper. The error has been fixed in the paper.
ABSTRACT
Cetuximab is a standard-of-care treatment for RAS wild-type metastatic colorectal cancer (mCRC) but not for those harbor a KRAS mutation since MAPK pathway is constitutively activated. Nevertheless, cetuximab also exerts its effect by its immunomodulatory activity despite the presence of RAS mutation. The aim of this study was to determine the impact of polymorphism FcγRIIIa V158F and killer immunoglobulin-like receptor (KIR) genes on the outcome of mCRC patients with KRAS mutations treated with cetuximab. This multicenter Phase II clinical trial included 70 mCRC patients with KRAS mutated. We found KIR2DS4 gene was significantly associated with OS (HR 2.27; 95% CI, 1.08-4.77; P = 0.03). In non-functional receptor homozygotes the median OS was 2.6 months longer than in carriers of one copy of full receptor. Multivariate analysis confirmed KIR2DS4 as a favorable prognostic marker for OS (HR 6.71) in mCRC patients with KRAS mutation treated with cetuximab. These data support the potential therapeutic of cetuximab in KRAS mutated mCRC carrying non-functional receptor KIR2DS4 since these patients significantly prolong their OS even after heavily treatment. KIR2DS4 typing could be used as predictive marker for identifying RAS mutated patients that could benefit from combination approaches of anti-EGFR monoclonal antibodies and other immunotherapies to overcome the resistance mediated by mutation in RAS.
Subject(s)
Antineoplastic Agents, Immunological/therapeutic use , Cetuximab/therapeutic use , Colorectal Neoplasms/drug therapy , Colorectal Neoplasms/genetics , Drug Resistance, Neoplasm/genetics , Proto-Oncogene Proteins p21(ras)/genetics , Receptors, IgG/genetics , Receptors, KIR/genetics , Adult , Aged , Aged, 80 and over , Biomarkers, Tumor/genetics , Female , Genes, MCC , Humans , Male , Middle Aged , Polymorphism, Genetic , Prospective Studies , Treatment OutcomeABSTRACT
BACKGROUND: Limited data are available regarding the ability of biomarkers to predict complete pathological response to neoadjuvant chemoradiotherapy in locally advanced rectal cancer. Complete response translates to better patient survival. DEK is a transcription factor involved not only in development and progression of different types of cancer, but is also associated with treatment response. This study aims to analyze the role of DEK in complete pathological response following chemoradiotherapy for locally advanced rectal cancer. METHODS: Pre-treated tumour samples from 74 locally advanced rectal-cancer patients who received chemoradiation therapy prior to total mesorectal excision were recruited for construction of a tissue microarray. DEK immunoreactivity from all samples was quantified by immunohistochemistry. Then, association between positive stained tumour cells and pathologic response to neoadjuvant treatment was measured to determine optimal predictive power. RESULTS: DEK expression was limited to tumour cells located in the rectum. Interestingly, high percentage of tumour cells with DEK positiveness was statistically associated with complete pathological response to neoadjuvant treatment based on radiotherapy and fluoropyrimidine-based chemotherapy and a marked trend toward significance between DEK positiveness and absence of treatment toxicity. Further analysis revealed an association between DEK and the pro-apoptotic factor P38 in the pre-treated rectal cancer biopsies. CONCLUSIONS: These data suggest DEK as a potential biomarker of complete pathological response to treatment in locally advanced rectal cancer.
Subject(s)
Biomarkers, Tumor/biosynthesis , Chromosomal Proteins, Non-Histone/biosynthesis , Oncogene Proteins/biosynthesis , Poly-ADP-Ribose Binding Proteins/biosynthesis , Rectal Neoplasms/metabolism , Rectal Neoplasms/therapy , Aged , Aged, 80 and over , Chemoradiotherapy , Female , Humans , Immunohistochemistry , Male , Middle Aged , Neoadjuvant Therapy , Predictive Value of Tests , Prognosis , Rectal Neoplasms/pathology , Treatment OutcomeABSTRACT
No disponible
Subject(s)
Humans , Male , Adult , Q Fever/etiology , Q Fever , Cytomegalovirus/isolation & purification , Coxiella burnetii/isolation & purification , Early Diagnosis , Abdomen , UltrasonographySubject(s)
Q Fever/complications , Splenic Infarction/etiology , Adult , Humans , Male , Q Fever/diagnosis , Splenic Infarction/diagnosisABSTRACT
Polo-like kinase 1 (PLK1) is a serine/threonine-protein kinase expressed during mitosis and overexpressed in multiple human cancers, including leukemia and also many solid tumors. PLK1 knockdown has been shown to block proliferation of leukemic cell lines and the clonogenic potential of tumor cells grown from patients with cancer. PLK1 inhibition is a promising strategy for the treatment of some tumors. We aim to analyze expression of PLK1 in metastatic colorectal carcinoma. Retrospective analysis of colorectal carcinomas with hepatic metastasis during follow-up receiving neoadjuvant chemotherapy (NAC), based on oxaliplatin. Immunohistochemistry for PLK-1 in paraffin-embedded tissue from the primary and also from the metastasis. 50 patients. 32% showed good histopathological response. 43% of the primaries were positive for PLK1, as opposed to 23.5% of the metastasis. Expression of PLK1 was significantly reduced in metastasis compared with the primaries (p = 0.05), what could be due to therapy or to a phenotypic change of the metastatic nodule. Analysis of the prognostic influence of PLK1 expression showed significant association between PLK1 expression in metastasis and lower overall survival (p = 0.000). We have also found a significant association between PLK1 expression and histopathological response (p = 0.02). All the tumors with high expression of PLK1 showed minor response (11/11). This study shows the association between survival and poor histopathological response to therapy and high expression of PLK1 in metastasis. Our results could open a new therapeutic approach through the inhibition of PLK1.
Subject(s)
Antineoplastic Combined Chemotherapy Protocols/therapeutic use , Biomarkers, Tumor/metabolism , Cell Cycle Proteins/metabolism , Colorectal Neoplasms/pathology , Liver Neoplasms/secondary , Neoadjuvant Therapy , Neoplasm Recurrence, Local/pathology , Protein Serine-Threonine Kinases/metabolism , Proto-Oncogene Proteins/metabolism , Colorectal Neoplasms/drug therapy , Colorectal Neoplasms/metabolism , Female , Follow-Up Studies , Humans , Immunoenzyme Techniques , Liver Neoplasms/drug therapy , Liver Neoplasms/metabolism , Lymphatic Metastasis , Male , Middle Aged , Neoplasm Invasiveness , Neoplasm Recurrence, Local/drug therapy , Neoplasm Recurrence, Local/metabolism , Neoplasm Staging , Prognosis , Retrospective Studies , Survival Rate , Polo-Like Kinase 1ABSTRACT
No disponible
Subject(s)
Female , Humans , Male , Osteoporosis/epidemiology , Osteoporosis/prevention & control , Osteoporotic Fractures/epidemiology , Osteoporotic Fractures/prevention & control , Risk Factors , Densitometry/instrumentation , Densitometry/methods , Vitamin D/therapeutic use , Osteoporosis/diagnosis , Osteoporosis/therapy , Diagnosis, Differential , Osteoporotic Fractures , Orthopedics/methods , Glucocorticoids/therapeutic use , AlgorithmsABSTRACT
Biliopancreatic cancer is one of the most aggressive solid neoplasms, and incidence is rising worldwide. It is known that ATF6α is one of the transmembrane proteins that acts crucially in endoplasmic reticulum stress response, and knockdown induces apoptosis of pancreatic cells. Apart from this, p-p38 has been previously correlated with better outcome in pancreatic cancer. Interestingly, ATF6α knockdown pancreatic cells showed increased p-p38. The aim of this study was to evaluate the expression of these 2 proteins, p-p38 and ATF6α, and their correlation with the outcome of biliopancreatic adenocarcinoma patients. Samples from patients with biliopancreatic adenocarcinoma that underwent pancreaticoduodenectomy from 2007 to 2013 were used to construct a tissue microarray to evaluate p-p38 and ATF6α proteins by immunohistochemistry. We observed that both markers showed a tendency to impact in the time to recurrence; then a combination of these 2 proteins was analyzed. Combination of ATF6α(high) and p-p38(low) was strongly associated with a higher risk of recurrence (hazard ratio 2.918, Pâ=â0.013). This 2-protein model remained significant after multivariate adjustment.We proposed a 2-protein signature based on ATF6α(high) and p-p38(low) as a potential biomarker of risk of recurrence in resected biliopancreatic adenocarcinoma patients.
Subject(s)
Activating Transcription Factor 6/metabolism , Adenocarcinoma/metabolism , Biliary Tract Neoplasms/metabolism , Biomarkers, Tumor/metabolism , Pancreatic Neoplasms/metabolism , p38 Mitogen-Activated Protein Kinases/metabolism , Adenocarcinoma/diagnosis , Adenocarcinoma/mortality , Adult , Aged , Aged, 80 and over , Biliary Tract Neoplasms/diagnosis , Biliary Tract Neoplasms/mortality , Female , Humans , Male , Middle Aged , Pancreatic Neoplasms/diagnosis , Pancreatic Neoplasms/mortality , Phosphorylation , Prognosis , Spain/epidemiologySubject(s)
Osteoporosis , Osteoporotic Fractures , Absorptiometry, Photon , Algorithms , Bone Density Conservation Agents/therapeutic use , Clinical Decision-Making , Combined Modality Therapy , Decision Support Techniques , Female , Fracture Fixation/methods , Health Status Indicators , Hip Fractures/diagnosis , Hip Fractures/etiology , Hip Fractures/therapy , Humans , Male , Osteoporosis/complications , Osteoporosis/diagnosis , Osteoporosis/therapy , Osteoporotic Fractures/diagnosis , Osteoporotic Fractures/epidemiology , Osteoporotic Fractures/etiology , Osteoporotic Fractures/therapy , Risk Assessment , Risk Factors , Spain/epidemiology , Spinal Fractures/diagnosis , Spinal Fractures/etiology , Spinal Fractures/therapy , Tomography, X-Ray Computed , Vitamin D/therapeutic use , Vitamins/therapeutic useABSTRACT
No disponible
Subject(s)
Humans , Male , Adult , Pericarditis , Chest Pain/etiology , Pericardial Effusion/etiology , Acute Disease , Primary Health Care/methods , Diagnosis, DifferentialSubject(s)
Fever/etiology , Pericarditis/diagnostic imaging , Ultrasonography/methods , Acute Disease , Adult , Humans , Male , Primary Health CareABSTRACT
BACKGROUND: Protein phosphatase 2A (PP2A) is a tumour suppressor frequently inactivated in human cancer and its tyrosine-307 phosphorylation has been reported as a molecular inhibitory mechanism. METHODS: Expression of phosphorylated PP2A (p-PP2A) was evaluated in 250 metastatic colorectal cancer (CRC) patients. Chi-square, Kaplan-Meier and Cox analyses were used to determine correlations with clinical and molecular parameters and impact on clinical outcomes. RESULTS: High p-PP2A levels were found in 17.2% cases and were associated with ECOG performance status (P=0.001) and presence of synchronous metastasis at diagnosis (P=0.035). This subgroup showed substantially worse overall survival (OS) (median OS, 6.0 vs 26.2 months, P<0.001) and progression-free survival (PFS) (median PFS, 3.8 vs 13.3 months, P<0.001). The prognostic impact of p-PP2A was particularly evident in patients aged <70 years (P<0.001). Multivariate analysis revealed that p-PP2A retained its prognostic impact for OS (hazard ratio 2.7; 95% confidence interval, 1.8-4.1; P<0.001) and PFS (hazard ratio 3.0; 95% confidence interval, 1.8-5.0; P<0.001). CONCLUSIONS: Phosphorylated PP2A is an alteration that determines poor outcome in metastatic CRC and represents a novel potential therapeutic target in this disease, thus enabling to define a subgroup of patients who could benefit from future treatments based on PP2A activators.
Subject(s)
Biomarkers, Tumor/metabolism , Colorectal Neoplasms/enzymology , Liver Neoplasms/enzymology , Phosphoprotein Phosphatases/metabolism , Aged , Colorectal Neoplasms/mortality , Colorectal Neoplasms/pathology , Female , Humans , Kaplan-Meier Estimate , Liver Neoplasms/mortality , Liver Neoplasms/secondary , Male , Multivariate Analysis , Phosphoproteins/metabolism , Phosphorylation , Proportional Hazards Models , Protein Phosphatase 2C , Protein Processing, Post-TranslationalABSTRACT
AIM: The relevance of the cytidine diphosphate-choline and Rho GTPases pathways in the pathogenesis of cancer has been previously demonstrated. We investigate by a case-control association study if genetics variants in these pathways are associated with risk of developing lung cancer. METHODS: Thirty-seven tag SNPs were evaluated as risk factor of NSCLC in 897 cases and 904 controls. RESULTS: Six SNPs were nominally associated with lung cancer risk, which were not significant after the Bonferroni correction for multiple comparisons. No association was observed with the remaining 31 analyzed SNPs, neither it was found significant in haplotype frequencies. CONCLUSIONS: Although the implication of the two pathways investigated in our study in carcinogenesis is well established, our null results suggest that common genetic variants in CDP-choline and Rho GTPases-related genes are not risk factors for lung cancer (AU)
No disponible
Subject(s)
Humans , Male , Female , Middle Aged , Aged , Carcinoma, Non-Small-Cell Lung/metabolism , Choline Kinase/genetics , Haplotypes , Lung Neoplasms/metabolism , Polymorphism, Single Nucleotide , rhoB GTP-Binding Protein/genetics , Carcinoma, Non-Small-Cell Lung/genetics , Genetic Predisposition to Disease/genetics , Lung Neoplasms/genetics , Phospholipids/metabolismABSTRACT
AIM: The relevance of the cytidine diphosphate-choline and Rho GTPases pathways in the pathogenesis of cancer has been previously demonstrated. We investigate by a case-control association study if genetics variants in these pathways are associated with risk of developing lung cancer. METHODS: Thirty-seven tag SNPs were evaluated as risk factor of NSCLC in 897 cases and 904 controls. RESULTS: Six SNPs were nominally associated with lung cancer risk, which were not significant after the Bonferroni correction for multiple comparisons. No association was observed with the remaining 31 analyzed SNPs, neither it was found significant in haplotype frequencies. CONCLUSIONS: Although the implication of the two pathways investigated in our study in carcinogenesis is well established, our null results suggest that common genetic variants in CDP-choline and Rho GTPases-related genes are not risk factors for lung cancer.
Subject(s)
Carcinoma, Non-Small-Cell Lung/genetics , Genetic Predisposition to Disease/genetics , Lung Neoplasms/genetics , Phospholipids/metabolism , Aged , Carcinoma, Non-Small-Cell Lung/metabolism , Choline Kinase/genetics , Female , Haplotypes , Humans , Lung Neoplasms/metabolism , Male , Middle Aged , Polymorphism, Single Nucleotide , rho GTP-Binding Proteins/geneticsABSTRACT
Endoplasmic reticulum (ER) is a central organelle in eukaryotic cells that regulates protein synthesis and maturation. Perturbation of ER functions leads to ER stress, which has been previously associated with a broad variety of diseases. ER stress is generally regarded as compensatory, but prolonged ER stress has been involved in apoptosis induced by several cytotoxic agents. Choline kinase α (ChoKα), the first enzyme in the Kennedy pathway, is responsible for the generation of phosphorylcholine (PCho) that ultimately renders phosphatidylcholine. ChoKα overexpression and high PCho levels have been detected in several cancer types. Inhibition of ChoKα has demonstrated antiproliferative and antitumor properties; however, the mechanisms underlying these activities remain poorly understood. Here, we demonstrate that ChoKα inhibitors (ChoKIs), MN58b and RSM932A, induce cell death in cancer cells (T47D, MCF7, MDA-MB231, SW620 and H460), through the prolonged activation of ER stress response. Evidence of ChoKIs-induced ER stress includes enhanced production of glucose-regulated protein, 78 kDa (GRP78), protein disulfide isomerase, IRE1α, CHOP, CCAAT/enhancer-binding protein beta (C/EBPß) and TRB3. Although partial reduction of ChoKα levels by small interfering RNA was not sufficient to increase the production of ER stress proteins, silencing of ChoKα levels also show a decrease in CHOP overproduction induced by ChoKIs, which suggests that ER stress induction is due to a change in ChoKα protein folding after binding to ChoKIs. Silencing of CHOP expression leads to a reduction in C/EBPß, ATF3 and GRP78 protein levels and abrogates apoptosis in tumor cells after treatment with ChoKIs, suggesting that CHOP maintains ER stress responses and triggers the pro-apoptotic signal. Consistent with the differential effect of ChoKIs in cancer and primary cells previously described, ChoKIs only promoted a transient and moderated ER stress response in the non-tumorogenic cells MCF10A. In conclusion, pharmacological inhibition of ChoKα induces cancer cell death through a mechanism that involves the activation of exaggerated and persistent ER stress supported by CHOP overproduction.
Subject(s)
Choline Kinase/metabolism , Endoplasmic Reticulum Stress/physiology , Transcription Factor CHOP/metabolism , Apoptosis/genetics , Apoptosis/physiology , Cell Line, Tumor , Cell Survival/genetics , Cell Survival/physiology , Choline Kinase/genetics , Endoplasmic Reticulum Chaperone BiP , Endoplasmic Reticulum Stress/genetics , Flow Cytometry , Fluorescent Antibody Technique , Humans , Phosphorylcholine/metabolism , Transcription Factor CHOP/geneticsABSTRACT
We have analyzed the response of primary cultures derived from tumor specimens of non small cell lung cancer (NSCLC) patients to choline kinase α (ChoKα) inhibitors. ChoKα inhibitors have been demonstrated to increase ceramides levels specifically in tumor cells, and this increase has been suggested as the mechanism that explain its proapoptotic effect in cancer cells. Here, we have investigated the molecular mechanism associated to the intrinsic resistance, and found that other enzyme involved in lipid metabolism, acid ceramidase (ASAH1), is specifically upregulated in resistant tumors. NSCLC cells with acquired resistance to ChoKα inhibitors also display increased levels of ASAH1. Accordingly, ASAH1 inhibition synergistically sensitizes lung cancer cells to the antiproliferative effect of ChoKα inhibitors. Thus, the determination of the levels of ASAH1 predicts sensitivity to targeted therapy based on ChoKα specific inhibition and represents a model for combinatorial treatments of ChoKα inhibitors and ASAH1 inhibitors. Considering that ChoKα inhibitors have been recently approved to enter Phase I clinical trials by the Food and Drug Administration (FDA), these findings are anticipating critical information to improve the clinical outcome of this family of novel anticancer drugs under development.
Subject(s)
Acid Ceramidase/antagonists & inhibitors , Antineoplastic Agents/pharmacology , Biomarkers, Tumor/metabolism , Carcinoma, Non-Small-Cell Lung/enzymology , Choline Kinase/antagonists & inhibitors , Drug Resistance, Neoplasm , Enzyme Inhibitors/pharmacology , Lung Neoplasms/enzymology , Acid Ceramidase/genetics , Acid Ceramidase/metabolism , Apoptosis/drug effects , Butanes/pharmacology , Carcinoma, Non-Small-Cell Lung/genetics , Carcinoma, Non-Small-Cell Lung/pathology , Cell Line, Tumor , Cell Proliferation/drug effects , Cell Survival/drug effects , Choline Kinase/metabolism , Dose-Response Relationship, Drug , Endocannabinoids , Ethanolamines/pharmacology , Humans , Inhibitory Concentration 50 , Lung Neoplasms/genetics , Lung Neoplasms/pathology , Molecular Targeted Therapy , Myristates/pharmacology , Oleic Acids , Propanolamines/pharmacology , Pyridinium Compounds/pharmacology , Tumor Cells, Cultured , Up-RegulationABSTRACT
El uso cada día más extendido de los anticoagulantes orales ha llevado al aumento del número de complicaciones con las que diariamente se enfrentan los servicios de urgencias (SU). El concentrado de complejo protrombínico (CCP) constituye una importante opción terapéutica cuando es urgente la reversión de la anticoagulación, ya que actúa de forma más rápida y completa que el plasma fresco congelado (PFC). A través del siguiente caso clínico, se revisa el uso e indicaciones del CCP en pacientes anticoagulados, y su utilización en procesos hemorrágicos intracraneales donde la rapidez de instauración del tratamiento es fundamental (AU)
The use of oral anticoagulants is increasing, leading to a rise in the number of complications emergency health services must cope with. A review of the literature showed that prothrombin complex is an important therapeutic option when emergency reversion of anticoagulation is required, as it acts more quickly and completely than fresh frozen plasma. In this case report we review the use and indications of prothrombin complex in patients on oral anticoagulants, noting that rapid onset of effect is particularly important in cases of intracerebral hemorrhage (AU)