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A report of two cases" ] ] "contieneResumen" => array:2 [ "es" => true "en" => true ] "contieneTextoCompleto" => array:1 [ "es" => true ] "contienePdf" => array:1 [ "es" => true ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0005" "etiqueta" => "Figura 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 4175 "Ancho" => 2869 "Tamanyo" => 726564 ] ] "descripcion" => array:1 [ "es" => "<p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Algoritmo diagnóstico-terapéutico de MAT.</p> <p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">CID: coagulación intravascular diseminada; ECG: electrocardiograma; ETEC: <span class="elsevierStyleItalic">Escherichia coli</span> enterotoxigénica; LDH: lactato deshidrogenasa; MAT: microangiopatía trombótica; PTT: púrpura trombocitopénica trombótica; SHU: síndrome hemolítico urémico; SHUa: SHU atípico; TC: tomografía computarizada.</p>" ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "R. 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D: Effacement of the cerebral sulci (arrows) and decreased size of both ventricles with poorly defined basal ganglia (arrows), suggestive of cerebral oedema.</p>" ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "P. Sánchez Zamora, B. Gómez del Pulgar Vázquez, S. Gholamian Ovejero" "autores" => array:3 [ 0 => array:2 [ "nombre" => "P." "apellidos" => "Sánchez Zamora" ] 1 => array:2 [ "nombre" => "B." "apellidos" => "Gómez del Pulgar Vázquez" ] 2 => array:2 [ "nombre" => "S." 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Documento de consenso de la Sociedad Española de Cirugía Cardiovascular y Endovascular y la Sociedad Española de Anestesiología, Reanimación y Terapeútica del Dolor" ] ] "contieneResumen" => array:2 [ "en" => true "es" => true ] "contieneTextoCompleto" => array:1 [ "en" => true ] "contienePdf" => array:1 [ "en" => true ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:8 [ "identificador" => "fig0035" "etiqueta" => "Figure 7" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr7.jpeg" "Alto" => 2422 "Ancho" => 2925 "Tamanyo" => 353878 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0035" "detalle" => "Figure " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0050" class="elsevierStyleSimplePara elsevierViewall">Algorithmic approach to the reversal of cerebral desaturation.</p> <p id="spar0055" class="elsevierStyleSimplePara elsevierViewall">Courtesy of Denault et al.<a class="elsevierStyleCrossRef" href="#bib0125"><span class="elsevierStyleSup">25</span></a>.</p>" ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "A. López Gómez, R. Rodríguez, N. Zebdi, R. Ríos Barrera, A. Forteza, J.J. Legarra Calderón, P. Garrido Martín, B. Hernando, A. Sanjuan, S. González Bardanca, M.Á. Varela Martínez, F.E. Fernández, R. Llorens, F.J. Valera Martínez, A. Gómez Felices, P.J. Aranda Granados, R. Sádaba Sagredo, J.R. Echevarría, R. Vicente Guillén, J. Silva Guisasola" "autores" => array:20 [ 0 => array:2 [ "nombre" => "A." "apellidos" => "López Gómez" ] 1 => array:2 [ "nombre" => "R." "apellidos" => "Rodríguez" ] 2 => array:2 [ "nombre" => "N." "apellidos" => "Zebdi" ] 3 => array:2 [ "nombre" => "R." "apellidos" => "Ríos Barrera" ] 4 => array:2 [ "nombre" => "A." "apellidos" => "Forteza" ] 5 => array:2 [ "nombre" => "J.J." "apellidos" => "Legarra Calderón" ] 6 => array:2 [ "nombre" => "P." "apellidos" => "Garrido Martín" ] 7 => array:2 [ "nombre" => "B." "apellidos" => "Hernando" ] 8 => array:2 [ "nombre" => "A." "apellidos" => "Sanjuan" ] 9 => array:2 [ "nombre" => "S." "apellidos" => "González Bardanca" ] 10 => array:2 [ "nombre" => "M.Á." "apellidos" => "Varela Martínez" ] 11 => array:2 [ "nombre" => "F.E." "apellidos" => "Fernández" ] 12 => array:2 [ "nombre" => "R." "apellidos" => "Llorens" ] 13 => array:2 [ "nombre" => "F.J." "apellidos" => "Valera Martínez" ] 14 => array:2 [ "nombre" => "A." "apellidos" => "Gómez Felices" ] 15 => array:2 [ "nombre" => "P.J." "apellidos" => "Aranda Granados" ] 16 => array:2 [ "nombre" => "R." "apellidos" => "Sádaba Sagredo" ] 17 => array:2 [ "nombre" => "J.R." "apellidos" => "Echevarría" ] 18 => array:2 [ "nombre" => "R." "apellidos" => "Vicente Guillén" ] 19 => array:2 [ "nombre" => "J." "apellidos" => "Silva Guisasola" ] ] ] ] ] "idiomaDefecto" => "en" "Traduccion" => array:1 [ "es" => array:9 [ "pii" => "S0034935621001043" "doi" => "10.1016/j.redar.2021.02.007" "estado" => "S300" "subdocumento" => "" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:1 [ "total" => 0 ] "idiomaDefecto" => "es" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S0034935621001043?idApp=UINPBA00004N" ] ] "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2341192922000440?idApp=UINPBA00004N" "url" => "/23411929/0000006900000003/v1_202204280534/S2341192922000440/v1_202204280534/en/main.assets" ] "en" => array:20 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Case report</span>" "titulo" => "Diagnostic-therapeutic algorithm for thrombotic microangiopathy. A report of two cases" "tieneTextoCompleto" => true "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "179" "paginaFinal" => "182" ] ] "autores" => array:1 [ 0 => array:4 [ "autoresLista" => "R. Rubio-Haro, M. Quesada-Carrascosa, J. Hernández-Laforet, C. Ferrer Gómez, J. De Andrés" "autores" => array:5 [ 0 => array:4 [ "nombre" => "R." "apellidos" => "Rubio-Haro" "email" => array:1 [ 0 => "rubenrubio1992@gmail.com" ] "referencia" => array:2 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] 1 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">*</span>" "identificador" => "cor0005" ] ] ] 1 => array:3 [ "nombre" => "M." "apellidos" => "Quesada-Carrascosa" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] ] ] 2 => array:3 [ "nombre" => "J." "apellidos" => "Hernández-Laforet" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] ] ] 3 => array:3 [ "nombre" => "C." "apellidos" => "Ferrer Gómez" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] ] ] 4 => array:3 [ "nombre" => "J." "apellidos" => "De Andrés" "referencia" => array:2 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] 1 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "aff0010" ] ] ] ] "afiliaciones" => array:2 [ 0 => array:3 [ "entidad" => "Servicio de Anestesiología, Reanimación y Tratamiento del Dolor, Consorcio Hospital General Universitario, Valencia, Spain" "etiqueta" => "a" "identificador" => "aff0005" ] 1 => array:3 [ "entidad" => "Unidad de Anestesia-Departamento de Cirugía, Facultad de Medicina, Universidad de Valencia, Valencia, Spain" "etiqueta" => "b" "identificador" => "aff0010" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "Corresponding author." ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Algoritmo diagnóstico-terapéutico de las microangiopatías trombóticas. A propósito de 2 casos" ] ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:8 [ "identificador" => "fig0005" "etiqueta" => "Figure 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 4175 "Ancho" => 2869 "Tamanyo" => 775008 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0005" "detalle" => "Figure " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">TMA diagnostic-therapeutic algorithm.</p> <p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">aHUS: atypical HUS; CT: computed tomography; DIC: disseminated intravascular coagulation; ECG: electrocardiogram; ETEC: <span class="elsevierStyleItalic">Escherichia coli</span> enterotoxigenic; HUS: haemolytic uremic syndrome; LDH: lactate dehydrogenase; TMA: thrombotic microangiopathy; TTP: thrombotic thrombocytopenic purpura.</p>" ] ] ] "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Introduction</span><p id="par0005" class="elsevierStylePara elsevierViewall">Thrombotic microangiopathy (TMA) is a pathological diagnosis secondary to vascular damage, endothelial abnormalities, and arteriolar and capillary thrombosis. It encompasses different syndromes, all of which are characterised by haemolytic anaemia, thrombocytopaenia and organ dysfunction, mainly renal or neurological. TMA is associated with significant mortality and morbidity, although early identification and immediate initiation of specific and supportive treatment can improve outcomes. TMAs can be classified as primary or secondary. Primary TMAs, such as thrombotic thrombocytopenic purpura (TTP) and haemolytic uremic syndrome (HUS), occur spontaneously with no underlying cause. Secondary forms occur in various clinical contexts, such as autoimmune disease, pregnancy (HELLP syndrome), disseminated intravascular coagulation (DIC), infection (influenza, HIV, EBV, parvovirus), malignant tumours, or the use of certain medications (calcineurin inhibitors, quinine), and treatment should be aimed at correcting the underlying cause<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a>.</p><p id="par0010" class="elsevierStylePara elsevierViewall">TTP is defined as TMA secondary to a severe ADAMTS13 deficiency (<10%), an enzyme responsible for cleaving von Willebrand factor multimers. These patients have unusually large von Willebrand factor multimers that bind to platelets, forming an intravascular network that leads to haemolysis and ischaemic tissue injury. TTP can be either congenital or acquired. The acquired form is thought to be secondary to autoantibodies against ADAMTS13. TTP is the only form of TMA in which renal dysfunction is rare and neurological involvement is far more frequent<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a>.</p><p id="par0015" class="elsevierStylePara elsevierViewall">HUS is a TMA associated with severe renal failure. The most common form is typical HUS, which is associated with a diarrhoeal illness caused by Shiga toxin–producing <span class="elsevierStyleItalic">E. coli.</span> Atypical HUS, less common, is caused by endothelial damage mediated by activation of C5 and the terminal complement complex (membrane attack complex). Genetic mutations in regulatory genes have been described in 50%–70% of patients with atypical HUS (aHUS), and anti-factor autoantibodies have been found in a small percentage of patients<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a>.</p><p id="par0020" class="elsevierStylePara elsevierViewall">Improved understanding of the pathophysiology of TMA has allowed clinicians to optimise management and treatment and improve outcomes<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a>. Although TMA can be diagnosed on the basis of several laboratory markers and clinical characteristics, a differential diagnosis with other haematological disorders, such as DIC or HELLP syndrome that share some clinical manifestations with TMA, will also be required.</p><p id="par0025" class="elsevierStylePara elsevierViewall">We report 2 clinical cases of interest.</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Case 1. Thrombotic thrombocytopenic purpura</span><p id="par0030" class="elsevierStylePara elsevierViewall">Our patient was a 55-year-old woman with a history of diabetes mellitus, dyslipidaemia, high blood pressure, and obesity. After returning from Romania, where she had been living in a rural environment with cattle, she went to the emergency room due to seizures with loss of consciousness. In the emergency department, she presented tonic-clonic seizures. The husband reported discomfort for the past 2 days with bloody diarrhoea, no fever and no abdominal or chest pain. She did not present haemoptysis or haematuria. On physical examination, the patient was in a postictal state, with global aphasia, haematomas, and scattered petechiae. A computed tomography (CT) scan was performed, but the findings were unremarkable. The only labs of interest were 10 × 10<span class="elsevierStyleSup">9</span>/l platelets (citrate), haemoglobin 10 g/dl normocytic, normochromic, indirect bilirubin 2.7 mg/dl, haptoglobin 1 mg/dl, LDH 1899 I/U. Coombs test negative. Haematology showed the presence of schistocytes in the blood smear.</p><p id="par0035" class="elsevierStylePara elsevierViewall">The PLASMIC score, which rates the risk of TTP on a scale of 0–7, was calculated<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a>:<ul class="elsevierStyleList" id="lis0005"><li class="elsevierStyleListItem" id="lsti0005"><span class="elsevierStyleLabel">-</span><p id="par0040" class="elsevierStylePara elsevierViewall">Platelets < 30 × 10<span class="elsevierStyleSup">9</span>/l</p></li><li class="elsevierStyleListItem" id="lsti0010"><span class="elsevierStyleLabel">-</span><p id="par0045" class="elsevierStylePara elsevierViewall">MCV < 90 fl</p></li><li class="elsevierStyleListItem" id="lsti0015"><span class="elsevierStyleLabel">-</span><p id="par0050" class="elsevierStylePara elsevierViewall">Creatinine < 2 mg/dl</p></li><li class="elsevierStyleListItem" id="lsti0020"><span class="elsevierStyleLabel">-</span><p id="par0055" class="elsevierStylePara elsevierViewall">INR < 1.5</p></li><li class="elsevierStyleListItem" id="lsti0025"><span class="elsevierStyleLabel">-</span><p id="par0060" class="elsevierStylePara elsevierViewall">Evidence of haemolysis: reticulocytes > 2.5%, indirect bilirubin > 2 mg/dl or undetectable haptoglobin</p></li><li class="elsevierStyleListItem" id="lsti0030"><span class="elsevierStyleLabel">-</span><p id="par0065" class="elsevierStylePara elsevierViewall">No active cancer</p></li><li class="elsevierStyleListItem" id="lsti0035"><span class="elsevierStyleLabel">-</span><p id="par0070" class="elsevierStylePara elsevierViewall">No history of solid organ or bone marrow transplantation</p></li></ul></p><p id="par0075" class="elsevierStylePara elsevierViewall">The patient met 7 out of a possible 7 criteria, so ADAMST13 and Shiga toxin tests were requested. We transferred the patient to the anaesthesia-ICU, conscious, oriented, sleepy, with right hemiparesis. A Mahurkar dialysis catheter was inserted into the right femoral vein and exchange with fresh frozen plasma was performed, with further plasmapheresis scheduled every 24 h/ for 5 consecutive days. Platelet transfusion was contraindicated, except in the event of life-threatening bleeding. The patient was given 1 mg/kg body weight methylprednisolone and folic acid supplements. The next day, diagnosis of TTP was confirmed with ADAMST13 of less than 0.5% (normal value: 40%–130%); inhibitory antibodies 21.8 IU/mL (positive if >15 U/mL), so acquired TTP with an unknown precipitating factor was diagnosed.</p><p id="par0080" class="elsevierStylePara elsevierViewall">Six days later, after 3 days with platelets > 150 × 10<span class="elsevierStyleSup">9</span>/l and normal LDH, regained mobility, and resolution of right hemiparesis, methylprednisolone was down-dosed to 0.5 mg/kg, and plasmapheresis was suspended the following day. Twenty four hours later (day 8), she presented an exacerbation (platelets 55 × 10<span class="elsevierStyleSup">9</span>/l), so plasmapheresis was restarted and steroids were updosed to 1 mg/kg. ADAMTS13 levels, which has increased to 26.7%, relapsed to below 0.5%. On day 14 of admission, ADAMTS13 levels were still below 0.5% (with platelets >150 × 10<span class="elsevierStyleSup">9</span>/l), so it was decided to add rituximab 375 mg/m<span class="elsevierStyleSup">2</span> once weekly for 4 consecutive weeks. Daily plasmapheresis was maintained until day 23, and ADAMTS13 and platelet levels recovered > 150 × 10<span class="elsevierStyleSup">9</span>/l (after 10 days). The patient was discharged from hospital 5 days later without incident, with platelets 268 × 10<span class="elsevierStyleSup">9</span>/l, with prednisone 80 mg/day.</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Case 2. Atypical haemolytic uraemic syndrome</span><p id="par0085" class="elsevierStylePara elsevierViewall">Our patient was a 22-year-old woman, 33 weeks pregnant, with no other history of interest, who went to the emergency room due to continuous, strong, uterine contractions. Placental abruption was diagnosed on the basis of clinical manifestations and ultrasound findings, and she was transferred urgently to the operating room where rapid sequence induction and orotracheal intubation was performed. A still born foetus was extracted. The patient presented complete (100%) placental abruption with abundant clots on the maternal side. Oozing haemorrhage was observed in subcutaneous cellular tissue, and the patient required 2.500 ml of crystalloids, 1 g tranexamic acid, 2 g of fibrinogen and 1 unit of fresh frozen plasma. Preoperative labs showed haemoglobin 12 g/dl, 277 × 10<span class="elsevierStyleSup">9</span>/l platelets (citrate), Quick Index (QI) 92%, APTT 26 s and fibrinogen 355 mg/dl. Intraoperative blood gas monitoring showed haemoglobin 9.8 g/dl, so no intraoperative blood transfusion or vasoactive drugs were required. The patient was extubated without incident and transferred to the anaesthesia ICU.</p><p id="par0090" class="elsevierStylePara elsevierViewall">The first postoperative labs showed haemoglobin 8.3 g/dl, QI 59%, platelets 149 × 10<span class="elsevierStyleSup">9</span>/l (citrate), APTT 37 s, derived fibrinogen 149 mg/dl (Clauss fibrinogen 40 mg/dl), creatinine 1.1 mg/dl. She was given 3 g fibrinogen, 10 mg K, 1000 mg iron carboxymaltose, and 1 unit of red blood cells.</p><p id="par0095" class="elsevierStylePara elsevierViewall">The next day, she presented severe acute renal failure (Cr 4.5 mg/dl, urea 58.6 mg/dl). Furosemide was administered to maintain urine output at >1 ml/kg/h. The patient also presented high blood pressure and oedema, together with hyperkalaemia (7 mEq/l) that responded to conservative therapy without haemodialysis, and required transfusion of 2 units of red blood cells. Clotting normalized, with QI 97%, APTT 27 s, fibrinogen 330 mg/dl and platelets 87 × 10<span class="elsevierStyleSup">9</span>/l (citrate). Labs showed elevated LDH (724 I/U), proteinuria (pr/cr ratio 4.9 g/g), hypoproteinaemia (4.2 g/dl), normal liver enzymes, and CPK 452 l/U. The initial complement study showed C3 65 mg/dl and C4 9 mg/dl (hypocomplementemia), with evidence of haemolysis with decreased haptoglobin (18 mg/dl) and negative Coombs test. Urine sediment showed 10–30 leukocytes per field. Antinuclear antibody test was negative. Preeclampsia was ruled out based on the previous ultrasound measurements made by the gynaecologist and supported by a normal sFlt-1/PIGF index. The smear showed 1–2 schistocytes per field.</p><p id="par0100" class="elsevierStylePara elsevierViewall">ADAMTS13 (normal: 99.6%), Shiga toxin (absent) and antiphospholipid antibody (normal) tests were ordered. We decided to start exchange with replacement of fresh plasma before starting eculizumab (Soliris®), given the suspicion of aHUS.</p><p id="par0105" class="elsevierStylePara elsevierViewall">Plasmapheresis was repeated 24 h later, and the first dose of eculizumab 900 mg was administered. Eculizumab, due to its mechanism of action, increases the patient’s susceptibility to meningococcal infection, so both meningococcal vaccines were administered. The third and last plasmapheresis was performed the following day.</p><p id="par0110" class="elsevierStylePara elsevierViewall">After starting eculizumab, the patient presented progressive and rapid recovery of platelets, haemoglobin and renal function, normalization of complement levels, and resolution of haemolysis. She was discharged after 7 days in the ICU. Eculizumab was continued as recommended in the package leaflet (starting with 900 mg/week/for 4 weeks and 1200 mg/every 15 days thereafter). The patient was given the result of the genetic study in the outpatient kidney clinic, which showed that she was the carrier of a homozygous deletion in the chromosomal region where the CFHR3 (OMIM#605336), CFHR1(OMIM#134371), and Chr1q31.3(196,743,929_196,801,319) genes are located. Factor H-related proteins comprise a group of 5 plasma proteins: CFHR1, CFHR2, CFHR3, CFHR4, and CFHR5, and each member of this group binds to the core complement component C3b. Mutations, genetic deletions, duplications, or rearrangements in individual CFHR genes are associated with a number of diseases, including aHUS.</p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Discussion</span><p id="par0115" class="elsevierStylePara elsevierViewall">TMAs are haematological emergencies that require urgent intervention. Targeted treatment relies on a rapid differential diagnosis, and diagnostic algorithms are very useful in clinical practice. The following is our diagnostic-therapeutic algorithm (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>), bearing in mind that a differential diagnosis with secondary causes of TMA must also be made.</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0120" class="elsevierStylePara elsevierViewall">Eculizumab is a humanized monoclonal antibody that inhibits C5 activation, generation of the proinflammatory molecule C5a, and formation of the membrane attack complex (C5b-C9); it preserves the first components of complement activation that are essential for the opsonization of microorganisms and the elimination of immune complexes. Its use in aHUS has greatly improved prognosis in this disease.</p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Conflict of interests</span><p id="par0125" class="elsevierStylePara elsevierViewall">The authors have no conflict of interest to declare.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:10 [ 0 => array:3 [ "identificador" => "xres1697480" "titulo" => "Abstract" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0005" ] ] ] 1 => array:2 [ "identificador" => "xpalclavsec1503523" "titulo" => "Keywords" ] 2 => array:3 [ "identificador" => "xres1697481" "titulo" => "Resumen" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0010" ] ] ] 3 => array:2 [ "identificador" => "xpalclavsec1503524" "titulo" => "Palabras clave" ] 4 => array:2 [ "identificador" => "sec0005" "titulo" => "Introduction" ] 5 => array:2 [ "identificador" => "sec0010" "titulo" => "Case 1. Thrombotic thrombocytopenic purpura" ] 6 => array:2 [ "identificador" => "sec0015" "titulo" => "Case 2. Atypical haemolytic uraemic syndrome" ] 7 => array:2 [ "identificador" => "sec0020" "titulo" => "Discussion" ] 8 => array:2 [ "identificador" => "sec0025" "titulo" => "Conflict of interests" ] 9 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "fechaRecibido" => "2020-07-28" "fechaAceptado" => "2020-11-30" "PalabrasClave" => array:2 [ "en" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec1503523" "palabras" => array:5 [ 0 => "Thrombotic microangiopathy" 1 => "Hemolytic uremic syndrome" 2 => "Thrombotic thrombocytopenic purpura" 3 => "Eculizumab" 4 => "ADAMTS13" ] ] ] "es" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec1503524" "palabras" => array:5 [ 0 => "Microangiopatía trombótica" 1 => "Síndrome hemolítico urémico" 2 => "Púrpura trombocitopénica trombótica" 3 => "Eculizumab" 4 => "ADAMTS13" ] ] ] ] "tieneResumen" => true "resumen" => array:2 [ "en" => array:2 [ "titulo" => "Abstract" "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Thrombotic microangiopathies (TMA) are a group of clinical syndromes associated with haemolytic anaemia, thrombocytopenia and organ dysfunction, mainly renal or neurological. They are associated with significant morbidity and mortality, so early diagnosis and treatment are essential. In this article we report two cases of TMA; a patient with thrombotic thrombocytopenic purpura (TTP) and a patient with atypical haemolytic uraemic syndrome (aHUS).</p></span>" ] "es" => array:2 [ "titulo" => "Resumen" "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">Las microangiopatías trombóticas (MAT) son un conjunto de síndromes clínicos que asocian anemia hemolítica, trombocitopenia y disfunción orgánica, principalmente renal o neurológica. Están asociados a una morbimortalidad significativa, por lo que su diagnóstico y tratamiento precoz son esenciales. En este artículo detallamos 2 casos de MAT; una paciente con una púrpura trombocitopénica trombótica (PTT) y otra paciente con un síndrome hemolítico urémico atípico (SHUa).</p></span>" ] ] "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: Rubio-Haro R, Quesada-Carrascosa M, Hernández-Laforet J, Ferrer Gómez C, De Andrés J. Algoritmo diagnóstico-terapéutico de las microangiopatías trombóticas. A propósito de 2 casos. Rev Esp Anestesiol Reanim. 2022. <span class="elsevierStyleInterRef" id="intr0005" href="https://doi.org/10.1016/j.redar.2020.11.016">https://doi.org/10.1016/j.redar.2020.11.016</span></p>" ] ] "multimedia" => array:1 [ 0 => array:8 [ "identificador" => "fig0005" "etiqueta" => "Figure 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 4175 "Ancho" => 2869 "Tamanyo" => 775008 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0005" "detalle" => "Figure " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">TMA diagnostic-therapeutic algorithm.</p> <p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">aHUS: atypical HUS; CT: computed tomography; DIC: disseminated intravascular coagulation; ECG: electrocardiogram; ETEC: <span class="elsevierStyleItalic">Escherichia coli</span> enterotoxigenic; HUS: haemolytic uremic syndrome; LDH: lactate dehydrogenase; TMA: thrombotic microangiopathy; TTP: thrombotic thrombocytopenic purpura.</p>" ] ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0005" "bibliografiaReferencia" => array:5 [ 0 => array:3 [ "identificador" => "bib0005" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Thrombotic microangiopathies: a general approach to diagnosis and management" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:3 [ 0 => "D.M. 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Diagnostic-therapeutic algorithm for thrombotic microangiopathy. A report of two cases
Algoritmo diagnóstico-terapéutico de las microangiopatías trombóticas. A propósito de 2 casos