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Coronal T1-weighted contrast-enhanced brain magnetic resonance showing a cystic lesion with contrast enhancement in its periphery, with an apparent nodule in its inferomedial part, with apparent central necrosis (arrow). B. Presence of severe lymphohistiocytic infiltrate and abundant macrophages, and centrally, a cross section of a larva with invaginations of its wall (arrow). Haematoxylin-eosin 4×. C. Cross section of cysticercus larva at the level of the scolex, showing the wavy tegument with microvilli and the presence of the hooks (arrow). 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(A) Langerhans cells have a monotonous morphology with a cleaved nucleus and large cytoplasm (H&E 400×). (B) Variable expression for nuclear/cytoplasmic positive S-100 (400×). (C) Intense CD1a-positive membrane (400×). (D) Confluent erythematous papules on the hard palate with a shiny, translucent appearance, corresponding to infiltration by histiocytosis. (E) Plain bone X-ray with osteolytic lesion in the distal femur. 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This pathology, described in 1953, is autosomally transmitted, so that both males and females can develop a haemorrhagic phenotype.<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> The <span class="elsevierStyleItalic">F11</span> gene is located on chromosome 4 (4q35) and is 23 kilobases in length.<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">Over the past 2 decades, more than 220 F11 gene mutations in FXI-deficient patients have been reported, of which only 7 showed a founder effect.<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> The wide range of clinical manifestations leads us to try to identify which mutations correlate with the haemorrhagic phenotype. This has a very important clinical influence, as it is difficult to establish which patients will need treatment and which will not.</p><p id="par0015" class="elsevierStylePara elsevierViewall">We report the case of a 60-year-old woman from the UK who has been living in Spain since 2020. She had no personal or family history of haemorrhage or thrombosis. In addition, she reported 2 dental extractions and an appendicitis operation without bleeding. No previous coagulation or genetic characterisation studies conducted in the UK were reported. In a routine laboratory control in January 2021, the automated coagulometer (TriniCLOTTM aPTT HS, Stago) detected an increased activated partial thromboplastin time (aPTT): aPTT 67.60 s (normal value: 20−40 s); aPTTr 2.11 (normal value: 0.8–1.25). Given the presence of a prolonged aPTT, a haemostasis study was performed to rule out the presence of lupus anticoagulant and the presence of inhibitor, and the lupus anticoagulant was negative: DVVR 0.97 (normal value < 1.2) and no inhibitor. Subsequently, an FXI level of 0.3% (normal value > 60%) was detected. The determination of FXI levels was obtained using an optical impedance coagulometer, which quantitatively determines FXI activity in citrated human plasma, based on the aPTT test in IL coagulation systems. The rest of the coagulation factors were within normal range.</p><p id="par0020" class="elsevierStylePara elsevierViewall">A second FXI value determination in February 2021 yielded a result of 1.3% and the genetic study was performed. The entire <span class="elsevierStyleItalic">F11</span> gene was sequenced by next generation sequencing.<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> The result was obtained in March 2022, which detected 2 heterozygous missense mutations in the <span class="elsevierStyleItalic">F11 gene</span>, one heterozygous in exon 6.c.508A>C(T152P) not previously described and the other heterozygous in exon 11,c.1247G>A(C398Y), previously described. The family study could not be completed because the patient did not have any living siblings or parents.</p><p id="par0025" class="elsevierStylePara elsevierViewall">We have described a new variant in the <span class="elsevierStyleItalic">F11</span> gene associated with FXI levels below 1% in a woman with a non-haemorrhagic phenotype with the previously described mutations. After reviewing all reported cases of the known mutation (exon 11,c.1247G>A(C398Y)) and its correlation with factor XI levels and clinical phenotype (<a href="http://www.factorxi.org/">http://www.factorxi.org/</a>), we observed that in this mutation FXI levels were between 40 and 58% in patients with no history of bleeding, according to the reported data. In 2 cases where it was present in homozygous form, levels were less than 1% and were associated with different types of bleeding. For patients with compound heterozygosity, values below 2% were associated with no bleeding. In our case, the known mutation would not explain the low FXI levels, but in heterozygotes with the new mutation in exon 6, the double heterozygous FXI levels were less than 1%, although this had no impact on the clinical presentation due to the absence of bleeding diathesis.</p><p id="par0030" class="elsevierStylePara elsevierViewall">In conclusion, we have conducted a case study whose literature review was carried out between December 2022 and January 2023 (<a href="http://www.factorxi.org/">http://www.factorxi.org/</a>). The descriptors used are factor XI deficiency; factor 11 gene; new mutation. Here we describe a novel mutation that, in compound heterozygosity with another known mutation, has FXI <1% levels and no familial or personal haemorrhagic or thrombotic symptoms. Hence the need to reconsider FXI deficiency as a rare haemorrhagic disease. Further studies are needed to know which genotype is associated with bleeding and which genotype is associated with protection against thromboembolic disease. In addition, the name described in the 20th century as haemophilia C should also be reconsidered, and a new nomenclature should be determined that better fits the associated clinical features.<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a></p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Ethical considerations</span><p id="par0035" class="elsevierStylePara elsevierViewall">Informed written consent was obtained from the patient for publication of this original article.</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0010">Funding</span><p id="par0040" class="elsevierStylePara elsevierViewall">None.</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0015">Conflict of interest</span><p id="par0045" class="elsevierStylePara elsevierViewall">None.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:4 [ 0 => array:2 [ "identificador" => "sec0005" "titulo" => "Ethical considerations" ] 1 => array:2 [ "identificador" => "sec0010" "titulo" => "Funding" ] 2 => array:2 [ "identificador" => "sec0015" "titulo" => "Conflict of interest" ] 3 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "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" => "Guideline for the diagnosis and management of the rare coagulation disorders: a United Kingdom Haemophilia Centre Doctors’ Organization guideline on behalf of the British Committee for Standards in Haematology" "autores" => array:1 [ 0 => array:2 [ "etal" => true "autores" => array:6 [ 0 => "A.D. Mumford" 1 => "S. Ackroyd" 2 => "R. Alikhan" 3 => "L. Bowles" 4 => "P. Chowdary" 5 => "J. Grainger" ] ] ] ] ] "host" => array:1 [ 0 => array:1 [ "Revista" => array:4 [ "tituloSerie" => "Br J Haematol" "fecha" => "2014" "volumen" => "167" "paginaInicial" => "304" ] ] ] ] ] ] 1 => array:3 [ "identificador" => "bib0010" "etiqueta" => "2" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Spectrum of factor XI (F11) mutations in the UK population – 116 index cases and 140 mutations" "autores" => array:1 [ 0 => array:2 [ "etal" => true "autores" => array:6 [ 0 => "M. Mitchell" 1 => "R. Mountford" 2 => "R. Butler" 3 => "A. Alhaq" 4 => "L. Dai" 5 => "G. Savidge" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1002/humu.9440" "Revista" => array:5 [ "tituloSerie" => "Hum Mutat" "fecha" => "2006" "volumen" => "27" "paginaInicial" => "829" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/16835902" "web" => "Medline" ] ] ] ] ] ] ] ] 2 => array:3 [ "identificador" => "bib0015" "etiqueta" => "3" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Congenital factor XI deficiency: an update" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:2 [ 0 => "S. Duga" 1 => "O. 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Martin-Fernández" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1182/blood.2019000055" "Revista" => array:6 [ "tituloSerie" => "Blood" "fecha" => "2019" "volumen" => "133" "paginaInicial" => "2618" "paginaFinal" => "2622" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/31043424" "web" => "Medline" ] ] ] ] ] ] ] ] 4 => array:3 [ "identificador" => "bib0025" "etiqueta" => "5" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Factor XI and contact activation as targets for antithrombotic therapy" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:3 [ 0 => "D. Gailani" 1 => "C.E. Bane" 2 => "A. Gruber" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1111/jth.13005" "Revista" => array:6 [ "tituloSerie" => "J Thromb Haemost" "fecha" => "2015" "volumen" => "13" "paginaInicial" => "1383" "paginaFinal" => "1395" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/25976012" "web" => "Medline" ] ] ] ] ] ] ] ] ] ] ] ] ] "idiomaDefecto" => "en" "url" => "/23870206/0000016100000004/v1_202308280911/S2387020623003145/v1_202308280911/en/main.assets" "Apartado" => array:4 [ "identificador" => "43309" "tipo" => "SECCION" "en" => array:2 [ "titulo" => "Letters to the Editor" "idiomaDefecto" => true ] "idiomaDefecto" => "en" ] "PDF" => "https://static.elsevier.es/multimedia/23870206/0000016100000004/v1_202308280911/S2387020623003145/v1_202308280911/en/main.pdf?idApp=UINPBA00004N&text.app=https://www.elsevier.es/" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2387020623003145?idApp=UINPBA00004N" ]
