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His apparent familial association does not seem casual, given the low prevalence of the disease. Familial sarcoidosis was first reported in 1923 by Martenstein,<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">2</span></a> who reported the case of two sisters affected by this disease. Although there are many series of sarcoidosis in Spanish literature, it is exceptional to find this association. Therefore, we present the case of two sisters affected by LS.</p><p id="par0010" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Case 1.</span> 31-year-old woman who presented with generalized joint pain, fever up to 38.5<span class="elsevierStyleHsp" style=""></span>°C and erythematous nodular lesions on the back of both legs. Purple nodules, painful on palpation stood out on physical examination, compatible with erythema nodosum. All analytical studies were normal. Chest radiography showed mediastinal widening indicative of bilateral lymphadenopathy. Spirometry, volumes, diffusion and walk test were normal. Computed tomography (CT) confirmed the bilateral hilar and mediastinal lymph nodes with normal lung parenchyma.</p><p id="par0015" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Case 2.</span> 32-year-old woman who consulted, 4 years after diagnosis of his sister, for painless swelling of the ankles, fever and nodules on the legs. Physical examination, except for the nodules, which were slightly painful on palpation, was normal. Lab results highlighted a ESR of 54<span class="elsevierStyleHsp" style=""></span>mm and a CRP of 65<span class="elsevierStyleHsp" style=""></span>mg/l. Biochemistry was normal, with angiotensin converting enzyme at 164<span class="elsevierStyleHsp" style=""></span>U/l (normal range 8–52<span class="elsevierStyleHsp" style=""></span>U/l) and polyclonal hypogammaglobinaemia. The chest radiograph showed bilateral hilar enlargement and right paratracheal mediastinal widening. Lung function tests were normal, and CT scan showed no interstitial lung disease.</p><p id="par0020" class="elsevierStylePara elsevierViewall">The presence of the typical triad (erythema nodosum, fever and bilateral hilar lymphadenopathy) confirmed the diagnosis in both cases without the need of histological studies. The outcome was favourable after treatment with NSAIDs.</p><p id="par0025" class="elsevierStylePara elsevierViewall">Estimates of sarcoidosis familial aggregation range from 0.8% in Spain<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">3</span></a> and 17% in the United States. <span class="elsevierStyleItalic">A Case Control Etiologic Study of Sarcoidosis</span> -ACCESS-<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">4</span></a> concluded that there is a high risk among first- and second-degree relatives of patients–especially between siblings–compared with relatives of controls. Although sarcoidosis is a genetically complex disease due to the involvement of several genes that contribute to the risk of its development, the strongest associations are found in the HLA region of the short arm of chromosome 6. Specifically, there has been a strong association between HLA-DRB1*0301, LS and good prognosis.<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">5</span></a> The <span class="elsevierStyleItalic">BTNL2</span> gen has a strong link with DRB1*15, which entails a higher risk of having sarcoidosis. The recent identification of a particular haplotype 2 -CCR2- in Spain and Sweden involves a separate genetic risk factor, which would support the idea of LS being treated as distinct entity within sarcoidosis. The 2 sisters were proposed to undergo a genetic study, but rejected the same.</p><p id="par0030" class="elsevierStylePara elsevierViewall">The cases described support studies of familial aggregation of sarcoidosis and consideration of LS as a subgroup associated with genetic factors that confer special characteristics to it, with a favourable clinical course and progression. The association between clinical manifestations and certain genetic factors that can help us predict the course of the disease and improve patient treatment should be highlighted.</p></span>" "pdfFichero" => "main.pdf" "tienePdf" => true "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: Rodríguez Martín C, Martín Asenjo M, Prieto de Paula JM. Síndrome de Löfgren familiar. Med Clin (Barc). 2016;147:374.</p>" ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0005" "bibliografiaReferencia" => array:5 [ 0 => array:3 [ "identificador" => "bib0030" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Medical progress: sarcoidosis" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:3 [ 0 => "M. Iannuzzi" 1 => "B. Rybicki" 2 => "A. 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Journal Information
Vol. 147. Issue 8.
Pages 374 (October 2016)
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Vol. 147. Issue 8.
Pages 374 (October 2016)
Letter to the Editor
Löfgren's familiar syndrome
Síndrome de Löfgren familiar
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Cristina Rodríguez Martín
, Miguel Martín Asenjo, José Maria Prieto de Paula
Corresponding author
Servicio de Medicina Interna, Hospital Clínico Universitario de Valladolid, Valladolid, Spain
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