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Letter to the Editor
Systemic capillary extravasation syndrome (Clarkson’s syndrome) in a patient with primary hypothyroidism
Síndrome de extravasación capilar sistémica (síndrome de Clarkson) en una paciente con hipotiroidismo primario
Felipe Blascoa,
Corresponding author
fblasco@torrevieja-salud.com

Corresponding author.
, Ana Elena Guillamóna, María Navarrob
a Unidad de Diagnóstico Médico y Enfermedades Minoritarias, Hospital Universitario de Torrevieja, Torrevieja, Alicante, Spain
b Servicio de Medicina Interna, Hospital Universitario de Torrevieja, Torrevieja, Alicante, Spain
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Systemic capillary leak syndrome &#40;SCLS&#41;&#44; also known as Clarkson&#8217;s syndrome&#44; is an extremely rare and potentially fatal process characterized by abrupt and recurrent episodes of anasarca&#44; hypotension&#44; hemoconcentration&#44; and hypoalbuminemia not associated with protein loss&#44; in the context of massive plasma extravasation into the extravascular space secondary to increased capillary permeability&#46; The underlying mechanism of this disease is unknown&#44; although 82&#37; of cases exhibit increased levels of immunoglobulin G subclass 1 &#40;IgG1&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">In this case report we describe how an elevation in the levels of vascular endothelial growth factor &#40;VEGF&#41;&#44; one of whose effects is to increase capillary permeability&#44; secondary to a sustained stimulus of thyroid stimulating hormone &#40;TSH&#41;&#44; may have triggered this process and explain the myxedema described in untreated primary hypothyroidism&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">We describe the case of a 52-year-old woman with clinical criteria of autoimmune polyglandular syndrome type 4 &#40;type 1 diabetes mellitus&#44; autoimmune hypothyroidism&#44; and pernicious anemia&#41; who visited the Emergency Department with anasarca of abrupt onset&#46; She reported that she had discontinued levothyroxine a few months earlier&#46; Laboratory tests performed on admission revealed TSH levels &#62;150&#160;uIU&#47;ml and thyroxine &#40;T4&#41; levels of 0&#46;38&#160;ng&#47;dl&#46; Because a chest X-ray showed severe bilateral pleural effusion&#44; a thoracocentesis was consequently performed&#44; extracting 900&#160;ml of fluid compatible with transudate&#46; An abdominal ultrasound revealed images of ascites&#44; but no signs of a chronic liver disease&#46; The diagnostic studies were completed with an echocardiogram that showed no valvular nor contractility alterations&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">Additional blood work revealed albumin levels of 2&#46;4&#160;g&#47;dl and baseline cortisol levels of 14&#160;&#181;g&#47;dl&#46; All other parameters fell within normal limits&#46; Because of the increased extravascular volume&#44; the abrupt onset associated with hypoalbuminemia&#44; but not albuminuria&#44; as well as the study findings ruling out a nephrotic syndrome&#44; liver cirrhosis&#44; or heart failure&#44; a potential diagnosis of SCLS was considered&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">Both a VEGF level above 1000&#160;pg&#47;ml &#40;normal value&#58; &#60;124&#160;pg&#47;ml&#41; and the existence of an IgG1 monoclonal component were confirmed&#46; After correcting the hypothyroidism and normalizing the TSH levels&#44; the VEGF levels dropped to 250&#160;pg&#47;ml&#44; but no changes were observed in the IgG1 levels&#46; The patient&#8217;s symptoms resolved within a few weeks&#44; and she has not experienced a relapse after one year of follow-up&#46;</p><p id="par0030" class="elsevierStylePara elsevierViewall">The VEGF comprises a set of proteins synthesized from a single gene that encodes 5 protein isoforms that interact with 3 tyrosine kinase receptors&#46; Activation of VEGF receptor 1 &#40;VEGFR-1&#41; by isoforms VEGF-C or VEGF-D leads to an increase in vascular permeability&#46; In a cohort of 20 patients with the classic form of SCLS&#44; all patients had significantly higher VEGF levels than the controls&#44; and short intervals of elevated VEGF levels coincided with episodes of SCLS&#46;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">This factor is also increased in the context of inflammation induced by interferon beta&#44; interleukins &#40;IL-1 and IL-6&#41;&#44; growth factors such as fibroblast growth factor 4 &#40;FFG-4&#41; and insulin-like growth factor 1 &#40;IGF-1&#41;&#44; and hypoxia&#46; Increased plasma levels of this factor have also been described with tumors secreting follicle-stimulating hormone &#40;FSH&#41; or luteinizing hormone &#40;LH&#41;&#44; as well as with oral contraceptives&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">With respect to the case described herein&#44; experimental studies carried out primarily with thyroid tumors have demonstrated how TSH induces the production of VEGF through increased expression of the gene regulating the synthesis of this protein&#46;<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> The suppression of this stimulus by means of treatment with levothyroxine and normalization of the TSH levels was followed by a marked decrease in the VEGF levels and resolution of the anasarca&#44; which has not recurred after one year of follow-up&#46;</p><p id="par0045" class="elsevierStylePara elsevierViewall">Coinciding with other authors&#44; we conclude that the role of IgG1 in the onset of this disease is debatable and that this parameter seems to be more related to an adaptive clinical response than being a triggering factor in itself&#46; This is supported by data from a case series published by Xie et al&#46;&#44;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> in which the levels of these antibodies showed no differences between active episodes and the remission phase&#46; Thus&#44; we hypothesize that IgG1 acts as a control mechanism in this context&#46; In their study on the angiogenesis suppression effect of humanized IgG1 antibodies&#44; Bogdanovich et al&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> suggest that endogenous antibodies&#44; such as IgG1&#44; may play a homeostatic role in modulating the action of the VEGF&#46; In this context&#44; an increase in IgG1 levels would entail nothing more than a modulatory response to block VEGF activity&#46; This response&#44; once triggered&#44; would persist over time&#46;</p></span>"
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        "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as&#58; Blasco F&#44; Guillam&#243;n AE&#44; Navarro M&#46; S&#237;ndrome de extravasaci&#243;n capilar sist&#233;mica &#40;s&#237;ndrome de Clarkson&#41; en una paciente con hipotiroidismo primario&#46; Med Clin &#40;Barc&#41;&#46; 2020&#46; <span class="elsevierStyleInterRef" id="intr0005" href="https://doi.org/10.1016/j.medcli.2020.05.056">https&#58;&#47;&#47;doi&#46;org&#47;10&#46;1016&#47;j&#46;medcli&#46;2020&#46;05&#46;056</span></p>"
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