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Ternero Vega, R.G. León, D.A. Delgado, M.O. Baturone" "autores" => array:4 [ 0 => array:4 [ "nombre" => "J.E." "apellidos" => "Ternero Vega" "email" => array:1 [ 0 => "jaraeloisa@hotmail.com" ] "referencia" => array:2 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] 1 => array:2 [ "etiqueta" => "*" "identificador" => "cor0005" ] ] ] 1 => array:3 [ "nombre" => "R.G." "apellidos" => "León" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] ] ] 2 => array:3 [ "nombre" => "D.A." "apellidos" => "Delgado" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "aff0010" ] ] ] 3 => array:3 [ "nombre" => "M.O." "apellidos" => "Baturone" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] ] ] ] "afiliaciones" => array:2 [ 0 => array:3 [ "entidad" => "Servicio de Medicina Interna, Hospital Universitario Virgen del Rocío, Sevilla, Spain" "etiqueta" => "a" "identificador" => "aff0005" ] 1 => array:3 [ "entidad" => "Servicio de Endocrinología y Nutrición, Hospital Universitario Virgen del Rocío, Sevilla, Spain" "etiqueta" => "b" "identificador" => "aff0010" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "Corresponding author." ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Síndrome de Guillain-Barré e hiponatremia" ] ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0005" "etiqueta" => "Figure 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 906 "Ancho" => 2201 "Tamanyo" => 87137 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Changes in our patient's sodium levels during hospitalisation.</p>" ] ] ] "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Hyponatraemia, the most prevalent electrolyte imbalance in clinical practice, is associated with increased morbidity and mortality. The association between hyponatraemia and Guillain-Barré syndrome (GBS) has been described in the literature, although few studies have analysed its prevalence, aetiology, pathophysiology, diagnosis, and treatment. We present the case of a patient with GBS and severe hyponatraemia.</p><p id="par0010" class="elsevierStylePara elsevierViewall">The patient was a 59-year-old man with type 2 diabetes mellitus and good metabolic control. He attended our hospital due to paraesthesia in the hands and feet and difficulty walking (2 falls at home), loss of sphincter control (requiring a urinary catheter), general discomfort, and drowsiness. Three weeks previously, the patient had presented diarrhoea, which lasted 3 days and resolved spontaneously. The examination revealed symmetric paraparesis, hypoaesthesia in both hands, and generalised areflexia. The patient was adequately hydrated and did not present oedema. A blood analysis revealed a low sodium concentration at 121<span class="elsevierStyleHsp" style=""></span>mEq/L (normal range, 135-145<span class="elsevierStyleHsp" style=""></span>mEq/L) and a glucose level of 168<span class="elsevierStyleHsp" style=""></span>mg/dL (normal range, 80-120<span class="elsevierStyleHsp" style=""></span>mg/dL), with normal potassium, urea, creatinine, and total protein concentrations; a head CT scan revealed no abnormalities. A CSF analysis detected albuminocytologic dissociation, a protein level of 2.34<span class="elsevierStyleHsp" style=""></span>g/L (normal range, 0.15-0.5<span class="elsevierStyleHsp" style=""></span>g/L), and a cell count of 8<span class="elsevierStyleHsp" style=""></span>cells/mm<span class="elsevierStyleSup">3</span>. The microbiological analysis yielded negative results. Based on these findings, the patient was diagnosed with acute inflammatory demyelinating polyradiculoneuropathy (a form of GBS) and euvolaemic hyponatraemia.</p><p id="par0015" class="elsevierStylePara elsevierViewall">We started treatment with immunoglobulins (Ig) dosed at 0.4<span class="elsevierStyleHsp" style=""></span>g/kg/day, in 5 boluses. However, treatment only achieved partial motor improvements, and an additional cycle was necessary 2 weeks later. Electroneurography and electromyography studies performed during hospitalisation confirmed the diagnosis. Neurological symptoms improved progressively; at discharge (a month after admission), however, the patient continued to display lower limb weakness, which prevented him from walking.</p><p id="par0020" class="elsevierStylePara elsevierViewall">Physical examination results were compatible with euvolaemic hyponatraemia. Plasma osmolality was 239<span class="elsevierStyleHsp" style=""></span>mOsm/kg (normal range, 275-295<span class="elsevierStyleHsp" style=""></span>mOsm/kg), urine osmolality was 591<span class="elsevierStyleHsp" style=""></span>mOsm/kg (normal range, 100-700<span class="elsevierStyleHsp" style=""></span>mOsm/kg), urine sodium concentration was 80 mEq/L (normal range, 20-200 mEq/L), and TSH concentration was 1.70<span class="elsevierStyleHsp" style=""></span>mIU/mL (normal range, 0.4-4mIU/mL); the patient showed a normal lipid profile and no monoclonal proteins in protein electrophoresis. Chest radiography revealed mediastinal widening; a chest and abdomen CT scan revealed no signs of tumour. The patient was diagnosed with euvolaemic hyponatraemia associated with syndrome of inappropriate antidiuretic hormone secretion (SIADH) secondary to GBS. The patient was initially treated with 3% hypertonic saline (500<span class="elsevierStyleHsp" style=""></span>cc/24<span class="elsevierStyleHsp" style=""></span>h) and water restriction (800<span class="elsevierStyleHsp" style=""></span>cc/24<span class="elsevierStyleHsp" style=""></span>h); we subsequently administered tolvaptan dosed at 15<span class="elsevierStyleHsp" style=""></span>mg/day due to lack of response. The drug was up-titrated to 30<span class="elsevierStyleHsp" style=""></span>mg/day, and progressively withdrawn on an outpatient basis until complete discontinuation 4 months later.</p><p id="par0025" class="elsevierStylePara elsevierViewall">One year later, lower limb weakness had improved with rehabilitation therapy, although the patient needed crutches to walk. Serum sodium levels were normal (141<span class="elsevierStyleHsp" style=""></span>mEq/L).</p><p id="par0030" class="elsevierStylePara elsevierViewall">Although some studies report an association between hyponatraemia and GBS, few studies have analysed the correlation. This association results in poorer hospital outcomes even at one year,<a class="elsevierStyleCrossRefs" href="#bib0055"><span class="elsevierStyleSup">1–5</span></a> longer hospital stays,<a class="elsevierStyleCrossRefs" href="#bib0055"><span class="elsevierStyleSup">1–3</span></a> and higher costs.<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">1</span></a> The association between hyponatraemia and GBS is even reported to be an independent predictor of mortality,<a class="elsevierStyleCrossRefs" href="#bib0060"><span class="elsevierStyleSup">2,5</span></a> which has also been described in other disorders.<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">1</span></a> Some studies suggest that patients with GBS and hyponatraemia are more likely to require ventilatory support,<a class="elsevierStyleCrossRefs" href="#bib0055"><span class="elsevierStyleSup">1,2</span></a> which may be explained by the fact that severe hyponatraemia can manifest as respiratory distress.<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">6</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">Most cases of hyponatraemia in the context of GBS develop during hospitalisation and are associated with Ig treatment; pseudohyponatraemia linked to increased protein levels may therefore play an important role. Another possibility is associated with water transport from the intracellular space to the intravascular space due to increased osmolality secondary to infusion of sugar-stabilised Ig. Palevsky et al.<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">7</span></a> analysed the effect of Ig infusion on sodium levels, measured with direct potentiometry to avoid diagnosis of pseudohyponatraemia. The authors observed hyponatraemia, despite using this technique. SIADH is a frequent cause of true hyponatraemia in patients with GBS.<a class="elsevierStyleCrossRefs" href="#bib0060"><span class="elsevierStyleSup">2,8,9</span></a> Other cases are due to cerebral salt-wasting syndrome, although this association is very rare.</p><p id="par0040" class="elsevierStylePara elsevierViewall">Our patient may meet the diagnostic criteria for SIADH as established in the latest European hyponatraemia guidelines (plasma osmolality<span class="elsevierStyleHsp" style=""></span><<span class="elsevierStyleHsp" style=""></span>275<span class="elsevierStyleHsp" style=""></span>mOsm/kg; urine osmolality<span class="elsevierStyleHsp" style=""></span>><span class="elsevierStyleHsp" style=""></span>100<span class="elsevierStyleHsp" style=""></span>mOsm/kg; euvolaemia; and absence of adrenal insufficiency, hypothyroidism, hypopituitarism, or kidney failure).<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">7</span></a> We did not determine cortisol levels in our patient; however, clinical and laboratory results were not compatible with adrenal insufficiency. The prevalence of SIADH in patients with GBS is not clear; case reports constitute the only available evidence. The pathophysiological mechanisms of the association between GBS and hyponatraemia are yet to be understood. Several hypotheses have been proposed: alterations of hypothalamic cells, causing ADH release into the bloodstream; alterations in osmoregulation; increased sensitivity of ADH receptors; and other mechanisms not related to ADH.<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">9</span></a> Other researchers support the involvement of interleukin 6, which may increase vasopressin release.<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">10</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall">Interestingly, our patient's sodium levels decreased following Ig administration (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>). This may indicate pseudohyponatraemia and/or water transport to the intravascular space, which play a role in true hyponatraemia. In retrospect, this may explain the patient's poor response to hypertonic saline and water restriction and the need to up-titrate tolvaptan to 30<span class="elsevierStyleHsp" style=""></span>mg/day to achieve normal sodium levels.</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0050" class="elsevierStylePara elsevierViewall">The available evidence on treatment with tolvaptan in patients with GBS and SIADH is strikingly scarce: to our knowledge, only one case has been published to date.</p><p id="par0055" class="elsevierStylePara elsevierViewall">Sodium levels should be monitored in patients with GBS. Pseudohyponatraemia, water transport, and SIADH should be considered in the differential diagnosis of hyponatraemia. In our case, hyponatraemia may have played a role in the need for an additional cycle of Ig and the slow motor recovery.</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: Ternero Vega JE, León RG, Delgado DA, Baturone MO. Síndrome de Guillain-Barré e hiponatremia. Neurología. 2020;35:282–284.</p>" ] ] "multimedia" => array:1 [ 0 => array:7 [ "identificador" => "fig0005" "etiqueta" => "Figure 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 906 "Ancho" => 2201 "Tamanyo" => 87137 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Changes in our patient's sodium levels during hospitalisation.</p>" ] ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0015" "bibliografiaReferencia" => array:10 [ 0 => array:3 [ "identificador" => "bib0055" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Hyponatremia in Guillain-Barré syndrome" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:4 [ 0 => "K. Rumalla" 1 => "A.Y. Reddy" 2 => "V. 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2024 August | 138 | 8 | 146 |
2024 July | 155 | 18 | 173 |
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2023 December | 176 | 5 | 181 |
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2023 July | 99 | 3 | 102 |
2023 June | 110 | 17 | 127 |
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2023 April | 81 | 1 | 82 |
2023 March | 97 | 17 | 114 |
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2022 December | 75 | 9 | 84 |
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2020 December | 63 | 15 | 78 |
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2019 December | 8 | 8 | 16 |
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