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Letter to the Editor
Guillain-Barré syndrome and hyponatraemia
Síndrome de Guillain-Barré e hiponatremia
J.E. Ternero Vegaa,
Corresponding author
jaraeloisa@hotmail.com

Corresponding author.
, R.G. Leóna, D.A. Delgadob, M.O. Baturonea
a Servicio de Medicina Interna, Hospital Universitario Virgen del Rocío, Sevilla, Spain
b Servicio de Endocrinología y Nutrición, Hospital Universitario Virgen del Rocío, Sevilla, Spain
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the patient had presented diarrhoea&#44; which lasted 3 days and resolved spontaneously&#46; The examination revealed symmetric paraparesis&#44; hypoaesthesia in both hands&#44; and generalised areflexia&#46; The patient was adequately hydrated and did not present oedema&#46; A blood analysis revealed a low sodium concentration at 121<span class="elsevierStyleHsp" style=""></span>mEq&#47;L &#40;normal range&#44; 135-145<span class="elsevierStyleHsp" style=""></span>mEq&#47;L&#41; and a glucose level of 168<span class="elsevierStyleHsp" style=""></span>mg&#47;dL &#40;normal range&#44; 80-120<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#41;&#44; with normal potassium&#44; urea&#44; creatinine&#44; and total protein concentrations&#59; a head CT scan revealed no abnormalities&#46; A CSF analysis detected albuminocytologic dissociation&#44; a protein level of 2&#46;34<span class="elsevierStyleHsp" style=""></span>g&#47;L &#40;normal range&#44; 0&#46;15-0&#46;5<span class="elsevierStyleHsp" style=""></span>g&#47;L&#41;&#44; and a cell count of 8<span class="elsevierStyleHsp" style=""></span>cells&#47;mm<span class="elsevierStyleSup">3</span>&#46; The microbiological analysis yielded negative results&#46; Based on these findings&#44; the patient was diagnosed with acute inflammatory demyelinating polyradiculoneuropathy &#40;a form of GBS&#41; and euvolaemic hyponatraemia&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">We started treatment with immunoglobulins &#40;Ig&#41; dosed at 0&#46;4<span class="elsevierStyleHsp" style=""></span>g&#47;kg&#47;day&#44; in 5 boluses&#46; However&#44; treatment only achieved partial motor improvements&#44; and an additional cycle was necessary 2 weeks later&#46; Electroneurography and electromyography studies performed during hospitalisation confirmed the diagnosis&#46; Neurological symptoms improved progressively&#59; at discharge &#40;a month after admission&#41;&#44; however&#44; the patient continued to display lower limb weakness&#44; which prevented him from walking&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">Physical examination results were compatible with euvolaemic hyponatraemia&#46; Plasma osmolality was 239<span class="elsevierStyleHsp" style=""></span>mOsm&#47;kg &#40;normal range&#44; 275-295<span class="elsevierStyleHsp" style=""></span>mOsm&#47;kg&#41;&#44; urine osmolality was 591<span class="elsevierStyleHsp" style=""></span>mOsm&#47;kg &#40;normal range&#44; 100-700<span class="elsevierStyleHsp" style=""></span>mOsm&#47;kg&#41;&#44; urine sodium concentration was 80 mEq&#47;L &#40;normal range&#44; 20-200 mEq&#47;L&#41;&#44; and TSH concentration was 1&#46;70<span class="elsevierStyleHsp" style=""></span>mIU&#47;mL &#40;normal range&#44; 0&#46;4-4mIU&#47;mL&#41;&#59; the patient showed a normal lipid profile and no monoclonal proteins in protein electrophoresis&#46; Chest radiography revealed mediastinal widening&#59; a chest and abdomen CT scan revealed no signs of tumour&#46; The patient was diagnosed with euvolaemic hyponatraemia associated with syndrome of inappropriate antidiuretic hormone secretion &#40;SIADH&#41; secondary to GBS&#46; The patient was initially treated with 3&#37; hypertonic saline &#40;500<span class="elsevierStyleHsp" style=""></span>cc&#47;24<span class="elsevierStyleHsp" style=""></span>h&#41; and water restriction &#40;800<span class="elsevierStyleHsp" style=""></span>cc&#47;24<span class="elsevierStyleHsp" style=""></span>h&#41;&#59; we subsequently administered tolvaptan dosed at 15<span class="elsevierStyleHsp" style=""></span>mg&#47;day due to lack of response&#46; The drug was up-titrated to 30<span class="elsevierStyleHsp" style=""></span>mg&#47;day&#44; and progressively withdrawn on an outpatient basis until complete discontinuation 4 months later&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">One year later&#44; lower limb weakness had improved with rehabilitation therapy&#44; although the patient needed crutches to walk&#46; Serum sodium levels were normal &#40;141<span class="elsevierStyleHsp" style=""></span>mEq&#47;L&#41;&#46;</p><p id="par0030" class="elsevierStylePara elsevierViewall">Although some studies report an association between hyponatraemia and GBS&#44; few studies have analysed the correlation&#46; This association results in poorer hospital outcomes even at one year&#44;<a class="elsevierStyleCrossRefs" href="#bib0055"><span class="elsevierStyleSup">1&#8211;5</span></a> longer hospital stays&#44;<a class="elsevierStyleCrossRefs" href="#bib0055"><span class="elsevierStyleSup">1&#8211;3</span></a> and higher costs&#46;<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&#44;<a class="elsevierStyleCrossRefs" href="#bib0060"><span class="elsevierStyleSup">2&#44;5</span></a> which has also been described in other disorders&#46;<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&#44;<a class="elsevierStyleCrossRefs" href="#bib0055"><span class="elsevierStyleSup">1&#44;2</span></a> which may be explained by the fact that severe hyponatraemia can manifest as respiratory distress&#46;<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&#59; pseudohyponatraemia linked to increased protein levels may therefore play an important role&#46; 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&#46; Palevsky et al&#46;<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">7</span></a> analysed the effect of Ig infusion on sodium levels&#44; measured with direct potentiometry to avoid diagnosis of pseudohyponatraemia&#46; The authors observed hyponatraemia&#44; despite using this technique&#46; SIADH is a frequent cause of true hyponatraemia in patients with GBS&#46;<a class="elsevierStyleCrossRefs" href="#bib0060"><span class="elsevierStyleSup">2&#44;8&#44;9</span></a> Other cases are due to cerebral salt-wasting syndrome&#44; although this association is very rare&#46;</p><p id="par0040" class="elsevierStylePara elsevierViewall">Our patient may meet the diagnostic criteria for SIADH as established in the latest European hyponatraemia guidelines &#40;plasma osmolality<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>275<span class="elsevierStyleHsp" style=""></span>mOsm&#47;kg&#59; urine osmolality<span class="elsevierStyleHsp" style=""></span>&#62;<span class="elsevierStyleHsp" style=""></span>100<span class="elsevierStyleHsp" style=""></span>mOsm&#47;kg&#59; euvolaemia&#59; and absence of adrenal insufficiency&#44; hypothyroidism&#44; hypopituitarism&#44; or kidney failure&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">7</span></a> We did not determine cortisol levels in our patient&#59; however&#44; clinical and laboratory results were not compatible with adrenal insufficiency&#46; The prevalence of SIADH in patients with GBS is not clear&#59; case reports constitute the only available evidence&#46; The pathophysiological mechanisms of the association between GBS and hyponatraemia are yet to be understood&#46; Several hypotheses have been proposed&#58; alterations of hypothalamic cells&#44; causing ADH release into the bloodstream&#59; alterations in osmoregulation&#59; increased sensitivity of ADH receptors&#59; and other mechanisms not related to ADH&#46;<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">9</span></a> Other researchers support the involvement of interleukin 6&#44; which may increase vasopressin release&#46;<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">10</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall">Interestingly&#44; our patient&#39;s sodium levels decreased following Ig administration &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46; This may indicate pseudohyponatraemia and&#47;or water transport to the intravascular space&#44; which play a role in true hyponatraemia&#46; In retrospect&#44; this may explain the patient&#39;s poor response to hypertonic saline and water restriction and the need to up-titrate tolvaptan to 30<span class="elsevierStyleHsp" style=""></span>mg&#47;day to achieve normal sodium levels&#46;</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&#58; to our knowledge&#44; only one case has been published to date&#46;</p><p id="par0055" class="elsevierStylePara elsevierViewall">Sodium levels should be monitored in patients with GBS&#46; Pseudohyponatraemia&#44; water transport&#44; and SIADH should be considered in the differential diagnosis of hyponatraemia&#46; In our case&#44; hyponatraemia may have played a role in the need for an additional cycle of Ig and the slow motor recovery&#46;</p></span>"
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