Letter to the Editor
Guillain-Barré syndrome after viral hepatitis A
Síndrome de Guillain-Barré tras infección por el virus de la hepatitis A
Rocío López Ruiz
, Julio Dotor García-Soto, Sara Eichau
Corresponding author
Unidad de Gestión Clínica de Neurología y Neurofisiología, Hospital Universitario Virgen Macarena, Sevilla, Spain
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The condition usually occurs after an infectious episode, more commonly after infection by <span class="elsevierStyleItalic">Campylobacter jejuni</span>, cytomegalovirus, Epstein-Barr virus, mycoplasma, HIV, <span class="elsevierStyleItalic">Shigella</span>, <span class="elsevierStyleItalic">Clostridium</span> or <span class="elsevierStyleItalic">Haemophilus influenza</span>.<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> It has also been described after hepatitis virus infection, being less common after hepatitis A virus infection.<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">We report the case of a 40-year-old male who went to the emergency department for general malaise and dysthermia 2 weeks after a trip to Bolivia.</p><p id="par0015" class="elsevierStylePara elsevierViewall">Jaundice stood out on physical examination. The lab tests showed total bilirubin levels of 6.30 mg/dl, GOT/GPT of 1,364/2,277 IU, INR 1.31 and CRP 16.82 mg/dl. Serology was performed with positive IgM results for hepatitis A virus. The rest of the lab and serology tests, including HIV and malaria, were negative. Ultrasound revealed no other findings.</p><p id="par0020" class="elsevierStylePara elsevierViewall">He was admitted with a hepatitis A virus diagnosis. After admission, he began with progressive ascending weakness, with distal paresthesias and blurred vision.</p><p id="par0025" class="elsevierStylePara elsevierViewall">On examination, he had bilateral facial weakness, diminished strength in the 4 limbs with MRC 4/5, decreased tone and areflexia. The initial nerve conduction study showed absence of F waves, motor and sensory demyelination in limbs and dysautonomia. Lumbar puncture showed albumin/cytological dissociation (albumin 152 mg/dl, 10 lymphocytes).</p><p id="par0030" class="elsevierStylePara elsevierViewall">The clinical findings and complementary tests were compatible with GBS, with a level 1 diagnostic accuracy according to the Brighton criteria.<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">A 5-day 0.4 g/kg/24 h treatment with intravenous immunoglobulins was initiated. The patient worsened clinically after 24 h with bradypsychia, 2/5 strength in limbs, dysphagia, dyspnoea and hemodynamic instability (hypertension and episodes of tachycardia with mobilization). Arterial blood gases showed global respiratory failure. The patient was transferred to the ICU, where he underwent orotracheal intubation and mechanical ventilation.</p><p id="par0040" class="elsevierStylePara elsevierViewall">The patient showed progressive neurological worsening for 2 weeks, developing a flaccid tetraplegia, preserving trunk flexion (3/5) and neck flexion-extension (2–3/5), involvement of lower cranial nerves with aphagia and dysautonomia. An immunoglobulin cycle was repeated 5 days after the end of the first one and subsequent plasmapheresis cycle at alternate days for 7 days. Subsequently, the patient progressed favourably, therefore, he was extubated and started rehabilitation treatment.</p><p id="par0045" class="elsevierStylePara elsevierViewall">Currently, the patient walks autonomously, with strength preserved in the limbs except deltoids 4+/5 and bilateral foot 3/5 eversion/inversion, with persistent areflexia.</p><p id="par0050" class="elsevierStylePara elsevierViewall">GBS is the most common cause of acquired acute polyradiculopathy. Under the eponym of GBS, all forms of acute inflammatory polyradiculopathies that can be classified as demyelinating, axonal or variant according to their clinical characteristics and the nerve conduction study are included.<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> The most common in Europe and the United States is the demyelinating variant; axonal variants are more common in eastern countries and have a worse prognosis. Variants of GBS include Miller-Fisher syndrome, Bickerstaff encephalitis or pharyngeal-cervical-brachial paralysis, among others.<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1,4</span></a></p><p id="par0055" class="elsevierStylePara elsevierViewall">In up to two thirds of cases, GBS occurs after a previous infectious or immune episode. It usually develops over days or weeks, with a subsequent recovery over months or years. Its in-depth pathogenesis is unknown, but given the relationship with infectious episodes, cross-immunity mechanisms are postulated through molecular mimicry between pathogen and nerve antigens.<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a></p><p id="par0060" class="elsevierStylePara elsevierViewall">The diagnosis of GBS is clinical, based on exploratory findings and supported by ancillary tests (albumin/cytological dissociation in CSF and abnormalities in nerve conduction studies),<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1,3</span></a> In axonal forms or variants of GBS, antiganglioside antibodies can be detected, which support the diagnosis. In demyelinating forms (the most common in our environment) these antibodies are usually negative and of little clinical utility.<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1,4</span></a></p><p id="par0065" class="elsevierStylePara elsevierViewall">The immunomodulatory treatment should be established as soon as the diagnosis is made, as it improves the prognosis. Intravenous immunoglobulins or plasmapheresis can be used, although the superiority of one against the other has not been demonstrated.<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a></p><p id="par0070" class="elsevierStylePara elsevierViewall">GBS is a serious condition, with a mortality of around 3–7% and need for ICU admission in up to 20–30% of cases.<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> Therefore, clinical suspicion, early diagnosis, hemodynamic monitoring and rapid immunomodulatory therapy initiation are the most effective therapeutic strategies to improve survival and prognosis.</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: López Ruiz R, Dotor García-Soto J, Eichau S. Síndrome de Guillain-Barré tras infección por el virus de la hepatitis A. Med Clin (Barc). 2020;154:238–239.</p>" ] ] "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" => "Guillain-Barre syndrome" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:3 [ 0 => "H.J. Willison" 1 => "B.C. 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