Letter to the Editor
Hyperammonemic encephalopathy in a patient with hereditary hemorrhagic telangiectasia
Encefalopatía hiperamoniémica en una paciente con telangiectasia hemorrágica hereditaria
Joana de Miguel Landiríbar, Oihane Orokieta Rincón, Alfonso Gutiérrez Macías
Corresponding author
Servicio de Medicina Interna, Hospital Universitario Basurto, Bilbao, Vizcaya, Spain
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Clinically characterized by cutaneous and mucosal telangiectasias and visceral vascular malformations (VM).<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> Mutations have been described in 5 different genes that encode proteins of the transforming growth factor ß (TGF-ß) family; however, most are produced in ENG genes (HHT type I) and ACVRL1 (HHT type II). Pulmonary VM is more common in type I, while in type II liver involvement is more prevalent.<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> Overall, liver involvement is the most common after epistaxis and is detected with imaging techniques in 41%–84% of cases; however, symptoms occur in less than 15% of cases.<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1–3</span></a> We report a case of HHT in which liver involvement in the form of hyperammonemic encephalopathy associated with hepatic VM was the most relevant clinical manifestation.</p><p id="par0010" class="elsevierStylePara elsevierViewall">We report he case of an 84-year-old woman with a history of arterial hypertension, atrial fibrillation, mitral regurgitation, and transient ischemic attack under treatment with acenocoumarol, furosemide, atenolol, and amlodipine. Diagnosed with HHT with common episodes of epistaxis. The molecular study showed a heterozygous deletion c. (772+1_773-1)_(1246+1_1247-1) in the ACVRL1 gene. Family history included frequent epistaxis in grandmother, mother and brother, and diagnosis of HHT with the same mutation in her son and a nephew.</p><p id="par0015" class="elsevierStylePara elsevierViewall">The patient was admitted due to an episode of fluctuating decreased level of consciousness, without involuntary movements, focal neurologic signs, or fever. Over the previous months she had numerous similar episodes, lasting several days and with no obvious trigger, which resolved spontaneously and left no sequelae. The neurological examination revealed a decrease in the level of consciousness, asterixis and hypotonia, without other abnormalities. Cardiac auscultation was arrhythmic, with a systolic murmur; in addition, multiple telangiectasias around the mouth, tongue and fingers were observed. Abdominal organomegaly or signs of heart failure were not detected.</p><p id="par0020" class="elsevierStylePara elsevierViewall">Laboratory data included haemoglobin 10.6<span class="elsevierStyleHsp" style=""></span>g/dl, gamma-glutamyl transferase 165<span class="elsevierStyleHsp" style=""></span>U/l and ammonaemia 127<span class="elsevierStyleHsp" style=""></span>μM/l (reference value: 19−87<span class="elsevierStyleHsp" style=""></span>μl/l). The cerebrospinal fluid study was normal. Brain computed tomography (CT) and magnetic resonance imaging revealed changes in chronic ischemic leukopathy. Abdomino-pelvic ultrasound and CT scan showed multiple hepatic arteriovenous fistulas, as well as tortuosity of the common hepatic and intrahepatic arteries, without signs of portal hypertension. The electroencephalogram showed a pattern of generalized periodic epileptiform discharges with short intervals, suggestive of metabolic encephalopathy. An etiological liver disease study showed no pathological results. It was concluded that the hyperammonemic encephalopathy was attributable to a portosystemic shunt associated with hepatic VMs and treatment with lactulose and rifaximin was initiated with clinical improvement and a parallel decrease in ammonemia values, as well as a decrease in the frequency and intensity of encephalopathy episodes in the follow-up.</p><p id="par0025" class="elsevierStylePara elsevierViewall">Hepatic involvement in HHT is related to the existence of hepatic VMs with shunts between the different vascular territories: arteriovenous (AV), arterioportal (AP) and portovenous (PV), which are not mutually exclusive and whose prevalence may change during follow-up.<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> The most common clinical manifestations are high output heart failure, attributable to excessive blood flow due to AV and/or PV shunts, portal hypertension, related to AP shunts, or nodular regenerative hyperplasia<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> and biliary ischemia associated with decreased hepatic artery flow.<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> Less frequently, cases such as the one described here have been reported, involving hyperammonemic encephalopathy due to PV shunts, which allow nitrogenous products to pass into the systemic circulation<a class="elsevierStyleCrossRefs" href="#bib0020"><span class="elsevierStyleSup">4,5</span></a> and mesenteric ischaemia associated with mesenteric arterial steal by the hepatic artery.<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">Ligation or embolization of the hepatic artery can be used in the treatment of symptomatic liver involvement in cases of high output heart failure and portal hypertension, although it provides a transient improvement and is associated with high morbidity and mortality, so it is reserved for patients for whom liver transplantation (LT) is not indicated.<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> LT is the only definitive therapeutic alternative for hepatic involvement in HHT refractory to symptomatic treatment.<a class="elsevierStyleCrossRefs" href="#bib0010"><span class="elsevierStyleSup">2,3</span></a> Experience with the antiangiogenic agent bevacizumab, which has shown its usefulness in other manifestations of the disease, is limited in liver involvement.<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> Treatment of encephalopathy is similar to that of hepatic encephalopathy with osmotic laxatives and rifaximin.<a class="elsevierStyleCrossRefs" href="#bib0020"><span class="elsevierStyleSup">4,5</span></a></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: de Miguel Landiríbar J, Orokieta Rincón O, Gutiérrez Macías A. Encefalopatía hiperamoniémica en una paciente con telangiectasia hemorrágica hereditaria. Med Clin (Barc). 2021;157:402–403.</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" => "Tratamiento de la telangiectasia hemorrágica hereditaria en el paciente adulto" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:3 [ 0 => "A. Riera-Mestre" 1 => "J. Ribas" 2 => "J. Castellote" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1016/j.medcli.2018.09.015" "Revista" => array:6 [ "tituloSerie" => "Med Clin (Barc)." 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