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Scientific letter
Intrahepatic cholestasis, sometimes benign recurrent
Colestasis intrahepática. A veces puede ser benigna y recurrente
Ruth García-Romeroa,
Corresponding author
ruthgarciaromero@yahoo.es

Corresponding author.
, Laura Morlan-Herradora, Ignacio Ros-Arnala, María Dolores Miramarb, Cristina Molera-Busonsc
a Servicio de Gastroenterología y Nutrición Pediátrica, Hospital Infantil Miguel Servet, Zaragoza, Spain
b Servicio de Genética, Hospital Infantil Miguel Servet, Zaragoza, Spain
c Servicio de Gastroenterología, Hepatología y Nutrición Pediátrica, Hospital Sant Joan de Déu, Barcelona, Spain
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">We present a case of atypical hepatic cholestasis in a paediatric patient&#46; A previously healthy five-year-old male&#44; of Romani ethnicity&#44; who came to the emergency department due to the appearance of generalised itching and jaundice over the previous four days&#44; together with acholia and choluria&#46; He had had chickenpox some 10 days earlier&#46; There were no previous similar personal or family episodes&#44; or previous illnesses or surgical interventions&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">The physical examination revealed cutaneous and conjunctival jaundice&#44; as well as chickenpox lesions in resolution phase&#46; The rest of the physical examination was normal&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">Given the symptoms&#44; a blood test was performed in the emergency department in which a cholestatic pattern was observed with total bilirubin of 8&#46;63&#8239;mg&#47;dl &#40;normal 0&#46;3&#8211;1&#46;2&#8239;mg&#47;dl&#41;&#44; direct bilirubin of 5&#46;61&#8239;mg&#47;dl &#40;normal 0&#8211;0&#46;2&#8239;mg&#47;dl&#41;&#44; alkaline phosphatase 739&#8239;U&#47;l &#40;normal 42&#8211;362&#8239;U&#47;l&#41;&#44; GGT 20&#8239;U&#47;l &#40;normal 3&#8211;22&#8239;U&#47;l&#41;&#44; GOT 71&#8239;U&#47;l &#40;normal 0&#8211;50&#8239;U&#47;l&#41;&#44; GPT 101&#8239;U&#47;l &#40;normal 0&#8211;50&#8239;U&#47;l&#41; and LDH 268&#8239;U&#47;l &#40;normal 0&#8211;248&#8239;U&#47;l&#41;&#46; A haemogram&#44; haemostasis test and a study of pancreatic and renal function were performed with normal results&#44; as well as serology tests&#46; The patient was referred to a paediatric gastroenterologist and a hepatobiliary ultrasound was requested in which mild diffuse hepatomegaly was found&#44; with normal echogenicity&#44; without focal lesions&#44; the rest of the abdominal ultrasound examination being normal&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">Treatment with ursodeoxycholic acid and colestyramine resin was prescribed&#46; Given the biochemical pattern of cholestasis and the normality of the GGT figures&#44; a genetic study was requested for type 1 familial cholestasis&#46; Progressive improvement of the symptoms was observed with a complete normalisation of cholestatic parameters in less than six weeks&#46; As a result&#44; no more complementary studies were carried out for the time being&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">The genetic study showed a pathogenic mutation in p&#46;Thr456Met in position 1367 of exon 12 of the ATP8B1 gene&#44; and a variant of uncertain clinical significance&#44; probably pathological&#44; p&#46;Asn1029Lys in position 3087 of exon 24 of the ATP8B1 gene&#44; both present in heterozygosity&#46; These mutations are diagnostic of benign recurrent intrahepatic cholestasis &#40;BRIC&#41;&#44; which is an atypical cause of cholestasis&#46;</p><p id="par0030" class="elsevierStylePara elsevierViewall">It was first described in 1959 by Summerskill and Wlashe&#44;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> and is characterised by self-limited and recurrent episodes of severe itching and jaundice that can last from weeks to several months&#44; sometimes triggered by viral infections&#46; The average duration is around three months for each episode&#44; and it can remain asymptomatic for highly variable periods&#44; ranging from months to years&#46;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">Its exact prevalence remains unknown&#44; but the estimated incidence is approximately 1 in 50&#44;000 to 100&#44;000 people worldwide&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> It is an autosomal recessive disease with incomplete penetrance&#44; of which two forms have been described&#46; Type 1 BRIC is secondary to a mutation in the ATP8B1 gene&#44; located on chromosome 18 &#40;18q21-q22&#41;&#44; which coincides with the genetic result of the patient presented&#46; This gene belongs to the ATP gene family &#40;ATPase superfamily&#41; and encodes a transporter protein &#40;aminophospholipid transferase&#41; that participates in the translocation of aminophospholipids at the hepatocyte level and contributes to maintaining an adequate balance of bile acids in the bile&#46; If defective&#44; it produces a decrease in the secretion of bile salts&#46;</p><p id="par0040" class="elsevierStylePara elsevierViewall">Type 2 BRIC is caused by a mutation in the ABCB11 gene&#44; located on chromosome 2 &#40;2q24&#41;&#44; which belongs to the ABC &#40;ATPBinding cassette transporters&#41; and ATP &#40;ATPase superfamily&#41; gene families&#46; This gene encodes a bile salt-exporting protein &#40;bile salt export pump&#44; BSEP&#41; that mobilises bile salts from hepatocytes&#46;</p><p id="par0045" class="elsevierStylePara elsevierViewall">Unlike progressive familial intrahepatic cholestasis &#40;PFIC-1&#41;&#44; whose altered gene is the same as in benign recurrent intrahepatic cholestasis&#44; penetrance is variable&#46; It occurs in the first decade of life&#44; in patients with normal psychomotor and physical development&#44; and it is usually benign&#44; without progression to fibrosis or liver failure&#44; or systemic involvement&#46; The pathophysiology of this condition is not clear&#44; and today the pathophysiological mechanisms are unknown&#44; although some triggers such as viral infections have been described&#46;<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a></p><p id="par0050" class="elsevierStylePara elsevierViewall">During the study of these patients&#44; serological studies should be included to exclude causes of acute and chronic viral hepatitis&#44; and medications that could cause cholestasis should be suspended&#46; Imaging studies are also necessary to exclude obstructive biliary pathologies&#46; In adolescents or adults&#44; endoscopic retrograde cholangiography can be used to exclude sclerosing cholangitis or other causes of biliary tree abnormalities&#46; Liver biopsy in the literature reviewed shows centrilobular cholestasis without liver lesions&#44; although inflammatory infiltrates can occasionally be observed&#46; In our patient&#44; a biopsy was not performed since the abnormal test results improved in a few weeks&#46;</p><p id="par0055" class="elsevierStylePara elsevierViewall">Currently&#44; there is no specific treatment to prevent or reduce the duration and severity of episodes&#46; Treatment is based on symptom relief&#44; until the episode resolves spontaneously&#46; Cholestyramine and ursodeoxycholic acid have been used in the treatment of these patients for the relief of symptoms&#44; with good response&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> Our patient has not experienced new episodes of cholestasis in the two years following his diagnosis&#46;</p></span>"
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