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Recurrent Hyperammonemia After Abernethy Malformation Type 2 Closure: a Case Report
Hui Li, Zhi Ma, Ying Xie, Feng Tian
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18940256110@126.com

Correspondence and reprint request:
Department of gastroenterology, Shengjing Hospital Affiliated to China Medical University, Shenyang, Liaoning, China
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    "textoCompleto" => "<span class="elsevierStyleSections"><span id="s0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="st0020">Introduction</span><p id="p0010" class="elsevierStylePara elsevierViewall">The Abernethy malformation is a rare congenital communication between the portal vein and systemic circulation&#59; it was first reported by John Abernethy in 1793&#46; According to the type of anastomosis and status of the portal vein&#44; it is classified into 2 types&#46;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">1</span></a> Type 1 is characterized by a complete absence of the portal vein and is predominantly &#40;74&#37; of cases&#41; found in females&#46;<a class="elsevierStyleCrossRefs" href="#bib0010"><span class="elsevierStyleSup">1-4</span></a> Type 1 malformation is further divided into subtypes A and B&#58;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">5</span></a> in type 1A&#44; the splenic vein and the superior mesenteric vein drain separately into the inferior vena cava&#59; in type 1B&#44; these veins form a common trunk&#46; Partial shunts between the portal vein and the systemic venous circulation are defined as type 2&#59; these allow for some potential portal per-fusion of the liver&#46; Various clinical presentations and some congenital malformations are associated with these abnormal shunts&#58;<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">6</span></a> hepatic encephalopathy&#44; portopulmonary syndrome&#44; hepatic masses&#44; cardiac defects&#44; and vascular anomalies have all been reported&#46;</p><p id="p0015" class="elsevierStylePara elsevierViewall">We report a patient with type 2 Abernethy malformation and hepatic encephalopathy&#46; Although she underwent successful interventional shunt closure&#44; her hyperammon-emia recurred 3 months postoperatively&#46; This is the first reported case of recurrent hyperammonemia after inter-ventional treatment&#59; we discuss herein the therapeutic options for Abernethy malformation&#46;</p><span id="s0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="st0025">Case report</span><p id="p0020" class="elsevierStylePara elsevierViewall">A 58-year-old female presented to the gastroenterology department of Shengjing Hospital &#40;affiliated with China Medical University&#41; with an 8-month history of dizziness&#44; sleepiness&#46; She was previously diagnosed&#44; at another institution&#44; with metabolic encephalopathy when she presented with elevated alanine transaminase levels without hepatic dysfunction&#46; She was otherwise healthy&#44; with a history significant only for a simple vocal-cord surgery&#46; Physical examination revealed lower-extremity edema but no splenomegaly or evidence of ascites&#46;</p><p id="p0025" class="elsevierStylePara elsevierViewall">Laboratory testing revealed aspartate aminotransferase level of 39 IU&#47;L &#40;normal range&#44; 5-34 IU&#47;L&#41;&#44; an alkaline phosphatase level of 180 IU&#47;L &#40;normal range&#44; 40-150 IU&#47; L&#41;&#44; a total bilirubin level of 24 &#956;mol&#47;L &#40;normal range&#44; 3&#46;4-20&#46;5 &#956;mol&#47;L&#41;&#44; and an indirect bilirubin level of 15&#46;7 &#956;mol&#47; L &#40;normal range&#44; 3&#46;4-11&#46;9 &#956;mol&#47;L&#41;&#46; Her white blood-cell count was 3&#46;9 x 10<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">9</span></a>&#47;L &#40;normal range&#44; 3&#46;5-9&#46;7 x 10<span class="elsevierStyleSup">9</span>&#47;L&#41;&#44; her hemoglobin level was 116 g&#47;L &#40;normal range&#44; 110-150 g&#47;L&#41;&#44; her platelet count was 180 x 10<span class="elsevierStyleSup">9</span>&#47;L &#40;normal range&#44; 135-350 x 10<span class="elsevierStyleSup">9</span>&#47;L&#41;&#44; and her coagulation profile was normal&#46; The tumor marker cancer antigen 19-9 &#40;CA19-9&#41; measured 58&#46;47 U&#47; mL &#40;normal range&#44; 0-37U&#47;mL&#41;&#46; Serological evaluation for ceruloplasmin&#44; hepatitis viruses A E&#44; and immunological markers was negative&#44; although her plasma ammonia level was 147&#46;6 &#956;mol&#47;L &#40;normal range&#44; 9-33 &#956;mol&#47;L&#41;&#46; Computed tomography of the abdomen was performed using a 64-row multidetector&#46; Multiplanar reconstruction and 3-dimensional volume-rendered images confirmed the presence of an abnormal shunt between the inferior vena cava and the superior mesenteric vein&#59; this shunt had a diameter of 33 mm &#40;<a class="elsevierStyleCrossRef" href="#f0010">Figure 1</a>&#41;&#46;</p><elsevierMultimedia ident="f0010"></elsevierMultimedia><p id="p0030" class="elsevierStylePara elsevierViewall">The patient subsequently underwent shunt closure&#44; using interventional angiography &#40;<a class="elsevierStyleCrossRef" href="#f0015">Figure 2</a>&#41;&#46; Her plasma ammonia level returned to normal range&#44; with complete resolution of encephalopathy and the lower-extremity edema&#46; However&#44; about 3 months after surgery&#44; routine follow-up examination revealed an elevated plasma ammonia level of 155 &#956;mol&#47;L&#59; repeat angiography confirmed successful shunt closure and did not reveal any other portal-venous vessels that could explain the recurrence of hyperammonemia&#40;<a class="elsevierStyleCrossRef" href="#f0015">Figure 2</a>&#41;&#46; However&#44; contrast-enhanced CT of the liver revealed that the portal vein was 1&#46;5 cm in diameter&#44; larger than the presurgical value &#40;<a class="elsevierStyleCrossRef" href="#f0020">Figure 3</a>&#41;&#46; Since she was asymptomatic&#44; conservative observation was recommended&#46; Over a year of follow-up&#44; the serological evaluation for liver function was normal&#44; while the plasma ammonia level was in the range of 60-80 &#956;mol&#47;L&#46;</p><elsevierMultimedia ident="f0015"></elsevierMultimedia><elsevierMultimedia ident="f0020"></elsevierMultimedia></span></span><span id="s0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="st0030">Discussion</span><p id="p0035" class="elsevierStylePara elsevierViewall">Abernethy malformation has a female dominance and is usually diagnosed during childhood&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">7</span></a> Hao&#44; <span class="elsevierStyleItalic">et al</span>&#46;&#44;<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">8</span></a> reviewed 101 previously reported patients with Abernethy malformation and found that 65&#46;3&#37; were female&#44; 69&#46;3&#37; were younger than 18 years of age&#44; and less than 10&#37; had type-2 malformations&#46;</p><p id="p0040" class="elsevierStylePara elsevierViewall">Some patients remain asymptomatic throughout life&#46;<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">9</span></a> When symptoms do occur&#44; the clinical manifestations are mainly associated with the hepatic shunt and associated congenital malformations&#46; In the Abernethy malformation&#44; diversion of the portal blood flow into the inferior vena cava leads to systemic hypertension&#44; which can explain the leg edema seen in our patient&#46; Metabolic and vasoactive substances bypass the liver through portosystemic collaterals and thus cause portopulmonary hypertension&#44; hyper-ammonemia&#44; and encephalopathy&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">10</span></a> Nodular liver lesions are seen in up to half of patients&#58; these include benign focal nodular hyperplasia&#44; hepatocellular adenoma&#44; and regenerative nodules<a class="elsevierStyleCrossRefs" href="#bib0025"><span class="elsevierStyleSup">4&#44;11</span></a> and may be explained by the absence of portal flow and compensatory increased hepatic arterial blood flow&#46; Although most of these lesions are benign&#44; there are several case reports in the literature describing the coexistence of hepatocellular carcinoma and hepatob-lastoma&#46; Therefore&#44; long-term follow-up and monitoring are recommended&#46;<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">12</span></a> Congenital hepatic shunts can also present with metabolic dysregulation&#44; such as hypoglyc-emia&#44; due to metabolic alterations in the liver&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">13</span></a></p><p id="p0045" class="elsevierStylePara elsevierViewall">Despite the existence of a direct connection between the portal and systemic venous systems&#44; hyperammonemia is found in only 26&#37; of patients with the Abernethy mal-formation&#44;<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">14</span></a> and only 15&#37; of all patients experience hepatic encephalopathy&#46;<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">15</span></a> A recent review identified 316 published cases and reported that hyperammonemia&#47;neu-rological abnormalities occurred in 35&#37; of patients with congenital portosystemic shunt&#46;<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">16</span></a> Hyperammonemia can be present without encephalopathy&#44; especially in younger patients&#59; clinical encephalopathy is more common at older ages&#46; Possible explanations for this phenomenon are an age-dependent increase in sensitivity to deleterious metabolites and the impact of the extent of shunting&#44; determined by the portal&#47;systemic shunt ratio-a shunt ratio of more than 60&#37; may predict the age of onset of encepha-lopathy&#46;<a class="elsevierStyleCrossRefs" href="#bib0090"><span class="elsevierStyleSup">17&#44;18</span></a></p><p id="p0050" class="elsevierStylePara elsevierViewall">Current treatment options&#44; including interventional or surgical shunt closure and liver transplantation&#44; are described in case reports&#59; however&#44; the therapeutic experience with Abernethy malformation is still limited&#46;<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">19</span></a> The choice of strategy depends on the type of shunt&#44; symptoms&#44; complications&#44; and comorbidities&#46; Shunt occlusion is not feasible in patients with type 1&#44; as the shunt is the only drainage route for the mesenteric venous blood&#46; Thus&#44; liver transplantation may be required to provide a patent portal system and to treat the metabolic abnormalities and liver disease in these patients&#46;<a class="elsevierStyleCrossRef" href="#bib0105"><span class="elsevierStyleSup">20</span></a> Kanamori&#44; <span class="elsevierStyleItalic">et al</span>&#46;<a class="elsevierStyleCrossRef" href="#bib0110"><span class="elsevierStyleSup">21</span></a> previously reported on a patient with type 2 Abernethy malformation who required liver transplantation after developing postoperative portal hypertension and another portosystemic shunt&#46; Thus&#44; it is important to ensure adequate portal vein capacity and normal portal pressure prior to closure&#44; in order to avoid postprocedure portal hypertension and subsequent mesenteric ischemia&#46;<a class="elsevierStyleCrossRef" href="#bib0115"><span class="elsevierStyleSup">22</span></a></p><p id="p0055" class="elsevierStylePara elsevierViewall">The balloon shunt occlusion test shows a visible intra-hepatic portal system &#40;IHPS&#41; in patients with both type 1 and type 2 Abernethy malformation&#46;<a class="elsevierStyleCrossRef" href="#bib0120"><span class="elsevierStyleSup">23</span></a> This finding could represent small portal vein branches which cannot be seen on ultrasonography but can be visualized on shunt angiog-raphy&#46;<a class="elsevierStyleCrossRefs" href="#bib0015"><span class="elsevierStyleSup">2&#44;24</span></a> Kanazawa H&#44; <span class="elsevierStyleItalic">et al</span>&#46;&#44;<a class="elsevierStyleCrossRef" href="#bib0120"><span class="elsevierStyleSup">23</span></a> proposed a new classification based on IHPS hypoplasia &#40;mild&#44; moderate&#44; and severe types&#41; under shunt occlusion&#59; this system guides the decision on whether to perform single-stage or 2-stage shunt closure&#46; Single-stage closure is recommended for mild and moderate types with crescent-shaped portal veins and a portal venous pressure below 25 mmHg&#46; This suggests that the intrahepatic portal vascular bed is able to accept sufficient blood flow immediately upon shunt closure&#46; Patients with the severe type&#44; with a small portal-triad area and a portal venous pressure over 25 mmHg&#44; are candidates for either 2-stage shunt closure or liver transplantation&#46; In the present case&#44; the intrahepatic portal vein system was well displayed under angiography&#44; similar to mild type of IHPS&#44; which indicated the possibility of shunt closure&#46; The balloon shunt occlusion test was not performed prior to operation and a direct shunt closure was carried out in this patient&#46; The treatment was proved effective in both the improvement of symptoms and laboratory results&#46; However&#44; her plasma ammonia level was elevated again just 3 months later&#46; Although repeat angiography showed persistent closure of the shunt&#44; an enlarged portal vein was confirmed&#59; thus&#44; we conjectured that the closure of the original large shunt caused a sudden increased inflow into the portal vein&#44; leading to portal hypertension&#44; when then resulted in the development of new collaterals between the portal and venous vessels&#46; As the diameter of shunt vessels grows with age&#44; the difficulty of intervention increases&#46; In our case&#44; the large diameter of the longstanding aberrant vessel increased the difficulty of the original operation and the chance of complications&#46; Therefore&#44; it is necessary to carefully assess the severity of the hypoplasia of IHPS as well as the PVP under the occlusion test&#44; and for cases with large abnormal vessel&#44; simple shunt closure may not be the first choice&#46;</p><p id="p0060" class="elsevierStylePara elsevierViewall">In conclusion&#44; the diagnosis of Abernethy malformation is challenging&#44; as it is an uncommon congenital malformation with nonspecific clinical symptoms&#46; However&#44; patients with unexplainable hyperammonemia and hepatic encephalopathy require evaluation for a potential porto-systemic shunt&#46; Since most significant presentations appear in older patients with large-diameter shunts&#44; as well as in those with severe portal dysplasia&#44; the incidence of postsurgical complications increases&#46; Thus&#44; it is necessary to evaluate the IHPS by angiography&#44; using the shunt-occlusion test&#44; and to measure the portal venous pressure under shunt occlusion in order to choose the optimal therapeutic approach&#46; Moreover&#44; in the present case&#44; although the repeat angiography failed to show the new collaterals between the portal and venous veins&#44; we couldn&#8217;t deny the existence of the recurrent shunts that might explain the recurrent hyperammonemia&#46; Additionally&#44; further tests should be done to explore the possible defects of urea cycle which might result in high ammonia&#46; Postoperative clinical improvement&#44; such as regression of benign liver masses and of pulmonary&#44; cardiac&#44; neurological&#44; and renal complications&#44; has been reported&#46;<a class="elsevierStyleCrossRef" href="#bib0125"><span class="elsevierStyleSup">24</span></a> However&#44; there are patients described in the literature with hepatic lesions that did not improve by 12 to 24 months after shunt closure&#46; These findings suggest that the malformation should be treated before a significant complication occurs and that long-term follow-up and monitoring for complications as well as malignancy are mandatory&#46;<a class="elsevierStyleCrossRef" href="#bib0120"><span class="elsevierStyleSup">23</span></a></p></span></span>"
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              "titulo" => "Case report"
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            0 => "Congenital malformation"
            1 => "Encephalopathy"
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        "titulo" => "Abstract"
        "resumen" => "<span id="abs0010" class="elsevierStyleSection elsevierViewall"><p id="sp0025" class="elsevierStyleSimplePara elsevierViewall">The Abernethy malformation is a rare congenital malformation defined by the presence of an extrahepatic portosystemic shunt&#46; Although most patients are asymptomatic&#44; clinical encephalopathy is present in 15&#37; of cases&#46; We present a patient with type 2 Aber-nethy malformation&#44; hyperammonemia&#44; and encephalopathy&#46; Shunt closure was performed successfully using interventional angiography&#59; however&#44; hyperammonemia recurred 3 months later&#46; The diagnosis of Abernethy malformation can be made easily&#44; but the ideal patient management strategy has not yet been established&#46; This is the first reported patient with recurrence of hyperam-monemia after interventional treatment&#59; we discuss the therapeutic options for Abernethy malformation&#46;</p></span>"
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          "en" => "<p id="sp0010" class="elsevierStyleSimplePara elsevierViewall">Coronal computed tomography &#40;<span class="elsevierStyleBold">A</span>&#41; and volume-rendering 3-dimensional &#40;<span class="elsevierStyleBold">B</span>&#41; images show the aberrant vessel traveling in a tortuous&#44; downward-right path&#46; Uneven thickening and an-eurysmal dilation with a diameter of 33 mm are seen &#40;white arrow&#41;&#46;</p>"
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          "en" => "<p id="sp0015" class="elsevierStyleSimplePara elsevierViewall">Angiographic images &#40;<span class="elsevierStyleBold">A</span>&#41; shows the intrahepatic portal system &#40;white arrow&#41; before shunt closure&#59; &#40;<span class="elsevierStyleBold">B</span>&#41; shows the aberrant drainage branches of superior mesenteric vein into the inferior vena cava prior to closure &#40;white arrow&#41;&#59; &#40;<span class="elsevierStyleBold">C</span>&#41; shows the successful closure of the shunt with coil embolization&#40;black arrow&#41;&#59; &#40;<span class="elsevierStyleBold">D</span>&#41; repeat angiographic image shows the persistent closure of the shunt&#46;</p>"
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          "en" => "<p id="sp0020" class="elsevierStyleSimplePara elsevierViewall">Axial contrast-enhanced CT images show the change in size of portal vein before &#40;<span class="elsevierStyleBold">A</span>&#41; and after &#40;<span class="elsevierStyleBold">B</span>&#41; shunt closure &#40;white arrow&#41;&#46;</p>"
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es en pt

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