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"documento" => "article" "crossmark" => 0 "licencia" => "http://creativecommons.org/licenses/by-nc-nd/4.0/" "subdocumento" => "mis" "cita" => "Ann Hepatol. 2012;11:128-9" "abierto" => array:3 [ "ES" => true "ES2" => true "LATM" => true ] "gratuito" => true "lecturas" => array:2 [ "total" => 58 "formatos" => array:3 [ "EPUB" => 7 "HTML" => 25 "PDF" => 26 ] ] "en" => array:11 [ "idiomaDefecto" => true "titulo" => "Glisson’s capsule blistering after hyperthermic intraperitoneal chemotherapy" "tienePdf" => "en" "tieneTextoCompleto" => "en" "tieneResumen" => "en" "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "128" "paginaFinal" => "129" ] ] "contieneResumen" => array:1 [ "en" => true ] "contieneTextoCompleto" => array:1 [ "en" => true ] "contienePdf" => array:1 [ "en" => true ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "f0005" "etiqueta" => "<span class="elsevierStyleBold">Figure 1</span>" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 948 "Ancho" => 1000 "Tamanyo" => 83960 ] ] "descripcion" => array:1 [ "en" => "<p id="sp0005" class="elsevierStyleSimplePara elsevierViewall">Liver surface after hyperthermic intraperitoneal chemotherapy. A. Blister. B. Reddish areas simulating a second degree skin burn.</p>" ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "Heriberto Medina-Franco, Daniel Zamora-Valdés, Ariadne Sánchez-Ramón, Gabriela Trejo-Gómez" "autores" => array:4 [ 0 => array:2 [ "nombre" => "Heriberto" "apellidos" => "Medina-Franco" ] 1 => array:2 [ "nombre" => "Daniel" "apellidos" => "Zamora-Valdés" ] 2 => array:2 [ "nombre" => "Ariadne" "apellidos" => "Sánchez-Ramón" ] 3 => array:2 [ "nombre" => "Gabriela" "apellidos" => "Trejo-Gómez" ] ] ] ] ] "idiomaDefecto" => "en" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S1665268119314966?idApp=UINPBA00004N" "url" => "/16652681/0000001100000001/v1_201906201317/S1665268119314966/v1_201906201317/en/main.assets" ] "en" => array:17 [ "idiomaDefecto" => true "titulo" => "Abnormal liver function tests in a patient with myotonic dystrophy type 1" "tieneTextoCompleto" => true "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "130" "paginaFinal" => "133" ] ] "autores" => array:1 [ 0 => array:4 [ "autoresLista" => "Maria Kalafateli, Christos Triantos, Athanasios Tsamandas, Gerasimos Kounadis, Chryssoula Labropoulou-Karatza" "autores" => array:5 [ 0 => array:4 [ "nombre" => "Maria" "apellidos" => "Kalafateli" "email" => array:1 [ 0 => "mariakalaf@hotmail.com" ] "referencia" => array:2 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">*</span>" "identificador" => "aff1" ] 1 => array:2 [ "etiqueta" => "*" "identificador" => "cor1" ] ] ] 1 => array:3 [ "nombre" => "Christos" "apellidos" => "Triantos" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">*</span>" "identificador" => "aff1" ] ] ] 2 => array:3 [ "nombre" => "Athanasios" "apellidos" => "Tsamandas" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">**</span>" "identificador" => "aff2" ] ] ] 3 => array:3 [ "nombre" => "Gerasimos" "apellidos" => "Kounadis" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">*</span>" "identificador" => "aff1" ] ] ] 4 => array:3 [ "nombre" => "Chryssoula" "apellidos" => "Labropoulou-Karatza" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">***</span>" "identificador" => "aff3" ] ] ] ] "afiliaciones" => array:3 [ 0 => array:3 [ "entidad" => "Department of Gastroenterology, University Hospital of Patras, Greece" "etiqueta" => "*" "identificador" => "aff1" ] 1 => array:3 [ "entidad" => "Department of Pathology, University Hospital of Patras, Greece" "etiqueta" => "**" "identificador" => "aff2" ] 2 => array:3 [ "entidad" => "Department of Internal Medicine, University Hospital of Patras, Greece" "etiqueta" => "***" "identificador" => "aff3" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor1" "etiqueta" => "*" "correspondencia" => "Correspondence and reprint request:" ] ] ] ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "f0005" "etiqueta" => "<span class="elsevierStyleBold">Figure 1</span>" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 1492 "Ancho" => 1000 "Tamanyo" => 148781 ] ] "descripcion" => array:1 [ "en" => "<p id="sp0005" class="elsevierStyleSimplePara elsevierViewall"><span class="elsevierStyleBold">A.</span> Microphotograph showing the presence of mild macrovesicular steatosis in the liver biopsy (arrows) (H&E × 250). <span class="elsevierStyleBold">B.</span> Microphotograph showing an area of bridging fibrosis in the liver biopsy (arrows) (H&E × 250).</p>" ] ] ] "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0010">Introduction</span><p id="p0005" class="elsevierStylePara elsevierViewall">Steinert’s disease (myotonic dystrophy type 1; MD) is an autosomal dominant multisystemic disorder with remarkable genetic heterogeneity, which is considered the most common form of adult-onset muscular dystrophy. Myotonic dystrophy affects skeletal muscles, particularly facial muscles, distal muscles of the forearm and ankle dorsiflexors leading to weakness, myotonia (slowed relaxation after muscle contraction) and muscle pain. Considering its multisystemic pattern, several other organ systems are involved such as heart, gonads, respiratory and gastrointestinal tract, endocrine system, central and peripheral nervous system. Consequently, patients may be presented with variable clinical features. As long as there is no disease-specific treatment available for Steinert’s disease, the management of these patients depends on clinical presentation and symptoms.</p><p id="p0010" class="elsevierStylePara elsevierViewall">Abnormal results of liver function tests have been reported in this setting but the pathophysiological mechanism is still unknown. We report on a patient who presented with elevated liver enzymes without indications of chronic liver disease, months before the diagnosis of Steinert’s disease.</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0015"><span class="elsevierStyleBold">Case Report</span></span><p id="p0015" class="elsevierStylePara elsevierViewall">A 49-year-old Caucasian female was seen at the outpatients-clinic because of abnormal liver function tests. Apart from debilitation, for a period of 3 months, she had been asymptomatic. She reported no alcohol consumption and she had given up smoking one month ago following a thirty years-smoking history. She was receiving thyrormone (T4) as hormone replacement therapy (partial thyroidectomy due to a thyroid nodule 4 years ago) and medication (risedronate, alfacalcidol) for osteoporosis. She had also been operated twice for uterine fibromyomas 16 and 7 years ago, whereas her family history was unremarkable.</p><p id="p0020" class="elsevierStylePara elsevierViewall">Clinical examination revealed a slim, tall woman (BMI 18, 3 kg/cm<span class="elsevierStyleSup">2</span>) without neurological findings or signs of chronic liver disease. Laboratory tests performed showed:</p><p id="p0025" class="elsevierStylePara elsevierViewall"><ul class="elsevierStyleList" id="li0005"><li class="elsevierStyleListItem" id="list0005"><span class="elsevierStyleLabel">•</span><p id="p0030" class="elsevierStylePara elsevierViewall">Alanine aminotransferase (ALT) 163 U/L (normal range between 0-45).</p></li><li class="elsevierStyleListItem" id="list0010"><span class="elsevierStyleLabel">•</span><p id="p0035" class="elsevierStylePara elsevierViewall">Aspartate aminotransferase (AST) 131 U/L (normal range 5-46).</p></li><li class="elsevierStyleListItem" id="list0015"><span class="elsevierStyleLabel">•</span><p id="p0040" class="elsevierStylePara elsevierViewall">Gamma glutamyl-transferase (GGT) 314 U/L (normal range 5-32).</p></li><li class="elsevierStyleListItem" id="list0020"><span class="elsevierStyleLabel">•</span><p id="p0045" class="elsevierStylePara elsevierViewall">Alkaline phosphatase (ALP) 414 U/L (normal range 100-290).</p></li><li class="elsevierStyleListItem" id="list0025"><span class="elsevierStyleLabel">•</span><p id="p0050" class="elsevierStylePara elsevierViewall">Total bilirubin 0.29 mg/dL (normal range 0, 1-0, 3).</p></li><li class="elsevierStyleListItem" id="list0030"><span class="elsevierStyleLabel">•</span><p id="p0055" class="elsevierStylePara elsevierViewall">Cholesterol 279 mg/dL (normal range 140-220).</p></li></ul></p><p id="p0060" class="elsevierStylePara elsevierViewall">Autoimmune screening was negative (AMA, ASMA, ANA, ANCA, anti-LKM) apart from a slight reduction of immunoglogulin M (IgM 36 mg/dL, normal range 40-300) and a great one of immunoglobulin G (IgG 339 mg/dL, normal range 700-1600).</p><p id="p0065" class="elsevierStylePara elsevierViewall">Tests for viral hepatitis and metabolic screening (a1-antitrypsin, caeruloplasmin, ferritin) were negative. IgM antibodies for viral infections (EBV, HSV I and II, CMV), screening for HIV 1, 2, anti-gliandin and transglutaminase antibodies were also negative. Thyroid function tests were between normal ranges.</p><p id="p0070" class="elsevierStylePara elsevierViewall">Ultrasound of upper abdomen showed no abnormal findings except from fatty liver infiltration. Magnetic retrograde cholangiopancreatography (MRCP) and computer tomography (CT) were also normal. A liver biopsy (<a class="elsevierStyleCrossRef" href="#f0005">Figure 1</a>) showed 5% steatosis, pericentric fibrosis, fibrous dilation of portal spaces and focuses of pericellular and bridging fibrosis, with absence of necroinflammation in portal spaces and lobules, neither microscopic disorders of small bile ductules; findings unable to correlate with a particular disease. No medication was prescribed and she was followed up regularly.</p><elsevierMultimedia ident="f0005"></elsevierMultimedia><p id="p0075" class="elsevierStylePara elsevierViewall">Eight months later she was presented with disequilibrium. The physical examination revealed slight ptosis of the eyelids, myotonia noted in face and jaw muscles, weakness of the neck muscles, distal upper limbs and lower limbs. Laboratory tests demonstrated:</p><p id="p0080" class="elsevierStylePara elsevierViewall"><ul class="elsevierStyleList" id="li0010"><li class="elsevierStyleListItem" id="list0035"><span class="elsevierStyleLabel">•</span><p id="p0085" class="elsevierStylePara elsevierViewall">ALT 134 U/L.</p></li><li class="elsevierStyleListItem" id="list0040"><span class="elsevierStyleLabel">•</span><p id="p0090" class="elsevierStylePara elsevierViewall">AST 102 U/L.</p></li><li class="elsevierStyleListItem" id="list0045"><span class="elsevierStyleLabel">•</span><p id="p0095" class="elsevierStylePara elsevierViewall">GGT 142 U/L.</p></li><li class="elsevierStyleListItem" id="list0050"><span class="elsevierStyleLabel">•</span><p id="p0100" class="elsevierStylePara elsevierViewall">ALP 107 U/L.</p></li><li class="elsevierStyleListItem" id="list0055"><span class="elsevierStyleLabel">•</span><p id="p0105" class="elsevierStylePara elsevierViewall">Total bilirubin 0.29 mg/dL.</p></li><li class="elsevierStyleListItem" id="list0060"><span class="elsevierStyleLabel">•</span><p id="p0110" class="elsevierStylePara elsevierViewall">Creatinine kinase was 295 U/L (normal range 0 to 142 U/L).</p></li></ul></p><p id="p0115" class="elsevierStylePara elsevierViewall">Tests for multiple myeloma (radiography for bone lytic lessions, urinary light chain excretion, beta-2 microglobulin, protein electrophoresis) were negative whereas the levels of vitamin 12, folic acid and aldolase were within normal range. Electromyography confirmed the diagnosis of myotonic dystrophy type 1 or Steinert disease. After diagnosis, she went through a cardiac echocardiography which did not show any heart conduction or structural abnormality. Spirometry showed the presence of a mild restrictive abnormality. Sixteen months later from her initial visit, patient remains in good clinical condition, without worsening of her neurological condition, whereas liver enzymes persist to be elevated (AST 58 U/L, ALT 48 U/L, GGT 193 U/L and ALP 329 U/L).</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0020">Discussion</span><p id="p0120" class="elsevierStylePara elsevierViewall">In the literature there are reports <a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1</span></a>-<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> that indicate liver involvement in already diagnosed MD (<a class="elsevierStyleCrossRef" href="#t0005">table 1</a>). We present a case of Steinert’s disease with abnormal liver function tests months before the presentation of clinical symptoms. Consequently physicians should include MD-although rarein the differential diagnosis of elevated liver and cholostatic enzymes. The pathophysiology should be further evaluated.</p><elsevierMultimedia ident="t0005"></elsevierMultimedia><p id="p0125" class="elsevierStylePara elsevierViewall">Myotonic dystrophy (MD) is a multisystemic, autosomal disorder with genetic and clinical heterogeneity. There are two forms, DM1 also called Steinert’s disease and DM2 which is generally milder in presentation with a later onset. DM1 is caused by an expansion of CTG trinucleotide repeat in the 3’-untranslated region of the dystrophia myotonica protein kinase gene (DMPK) on chromosome 19q 13.3,<a class="elsevierStyleCrossRefs" href="#bib0030"><span class="elsevierStyleSup">6</span></a>-<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">10</span></a> whereas DM2 results from an expansion of CCTG tetranucleotide repeat expansion located in intron 1 of the zinc finger protein 9 gene (ZNF9) on chromosome 3q 21.3.<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">11</span></a> In each case, the genes are transcribed to RNA but are not translated.<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">12</span></a> The mutant RNA results in abnormal function of several genes<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">13</span></a> such as the skeletal muscle choride channel,<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">14</span></a> the insulin receptor<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">15</span></a> and cardiac troponin T.<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">16</span></a> Both forms are presented as muscle weakness, myotonia, cataract, cardiac conduction abnormalities, insulin resistance, primary hypogonadism, hypogammaglobulinemia and respiratory abnormalities. Gastrointestinal manifestations include colicky abdominal pain, constipation, diarrhea, pseudo-obstruction and swallowing difficulties, all related to smooth muscle involvement.<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">17</span></a></p><p id="p0130" class="elsevierStylePara elsevierViewall">There is some evidence of liver involvement in MD but the pathophysiology is still uncertain. Ronnemaa, <span class="elsevierStyleItalic">et al.</span><a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> studied the activity of serum GGT in 17 patients with MD. GGT activity was found elevated in 11 (65%) patients whereas most of them had one or more other pathological liver tests. In a later study,<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> the authors evaluated prospectively liver and gallbladder function in 53 patients with MD. Abnormal activity of at least one liver enzyme was found in 35 patients (66%). Liver abnormalities were not correlated to disease severity or CTG expansion. Heatwole, <span class="elsevierStyleItalic">et al.</span><a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> studied 126 MD patients mild to moderately affected. Patients demonstrated abnormal values in all liver enzyme levels tested (lactate dehydrogenase-LDH, GGT, AST, ALT and ALP).</p><p id="p0135" class="elsevierStylePara elsevierViewall">It has been suggested that abnormal liver tests represent a cell membrane defect affecting the contractility of bile canaliculli and bile ductules.<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">18</span></a>,<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">19</span></a> An alternative explanation is that the elevation of GGT results from dysfunction of the hepatocytes whereas the elevation of ALT, AST and LDH results from abnormal skeletal muscle.<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> In another study,<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> authors suggested that oxidative stress may play a role in the pathogenesis of MD. They investigated 39 patients with MD to assess the plasma concentration of advanced oxidation protein products (AOPPs) and GGT and related them to clinical severity scores. GGT and AOPPs were significantly higher in patients than in controls and, moreover, a correlation was found between serum GGT levels and AOPPs as well as between AOPPs and extra-muscular signs of the disease. GGT is known for catalyzing free radical formation and oxidative damage<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">20</span></a> and its increase could result from the oxidative stress status.</p><p id="p0140" class="elsevierStylePara elsevierViewall">To conclude, our patient presented with elevated liver enzymes without indications of chronic liver disease, months before the diagnosis of Steinert’s disease. Consequently, we demonstrate that abnormal liver tests may be the presenting feature of MD and this disorder should be included in the differential diagnosis of elevated liver enzymes. Moreover, considering these abnormal values as indications of liver dysfunction, medications undergoing metabolic clearance should be prescribed cautiously in this setting.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:6 [ 0 => array:3 [ "identificador" => "xres1209102" "titulo" => "Abstract" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abs0005" ] ] ] 1 => array:2 [ "identificador" => "xpalclavsec1125770" "titulo" => "Key words" ] 2 => array:2 [ "identificador" => "sec0005" "titulo" => "Introduction" ] 3 => array:2 [ "identificador" => "sec0010" "titulo" => "Case Report" ] 4 => array:2 [ "identificador" => "sec0015" "titulo" => "Discussion" ] 5 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "fechaRecibido" => "2011-07-08" "fechaAceptado" => "2011-08-01" "PalabrasClave" => array:1 [ "en" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Key words" "identificador" => "xpalclavsec1125770" "palabras" => array:3 [ 0 => "Myotonic dystrophy" 1 => "Steinert's disease" 2 => "Liver function tests" ] ] ] ] "tieneResumen" => true "resumen" => array:1 [ "en" => array:2 [ "titulo" => "Abstract" "resumen" => "<span id="abs0005" class="elsevierStyleSection elsevierViewall"><p id="sp0015" class="elsevierStyleSimplePara elsevierViewall">Myotonic dystrophy type 1, also known as Steinert's disease, is a multisystemic disorder with significant genetic and clinical heterogeneity. Apart from skeletal muscles' myotonia and wasting, a variety of system organs can be affected. We report on a 49 years old female patient with unremarkable medical and family history, who presented with elevated liver enzymes without signs or symptoms of chronic liver disease neither neurological features. Initial assessment, including liver biopsy, did not reveal the cause of these abnormalities. Eight months later, she complained for disequilibrium and eventually electromyography confirmed the diagnosis of Steinert's disease. Steinert's disease should be considered in the differential diagnosis of patients with elevated liver enzymes, as long as abnormal liver tests may be the initial presentation. The pathophysiological mechanism of this abnormality remains unclear.</p></span>" ] ] "multimedia" => array:2 [ 0 => array:7 [ "identificador" => "f0005" "etiqueta" => "<span class="elsevierStyleBold">Figure 1</span>" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 1492 "Ancho" => 1000 "Tamanyo" => 148781 ] ] "descripcion" => array:1 [ "en" => "<p id="sp0005" class="elsevierStyleSimplePara elsevierViewall"><span class="elsevierStyleBold">A.</span> Microphotograph showing the presence of mild macrovesicular steatosis in the liver biopsy (arrows) (H&E × 250). <span class="elsevierStyleBold">B.</span> Microphotograph showing an area of bridging fibrosis in the liver biopsy (arrows) (H&E × 250).</p>" ] ] 1 => array:7 [ "identificador" => "t0005" "etiqueta" => "<span class="elsevierStyleBold">Table 1</span>" "tipo" => "MULTIMEDIATABLA" "mostrarFloat" => true "mostrarDisplay" => false "tabla" => array:1 [ "tablatextoimagen" => array:1 [ 0 => array:2 [ "tabla" => array:1 [ 0 => """ <table border="0" frame="\n \t\t\t\t\tvoid\n \t\t\t\t" class=""><thead title="thead"><tr title="table-row"><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Author \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Year of publication \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Type of publication \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Main findings \t\t\t\t\t\t\n \t\t\t\t\t\t</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="top">Ronnemaa T, <span class="elsevierStyleItalic">et al.</span><span class="elsevierStyleSup">1</span> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="middle">1987 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="middle">Prospective study \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="top">Elevated GGT in 65% patients with MD. \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="top">Achiron A, <span class="elsevierStyleItalic">et al.</span><span class="elsevierStyleSup">2</span> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="middle">1998 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="middle">Prospective study \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="top">Abnormal liver enzymes in 66% patients with MD. \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="top">Heatwole C, <span class="elsevierStyleItalic">et al.</span><span class="elsevierStyleSup">3</span> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="middle">2006 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="middle">Prospective study \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="top">Abnormal values in all liver enzyme tested; 45% elevated GGT. \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="top">Siciliano G, <span class="elsevierStyleItalic">et al.</span><span class="elsevierStyleSup">4</span> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="middle">2005 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="middle">Prospective study \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="top">Elevated GGT and advanced oxidation protein products (AOPPs) in patients with MD1; possible role of oxidative stress in the pathogenesis. \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="top">Syn JK, <span class="elsevierStyleItalic">et al</span><span class="elsevierStyleSup">5</span> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="middle">2009 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="middle">Case presentation \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="top">Elevated liver enzymes years before the onset of Steinert’s disease in a 53 years old male. \t\t\t\t\t\t\n \t\t\t\t</td></tr></tbody></table> """ ] "imagenFichero" => array:1 [ 0 => "xTab2064158.png" ] ] ] ] "descripcion" => array:1 [ "en" => "<p id="sp0010" class="elsevierStyleSimplePara elsevierViewall">Liver involvement in myotonic dystrophy type 1.</p>" ] ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bs0005" "bibliografiaReferencia" => array:20 [ 0 => array:3 [ "identificador" => "bib0005" "etiqueta" => "1." 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Year/Month | Html | Total | |
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2024 October | 56 | 13 | 69 |
2024 September | 55 | 24 | 79 |
2024 August | 82 | 24 | 106 |
2024 July | 92 | 19 | 111 |
2024 June | 64 | 16 | 80 |
2024 May | 48 | 12 | 60 |
2024 April | 67 | 14 | 81 |
2024 March | 85 | 12 | 97 |
2024 February | 75 | 18 | 93 |
2024 January | 98 | 12 | 110 |
2023 December | 52 | 20 | 72 |
2023 November | 63 | 24 | 87 |
2023 October | 61 | 28 | 89 |
2023 September | 53 | 4 | 57 |
2023 August | 50 | 4 | 54 |
2023 July | 53 | 11 | 64 |
2023 June | 58 | 3 | 61 |
2023 May | 77 | 9 | 86 |
2023 April | 68 | 6 | 74 |
2023 March | 84 | 4 | 88 |
2023 February | 36 | 12 | 48 |
2023 January | 31 | 6 | 37 |
2022 December | 33 | 17 | 50 |
2022 November | 26 | 5 | 31 |
2022 October | 21 | 15 | 36 |
2022 September | 19 | 20 | 39 |
2022 August | 6 | 10 | 16 |
2022 July | 15 | 13 | 28 |
2022 June | 22 | 11 | 33 |
2022 May | 23 | 23 | 46 |
2022 April | 33 | 16 | 49 |
2022 March | 30 | 21 | 51 |
2022 February | 43 | 9 | 52 |
2022 January | 49 | 16 | 65 |
2021 December | 11 | 20 | 31 |
2021 November | 19 | 19 | 38 |
2021 October | 21 | 28 | 49 |
2021 September | 17 | 18 | 35 |
2021 August | 14 | 15 | 29 |
2021 July | 9 | 24 | 33 |
2021 June | 8 | 10 | 18 |
2021 May | 13 | 11 | 24 |
2021 April | 58 | 19 | 77 |
2021 March | 25 | 22 | 47 |
2021 February | 10 | 22 | 32 |
2021 January | 5 | 9 | 14 |
2020 December | 12 | 8 | 20 |
2020 November | 6 | 15 | 21 |
2020 October | 9 | 11 | 20 |
2020 September | 17 | 6 | 23 |
2020 August | 8 | 12 | 20 |
2020 July | 4 | 3 | 7 |
2020 June | 5 | 6 | 11 |
2020 May | 3 | 10 | 13 |
2020 April | 1 | 1 | 2 |
2020 March | 8 | 3 | 11 |
2020 February | 2 | 10 | 12 |
2020 January | 6 | 13 | 19 |
2019 December | 5 | 11 | 16 |
2019 November | 6 | 4 | 10 |
2019 October | 4 | 4 | 8 |
2019 September | 4 | 8 | 12 |
2019 August | 1 | 4 | 5 |
2019 July | 1 | 4 | 5 |
2019 June | 1 | 5 | 6 |