Scielo RSS <![CDATA[Revista Española de Enfermedades Digestivas]]> http://scielo.isciii.es/rss.php?pid=1130-010820090011&lang=en vol. 101 num. 11 lang. en <![CDATA[SciELO Logo]]> http://scielo.isciii.es/img/en/fbpelogp.gif http://scielo.isciii.es <![CDATA[<B>Infection with <I>Helicobacter pylori</B></I>: <B>Prevalence, research and impact of antibiotic resistance</B>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082009001100001&lng=en&nrm=iso&tlng=en <![CDATA[<B>Antimicrobial susceptibility of <I>Helicobacter pylori</I> and mechanisms of clarithromycin resistance in strains isolated from patients in Uruguay</B>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082009001100002&lng=en&nrm=iso&tlng=en The prevalence and mechanisms of antibiotic resistance of Helicobacter pylori have not yet been investigated in Uruguay. The objective of this study was to assess the susceptibility of H. pylori to the most frequently used antibiotics and to determine the mechanism of resistance to clarithromycin. Seventy-nine isolates were obtained from gastric biopsies of 50 adult patients during two periods, 2001 and 2006. The former group enrolled the general population (GP), the latter group Afro-descendant (AD) subjects. The minimum inhibitory concentrations of clarithromycin, amoxicillin, tetracycline, metronidazole, and levofloxacin were determined using the E-test technique. Amplification was achieved through PCR and nucleic acid sequencing to detect mutations in the site of action of clarithromycin in the rRNA gene 23S. No amoxicillin or tetracycline-resistant strains were found. Clarithromycin resistance was found in 12% of the patients overall: 19.4% resistance in AD patients and no resistance in the GP group. This difference was statistically significant. The highest resistance was seen with metronidazole (36%), present in similar proportions in the two groups: 36.8% (GP) and 35.5% (AD). One GP patient and one AD patient had levofloxacin-resistant strains. Sequencing analysis of gene 23S rRNA showed that only mutation in position 2143 was presented in all clarithromycin-resistant strains. <![CDATA[<B>Decrease in viral load at weeks 12 and 24 in patients with chronic hepatitis B treated with lamivudine or adefovir predicts virological response at week 48</B>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082009001100003&lng=en&nrm=iso&tlng=en Aim: the aim of our study was to evaluate the decrease in viral load (VL) that is able to predict antiviral treatment response at one year in patients with chronic hepatitis B. Methods: the clinical records of 66 patients, 31 treated with lamivudine (LAM) and 35 treated with adefovir (ADF), were retrospectively reviewed. We measured viral DNA at months 1, 3 and 6. Results: the LAM group showed virological response (VR) in 51.6% of patients. Baseline VL was higher in non responders (5.37 &plusmn; 1.16 vs. 7.01 &plusmn; 1.05; p < 0.001). Responders showed a higher percentage of VL decrease at month 3 from baseline (49.2 vs. 38.3%; p = 0.03). We designed a ROC curve and established a cutoff point for decrease of 30% that had 80% of negative predictive value (NPV). The ADF group showed VR in 57.1% of patients. Baseline VL was higher in nonresponders (4.67 &plusmn; 1.22 vs. 5.78 &plusmn; 1.34; p = 0.01). We observed a significant decrease in VL (log) at months 3 (2.6 &plusmn; 1.1 vs. 1.3 &plusmn; 1.3; p = 0.03) and 6 (2.6 &plusmn; 1.2 vs. 1.3 &plusmn; 1.2; p = 0.006). The percentage of decrease of VL from baseline was also statistically significant. We created ROC curves at months 3 and 6, and established the best cutoff points. At month 6 a decrease of 1 log in VL had a NPV of 80%, and a decrease of 20% in VL from baseline had 100% NPV. Conclusion: the decrease in viral DNA at weeks 12 and 24 can predict VR at one year in patients with chronic hepatitis B treated with LAM or ADF. This could optimize treatment. <![CDATA[<B>Epidemiologic study on the current incidence of inflammatory bowel disease in Madrid</B>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082009001100004&lng=en&nrm=iso&tlng=en Introduction: the incidence of inflammatory bowel disease (IBD) varies widely according to geographical area and has been reported to have increased in the last few years. No data are available on the current incidence of this disease in Madrid (Spain). Aim: to determine the incidence of inflammatory bowel disease in the area of influence of University Hospital Fundación Alcorcón (Madrid), and to compare our results with those from other Spanish and European series. Patients and methods: a prospective, population-based study was performed to determine the incidence of IBD in the area of University Hospital Fundación Alcorcón in Madrid between 2003 and 2005. Total population: 213,587 inhabitants (177,490 older than 14 years). Crude rates and age- and sex-specific rates adjusted to the European standard population were calculated. A retrospective study (1998-2003) was also performed. Results: a total of 69 cases were diagnosed -Crohn's disease (CD): 35, ulcerative colitis (UC): 33, indeterminate colitis: 1- in the prospective period. Crude rates of CD and UC were 7.92 and 7.47 cases/100,000 inhabitants/year, respectively (the population aged 0-14 years). Specific rates were 8.0 (95% CI, 7.03-8.97) and 7.47 (95% CI, 6.5-8.4), respectively. Mean age at diagnosis was 31.02&plusmn; 10.76 and 39.91&plusmn;16.19 years for CD and UC, respectively. Incidence in the retrospective study was 7.13 and 6.22 cases/100,000 inhabitants/year, respectively for CD and UC. Conclusions: the incidence of CD and UC in Madrid has increased in the last decades, with rates close to those in northern European countries for CD, higher than those recently published in Spanish prospective studies and similar to those previously described in Spain and southern countries for UC. Rates were higher in the prospective period than in the retrospective one. <![CDATA[<B>Ultrasonography is an accurate technique for the diagnosis of gastrointestinal tumors in patients without localizing symptoms</B>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082009001100005&lng=en&nrm=iso&tlng=en Introduction and objectives: this study compared the accuracy of ultrasonography in the diagnosis of gastrointestinal tumors in patients with several degrees of clinical suspicion. Material and methods: we recruited patients that were suspect for gastrointestinal neoplasia but with no evidence of localizing symptoms (group A), and patients that were suspect for colon cancer (group B) or for gastric cancer (group C). Accuracy in the diagnosis was compared for: gastric cancer in groups A and C, and for colon cancer in groups A and B. The comparison was made by using the contingency coefficient, which quantifies coincidence of endoscopic and ultrasonographic diagnoses. Results: seventy-nine patients were included in group A (48 males), wherein 12 colon and 5 gastric neoplasms were detected. Group B was comprised of 153 patients (78 males) and included 66 patients with colorectal cancer (CCR). Group C contained 58 patients (35 males), 31 of whom were diagnosed with gastric cancer. The accuracy of sonography for diagnosing colon cancer was 95.5% for group A and 87.5% for group B. The contingency coefficient for endoscopy vs. ultrasonography was greater for group A: 0.658 than for group B: 0.549. The diagnostic accuracy for gastric cancer was 97.4% for group A and 86.2% for group C. The contingency coefficient between endoscopic and ultrasonographic diagnoses was also greater in group A (0.618) than in group C (0.588). Conclusions: the accuracy of ultrasonography in diagnosing colon and gastric cancer is not lower in patients without localizing symptoms.<hr/>Introducción y objetivos: en todos los estudios publicados hasta la fecha se ha evaluado la precisión de la ecografía en el diagnóstico del cáncer de colon y del cáncer gástrico en pacientes en los que esta era la sospecha diagnóstica o ya con un diagnóstico establecido de esta patología. Nosotros, en este estudio, comparamos la sensibilidad de la ecografía en pacientes con diferentes grados de sospecha clínica. Material y método: reclutamos pacientes con sospecha de neoplasia digestiva, sin evidencia de síntomas localizadores (grupo A), pacientes con sospecha de cáncer de colon (grupo B) y pacientes con sospecha de cáncer gástrico (grupo C). Comparamos la precisión de la ecografía en el diagnóstico del cáncer gástrico en los grupos A y C, y la precisión en el diagnóstico del cáncer de colon en los grupos A y B. El parámetro usado en la comparación es el coeficiente de contigencia que cuantifica la coincidencia de diagnóstico endoscópico y ecográfico. Resultados: se han incluido 79 pacientes en el grupo A (48 varones y 31 mujeres, con una edad media de 69,3 años), en los que se han diagnosticado 12 neoplasias colónicas y 5 gástricas. El grupo B se compone de 153 pacientes (78 varones y 75 mujeres, con una edad media de 66,5 años) e incluye 66 pacientes con CCR. Finalmente, el grupo C está formado por 58 pacientes (35 varones y 23 mujeres, con una edad media de 67,4 años), siendo diagnosticados de cáncer gástrico 31 pacientes. La precisión de la ecografía en el diagnóstico del cáncer de colon fue del 95,5% en el grupo A y del 87,5% en el grupo B. El coeficiente de contingencia entre los diagnósticos endoscópico y ecográfico también fue superior en el grupo A: 0,658 frente a 0,549. La precisión de la ecografía en el diagnóstico del cáncer gástrico fue del 97,4% en el grupo A y del 86,2% en el grupo C. El coeficiente de contingencia entre los diagnósticos endoscópico y ecográfico también fue mayor en el grupo A (0,618) que en el grupo C (0,588). Conclusiones: la precisión de la ecografía digestiva en el diagnóstico del cáncer de colon y del cáncer gástrico no es inferior en los pacientes en los que no hay una sospecha específica de estas patologías. <![CDATA[<B>Noninvasive assessment of liver fibrosis</B>: <B>Serum markers and transient elastography (FibroScan)</B>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082009001100006&lng=en&nrm=iso&tlng=en Both the prognosis and potential treatment of chronic liver disease greatly depend on the progression of liver fibrosis, which is the ultimate outcome of chronic liver damage. Historically, liver biopsy has been instrumental in adequately assessing patients with chronic liver disease. Histological assessment allows clinicians both to obtain diagnostic information and initiate adequate therapy. However, the technique is not exempt of deleterious effects. Multiple diagnostic tests have been developed for the staging of fibrosis using noninvasive methods, most of them in the setting of chronic hepatitis C. The goal of this paper is to review available data on the staging and assessment of liver fibrosis with two methods: serum markers and transient elastography (FibroScan®). <![CDATA[<B>Abdominal mass, multiple lymphadenopathies, and polyposis</B>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082009001100007&lng=en&nrm=iso&tlng=en Both the prognosis and potential treatment of chronic liver disease greatly depend on the progression of liver fibrosis, which is the ultimate outcome of chronic liver damage. Historically, liver biopsy has been instrumental in adequately assessing patients with chronic liver disease. Histological assessment allows clinicians both to obtain diagnostic information and initiate adequate therapy. However, the technique is not exempt of deleterious effects. Multiple diagnostic tests have been developed for the staging of fibrosis using noninvasive methods, most of them in the setting of chronic hepatitis C. The goal of this paper is to review available data on the staging and assessment of liver fibrosis with two methods: serum markers and transient elastography (FibroScan®). <![CDATA[<B>Presacral mass as a cause of constipation</B>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082009001100008&lng=en&nrm=iso&tlng=en Both the prognosis and potential treatment of chronic liver disease greatly depend on the progression of liver fibrosis, which is the ultimate outcome of chronic liver damage. Historically, liver biopsy has been instrumental in adequately assessing patients with chronic liver disease. Histological assessment allows clinicians both to obtain diagnostic information and initiate adequate therapy. However, the technique is not exempt of deleterious effects. Multiple diagnostic tests have been developed for the staging of fibrosis using noninvasive methods, most of them in the setting of chronic hepatitis C. The goal of this paper is to review available data on the staging and assessment of liver fibrosis with two methods: serum markers and transient elastography (FibroScan®). <![CDATA[<b>Acquired chronic hepatocerebral degeneration due to cirrhosis from non-alcoholic steatohepatitis</b>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082009001100009&lng=en&nrm=iso&tlng=en Introduction and objective: acquired chronic hepatocerebral degeneration, acquired hepatolenticular degeneration or pseudo-Wilson is an infrequent disorder with a hepatic origin. Cases in the literature are scarce and it is frequently confused with hepatic encephalopathy and Wilson's disease. The aim of this essay is to report a patient suffering from this disorder due to cirrhosis from non-alcoholic steatohepatitis. Case report: we present a 54-year-old man diagnosed from cirrhosis grade B9 of the Child Pugh classification. He progressively developed a picture with bradylalia, mild postural and action tremor and spatial and temporal disorientation. Further studies demonstrated an increase of the values of hepatic transaminases and a hiperintensity in the basal nuclei in the cerebral magnetic resonance imaging. Clinical and radiological data established the diagnosis of hepatocerebral degeneration. Conclusions: acquired chronic hepatocerebral degeneration is a disorder rarely reported in the literature that it is usually confused with other diseases. We alert about the need of having this diagnosis into account with patients developing neurological symptoms after hepatic disease.<hr/>Fundamento y objetivo: el síndrome hepatocerebral crónico, también denominado degeneración hepatolenticular crónica adquirida (DHCA) o pseudo-Wilson, es un trastorno poco frecuente de origen hepático. Los casos recogidos en la literatura son escasos y frecuentemente es confundido con la encefalopatía hepática y con la enfermedad de Wilson. El objetivo de este artículo es presentar un paciente que sufre este trastorno de forma secundaria a una cirrosis por esteatohepatitis no alcohólica. Caso clínico: se trata de un varón de 54 años diagnosticado de cirrosis en grado funcional de Child-Pugh B9 que presentó un cuadro progresivo de bradilalia, temblor postural y de acción leve y, en ocasiones, desorientación temporoespacial. Los estudios complementarios evidenciaron una elevación de las transaminasas hepáticas y una hiperintensidad de los núcleos basales en la resonancia magnética cerebral estableciéndose el diagnóstico de DHCA. Conclusiones: la DHCA es un trastorno poco descrito en la literatura que en ocasiones es confundido con otras entidades. Es necesario descartar la presencia de esta patología en los pacientes cirróticos con alteraciones neurológicas tras una enfermedad hepática. <![CDATA[<B>Benign liver tumors</B>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082009001100010&lng=en&nrm=iso&tlng=en Introduction and objective: acquired chronic hepatocerebral degeneration, acquired hepatolenticular degeneration or pseudo-Wilson is an infrequent disorder with a hepatic origin. Cases in the literature are scarce and it is frequently confused with hepatic encephalopathy and Wilson's disease. The aim of this essay is to report a patient suffering from this disorder due to cirrhosis from non-alcoholic steatohepatitis. Case report: we present a 54-year-old man diagnosed from cirrhosis grade B9 of the Child Pugh classification. He progressively developed a picture with bradylalia, mild postural and action tremor and spatial and temporal disorientation. Further studies demonstrated an increase of the values of hepatic transaminases and a hiperintensity in the basal nuclei in the cerebral magnetic resonance imaging. Clinical and radiological data established the diagnosis of hepatocerebral degeneration. Conclusions: acquired chronic hepatocerebral degeneration is a disorder rarely reported in the literature that it is usually confused with other diseases. We alert about the need of having this diagnosis into account with patients developing neurological symptoms after hepatic disease.<hr/>Fundamento y objetivo: el síndrome hepatocerebral crónico, también denominado degeneración hepatolenticular crónica adquirida (DHCA) o pseudo-Wilson, es un trastorno poco frecuente de origen hepático. Los casos recogidos en la literatura son escasos y frecuentemente es confundido con la encefalopatía hepática y con la enfermedad de Wilson. El objetivo de este artículo es presentar un paciente que sufre este trastorno de forma secundaria a una cirrosis por esteatohepatitis no alcohólica. Caso clínico: se trata de un varón de 54 años diagnosticado de cirrosis en grado funcional de Child-Pugh B9 que presentó un cuadro progresivo de bradilalia, temblor postural y de acción leve y, en ocasiones, desorientación temporoespacial. Los estudios complementarios evidenciaron una elevación de las transaminasas hepáticas y una hiperintensidad de los núcleos basales en la resonancia magnética cerebral estableciéndose el diagnóstico de DHCA. Conclusiones: la DHCA es un trastorno poco descrito en la literatura que en ocasiones es confundido con otras entidades. Es necesario descartar la presencia de esta patología en los pacientes cirróticos con alteraciones neurológicas tras una enfermedad hepática. <![CDATA[<B>Syphilitic hepatitis</B>: <B>case report</B>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082009001100011&lng=en&nrm=iso&tlng=en Introduction and objective: acquired chronic hepatocerebral degeneration, acquired hepatolenticular degeneration or pseudo-Wilson is an infrequent disorder with a hepatic origin. Cases in the literature are scarce and it is frequently confused with hepatic encephalopathy and Wilson's disease. The aim of this essay is to report a patient suffering from this disorder due to cirrhosis from non-alcoholic steatohepatitis. Case report: we present a 54-year-old man diagnosed from cirrhosis grade B9 of the Child Pugh classification. He progressively developed a picture with bradylalia, mild postural and action tremor and spatial and temporal disorientation. Further studies demonstrated an increase of the values of hepatic transaminases and a hiperintensity in the basal nuclei in the cerebral magnetic resonance imaging. Clinical and radiological data established the diagnosis of hepatocerebral degeneration. Conclusions: acquired chronic hepatocerebral degeneration is a disorder rarely reported in the literature that it is usually confused with other diseases. We alert about the need of having this diagnosis into account with patients developing neurological symptoms after hepatic disease.<hr/>Fundamento y objetivo: el síndrome hepatocerebral crónico, también denominado degeneración hepatolenticular crónica adquirida (DHCA) o pseudo-Wilson, es un trastorno poco frecuente de origen hepático. Los casos recogidos en la literatura son escasos y frecuentemente es confundido con la encefalopatía hepática y con la enfermedad de Wilson. El objetivo de este artículo es presentar un paciente que sufre este trastorno de forma secundaria a una cirrosis por esteatohepatitis no alcohólica. Caso clínico: se trata de un varón de 54 años diagnosticado de cirrosis en grado funcional de Child-Pugh B9 que presentó un cuadro progresivo de bradilalia, temblor postural y de acción leve y, en ocasiones, desorientación temporoespacial. Los estudios complementarios evidenciaron una elevación de las transaminasas hepáticas y una hiperintensidad de los núcleos basales en la resonancia magnética cerebral estableciéndose el diagnóstico de DHCA. Conclusiones: la DHCA es un trastorno poco descrito en la literatura que en ocasiones es confundido con otras entidades. Es necesario descartar la presencia de esta patología en los pacientes cirróticos con alteraciones neurológicas tras una enfermedad hepática. <![CDATA[<B>Desmoid tumor arising in a laparoscopic trocar site after cholectomy</B>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082009001100012&lng=en&nrm=iso&tlng=en Introduction and objective: acquired chronic hepatocerebral degeneration, acquired hepatolenticular degeneration or pseudo-Wilson is an infrequent disorder with a hepatic origin. Cases in the literature are scarce and it is frequently confused with hepatic encephalopathy and Wilson's disease. The aim of this essay is to report a patient suffering from this disorder due to cirrhosis from non-alcoholic steatohepatitis. Case report: we present a 54-year-old man diagnosed from cirrhosis grade B9 of the Child Pugh classification. He progressively developed a picture with bradylalia, mild postural and action tremor and spatial and temporal disorientation. Further studies demonstrated an increase of the values of hepatic transaminases and a hiperintensity in the basal nuclei in the cerebral magnetic resonance imaging. Clinical and radiological data established the diagnosis of hepatocerebral degeneration. Conclusions: acquired chronic hepatocerebral degeneration is a disorder rarely reported in the literature that it is usually confused with other diseases. We alert about the need of having this diagnosis into account with patients developing neurological symptoms after hepatic disease.<hr/>Fundamento y objetivo: el síndrome hepatocerebral crónico, también denominado degeneración hepatolenticular crónica adquirida (DHCA) o pseudo-Wilson, es un trastorno poco frecuente de origen hepático. Los casos recogidos en la literatura son escasos y frecuentemente es confundido con la encefalopatía hepática y con la enfermedad de Wilson. El objetivo de este artículo es presentar un paciente que sufre este trastorno de forma secundaria a una cirrosis por esteatohepatitis no alcohólica. Caso clínico: se trata de un varón de 54 años diagnosticado de cirrosis en grado funcional de Child-Pugh B9 que presentó un cuadro progresivo de bradilalia, temblor postural y de acción leve y, en ocasiones, desorientación temporoespacial. Los estudios complementarios evidenciaron una elevación de las transaminasas hepáticas y una hiperintensidad de los núcleos basales en la resonancia magnética cerebral estableciéndose el diagnóstico de DHCA. Conclusiones: la DHCA es un trastorno poco descrito en la literatura que en ocasiones es confundido con otras entidades. Es necesario descartar la presencia de esta patología en los pacientes cirróticos con alteraciones neurológicas tras una enfermedad hepática. <![CDATA[<B>Giant lipoma and intestinal intussusception</B>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082009001100013&lng=en&nrm=iso&tlng=en Introduction and objective: acquired chronic hepatocerebral degeneration, acquired hepatolenticular degeneration or pseudo-Wilson is an infrequent disorder with a hepatic origin. Cases in the literature are scarce and it is frequently confused with hepatic encephalopathy and Wilson's disease. The aim of this essay is to report a patient suffering from this disorder due to cirrhosis from non-alcoholic steatohepatitis. Case report: we present a 54-year-old man diagnosed from cirrhosis grade B9 of the Child Pugh classification. He progressively developed a picture with bradylalia, mild postural and action tremor and spatial and temporal disorientation. Further studies demonstrated an increase of the values of hepatic transaminases and a hiperintensity in the basal nuclei in the cerebral magnetic resonance imaging. Clinical and radiological data established the diagnosis of hepatocerebral degeneration. Conclusions: acquired chronic hepatocerebral degeneration is a disorder rarely reported in the literature that it is usually confused with other diseases. We alert about the need of having this diagnosis into account with patients developing neurological symptoms after hepatic disease.<hr/>Fundamento y objetivo: el síndrome hepatocerebral crónico, también denominado degeneración hepatolenticular crónica adquirida (DHCA) o pseudo-Wilson, es un trastorno poco frecuente de origen hepático. Los casos recogidos en la literatura son escasos y frecuentemente es confundido con la encefalopatía hepática y con la enfermedad de Wilson. El objetivo de este artículo es presentar un paciente que sufre este trastorno de forma secundaria a una cirrosis por esteatohepatitis no alcohólica. Caso clínico: se trata de un varón de 54 años diagnosticado de cirrosis en grado funcional de Child-Pugh B9 que presentó un cuadro progresivo de bradilalia, temblor postural y de acción leve y, en ocasiones, desorientación temporoespacial. Los estudios complementarios evidenciaron una elevación de las transaminasas hepáticas y una hiperintensidad de los núcleos basales en la resonancia magnética cerebral estableciéndose el diagnóstico de DHCA. Conclusiones: la DHCA es un trastorno poco descrito en la literatura que en ocasiones es confundido con otras entidades. Es necesario descartar la presencia de esta patología en los pacientes cirróticos con alteraciones neurológicas tras una enfermedad hepática. <![CDATA[<B>Intestinal obstruction due to metastasis in mesentery from squamous cell lung carcinoma</B>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082009001100014&lng=en&nrm=iso&tlng=en Introduction and objective: acquired chronic hepatocerebral degeneration, acquired hepatolenticular degeneration or pseudo-Wilson is an infrequent disorder with a hepatic origin. Cases in the literature are scarce and it is frequently confused with hepatic encephalopathy and Wilson's disease. The aim of this essay is to report a patient suffering from this disorder due to cirrhosis from non-alcoholic steatohepatitis. Case report: we present a 54-year-old man diagnosed from cirrhosis grade B9 of the Child Pugh classification. He progressively developed a picture with bradylalia, mild postural and action tremor and spatial and temporal disorientation. Further studies demonstrated an increase of the values of hepatic transaminases and a hiperintensity in the basal nuclei in the cerebral magnetic resonance imaging. Clinical and radiological data established the diagnosis of hepatocerebral degeneration. Conclusions: acquired chronic hepatocerebral degeneration is a disorder rarely reported in the literature that it is usually confused with other diseases. We alert about the need of having this diagnosis into account with patients developing neurological symptoms after hepatic disease.<hr/>Fundamento y objetivo: el síndrome hepatocerebral crónico, también denominado degeneración hepatolenticular crónica adquirida (DHCA) o pseudo-Wilson, es un trastorno poco frecuente de origen hepático. Los casos recogidos en la literatura son escasos y frecuentemente es confundido con la encefalopatía hepática y con la enfermedad de Wilson. El objetivo de este artículo es presentar un paciente que sufre este trastorno de forma secundaria a una cirrosis por esteatohepatitis no alcohólica. Caso clínico: se trata de un varón de 54 años diagnosticado de cirrosis en grado funcional de Child-Pugh B9 que presentó un cuadro progresivo de bradilalia, temblor postural y de acción leve y, en ocasiones, desorientación temporoespacial. Los estudios complementarios evidenciaron una elevación de las transaminasas hepáticas y una hiperintensidad de los núcleos basales en la resonancia magnética cerebral estableciéndose el diagnóstico de DHCA. Conclusiones: la DHCA es un trastorno poco descrito en la literatura que en ocasiones es confundido con otras entidades. Es necesario descartar la presencia de esta patología en los pacientes cirróticos con alteraciones neurológicas tras una enfermedad hepática. <![CDATA[<B>Bowel subocclusion due to <I>Anisakis</B></I>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082009001100015&lng=en&nrm=iso&tlng=en Introduction and objective: acquired chronic hepatocerebral degeneration, acquired hepatolenticular degeneration or pseudo-Wilson is an infrequent disorder with a hepatic origin. Cases in the literature are scarce and it is frequently confused with hepatic encephalopathy and Wilson's disease. The aim of this essay is to report a patient suffering from this disorder due to cirrhosis from non-alcoholic steatohepatitis. Case report: we present a 54-year-old man diagnosed from cirrhosis grade B9 of the Child Pugh classification. He progressively developed a picture with bradylalia, mild postural and action tremor and spatial and temporal disorientation. Further studies demonstrated an increase of the values of hepatic transaminases and a hiperintensity in the basal nuclei in the cerebral magnetic resonance imaging. Clinical and radiological data established the diagnosis of hepatocerebral degeneration. Conclusions: acquired chronic hepatocerebral degeneration is a disorder rarely reported in the literature that it is usually confused with other diseases. We alert about the need of having this diagnosis into account with patients developing neurological symptoms after hepatic disease.<hr/>Fundamento y objetivo: el síndrome hepatocerebral crónico, también denominado degeneración hepatolenticular crónica adquirida (DHCA) o pseudo-Wilson, es un trastorno poco frecuente de origen hepático. Los casos recogidos en la literatura son escasos y frecuentemente es confundido con la encefalopatía hepática y con la enfermedad de Wilson. El objetivo de este artículo es presentar un paciente que sufre este trastorno de forma secundaria a una cirrosis por esteatohepatitis no alcohólica. Caso clínico: se trata de un varón de 54 años diagnosticado de cirrosis en grado funcional de Child-Pugh B9 que presentó un cuadro progresivo de bradilalia, temblor postural y de acción leve y, en ocasiones, desorientación temporoespacial. Los estudios complementarios evidenciaron una elevación de las transaminasas hepáticas y una hiperintensidad de los núcleos basales en la resonancia magnética cerebral estableciéndose el diagnóstico de DHCA. Conclusiones: la DHCA es un trastorno poco descrito en la literatura que en ocasiones es confundido con otras entidades. Es necesario descartar la presencia de esta patología en los pacientes cirróticos con alteraciones neurológicas tras una enfermedad hepática.