Colon necrosis in acute severe pancreatitis.

A 78 year-old woman was admitted for biliary acute pancreatitis (AP). Fluid and analgesia were initially administered. Her clinical course was poor with persisting abdominal pain, intestinal paresis and fever development. On her 7th admission day a contrast-enhanced computed tomography scan was performed where a huge necrotic peripancreatic collection was found with gastric compression .

Hepatitis E seroprevalence in inflammatory bowel disease.

BACKGROUND AND AIMS: Several cases of chronic infection by hepatitis E virus (HEV) in immunocompromised patients have been described recently. Patients with inflammatory bowel disease (IBD) are frequently immunocompromised because of the disease itself or due to therapy. Our aims were to determine HEV seroprevalence in patients with IBD and to detect possible chronic forms. METHODS: We prospectively selected a random sample of 87 patients from our local IBD clinic database at the Gastroenterology Service, Hospital Ramón y Cajal, in Madrid, Spain. Patients completed an oral epidemiologic interview. Anti-HEV IgG and IgM antibodies and HEV-RNA were determined. Medical records were reviewed, focusing on drug exposure. RESULTS: We included 87 patients, with a mean age of 44.7 years (SD 16) and a mean of 10.4 years (SD 8.4) with IBD. Fifty-seven percent were diagnosed with Crohn's disease, 41.4% with ulcerative colitis and 1.1% with unclassified IBD. A total of 41.4% had received systemic glucocorticoids for more than 3 months, 32.2% had been treated with thiopurines, 16.1% with biological drugs, and 3.4% with methotrexate. Anti HEV-IgM was determined in 75 patients and IgG in 80, and were positive in 2.7% and 1.3%, respectively. HEV-RNA was analyzed in a random subset of 46 patients, and all determinations were negative. Therefore, no case of chronic HEV infection was detected. CONCLUSIONS: We found a low HEV seroprevalence of just 1.14% in patients with IBD, similar to that in the general population. This could be due to the lower degree of immunosuppression in this group, or to different dietary habits.

[Acute liver ischaemia after gastro-oesophageal variceal bleeding]. / Isquemia hepática aguda tras hemorragia digestiva alta por varices esofagogástricas.

INTRODUCTION: Variceal upper gastrointestinal bleeding (UGIB) can trigger acute hypoxic hepatitis (AHH). The aim of this study was to analyse the incidence, associated risk factors and mortality of AHH after variceal UGIB. PATIENTS AND METHODS: Retrospective study of cirrhotic patients with variceal UGIB, classified into 2 groups according to the development of AHH. AHH was diagnosed when AST and ALT reached levels 10 times above the upper limit of normal, after ruling out other causes of hepatitis. The standard initial treatment consisted of haemodynamic support, emergency endoscopy with rubber band ligation, somatostatin and antibiotics. In the case of failure of primary haemostasis, a transjugular intrahepatic portosystemic shunt (TIPS) was implanted. Both groups (AHH and non-AHH) were compared. RESULTS: Sixty-eight cirrhotic patients with variceal UGIB admitted to the gastroenterology department of Hospital Ramón y Cajal between January 2007 and March 2012 were analysed. Eleven of these patients (16.2%) developed AHH. Univariate analysis showed the following items as risk factors: diabetes (OR: 7.5; CI: 1.9-29), shock (OR: 8.5; CI: 2.06-34) and persistent bleeding (OR: 9.0, CI: 1.6-49, P=.03). However, multivariate analysis confirmed only diabetes (OR: 8.61; CI: 1.4-52.5) and shock (OR: 7.58; CI: 1.26-45.51) as risk factors. Mortality rate in the AHH group was 45%, compared to 10.5% in the non-HAA group (P=.012). CONCLUSIONS: AHH after variceal UGIB occurred in 16.2% of cirrhotic patients and was associated with a poorer prognosis, with a mortality rate of 45%. Our findings suggest that diabetes and shock are risk factors for the development of AHH. Early identification of at-risk patients could therefore help prevent AHH.

[Acute hypertrygliceridemic pancreatitis]. / Pancreatitis aguda por hipertrigliceridemia.

Acute hypertriglyceridemic pancreatitis is the third cause of acute pancreatitis in the Western population. There is usually an underlying alteration in lipid metabolism and a secondary factor. Clinical presentation is similar to that of pancreatitis of other etiologies, but the course of acute hypertriglyceridemic pancreatitis seems to be worse and more recurrent. Some laboratory data can be artefacts, leading to diagnostic errors. This is the case of amylase, which can show false low levels. Treatment is based on intense fluidotherapy and analgesia. When there is no response to conservative management, other methods to lower triglyceride levels should be used. Several options are available, such as plasmapheresis, insulin, and heparin. The present article provides a review of the current literature on this entity.

Black esophagus and diabetes: a close relationship.

The black esophagus is a rare clinical entity, down to 0.2% in autopsy series and 0.001-0.2% in series of endoscopies. Although it is an entity that has already been reported in the literature, its etiopathogenesis is not completely known. Different theories have been proposed to clarify their cause. One of these theories makes a hypothesis of a viral infection as the underlying cause; this theory can be seen in the literature extensively, but only two cases were reported. The first case is a case with histopathological confirmation of Herpes virus infection. The second is a case in which vascular deterioration has been the main cause of esophageal necrosis. In both cases, diabetes is the factor that determines a bad evolution of the disease.

Histopathological differences in patients with biopsy-proven non-alcoholic fatty liver disease with and without type 2 diabetes.

BACKGROUND AND AIMS: Prevalence of non-alcoholic fatty liver disease (NAFLD) in developed countries is 30% in the general population and 50% in patients with type 2 diabetes mellitus (T2DM). The aim of this study was to compare the severity of NAFLD, as assessed by liver biopsy and using the non-invasive index NAFLD Fibrosis Score (NFS), in subjects with and without T2DM. PATIENTS AND METHODS: The study sample consisted of 217 patients with biopsy-proven NAFLD. Anthropometric assessments, laboratory tests, histological criteria established by the Non-alcoholic Steatohepatitis Clinical Research Network (NASH CRN), and the NFS were recorded. RESULTS: Patients with T2DM (n=36; 16.5%) had higher HOMA-IR values (6.3±3.6 vs. 3.3±2.4; p<0.0001), GGT levels (125.2±102.3 vs. 82.5±70.6IU/l; p<005), and NFS index (-0.6±0.2 vs. -1.8±0.1; p<0.001) than subjects with no T2DM. Patients with T2DM were found higher rates of NASH (72.2% vs. 48.6%; p<0.05), advanced steatosis (80.6% vs. 63%; p<0.05), and liver fibrosis (75% vs. 43.1%, p<0.05) than patients with no T2DM. Patients with T2DM also had higher NFS values (-0.6±1.2 vs. -1.8±1.8: p=0.01). A logistic regression analysis adjusting for age, gender and BMI showed a significant independent association between NASH and presence of T2DM (OR=4.2: 95% CI: 1.4-12.1; p=0.007). A second model adjusting for the same covariates showed T2DM to be an independent factor associated to advanced fibrosis (OR=4.1; 95% CI: 1.7-9.7). CONCLUSION: Patients with T2DM have more advanced degrees of NAFLD and advanced fibrosis as assessed by liver biopsy and the NFS index. Particular attention should be paid to the study and monitoring of NASH in patients with T2DM.

Incidence, management, and course of cancer in patients with inflammatory bowel disease.

BACKGROUND AND AIMS: Patients with inflammatory bowel disease [IBD] are at increased risk for developing some types of neoplasia. Our aims were to determin the risk for cancer in patients with IBD and to describe the relationship with immunosuppressive therapies and clinical management after tumor diagnosis. METHODS: Retrospective, multicenter, observational, 5-year follow-up, cohort study. Relative risk [RR] of cancer in the IBD cohort and the background population, therapeutic strategies, and cancer evolution were analyzed. RESULTS: A total of 145 cancers were diagnosed in 133 of 9100 patients with IBD (global cumulative incidence 1.6% vs 2.4% in local population; RR = 0.67; 95% confidence interval [CI]: 0.57-0.78). Patients with IBD had a significantly increased RR of non-melanoma skin cancer [RR = 3.85; 2.53-5.80] and small bowel cancer [RR = 3.70; 1.23-11.13]. After cancer diagnosis, IBD treatment was maintained in 13 of 27 [48.1%] patients on thiopurines, in 2 of 3 on methotrexate [66.6%], none on anti-TNF-α monotherapy [n = 6] and 4 of 12 [33.3%] patients on combined therapy. Rate of death and cancer remission during follow-up did not differ [p > 0.05] between patients who maintained the treatment compared with patients who withdrew [5% vs 8% and 95% vs 74%, respectively]. An association between thiopurines [p = 0.20] or anti-TNF-α drugs [p = 0.77] and cancer was not found. CONCLUSIONS: Patients with IBD have an increased risk for non-melanoma skin cancer and small bowel cancer. Immunosuppresive therapy is not related to a higher overall risk for cancer or worse tumor evolution in patients who maintain these drugs after cancer diagnosis.

Histopathological differences in patients with biopsy-proven non-alcoholic fatty liver disease with and without type 2 diabetes / Diferencias histopatológicas en pacientes con diabetes mellitus tipo 2 y no diabéticos con enfermedad hepática grasa no alcohólica diagnosticada con biopsia

Background and aims: Prevalence of non-alcoholic fatty liver disease (NAFLD) in developed countries is 30% in the general population and 50% in patients with type 2 diabetes mellitus (T2DM). The aim of this study was to compare the severity of NAFLD, as assessed by liver biopsy and using the non-invasive index NAFLD Fibrosis Score (NFS), in subjects with and without T2DM. Patients and methods: The study sample consisted of 217 patients with biopsy-proven NAFLD. Anthropometric assessments, laboratory tests, histological criteria established by the Non-alcoholic Steatohepatitis Clinical Research Network (NASH CRN), and the NFS were recorded. Results: Patients with T2DM (n=36; 16.5%) had higher HOMA-IR values (6.3±3.6 vs. 3.3±2.4; p<0.0001), GGT levels (125.2±102.3 vs. 82.5±70.6IU/l; p<005), and NFS index (−0.6±0.2 vs. −1.8±0.1; p<0.001) than subjects with no T2DM. Patients with T2DM were found higher rates of NASH (72.2% vs. 48.6%; p<0.05), advanced steatosis (80.6% vs. 63%; p<0.05), and liver fibrosis (75% vs. 43.1%, p<0.05) than patients with no T2DM. Patients with T2DM also had higher NFS values (−0.6±1.2 vs. −1.8±1.8: p=0.01). A logistic regression analysis adjusting for age, gender and BMI showed a significant independent association between NASH and presence of T2DM (OR=4.2: 95% CI: 1.4-12.1; p=0.007). A second model adjusting for the same covariates showed T2DM to be an independent factor associated to advanced fibrosis (OR=4.1; 95% CI: 1.7-9.7). Conclusion: Patients with T2DM have more advanced degrees of NAFLD and advanced fibrosis as assessed by liver biopsy and the NFS index. Particular attention should be paid to the study and monitoring of NASH in patients with T2DM

Antecedentes y objetivos: La prevalencia de la enfermedad hepática grasa no alcohólica (NAFLD) en los países desarrollados es del 30% de la población general y del 50% de los pacientes con diabetes mellitus tipo 2 (DM2). El objetivo de este estudio fue comparar la gravedad de NAFLD evaluado por biopsia hepática y con un índice no invasivo NAFLD Fibrosis Score (NFS) en sujetos con DM2 frente a pacientes no diabéticos. Pacientes y métodos: Este estudio se llevó a cabo entre 217 pacientes con diagnostico mediante biopsia de NAFLD. Se registraron la valoración antropométrica, pruebas de laboratorio, criterios histológicos establecidos por la Red de Investigación Clínica de Esteatohepatitis No Alcohólica (NASH) y NFS. Resultados: Los pacientes con DM2 (n=36; 16,5%) tuvieron más HOMA-IR (6,3±3,6 vs. 3,3±2,4; p<0,0001), GGT (125,2±102,3 vs. 82,5±70,6UI/L); p<0,05) e índice NFS (−0,6±0,2 vs. −1,8±0,1; p<0,001) que los sujetos sin DM2. Los pacientes con DM2 presentaron mayor porcentaje de EHNA (72,2 vs. 48,6%; p<0,05), grado avanzado de esteatosis (80,6 vs. 63%; p<0,05) y fibrosis hepática (75 vs. 43,1%; p<0,05) que los pacientes sin DM2. Los pacientes con DM2 presentaron también valores más altos de NFS (−0,6±1,2 vs. −1,8±1,8; p=0,01). El análisis de regresión logística ajustado por edad, sexo e IMC mostró asociación significativa independiente entre la esteatohepatitis y la presencia de DM2 (OR=4,2; IC 95%: 1,4-12,1; p=0,007). Un segundo modelo ajustado por las mismas covariables mostró que la DM2 fue un factor independiente asociado a la fibrosis avanzada (OR=4,1; IC 95%: 1,7-9,7). Conclusión: Los pacientes con DM2 tienen grados más avanzados de NAFLD y fibrosis avanzada evaluados mediante biopsia hepática y el índice NFS. Debe prestarse especial atención al estudio y seguimiento de la esteatohepatitis en pacientes con DM2

Hepatitis E seroprevalence in inflammatory bowel disease / Seroprevalencia de la hepatitis E en la enfermedad inflamatoria intestinal

BACKGROUND AND AIMS: Several cases of chronic infection by hepatitis E virus (HEV) in immunocompromised patients have been described recently. Patients with inflammatory bowel disease (IBD) are frequently immunocompromised because of the disease itself or due to therapy. Our aims were to determine HEV seroprevalence in patients with IBD and to detect possible chronic forms. Methods: We prospectively selected a random sample of 87 patients from our local IBD clinic database at the Gastroenterology Service, Hospital Ramón y Cajal, in Madrid, Spain. Patients completed an oral epidemiologic interview. Anti-HEV IgG and IgM antibodies and HEV-RNA were determined. Medical records were reviewed, focusing on drug exposure. Results: We included 87 patients, with a mean age of 44.7 years (SD 16) and a mean of 10.4 years (SD 8.4) with IBD. Fifty-seven percent were diagnosed with Crohn's disease, 41.4% with ulcerative colitis and 1.1% with unclassified IBD. A total of 41.4% had received systemic glucocorticoids for more than 3 months, 32.2% had been treated with thiopurines, 16.1% with biological drugs, and 3.4% with methotrexate. Anti HEV-IgM was determined in 75 patients and IgG in 80, and were positive in 2.7% and 1.3%, respectively. HEV-RNA was analyzed in a random subset of 46 patients, and all determinations were negative. Therefore, no case of chronic HEV infection was detected. Conclusions: We found a low HEV seroprevalence of just 1.14% in patients with IBD, similar to that in the general population. This could be due to the lower degree of immunosuppression in this group, or to different dietary habits

INTRODUCCIÓN Y OBJETIVOS: Recientemente se han descrito varios casos de infección crónica por el virus de la hepatitis E (VHE) en pacientes inmunodeprimidos. Los pacientes con enfermedad inflamatoria intestinal (EII) suelen estar inmunodeprimidos debido a la enfermedad en sí o debido a los tratamientos recibidos. Nuestro objetivo fue determinar la seroprevalencia de VHE en pacientes con EII y detectar posibles formas crónicas. MÉTODOS: Analizamos de forma retrospectiva una muestra aleatorea de 87 pacientes de nuestra base de datos de la consulta de EII en el Servicio de Gastroenterología del Hospital Ramón y Cajal, en Madrid, España. Los pacientes respondieron una encuesta epidemiológica oral y se determinaron anticuerpos IgG e IgM frente al VHE, así como RNA de VHE. Se revisaron las historias médicas, haciendo especial hincapié en los tratamientos recibidos. RESULTADOS: Incluimos 87 pacientes con una edad media de 44,7 años (D.E.16) y una media de 10,4 (D.E. 8,4) años de enfermedad. El 57% tenían una enfermedad de Crohn, 41,4% colitis ulcerosa y 1,1% colitis indeterminada. El 41,4% de ellos habían recibido corticoides sistémicos durante más de 3 meses, el 32,3% habían sido tratados con tiopurinas, el 16,1% con fármacos biológicos y el 3,4% con metotrexato. Se determinó la IgM frente a VHE en 75 pacientes y la IgG en 80, resultando positivos en 2,7% y 1,3% respectivamente. El RNA de VHE se analizó en un subgrupo aleatorio de 46 pacientes, y todas las determinaciones fueron negativas, así que no se detectó ningún caso de infección crónica por VHE. CONCLUSIONES: Encontramos una baja seroprevalencia de tan sólo 1,14% en los pacientes con EII, dato similar al de la población general. Esto podría explicarse por un menor grado de inmunosupresión en este grupo, o a diferentes hábitos dietéticos

Isquemia hepática aguda tras hemorragia digestiva alta por varices esofagogástricas / Acute liver ischaemia after gastro-oesophageal variceal bleeding

INTRODUCCIÓN: La hemorragia digestiva alta por varices esofagogástricas (HDA por VEG) puede desencadenar una isquemia hepática aguda (IHA). El objetivo de este estudio fue analizar la incidencia de IHA tras una HDA por VEG, los factores de riesgo y su mortalidad. PACIENTES Y MÉTODOS: Estudio retrospectivo sobre pacientes cirróticos con HDA por VEG. Se clasificaron en 2 grupos, determinados por el desarrollo o no de una IHA. Definimos IHA como AST y ALT por encima de 10 veces el valor basal, descartando otras causas de hepatitis aguda. El tratamiento inicial estándar fue soporte hemodinámico, endoscopia urgente con ligadura con bandas y/o escleroterapia, somatostatina y antibióticos. En caso de fracaso de estas medidas, se recurrió a la implantación de una derivación portosistémcica percutánea intrahepática (DPPI). Ambos grupos (IHA y no-IHA) fueron comparados. RESULTADOS: Durante un periodo de 5 años, se recogieron 68 pacientes con HDA por VEG. La incidencia de IHA fue del 16,2%. Tras el análisis univariante, los factores asociados con IHA fueron la diabetes mellitus (OR: 7,5; IC: 1,9-29), shock (OR: 8,5; IC: 2,06-34) y la persistencia de la hemorragia (OR: 9, IC: 1,6-49, p = 0,03). En el análisis multivariante solo mostraron significación estadística la diabetes mellitus (OR: 8,61; IC: 1,4-52,5) y el shock (OR: 7,58; IC: 1,26-45,51). La mortalidad del grupo de IHA fue mayor (45%) que en el grupo no-IHA (10,5%) (p = 0,012). CONCLUSIONES: La IHA tras una hemorragia digestiva por VEG en el paciente cirrótico ocurrió en el 16,2%, asociándose con un peor pronóstico y una mortalidad del 45%. Nuestros resultados sugieren que la diabetes mellitus y el shock hipovolémico son factores de riesgo para el desarrollo de IHA. La detección precoz de estos pacientes en riesgo podría por tanto ayudar a prevenir la IHA

INTRODUCTION: Variceal upper gastrointestinal bleeding (UGIB) can trigger acute hypoxic hepatitis (AHH). The aim of this study was to analyse the incidence, associated risk factors and mortality of AHH after variceal UGIB. PATIENTS AND METHODS: Retrospective study of cirrhotic patients with variceal UGIB, classified into 2 groups according to the development of AHH. AHH was diagnosed when AST and ALT reached levels 10 times above the upper limit of normal, after ruling out other causes of hepatitis. The standard initial treatment consisted of haemodynamic support, emergency endoscopy with rubber band ligation, somatostatin and antibiotics. In the case of failure of primary haemostasis, a transjugular intrahepatic portosystemic shunt (TIPS) was implanted. Both groups (AHH and non-AHH) were compared. RESULTS: Sixty-eight cirrhotic patients with variceal UGIB admitted to the gastroenterology department of Hospital Ramón y Cajal between January 2007 and March 2012 were analysed. Eleven of these patients (16.2%) developed AHH. Univariate analysis showed the following items as risk factors: diabetes (OR: 7.5; CI: 1.9-29), shock (OR: 8.5; CI: 2.06-34) and persistent bleeding (OR: 9.0, CI: 1.6-49, P = .03). However, multivariate analysis confirmed only diabetes (OR: 8.61; CI: 1.4-52.5) and shock (OR: 7.58; CI: 1.26-45.51) as risk factors. Mortality rate in the AHH group was 45%, compared to 10.5% in the non-HAA group (P = .012). CONCLUSIONS: AHH after variceal UGIB occurred in 16.2% of cirrhotic patients and was associated with a poorer prognosis, with a mortality rate of 45%. Our findings suggest that diabetes and shock are risk factors for the development of AHH. Early identification of at-risk patients could therefore help prevent AHH

Pancreatitis aguda por hipertrigliceridemia / Acute hypertrygliceridemic pancreatitis

La pancreatitis aguda por hipertrigliceridemia es la tercera causa de pancreatitis aguda en la población occidental. Normalmente hay una alteración subyacente del metabolismo lipidémico, sobre la que actúa un factor secundario. La presentación clínica es similar a la de las pancreatitis agudas de otras etiologías, aunque su curso parece ser más tórpido y recurrente. Para su diagnóstico hay que saber que algunos parámetros de la analítica pueden estar artefactados, lo que puede conducir a un fallo en el diagnóstico. Tal es el caso de la amilasa, que puede estar falsamente descendida. El tratamiento se basa en sueroterapia intensa y analgesia. Cuando no responde al tratamiento conservador, deben utilizarse otros métodos para disminuir el nivel de triglicéridos. Para ello disponemos de la plasmaféresis, la insulina y la heparina. Este artículo pretende mostrar una revisión de la literatura actual sobre esta patología (AU)

Acute hypertriglyceridemic pancreatitis is the third cause of acute pancreatitis in the Western population. There is usually an underlying alteration in lipid metabolism and a secondary factor. Clinical presentation is similar to that of pancreatitis of other etiologies, but the course of acute hypertriglyceridemic pancreatitis seems to be worse and more recurrent. Some laboratory data can be artefacts, leading to diagnostic errors. This is the case of amylase, which can show false low levels. Treatment is based on intense fluidotherapy and analgesia. When there is no response to conservative management, other methods to lower triglyceride levels should be used. Several options are available, such as plasmapheresis, insulin, and heparin. The present article provides a review of the current literature on this entity (AU)