Hepatic splenosis, description of an unusual behavior at contrast-enhanced ultrasonography (CEUS).

The case was a 47-year-old male, asymptomatic, with a personal history of splenectomy in childhood. He was referred to our outpatient clinic to complete the study of space-occupying liver lesion. The initial diagnostic suspicion was liver adenoma, given its behavior on magnetic resonance imaging and the absence of previous liver disease. We performed an intravascular contrast-enhanced ultrasound (CEUS) (SonoVue©). The lesion showed rapid centripetal enhancement, remaining enhanced in the portal phase with dim washout in the late venous phase. Given the therapeutic implications of the diagnosis of a hepatic adenoma, an ultrasound-guided percutaneous biopsy with an 18-gauge core needle was performed. The anatomopathological study confirmed the presence of hepatic splenosis. Hepatic splenosis can present as isolated or multiple foci (1). There is little published information on the behavior of hepatic splenosis in CEUS (2, 3, 4), which prevents any behavior from being generalized. The most frequently described behavior is hyperenhancement in the arterial phase without subsequent washout, not a specific behavior that can lead to the misdiagnosis of other entities such as hemangioma. In our case, it was caused by an isolated focus of splenosis that did not show the most frequent described behavior at CEUS, since it presented a faint washout in the venous phase, making it necessary to rule out malignancy.

Fontan protein-losing enteropathy is associated with advanced liver disease and a proinflammatory intestinal and systemic state.

BACKGROUND AND AIMS: Protein-losing enteropathy (PLE) after Fontan surgery carries significant morbimortality. Its pathophysiology and association with other Fontan complications are poorly understood. Our aims were to examine whether Fontan-PLE is associated with greater liver damage and to assess the presence of systemic and intestinal inflammation. METHODS: Fontan patients with PLE and Fontan controls without PLE matched for age and Fontan surgery procedure were included. Data were prospectively compiled on blood and stool tests, liver imaging, elastography, cardiac-MRI and cardiac catheterization. RESULTS: Twenty-nine Fontan patients were enrolled (14 with PLE and 15 controls without PLE). Patients with PLE had more advanced liver disease estimated by non-invasive methods: blunt liver margins on ultrasonography (71.4% vs 26.7%, P = .027), greater median liver stiffness (25.4 vs 14.5 kPa, P = .003) and higher FIB-4 (P = .016). Portal hypertension-related signs were more common in patients with PLE including ascites (P = .035), larger spleen size (P = .005), oesophageal varices/splanchnic collateral shunts (P = .03), higher liver stiffness-spleen size-to-platelet ratio risk score (P < .001) and lower platelet count (P = .01). Systemic proinflammatory cytokines (TNF-α, interleukin-6), biomarkers of intestinal permeability (intestinal fatty-acid binding protein) and faecal calprotectin concentrations were also significantly increased in Fontan-PLE (P < .05). Faecal calprotectin directly correlated with alpha-1 antitrypsin clearance and inversely with cardiac index, total serum proteins and body mass index. CONCLUSION: Fontan-PLE is associated with advanced liver disease and increased markers of systemic inflammation and intestinal permeability. Faecal calprotectin is elevated and correlates with Fontan-PLE severity. Liver assessment is mandatory in all Fontan patients, and especially in those with PLE.

Adenocarcinoma de bulbo duodenal, un diagnóstico poco sospechado / Bulbar duodenal adenocarcinoma. An unsuspected diagnosis

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Trastornos linfoproliferativos en una unidad de enfermedad inflamatoria intestinal / Lymphoproliferative disorders in an inflammatory bowel disease unit

IntroducciónLa relación entre la enfermedad inflamatoria intestinal (EII) y los trastornos linfoproliferativos (TL) se ha reportado previamente.ObjetivosEstablecer la incidencia de TL en una unidad de EII y describir sus características clínicas.Material y métodosSe utilizaron el registro de datos de la consulta monográfica de EII y las historias clínicas. En todos los casos, el diagnóstico de EII se realizó mediante los criterios habituales.ResultadosSe identificaron 7 casos de TL en 911 pacientes con EII. Cinco eran varones, 4 tenían colitis ulcerosa y 3, enfermedad de Crohn. El tiempo medio entre el diagnóstico de la EII y el TL fue de 4,82 años (rango [r]: 0–20). La edad media al diagnóstico del TL fue de 53 años (r: 33–76). Cuatro de los TL estaban limitados al tracto gastrointestinal. Sólo uno fue linfoma de Hodgkin. Cinco pacientes habían recibido tiopurinas y 4 habían recibido, además, agentes biológicos. Tres de los casos se encontraron asociados a infección por el virus de Epstein Barr (VEB). La incidencia estimada de TL en esta serie de pacientes fue de 81,74/100.000. Tras un tiempo medio de 32,3 meses (r: 5–57) después del último tratamiento para el TL, todos los pacientes menos uno se encuentran en remisión de su enfermedad hematológica.DiscusiónLa incidencia de TL en pacientes con EII fue más elevada que la esperada para la población general (81,74 versus 22). Posiblemente en su patogénesis participen la inflamación crónica, el uso de medicamentos modificadores de la respuesta inmunitaria y la infección por el VEB(AU)

IntroductionThe relationship between inflammatory bowel disease (IBD) and lymphoproliferative disorders (LD) has been previously reported.AimsTo establish the local incidence of LD in an IBD unit, and to describe the clinical characteristics of observed cases.Material and methodsAll the clinical records of patients with ulcerative colitis (UC) or Crohn's disease (CD) followed-up in a tertiary center were reviewed. In all cases, IBD had been diagnosed according to standard criteria.ResultsOf 911 patients with IBD, we identified seven with lymphoma. Five of the patients were men, four had been diagnosed with UC and three with Crohn's disease. The mean time from IBD to lymphoma diagnosis was 4.82 years (r: 0–20). The mean age at lymphoma diagnosis was 53 years (r: 33–76). Four were colorectal lymphomas. There was only one case of Hodgkin's disease. Five patients had been treated with thiopurines, and four of these had also been treated with biological agents. Three cases were associated with Epstein-Barr (EBV) virus infection. The estimated incidence of LD in these IBD patients was 81.74/100,000/year. After a mean follow-up of 32.3 months (r: 5–57) following the last treatment for LD, all patients except one are in remission.DiscussionThe incidence rate of LD was much higher than the expected rate for the general population (81.74 vs. 22). Chronic inflammation, immune-modifying drugs and Epstein Barr virus infection may be implicated in the pathogenesis of this disease(AU)

[Lymphoproliferative disorders in an inflammatory bowel disease unit]. / Trastornos linfoproliferativos en una unidad de enfermedad inflamatoria intestinal.

INTRODUCTION: The relationship between inflammatory bowel disease (IBD) and lymphoproliferative disorders (LD) has been previously reported. AIMS: To establish the local incidence of LD in an IBD unit, and to describe the clinical characteristics of observed cases. MATERIAL AND METHODS: All the clinical records of patients with ulcerative colitis (UC) or Crohn's disease (CD) followed-up in a tertiary center were reviewed. In all cases, IBD had been diagnosed according to standard criteria. RESULTS: Of 911 patients with IBD, we identified seven with lymphoma. Five of the patients were men, four had been diagnosed with UC and three with Crohn's disease. The mean time from IBD to lymphoma diagnosis was 4.82 years (r: 0-20). The mean age at lymphoma diagnosis was 53 years (r: 33-76). Four were colorectal lymphomas. There was only one case of Hodgkin's disease. Five patients had been treated with thiopurines, and four of these had also been treated with biological agents. Three cases were associated with Epstein-Barr (EBV) virus infection. The estimated incidence of LD in these IBD patients was 81.74/100,000/year. After a mean follow-up of 32.3 months (r: 5-57) following the last treatment for LD, all patients except one are in remission. DISCUSSION: The incidence rate of LD was much higher than the expected rate for the general population (81.74 vs. 22). Chronic inflammation, immune-modifying drugs and Epstein Barr virus infection may be implicated in the pathogenesis of this disease.

[Epiploic appendicitis: the other appendicitis]. / Apendicitis epiploica: la otra apendicitis.

Epiploic appendages are fat-filled, serosa-covered pediculated formations originating in the external wall of the bowel, toward the peritoneal cavity. Torsion of the epiploic appendages produces strangulation and infarction of the pedicle, initially venous and, when prolonged, ischemic, resulting in epiploic appendagitis. The main clinical manifestation is abdominal pain. Diagnosis is established through imaging techniques (ultrasound and computed tomography). Treatment is conservative and the prognosis is excellent.

Apendicitis epiploica: la otra apendicitis / Epiploic appendicitis: the other appendicitis

Los apéndices epiploicos son formaciones grasas, pediculadas, recubiertas de serosa que se encuentran en la superficie externa del colon, hacia la cavidad peritoneal. Cuando uno de estos apéndices se torsiona, se produce el estrangulamiento del pedículo y un infarto de éste, que al principio es venoso y, si se prolonga en el tiempo, se hace isquémico, lo que de lugar a la apendicitis epiploica. La manifestación clínica fundamental es el dolor. Su diagnóstico se realiza a través de las pruebas de imagen (ecografía, tomografía computarizada). El tratamiento es conservador y su pronóstico, excelente

Epiploic appendages are fat-filled, serosa-covered pediculated formations originating in the external wall of the bowel, toward the peritoneal cavity. Torsion of the epiploic appendages produces strangulation and infarction of the pedicle, initially venous and, when prolonged, ischemic, resulting in epiploic appendagitis. The main clinical manifestation is abdominal pain. Diagnosis is established through imaging techniques (ultrasound and computed tomography). Treatment is conservative and the prognosis is excellent

Idiopathic pancreatitis in inflammatory bowel disease.

BACKGROUND AND AIMS: The incidence of pancreatitis is increased in inflammatory bowel disease. However, pancreatitis as an extraintestinal manifestation of the intestinal disease is exceedingly rare. We have retrospectively analyzed the prevalence of pancreatitis in a combined hospital cohort, and specifically studied cases in which no other cause than the intestinal disease itself could be found. METHODS: The prevalence of pancreatitis in 1057 inflammatory bowel disease patients from two hospitals in the Community of Madrid, Spain, was determined by means of database examination. RESULTS: The prevalence of pancreatitis was 2.74% (29 cases); only in four patients (0.38%) it was considered idiopathic and thus a possible extraintestinal manifestation. Underlying chronic pancreatitis was identified in three of these four patients. CONCLUSIONS: In inflammatory bowel disease patients, pancreatitis is more often due to a nonrelated cause, and cases that can be adscribed to extraintestinal manifestation of the intestinal disease are comparatively rare.

[Filgrastim in refractory Crohn's disease with an intra-abdominal abscess]. / Filgrastim en la enfermedad de Crohn refractaria con absceso intraabdominal.

The application of recombinant human granulocyte colony-stimulating factor (filgrastim) seems to be a safe, well tolerated and potentially effective therapy for active Crohn's disease. We report the case of an adolescent boy with Crohn's disease and intra-abdominal abscess associated who had a significant response to treatment with recombinant human granulocyte colony-stimulating factor after all standard treatments had failed.

[Pain originating from the abdominal wall: a forgotten diagnostic option]. / Dolor originado en la pared abdominal: una alternativa diagnóstica olvidada.

Chronic abdominal pain is a common clinical problem in primary care, and is usually referred to gastroenterologists or general surgeons. Although up to 20% of cases of idiopathic abdominal pain arise in structures of the abdominal wall, this is frequently overlooked as a possible cause. It includes pain arising from structures of the abdominal wall including skin, parietal peritoneum, cellular subcutaneous tissue, aponeuroses, abdominal muscles and somatosensorial innervation from lower dorsal roots. The diagnosis is based on anamnesis and physical examination. Carnett's sign is a simple maneuver that discriminates between parietal and visceral pain. Management with topical anesthesia is effective in a majority of patients and can help to confirm the diagnosis.

Filgrastim en la enfermedad de Crohn refractaria con absceso intraabdominal / Filgrastim in refractory Crohn’s disease with an intra-abdominal abscess

El tratamiento con factor recombinante estimulante de progenitores granulocíticos (filgrastim) parece ser una alternativa terapéutica segura, bien tolerada y potencialmente efectiva en pacientes con una enfermedad de Crohn activa. Presentamos el caso de un varón adolescente con enfermedad de Crohn y absceso intraabdominal asociado, en el que los tratamientos convencionales habían fracasado, que experimentó una importante respuesta al tratamiento con factor recombinante estimulante de progenitores granulocíticos

The aplication of recombinant human granulocyte colony-stimulating factor (filgrastim) seems to be a safe, well tolerated and potentially effective therapy for active Crohn's disease. We report the case of an adolescent boy with Crohn's disease and intra-abdominal abscess associated who had a significant response to treatment with recombinant human granulocyte colony-stimulating factor after all standard treat-ments had failed

Dolor originado en la pared abdominal: una alternativa diagnóstica olvidada / Pain originating from the abdominal wall: a forgotten diagnostic option

El dolor abdominal crónico es un problema clínico muy frecuente abordado en atención primaria, habitualmente remitido a los especialistas de gastroenterología y cirugía general. A pesar de que, según los estudios publicados, hasta un 20% de los pacientes estudiados por dolor abdominal crónico no filiado se corresponden con una enfermedad de la pared abdominal, pocos médicos plantean esta entidad dentro del diagnóstico diferencial. Incluye todas las enfermedades originadas en estructuras de la pared abdominal: piel, peritoneo parietal, tejido celular subcutáneo, aponeurosis y grupos musculares abdominales e inervación somatosensorial de las raíces nerviosas T7 a T12. Su diagnóstico se basa en la historia clínica y la exploración física. El signo de Carnett es una maniobra exploratoria sencilla que discrimina entre enfermedad visceral y de la pared. El tratamiento con anestésicos tópicos es efectivo en la mayoría de los pacientes y puede ayudar a confirmar el diagnóstico de sospe

Chronic abdominal pain is a common clinical problem in primary care, and is usually referred to gastroenterologists or general surgeons. Although up to 20% of cases of idiopathic abdominal pain arise in structures of the abdominal wall, this is frequently overlooked as a possible cause. It includes pain arising from structures of the abdominal wall including skin, parietal peritoneum, cellular subcutaneous tissue, aponeuroses, abdominal muscles and somatosensorial innervation from lower dorsal roots. The diagnosis is based on anamnesis and physical examination. Carnett's sign is a simple maneuver that discriminates between parietal and visceral pain. Management with topical anesthesia is effective in a majority of patients and can help to confirm the diagnosis