Tumores neuroendocrinos gástricos: presentación clínica, endoscópica y alternativas de tratamiento / Clinical and endoscopic presentation of gastric neuroendocrine tumors

Background: Gastric neuroendocrine tumors correspond to less than 1 percent of all gastric tumors. These tumors can be of three types. Seventy five percent are type I and are associated to chronic atrophic gastritis type A (CAG- A). Half of them are associated with pernicious anemia. Type II tumors are associated with Zollinger Ellison syndrome and type I multiple endocrine neoplasia. Type III are sporadic tumors. Aim: To report the clinical, endoscopical features and response to the treatment of gastric neuroendocrine tumors. Patients and methods: A retrospective study of eleven patients (seven male, aged 38 to 72 years old) with a pathological diagnosis of gastric neuroendocrine tumor. Their clinical presentation, associated diseases, treatment and follow up were reviewed. Results: Epigastric pain was present in eight patients, weight loss in three, epigastric pain and weight loss in one and post prandial abdominal pain in two. At endoscopy, multiple polyps in the fundus were observed in six, verrucose gastritis in one, polyps in the antrum in one, two subcardial polyps in 1, a fundus ulcer in one and a Bormann III type lesion in one. Chronic atrophic gastritis was diagnosed in seven patients and pernicious anemia in five. Serum gastrin levels were determined in 4 patients and were high in all. Four subjects were treated with endoscopic polipectomy only. A partial or total gastrectomy was done in seven patients. No complications or mortality occurred during the follow up. Conclusions: Abdominal pain is a common presentation of patients with gastric neuroendocrine neoplasia. Polyps predominantly in the fundus are the most common endoscopic finding. Surgical treatment or endoscopical polypectomy, depending of the extension of the disease, yield satisfactory results

Obesidad: factor de riesgo para esteatohepatitis y fibrosis hepática / Obesity as a risk factor for steatohepatitis and hepatic fibrosis

Background: Nonalcoholic fatty liver (NAFL) has been recognized as a cause of chronic liver disease. Its main risk factor is obesity. Aim: To describe the clinical and liver pathological findings in a group of patients who underwent surgery as obesity treatment. Patients and Methods: Sixty eight patients with severe or morbid obesity were subjected to surgery as obesity treatment. Each patient was evaluated with a complete clinical and laboratory medical assessment. A wedge of liver was excised during surgery. Liver biopsies were analyzed without knowledge of clinical and laboratory findings. The presence of steatosis, inflammation (portal or lobular), fibrosis and cirrhosis were recorded in the pathological analysis. Age and body mass index (BMI) were correlated with pathological data. Significance was set at a p value of less than 0.05. Results: Ninety one percent of patients had steatosis, 45 percent inflammation and 47 percent fibrosis. One patient had cirrhosis (1,4 percent). There was a statistically significant association between BMI and moderate or severe steatosis (p <0.03). There was also an association between BMI and portal (p=0.017) and lobular inflammation (p=0.034). A BMI over 40 kg/m2 (morbid obesity) was significantly associated with the presence of fibrosis (p=0.032). Moreover, the presence of moderate or severe steatosis was a risk factor for the development of hepatic fibrosis (p=0.026). Conclusions: Obesity is a major and independent risk factor for steatohepatitis and fibrosis. The degree of steatosis in the liver biopsy, is a risk factor for the development of fibrosis

Insuficiencia hepática fulminante / Fulminant hepatic failure

Fulminant hepatic failure (FHF) is an acute and eventually fatal illness, caused by a severe hepatocyte damage with massive necrosis. Its hallmarks are hepatic encephalopathy and a prolonged prothrombin time (<40 percent). FHF is currently defined as hyperacute (encephalopathy appearing within 7 days of the onset of jaundice), acute (encephalopathy appearing between 8 and 28 days) or subacute (encephalopathy appearing between 5 and 12 weeks). FHF can be caused by viruses, drugs, toxins, and miscellaneous conditions such as Wilson's disease, Budd-Chiari syndrome, ischemia and others. However, a single most common etiology is still not defined. Factors that are valuable in assessing the likelihood of spontaneous recovery are age, etiology, degree of encephalopathy, prothrombin time and serum bilirubin. The management is based in the early treatment of infections, hemodynamic abnormalities, cerebral edema, and other associated conditions. Liver transplant has emerged as the most important advance in the therapy of FHF, with a survival rate that ranges between 60 and 80 percent. The use of hepatic support systems, extracorporeal liver support and auxiliary liver transplantation are innovative therapies

Características clínicas y factores pronósticos en la insuficiencia hepática fulminante en adultos y niños / Clinical features and prognostic factors in fulminant hepatic failure in adults and children

La Insuficiencia Hepática Fulminante (IHF) es una entidad rápidamente fatal, secundaria a múltiples causas y se clasifica en hiperaguda, aguda y subaguda. El único tratamiento que modifica su pronóstico es el trasplante hepático ortotópico (THO). Objetivo: describir las características clínicas, manejo y evolución de pacientes adultos y niños con IHF. Pacientes y métodos: 51 casos de IHF, evaluando evolución, factores pronósticos, posible etiología y tratamientos realizados en el Hospital Clínico de la Universidad de Chile y Roberto del Río entre abril de 1990 y febrero del 2002. Resultados: 34 adultos (67 por ciento), edad de 46 ñ 17,6. Las causas principales fueron isquemia 29 por ciento, criptogénica 20 por ciento, drogas 14 por ciento y viral 11 por ciento. La presentación fue hiperaguda 53 por ciento, aguda 38 por ciento y subaguda 9 por ciento. Las complicaciones más frecuentes fueron respiratorias 67 por ciento, renal 67 por ciento, hematológicas 61 por ciento e infecciosas 55 por ciento. Diecisiete niños (33 por ciento), edad de 5 ñ 4,3. Las causas principales fueron viral 41,2 por ciento, criptogénica 29 por ciento, hepatitis autoinmune 17 por ciento. Las complicaciones más frecuentes fueron infecciosas 88 por ciento, cardiovascular 71 por ciento, respiratorias 65 por ciento y hematológicas 65 por ciento. Ingresaron a una Unidad de Pacientes Críticos 33 adultos y 17 niños. Sólo se transplantaron 3 (6 por ciento) pacientes (2 niños y un adulto), todos vivos hasta la fecha. La sobrevida sin transplante fue de 15 por ciento en los adultos y 20 por ciento en los niños. Conclusión: la IHF es una enfermedad de variada etiología y alta mortalidad, que requiere un manejo multidisciplinario y en que debería plantearse el THO como la única alternativa posible, si no hay contraindicación

Enfermedad de Wilson / Wilsonïs disease

La enfermedad de Wilson (EW) es un defecto autosómico recesivo del transporte celular del cobre desde el hígado. Hasta la fecha, se han identificado más de 100 mutaciones en el gen de EW, siendo más común la sustitución His 1069Gln, que puede presentarse en más de 40 por ciento de los casos. La reducción en la excreción biliar lleva a la acumulación de cobre, inicialmente en el hígado y luego en otros tejidos, particularmente el cerebro. Los depósitos tisulares de cobre causan variados síntomas y signos que reflejan deterioro hepático, neurológico, hematológico y renal. Los pacientes con EW frecuentemente se presentan como enfermedad hepática o con síntomas neuropsiquiátricos. Aún en ausencia de historia familiar, la EW debe ser sospechada cuando aparecen estos síntomas sin otra explicación, particularmente en pacientes jóvenes. A pesar de los avances en terapéutica médica, aún se observan significativas tasas de mortalidad en algunos grupos de pacientes con EW

Ecotomografía doppler arterial intrarrenal en pacientes cirróticos con ascitis, con y sin síndrome hepatorrenal / Intrarenal arterial doppler ultrasonography in cirrhotic patients with ascites, with and without hepatorenal syndrome

Background: The pathophysiological hallmark of the hepatorenal syndrome (HRS) is renal vasoconstriction. Doppler ultrasonography can be used to assess the vascular resistance in small renal intraparenchymal vessels through analysis of the Doppler waveform by a parameter termed Resistive Index (RI). We postulated that the RI could be important for the diagnosis and prognosis of HRS. Aims: to assess the RI in cirrhotic patients with ascites, with and without HRS. Patients and methods: We studied 48 cirrhotics with ascites, of whom 12 were with and 36 without HRS and other 23 were normal subjects. We measured the intrarenal arterial RI (Resistive index = Peak systolic velocity - Minimum diastolic velocity/Peak systolic velocity) with color Doppler ultrasonography after visualization of interlobular or arcuate arteries. It was considered abnormal when higher than 0.70. Results: The RI values, mean and SD) were: normal subjects: 0.58 ñ 0.05, cirrhotics with ascites: 0.65 ñ 0.05 and cirrhotics with ascites and HRS: 0.78 ñ 0.11. Patients with HRS had significantly higher values than those without HRS (p < 0.001). The Relative Risk of developing the HRS in patients with a RI ü 0.70 were 3.32 (CI 95 percent = 1.79 - 6.2) Conclusions: The RI was useful in patients with cirrhosis and ascites for the prognosis of HRS and could suggest diagnosis of HRS with values of 0.78 or higher, if other clinical conditions that produce renal vasoconstriction are excluded

Heparina e insulina en el tratamiento de la pancreatitis aguda por hipertrigliceridemia: experiencia en 5 casos / Heparin and/or insulin treatment of acute pancreatitis caused by hypertriglyceridemia

Background: Hypertriglyceridemia over 1,000 mg/dl can provoke acute pancreatitis and its persistence can worsen the clinical outcome. On the contrary, a rapid decrease in triglyceride level is beneficial. Plasmapheresis has been performed in some patients to remove chylomicrons from the circulation, while heparin and/or insulin have been administered in some other cases to rapidly reduce blood triglycerides. Heparin and insulin stimulate lipoprotein-lipase activity and accelerate chylomicron degradation. Aim: To report five patients with acute pancreatitis treated with heparin and insulin. Patients and methods: Five patients (4 females and 1 male) seen in the last two years, who suffered acute pancreatitis induced by hypertriglyceridemia are reported. Initial blood triglyceride levels were above 1,000 mg/dl (range 1,590-8,690 mg/dl). Besides the usual treatment of acute pancreatitis, heparin and/or insulin were administered intravenously in continuous infusion. Heparin dose was guided by usual parameters of blood coagulation, and insulin dose, by serial determinations of blood glucose. Pancreatic necrosis was demonstrated in 4 patients. Results: Serum triglyceride levels decreased to <500 mg/dl within 3 days in all cases. No complication of treatment was observed and all patients survived. Early and late complications of pancreatitis occurred in one patient. Conclusion: Administration of heparin and/or insulin is an efficient alternative to reduce triglyceride levels in patients with acute pancreatitis and hypertriglyceridemia

Coagulación endoscópica con plasma de argón: una opción terapéutica en la ectasia vascular antral / Endoscopic coagulation with argon plasma: a therapeutic option in vascular antral ectasia

Background: Gastric Antral Vascular Ectasia or Watermelon stomach is a rare cause of chronic gastrointestinal bleeding, often presenting as a chronic iron deficiency anemia. This condition can be associated with some other diseases such as cirrhosis, autoimmune diseases and others. We report two patients treated with Argon Plasma Coagulation, a 68 years old male with an ethanol related cirrhosis and a 72 years old female with an idiopathic Gastric Antral Vascular Ectasia. The characteristic endoscopic features were mistaken for many years as gastritis. Both patients presented with severe anemia requiring multiple transfusions as treatment. Due to the poor operative risk, both patients were treated with Argon Plasma Coagulation with good results

Hígado graso agudo del embarazo: estudio retrospectivo clínico-patológico de 10 casos / Acute fatty liver of pregnancy: retrospective clinical-pathological study in 10 cases

Se estudiaron retrospectivamente 10 casos de Hígado Graso Agudo del Embarazo (HGAE) entre los años 1990 y 2001. Se describen los hallazgos clínicos y de laboratorio de la enfermedad, analizando su asociación con el síndrome hipertensivo del embarazo (SHE) y estableciendo el rol diagnóstico de la biopsia hépatica percutánea de esta patología. Se propone que el desenlace en falla hepática aguda podría gatillarse por eventos precipitantes compartidos por un mismo espectro de enfermedades (HGAE y SHE). Se concluye que el estudio anatomopatológico hépatico es discutido como pilar diagnóstico y se ofrece una aproximación actual al enfrentamiento de esta entidad