Joel Omar Jáquez-Quintana

Predictors of in-hospital mortality in patients with non-variceal upper gastrointestinal bleeding

OBJECTIVE to determine the independent predictors of in-hospital death of Hispanic patients with nonvariceal upper gastrointestinal bleeding (NVUGB). EXPERIMENTAL DESIGN prospective and observational trial. PATIENTS in a period between 2000 and 2009, all patients with NVUGB admitted to our hospital were studied. Demographical and clinical characteristics, endoscopic findings and laboratory tests were evaluated χ² and Mann-Whitney U analyses were per-formed for comparisons, and binary logistic regression was employed to identify independent predictors of in-hospital mortality. RESULTS 1,067 patients were included, 65% male with a mean age of 58.8 years. Mean number of comorbidities per patient was 1.6 ± 0.76. The most frequent cause of bleeding were gastric and duodenal ulcers (55.4%); 278 patients (25.8%) received endoscopic treatment of which 69.1% had combined therapy. Rebleeding occurred in 36 patients (3.4%) of which 50% died. In-hospital mortality was 10.2%, of which only 3.1% was associated to bleeding. When comparing causes of death among patients with and without comorbidities, only hypovolemic shock was found significative (48.3 vs. 25%; p = 0.020). Binary logistic regression found that the number of comorbidities, Rockall scale score; serum albumin < 2.6 g/dL on admission; rebleeding and length of hospital stay were independent risk factors of in-hospital mortality. CONCLUSION the number of comorbidities, the Rockall scales core, an albumin level < 2.6 g/dL, the presence of rebleeding and hospital stay were predictors of in-hospital mortality in patients with NVUGB.

Subclinical abnormal glucose tolerance is a predictor of death in liver cirrhosis

AIM To determine if subclinical abnormal glucose tolerance (SAGT) has influence on survival of non-diabetic patients with liver cirrhosis. METHODS In total, 100 patients with compensated liver cirrhosis and normal fasting plasma glucose were included. Fasting plasma insulin (FPI) levels were measured, and oral glucose tolerance test (OGTT) was performed. According to OGTT results two groups of patients were formed: those with normal glucose tolerance (NGT) and those with SAGT. Patients were followed every three months. The mean follow-up was 932 d (range of 180-1925). Survival was analyzed by the Kaplan-Meyer method, and predictive factors of death were analyzed using the Cox proportional hazard regression model. RESULTS Of the included patients, 30 showed NGT and 70 SAGT. Groups were significantly different only in age, INR, FPI and HOMA2-IR. Patients with SAGT showed lower 5-year cumulated survival than NGT patients (31.7% vs 71.6%, P = 0.02). Differences in survival were significant only after 3 years of follow-up. SAGT, Child-Pugh B, and high Child-Pugh and Model for End-Stage Liver Disease (MELD) scores were independent predictors of death. The causes of death in 90.3% of cases were due to complications related to liver disease. CONCLUSION SAGT was associated with lower survival. SAGT, Child-Pugh B, and high Child-Pugh and MELD scores were independent negative predictors of survival.

Diabetic myonecrosis in a patient with hepatic cirrhosis: a case report and review of the literature

IntroductionDiabetic myonecrosis was first reported by Angervall and Stener in 1965. In its classical clinical expression, it affects type 1 diabetes mellitus patients with long-standing poor metabolic control and advanced chronic microvascular complications. A sudden-onset of severe pain in the region of the involved muscle, usually the quadriceps, is the typical clinical manifestation. Magnetic resonance imaging (MRI) confirms the clinical diagnosis; in some cases of diagnostic uncertainty, a muscle biopsy may be required.Case PresentationWe present the case of a 38 year-old Hispanic male from Mexico, with alcohol-induced hepatic cirrhosis (Child-Pugh C/MELD 45) and type 2 diabetes mellitus admitted to the emergency room due to hepatic encephalopathy with intense pain and an increase in volume of the left thigh. MRI showed edema and inflammatory changes of the quadriceps muscle with a hyperintense signal on T2-weighted images; in addition, there was a subacute hematoma.ConclusionTo the best of our knowledge, this is the first case of diabetic myonecrosis associated with and complicated by advanced hepatic cirrhosis reported in the literature.

Wernicke Encephalopathy Presenting in a Patient with Severe Acute Pancreatitis

CONTEXT Acute pancreatitis can lead to prolonged fasting and malnutrition. Many metabolic changes, including thiamine deficiency, may lead to the well know pancreatic encephalopathy. In this condition however the thiamine deficiency is rarely suspected. CASE REPORT We report the case of a 17-year-old woman with severe acute pancreatitis who developed mental status changes and ophthalmoplegia. A magnetic resonance image showed hyperintensive signals in periventricular areas, medial thalamus, and mammillary bodies, findings consistent with the diagnosis of Wernicke encephalopathy. Thiamine treatment reversed neurological complications. CONCLUSION Wernicke encephalopathy secondary to thiamine deficiency should be considered as a possible cause of acute mental status changes in patients with acute pancreatitis and malnutrition. Prophylactic doses of thiamine could be considered in susceptible patients.

Vólvulo sigmoideo como presentación de una displasia neuronal intestinal tipo B en un adolescente

We report a 17-year-old man admitted to emergency department due to abdominal pain and distension. He referred a history of 18 months with constipation. Computerized tomography showed dilatation of the colon and coprostasis. The patient improved after disimpaction with enemas. Colonoscopy and anorectal manometry were reported normal. A full thickness rectal biopsy revealed normal ganglion cells. The patient was readmitted with a sigmoid volvulus. Sigmoidectomy and a termino-terminal anastomosis (descending colon-rectum) were performed (Figs. 1A and B). Histologically, neuronal intestinal dysplasia type B (NID-B) (NID) was reported (Fig. 1 C). Dehiscence and anastomatic leakage were found along with dilatation of the descending and transverse colon. Subtotal colectomy with a colostomy of the ascending colon and Hartmann’s pouch were performed. The resected segments showed NID-B.

Multiple Biliary Hamartomas, The ‘‘Von Meyenburg Complexes’’

Multiple biliary hamartomas are rare benign malformations of the intrahepatic bile ducts first described by von Meyenburg in 1918. They originate from embryonic bile ducts that fail to involute. These are generally asymptomatic and usually encountered as an incidental finding at imaging, laparotomy or autopsy.Abstract Multiple biliary hamartomas are rare benign malformations of the intrahepatic bile ducts first described by von Meyenburg in 1918. They originate from embryonic bile ducts that fail to involute. These are generally asymptomatic and usually encountered as an incidental finding at imaging, laparotomy or autopsy.

Mo1976 Plasma Levels Cytokine Imbalance in Compensated Cirrhotic Patients With Impaired Glucose Tolerance and Diabetes Mellitus. A Prospective Study

Background and Aims: To define if there is an imbalance in plasma levels of some proinflammatory, fibrogenic and antifibrogenic cytokines of patients with liver cirrhosis (LC) and impaired glucose tolerance (IGT) or Diabetes Mellitus (DM) . Methods: We studied 54 patients with compensated LC who had normal fasting plasma glucose (FPG) levels. An oral glucose tolerance test (OGTT) was carried out:18 patients were normal, 18 had IGT, and 18 had DM. Plasma levels of the following cytokines were measured: TNF-α, Soluble Tumor Necrosis Factor Receptor 1 (sTNF-R1), Leptin, TGF-β1, and Hepatocyte Growth Factor (HGF). Also, fasting plasma insulin (FPI) levels were measured and HOMA2-IR was calculated. Results were compared with those of a control group of 18 patients without liver disease or DM. Data were expressed as medians and interquartile ranges. Intergroup comparison was performed using non parametric tests. Results:. Patients with IGT and DM had significantly higher sTNF-R1 (p = 0.0043 and 0.0045 respectively) (Figure 1) and significantly lower TGF-β1 (p = 0.001 and 0.001 respectively) (Figure 2) compared to controls. Leptin , HGF, and TNF-α showed no significant differences among cirrhotic patient and controls. Correlations between sTNF-R1 and HOMA2-IR and between leptin and HOMA2-IR were found. Conclusions: IGT and DM were associated to an imbalance of sTNF-R1 and TGFβ1 in cirrhotic patients. At the same time sTNF-R1and leptin correlated with IR. These findings may suggest that sTNF-R1 might be implicated in the development of DM or in the deterioration of liver function in cirrhotic patients with DM.

Endoscopic management of esophago-mediastinal fistula secondary to mediastinal tuberculosis infection.

A 45-year-old male with chronic myeloid leukemia (bcr/abl positive) was treated with imatinib mesylate. After 2 months of treatment, the patient presented with fever, diaphoresis, cough, thoracic pain, and progressive dyspnea. Melena developed subsequently. An upper endoscopy was performed, showing an extrinsic compression in the middle third of the esophagus and a 10 mm-diameter, oval-shaped fistula with clear borders (A). The CT scan showed a cluster of nodules, subcarinal air bubbles, and massive pericardial effusion and was without alterations in the lung parenchyma (B). A covered, self-expandable, metal stent (Covered Wallflex 10 cm; Boston Scientific, Natick, Mass) was placed in the esophagus within 24 hours of these findings. The postprocedure esophagogram showed no leaks of contrast material (C). Adenosine deaminase levels of the pericardial fluid were 130 U/L (normal <40 U/L), so the diagnosis of tuberculosis was made. Appropriate antituberculous

Hemorragia de intestino medio causada por uncinariasis y diagnosticada por cápsula endoscópica. Caso clínico

En nuestro país, el 85% de las hemorragias de intestino medio (HIM) son secundarias a angiodisplasias, úlceras y tumores benignos y malignos1. La parasitosis intestinal es una causa poco frecuente de HIM. La uncinariasis es una parasitosis intestinal producida por Necator americanus (N. americanus) y Ancylostoma duodenale, las cuales se distribuyen en todo el mundo pero N. americanus se observa comúnmente en el sur de Norteamérica, Centroamérica y Suramérica, África y Asia tropical2. En este informe se presenta el primer caso de HIM causada por uncinariasis y diagnosticada por cápsula endoscópica (CE) en nuestro país. Mujer de 43 años, proveniente de medio semirrural de la frontera entre México y EE. UU. (Estado de Tamaulipas), con retraso mental y parálisis de los miembros inferiores de causa desconocida, enviada a nuestro centro por hematoquecia intermitente de 3 años de evolución. Negó antecedentes de dolor abdominal o consumo crónico de antiinflamatorios no esteroideos. Independientemente de la palidez de piel y tegumentos, no se encontraron datos relevantes en la exploración física. En los exámenes de laboratorio, la hemoglobina fue de 8 g/dL (normal: 13-16), VGM 72 fl (normal: 78-100), leucocitos normales y eosinofilia del 18% (normal: 0-8). La esofagogastroduodenoscopia (EGD) no mostró lesiones vasculares ni de la mucosa, y en la ileocolonoscopia los hallazgos fueron de úlceras en el íleon terminal, sin reporte histopatológico. La paciente fue tratada con mesalazina por vía oral a dosis y tiempo no especificados y cursó con episodios intermitentes de hematoquecia (sangre roja, fresca, brillante e indolora) y anemia ferropénica persistente en más de 3 determinaciones. Un año más tarde, el control endoscópico (EGD y colonoscopia) y la angiografía mesentérica no evidenciaron el sitio de hemorragia. Posterior a la resección de un segmento intestinal por divertículo de Meckel durante laparotomía exploradora, la paciente presentó nuevos episodios de hematoquecia y persistencia de la anemia, requiriendo hemotransfusiones en los 2 últimos años (40 U de sangre en paquete globular). En la enteroscopia con CE (Pillcam SB, GIVEN Imaging Ltd, Yokneam, Israel), se observaron eritema, múltiples erosiones y edema de la mucosa yeyunal; abundantes parásitos adheridos a la mucosa intestinal, sangre en el interior de algunos de ellos y hemorragia intestinal secundaria a úlceras (fig. 1 A y B). La paciente fue tratada con un antiparasitario (albendazol) y suplementos de hierro; 12 meses después se encuentra en buenas condiciones generales, sin evidencia de hematoquecia ni datos clínicos o de laboratorio de anemia. Las uncinarias afectan específicamente a los humanos. La larva filariforme, forma infectiva, presente en los suelos húmedos, penetra la piel cuando los individuos se ponen en contacto con el parásito, produciendo una erupción dérmica pruriginosa, eritematosa y papular. Las larvas pasan a la circulación sanguínea y de allí a los alvéolos pulmonares de donde, mediante las secreciones bronquiales, son deglutidas al tracto digestivo3. La eosinofilia ha sido reportada en entre el 30 y el 40% de los casos. Ambos tipos de uncinarias parasitan la parte proximal del intestino delgado en sus formas adultas, las cuales miden alrededor de 10 a 15 mm de largo y se adhieren con firmeza a la mucosa intestinal mediante unas placas cortantes bucales, succionando sangre al mismo tiempo que secretan enzimas anticoagulantes para mantener el flujo de sangre. La gravedad de la enfermedad dependerá de la cantidad de parásitos4. En este reporte de caso especial, presentamos la evidencia de HIM crónica secundaria a uncinariasis documentada por las manifestaciones clínicas (hematoquecia intermitente), laboratorio (anemia y eosinofilia persistentes), úlceras sangrantes yeyunales (cápsula endoscópica) y buena respuesta a tratamiento en el seguimiento a 12 meses posterior al tratamiento antiparasitario y suplementos de hierro. Aunque es una causa poco frecuente de HIM, la parasitosis debe ser considerada como una causa posible en sujetos con factores de riesgo (retardo mental y residencia en medio rural) y eosinofilia persistente, independientemente de la región geográfica. Este caso representa un verdadero reto diagnóstico. Cuando no se sigue el protocolo de estudio de la HIM, el diagnóstico se hace más difícil, la atención médica se encarece y el paciente tiene más riesgo de morbilidad por decisiones no bien fundamentadas. Actualmente, hay consenso de realizar una enteroscopia mediante cápsula endoscópica, ante la sospecha de HIM. Un examen coprológico puede identificar los huevecillos del parásito; en nuestro caso, no fue reportado.

La diabetes en la cirrosis hepática

The prevalence of overt diabetes mellitus (DM) in liver cirrhosis is about 30%. However, DM or impaired glucose tolerance can be observed in 90% after an oral glucose tolerance test in patients with normal fasting plasma glucose. Type 2 DM may produce cirrhosis, whereas DM may be a complication of cirrhosis. The latter is known as «hepatogenous diabetes». Overt and subclinical DM is associated with liver complications and death in cirrhotic patients. Treating diabetes is difficult in cirrhotic patients because of the metabolic impairments due to liver disease and because the most appropriate pharmacologic treatment has not been defined. It is also unknown if glycemic control with hypoglycemic agents has any impact on the course of the liver disease.