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INTRODUCTION: Gastrocolic fistula is a rare complication of adenocarcinoma of the colon. Despite radical resections, these patients usually have a poor prognosis with a mean survival of 23 months and long-term survival is rarely reported. CASE PRESENTATION: A 48-year-old Latino-American man presented with watery diarrhea, diffuse abdominal pain and weight loss for 3 months. A computed tomography scan revealed a mass in the splenic flexure that had infiltrated his stomach and diaphragm. Panendoscopy and colonoscopy confirmed the presence of a fistula between the distal transverse colon and the stomach, which was secondary to a colon cancer. His colon, stomach and left diaphragm were resected en bloc. A histological examination revealed a moderately differentiated adenocarcinoma of the colon that had infiltrated the full width of the gastric wall with 37 negative lymph nodes and clear surgical margins. Adjuvant chemotherapy with capecitabine and oxaliplatin was administered after surgery. Our patient is alive and without any recurrence 5 years after surgery. CONCLUSIONS: En bloc resection with adjuvant chemotherapy offers the best treatment option for gastrocolic fistulas. This is one of the patients with greater survival reported in the medical literature.
Assuntos
Adenocarcinoma/complicações , Colo Transverso/patologia , Neoplasias do Colo/complicações , Fístula Gástrica/etiologia , Fístula Intestinal/etiologia , Dor Abdominal/etiologia , Adenocarcinoma/diagnóstico , Adenocarcinoma/cirurgia , Quimioterapia Adjuvante , Neoplasias do Colo/diagnóstico , Neoplasias do Colo/cirurgia , Colonoscopia , Fístula Gástrica/diagnóstico , Fístula Gástrica/cirurgia , Gastroscopia , Humanos , Fístula Intestinal/diagnóstico , Fístula Intestinal/cirurgia , Masculino , Pessoa de Meia-Idade , Recidiva Local de Neoplasia/patologia , Tomografia Computadorizada por Raios X , Resultado do Tratamento , Redução de PesoRESUMO
AIM: We aimed to examine the prevalence of early changes in some components of metabolic syndrome after smoking cessation. METHODS: Forty-eight heavy smokers from the Tobacco Cessation Clinic (24 women/24 men), average age of 49.4 years, were included in this study. They smoked a mean of 19.92 cigarettes per day and had smoked 33.23 packages per year during 33.4 years. Participants were included in a treatment group based on cognitive behavior therapy (CBT); 16 participants received varenicline and the other 16 nicotine replacement therapy (NRT). The target quit day was scheduled for week 3 through abrupt cessation. Abstinence was confirmed with exhaled carbon monoxide (CO) levels. Blood pressure, body mass index (BMI), and waist circumference (WC) were evaluated weekly. Glucose, triglycerides, high density lipoproteins (HDL-C), and insulin to determine the homeostasis model assessment (HOMA) index were determined in blood samples at weeks 1, 4, and 10. As a control group 96 healthy nonsmokers were matched by age and sex. RESULTS: The mean BMI in smokers was 26.94 kg/m(2) and in nonsmokers 26.23 kg/m(2). Smokers showed hypertension, hypertriglyceridemia, and lower levels of HDL-C than nonsmokers. Percentages of cessation in week 3 were 81% for NRT and 93% for CBT and varenicline. The mean weight increase at the end of the treatment was 1.09 kg in the CBT group, 1.06 kg in the NRT group, and 1.17 kg in the varenicline group. The prevalence of metabolic syndrome was 31.25% in week 1 and 29.16% at the end. There were reductions in the number of subjects with hypertension, glucose alterations, hypertriglyceridemia, and low HDL levels. CONCLUSIONS: Benefits of quitting smoking exceeded by far the risks associated with the amount of weight gained.
Assuntos
Síndrome Metabólica/tratamento farmacológico , Abandono do Hábito de Fumar , Adolescente , Adulto , Idoso , Glicemia/análise , Pressão Sanguínea , Índice de Massa Corporal , Monóxido de Carbono/análise , HDL-Colesterol/metabolismo , Terapia Cognitivo-Comportamental , Feminino , Homeostase , Humanos , Insulina/metabolismo , Masculino , Síndrome Metabólica/complicações , Síndrome Metabólica/epidemiologia , Pessoa de Meia-Idade , Nicotina/uso terapêutico , Prevalência , Fumar , Circunferência da Cintura , Aumento de Peso , Adulto JovemRESUMO
BACKGROUND: Endothelial dysfunction has been previously described in metabolic syndrome patients. The levels of circulating endothelial progenitor cells (EPCs) inversely correlates with the incidence of cardiovascular disease. The aim of this study was to investigate the association between NAFLD, metabolic syndrome and EPC levels. MATERIAL AND METHODS: A cross-sectional pilot study was performed at a university hospital in Mexico. Two groups of patients without previously known chronic diseases were studied and classified according to the presence of NAFLD. Anthropometric, dietary, and biochemical variables, and circulating EPC number were measured and compared between the groups. RESULTS: Forty subjects were included and classified into two groups: patients with NAFLD (n = 20) and a control group (n = 20). The overall prevalence of insulin resistance and metabolic syndrome was 25% and 17.5%, respectively. EPC levels were found to be higher in the NAFLD group (p < 0.05) as in the patients with insulin resistance (p < 0.01) and metabolic syndrome (p < 0.01). These levels showed correlation with the severity of steatosis. CONCLUSIONS: Patients with NAFLD have increased levels of EPC, such levels are associated with the severity of NAFLD. These findings may suggest that these cells may play a role in the early natural history of NAFLD. EPC might be increased in an attempt to repair the endothelial damage resulting from metabolic alterations accompanying NAFLD. Further studies are needed to establish the dynamics of these cells in NAFLD.
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Células Endoteliais/patologia , Fígado Gorduroso/patologia , Síndrome Metabólica/patologia , Células-Tronco/patologia , Antígeno AC133 , Antígenos CD/sangue , Antígenos CD34/sangue , Biomarcadores/sangue , Estudos de Casos e Controles , Estudos Transversais , Células Endoteliais/metabolismo , Fígado Gorduroso/sangue , Glicoproteínas/sangue , Hospitais Universitários , Humanos , Resistência à Insulina , Antígenos Comuns de Leucócito/sangue , Síndrome Metabólica/sangue , México , Pessoa de Meia-Idade , Hepatopatia Gordurosa não Alcoólica , Peptídeos/sangue , Projetos Piloto , Índice de Gravidade de Doença , Células-Tronco/metabolismo , Receptor 2 de Fatores de Crescimento do Endotélio Vascular/sangueRESUMO
Background and Aim. Levetiracetam is a second-generation antiepileptic drug. It is approved as an adjunctive treatment of partial onset seizures with or without secondary generalization. It is considered safe with less than 1% of patients with transient elevations of liver enzymes. Methods. We report a case of acute liver failure secondary to Levetiracetam in combination with Lacosamide documented with a liver biopsy. Results. Liver biopsy demonstrated acute liver injury with a predominant submassive necrosis pattern and features of a drug-induced hepatitis. Conclusions. This is the first published case of acute liver failure due to antiepileptic therapy with Levetiracetam in combination with Lacosamide.
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The differential diagnosis of fever of unknown origin (FUO) includes infectious, neoplastic, rheumaticinflammatory and miscellaneous diseases. We report the case of a 35-year-old man with FUO caused by Q fever. A liver biopsy showed the characteristic fibrin-ring lipogranulomas compatible with Q fever. The serologic tests confirmed the diagnosis of acute infection by Coxiella burnetii. The therapeutic response was excellent. In conclusion, we described a patient with acute Q fever and granulomatous hepatitis.
Assuntos
Febre de Causa Desconhecida/etiologia , Febre Q/complicações , Adulto , Biópsia , Diagnóstico Diferencial , Granuloma/patologia , Hepatite Viral Humana/patologia , Humanos , Fígado/patologia , Masculino , Febre Q/patologiaRESUMO
BACKGROUND & AIMS: Some phytochemicals present in coffee have a potential antioxidant role which seems to protect the human body against cardiovascular diseases, liver disease and malignancies. Nonalcoholic fatty liver disease is a common disease with limited therapeutic options. This study investigated the antioxidant effect of coffee by measuring antioxidant enzymes and lipid peroxidation markers in patients with nonalcoholic fatty liver disease. MATERIAL AND METHODS: We performed a case-control study at the University Hospital, Mexico City. Anthropometric, metabolic, dietary and biochemical variables of all patients were determined and compared. The presence of nonalcoholic fatty liver disease was established by ultrasonography. All patients completed a dietary questionnaire in order to determine their of coffee consumption. Catalase, superoxide dismutase and thiobarbituric acid reactive substances were measured in all of the patients. RESULTS: Seventy-three subjects with and 57 without nonalcoholic fatty liver disease were included. Patients with nonalcoholic fatty liver disease had significantly higher body mass index, blood glucose, homeostasis model of assessment-insulin resistance and insulin values in comparison to patients without nonalcoholic fatty liver disease. On the one hand, there was a significant difference in coffee intake between the groups (p < 0.05, for all comparisons). There was no significant difference between groups in catalase (0.39 ± 0.74 vs. 0.28 ± 0.69 nM/min/mL), superoxide dismutase (5.4 ± 3.45 vs. 4.7 ± 2.1 U/mL) or thiobarbituric acid-reactive substances (4.05 ± 1.87 vs. 3.94 ± 1.59 µM/mL). CONCLUSIONS: A high intake of coffee has a protective effect against nonalcoholic fatty liver disease however there was no significant difference in the antioxidant variables analyzed.
Assuntos
Antioxidantes/metabolismo , Café , Fígado Gorduroso/sangue , Fígado Gorduroso/prevenção & controle , Índice de Gravidade de Doença , Adulto , Glicemia/metabolismo , Estudos de Casos e Controles , Catalase/sangue , Estudos Transversais , Fígado Gorduroso/epidemiologia , Humanos , Incidência , Resistência à Insulina/fisiologia , Peroxidação de Lipídeos/fisiologia , México , Pessoa de Meia-Idade , Hepatopatia Gordurosa não Alcoólica , Superóxido Dismutase/sangue , Substâncias Reativas com Ácido Tiobarbitúrico/metabolismoRESUMO
Viral hepatitis is a common cause of morbidity in Mexico. Insulin resistance (IR) is related to the liver damage caused by some viral infections, especially chronic infections. Chronic viral infection is an important risk factor for the development of type 2 diabetes mellitus, disease that is currently among the 10 main causes of morbidity and the most common cause of mortality. Although several studies have reported an association between IR and hepatitis B virus or hepatitis C virus (HCV) infection, the pathophysiology has been studied thoroughly only for the association between IR and HCV infection. It is thought that HCV infection causes direct damage through the action of the core proteins, which induces an inflammatory state characterized by secretion of proinflammatory cytokines that interfere with normal insulin signaling and disturb glucose, lipid and protein metabolism. This review summarizes the mechanisms by which viral infection is thought to induce IR.
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Hepatite Viral Humana/fisiopatologia , Resistência à Insulina , Adulto , Idoso , Comorbidade , Citocinas/metabolismo , Diabetes Mellitus Tipo 2/epidemiologia , Diabetes Mellitus Tipo 2/etiologia , Metabolismo Energético , Ácidos Graxos/metabolismo , Frutosedifosfatos/biossíntese , Genótipo , Gluconeogênese , Hepatite Viral Humana/epidemiologia , Humanos , Hepatopatias/epidemiologia , Hepatopatias/fisiopatologia , México/epidemiologia , Pessoa de Meia-Idade , Sobrepeso/epidemiologia , Prevalência , Fatores de Risco , Proteínas Virais/fisiologiaRESUMO
Acute, acute-on-chronic and chronic liver diseases are major health issues worldwide, and most cases end with the need for liver transplantation. Up to 90% of the patients die waiting for an organ to be transplanted. Hepatic encephalopathy is a common neuropsychiatric syndrome that usually accompanies liver failure and impacts greatly on the quality of life. The molecular adsorbent recirculating system (MARS) is a recently developed form of artificial liver support that functions on a base of albumin dialysis. It facilitates the dialysis of albumin-bound and water-soluble toxins, allowing the patient to survive and even improving some clinical features of liver failure. The following manuscript reviews the technical features of MARS operation and some of the clinical trials that analyze the efficacy of the system in the therapy of liver diseases.
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Encefalopatia Hepática/etiologia , Encefalopatia Hepática/terapia , Falência Hepática/complicações , Fígado Artificial , Diálise Renal/métodos , Albuminas , Humanos , Desintoxicação por Sorção/métodos , Resultado do TratamentoRESUMO
Viral hepatitis is a common cause of morbidity in Mexico. Insulin resistance (IR) is related to the liver damage caused by some viral infections, especially chronic infections. Chronic viral infection is an important risk factor for the development of type 2 diabetes mellitus, disease that is currently among the 10 main causes of morbidity and the most common cause of mortality. Although several studies have reported an association between IR and hepatitis B virus or hepatitis C virus (HCV) infection, the pathophysiology has been studied thoroughly only for the association between IR and HCV infection. It is thought that HCV infection causes direct damage through the action of the core proteins, which induces an inflammatory state characterized by secretion of proinflammatory cytokines that interfere with normal insulin signaling and disturb glucose, lipid and protein metabolism. This review summarizes the mechanisms by which viral infection is thought to induce IR.
Las hepatitis virales son una causa común de morbilidad en México. La resistencia a la insulina (RI) ha sido relacionada con el daño hepático causado por infecciones virales crónicas, haciendo de ellas un factor de riesgo para el desarrollo de diabetes mellitus tipo 2, problema de salud que se encuentra entre las primeras 10 causas de morbilidad y es la primera de mortalidad. Aunque varios estudios han reportado una asociación entre la RI y la infección con virus de la hepatitis B y virus de la hepatitis C, sólo con el último se ha estudiado su fisiopatología. Se ha sugerido que produce daño directo a través de proteínas de su núcleo e induce un estado inflamatorio que interfiere con la señalización normal de insulina, resultando en una alteración del metabolismo de glucosa, lípidos y proteínas. Esta revisión resume los mecanismos por los que se sugiere que estas infecciones inducen RI.