RESUMEN
Ulcerative colitis is one of the inflammatory bowel disease (IBD) consequences characterized by chronic inflammation of the gastrointestinal (GI) tract. The current study aims to determine the changes in colon tissue caused by induced Ulcerative Colitis and reduce these changes by worms' antigen. The study included 45 adult male albino mice (Mus musculus), with ages ranging between 8-10 weeks; the average weights ranged between 18-32 g. Ulcerative colitis was induced by intracolonic administration of 100 µL of 4% after they had been starved for 18 h. The animals were dissected after one week, and routine histological sections were conducted. The results of the histological study showed that in the colon of white mice treated with 4% acetic acid occurred, many histological changes were represented by the appearance of inflammatory cells in the mucous layer around the goblet cells, and the formation of vacuoles, necrosis at epithelium and intense congestion under the surface epithelium. The marked histological sections of the colon in mice with induced ulcerative colitis treated with helminth extract at a concentration of 0.1 mg/kg for a week, were showed that the histological changes began to decrease in the colon tissue, with the presence of a few inflammatory cells as well as little mucus secretion.
Asunto(s)
Colitis Ulcerosa , Animales , Masculino , Ratones , Ácido Acético/efectos adversos , Colitis Ulcerosa/inducido químicamente , Colitis Ulcerosa/patología , InflamaciónRESUMEN
We describe the clinical and liver biopsy morphologic features for 4 patients with minocycline-induced autoimmune hepatitis (group 1). We compared the serum laboratory values and liver biopsy findings from group 1 with those from 10 patients with sporadic autoimmune hepatitis (group 2). All patients in group 1 had positive serum antinuclear antibody titers, but none had positive serum anti-smooth muscle antibody titers. The morphologic findings of group 1 biopsies were those of autoimmune hepatitis in all 4 patients. In addition, 1 of these biopsy specimens also had scattered single eosinophils, unlike autoimmune hepatitis. The mean histologic activity index scores for patients in groups 1 and 2, respectively, were 6.7 and 5.4. No patients in group 1 had marked bridging fibrosis or cirrhosis, compared with 4 of 10 patients in group 2. Minocycline-induced autoimmune hepatitis is usually identical to sporadic autoimmune hepatitis. The absence of eosinophils does not exclude the possibility of a minocycline cause. In the absence of clinical or morphologic differences, a recent ingestion of minocycline should be excluded before the diagnosis of sporadic autoimmune hepatitis is established. Whether the drug is unmasking latent autoimmune hepatitis is unclear.
Asunto(s)
Antibacterianos/efectos adversos , Enfermedad Hepática Inducida por Sustancias y Drogas/etiología , Hepatitis Autoinmune/etiología , Hígado/efectos de los fármacos , Minociclina/efectos adversos , Adolescente , Adulto , Anticuerpos Antinucleares/sangre , Biopsia , Sedimentación Sanguínea , Enfermedad Hepática Inducida por Sustancias y Drogas/sangre , Enfermedad Hepática Inducida por Sustancias y Drogas/tratamiento farmacológico , Enfermedad Hepática Inducida por Sustancias y Drogas/patología , Femenino , Glucocorticoides/uso terapéutico , Hepatitis Autoinmune/sangre , Hepatitis Autoinmune/tratamiento farmacológico , Hepatitis Autoinmune/patología , Humanos , Hígado/patología , Pruebas de Función Hepática , Masculino , Persona de Mediana Edad , Músculo Liso/inmunologíaRESUMEN
Patients with chronic viral hepatitis and cirrhosis often have elevated serum alpha-fetoprotein (AFP) values, the causes of which are unclear. We studied 81 patients with chronic hepatitis C and the relationships of serum AFP and alanine aminotransferase (ALT) values, hepatic histologic features, and hepatocyte proliferation activity scores. Twenty-two patients had nil to mild fibrosis, 34 had moderate fibrosis, and 25 had marked fibrosis-cirrhosis. The mean serum AFP value was significantly greater in patients with more fibrosis. Serum ALT values were slightly greater in the marked fibrosis-cirrhosis patient group. The differences in the HAI and in hepatocyte MIB-1 scores were not significant. Among all patients, increasing serum AFP values significantly correlated with increasing ALT values. However, there were no significant correlations with serum ALT or HAI and serum AFP values. There was no association between serum AFP values and immunohistochemical staining for AFP within hepatocytes. These results suggest that elevated serum AFP values are the result of altered hepatocyte-hepatocyte interaction and loss of normal architectural arrangements. The presence of marked fibrosis or cirrhosis, a state of significant altered hepatocyte architecture, may be the underlying cause of increased serum AFP, rather than necrosis or active regeneration.
Asunto(s)
Alanina Transaminasa/sangre , Hepatitis C Crónica/sangre , Hepatitis C Crónica/patología , alfa-Fetoproteínas/análisis , Antígenos Nucleares , División Celular , Hepatitis C Crónica/metabolismo , Humanos , Técnicas para Inmunoenzimas , Antígeno Ki-67 , Proteínas Nucleares/metabolismoRESUMEN
OBJECTIVE: The clinical and morphological significance of a raised alpha-fetoprotein (AFP) level in patients with chronic hepatitis C is undefined. We sought to determine the relation between serum AFP level and liver histology in this population. METHODS: We reviewed the clinical and histological records of 200 consecutively evaluated patients with chronic hepatitis C whose serum AFP levels were recorded. Two groups were studied: group I = 125/200 (62%) patients with normal AFP, < 10 ng/ml; and group II = 75/200 (38%) patients with raised AFP, > 10 ng/ml. The groups were compared according to age, gender, duration of disease, histology, and history of alcohol abuse. RESULTS: There was no significant difference in serum AFP based on age, gender, alcohol consumption, or disease duration. Significant histological differences were observed: cirrhosis was present in 57 (45%) patients in group I versus 51 (68%) in group II (p < 0.001). Hepatocellular carcinoma was more frequent in group II (14/75 [19%]) than in group I (1/125 [1%]) (p < 0.001). Ten of 77 (13%) noncirrhotic patients and 51/108 (47%) cirrhotic patients had a raised AFP (p < 0.002; relative risk, 3.262; confidence interval [C.I.], 1.912-5.564). A derived AFP level of 17.8 ng/ml maximized specificity for predicting histological outcome: one of 76 (1.3%), 29/108 (26.8%), and 14/15 (93.3%) patients were noncirrhotic, cirrhotic, or had HCC, respectively. This derived AFP value is 35% sensitive and 98.6% specific for cirrhosis, with a positive predictive value of 97.7%. CONCLUSION: A serum AFP level >17.8 ng/ml strongly suggests the diagnosis of cirrhosis in a population of patients with chronic hepatitis C.
Asunto(s)
Hepatitis C Crónica/sangre , Hepatitis C Crónica/patología , Hígado/patología , alfa-Fetoproteínas/análisis , Anciano , Biomarcadores , Carcinoma Hepatocelular/complicaciones , Femenino , Hepatitis C Crónica/complicaciones , Humanos , Cirrosis Hepática/complicaciones , Neoplasias Hepáticas/complicaciones , Masculino , Persona de Mediana Edad , Sensibilidad y EspecificidadRESUMEN
Several reports suggest that posttransfusion hepatitis C causes more aggressive histological activity than disease that is acquired via other routes. We sought to determine whether mode of transmission affects disease outcome. We studied the demographics, presenting laboratory data, and clinical course of 627 consecutively evaluated nonalcoholic patients with chronic hepatitis C. Two hundred eighty-two patients (45%) were transfusion recipients, 262 (42%) acquired the disease via other routes of percutaneous exposure, and 83 (13%) were without risks. Liver histology was available in 463 patients (215 transfusion recipients, 195 non-transfusion recipients, and 53 who were were without risks) and showed noncirrhosis in 274 (59%), cirrhosis in 173 (37%), and hepatocellular carcinoma in 16 patients (4%) who also had underlying cirrhosis. Duration of follow-up was 1 to 25 years (mean, 48 months; median, 21 years). One hundred eighteen of 173 (68%) cirrhotic patients were transfusion recipients; 40 of 173 (23%) cirrhotic patients acquired infection via other percutaneous exposure, and the remainder were without known risk factors (P < .001). Among the 215 patients with blood transfusions for whom histology was available, 118 of 215 (55%) had cirrhosis and 89 of 215 (41%) were noncirrhotic (P < .001); 8 transfused patients (4%) had hepatocellular carcinoma. In the percutaneous group, 40 of 195 (21%) of the patients were cirrhotic versus 153 of 195 (78%) who were noncirrhotic (P < .001); 2 patients (1%) had hepatocellular carcinoma. During the follow-up period, 59 of 189 (31%) of the cirrhotic patients (including those 16 individuals with hepatocellular carcinoma) developed hepatic decompensation. By univariate analysis, the risk of liver failure was related to age at viral acquisition, but by logistic regression analysis, only mode of transmission, and not age or estimated disease duration, predicted risk of liver failure. Patients with posttransfusion hepatitis C were more likely to develop decompensation than individuals who were not transfusion recipients (relative risk, 3.921; CI = 2.205 to 7.015). Serum albumin, prothrombin time, and platelet count at presentation were independent laboratory predictors of subsequent hepatic decompensation. The rate of hepatocellular carcinoma development among all cirrhotic patients during the follow-up period was 1.2% per year. Patients with posttransfusion hepatitis C are at greater risk of cirrhotic decompensation than those individuals with non-transfusion-acquired disease. The risk of liver failure is more closely related to the mode of transmission than to age at viral acquisition or to the duration of infection.
Asunto(s)
Hepatitis C/tratamiento farmacológico , Hepatitis C/transmisión , Adolescente , Adulto , Anciano , Anciano de 80 o más Años , Antivirales/uso terapéutico , Estudios de Cohortes , Femenino , Hepatitis C/epidemiología , Hepatitis C/etiología , Humanos , Hígado/patología , Cirrosis Hepática/etiología , Masculino , Persona de Mediana Edad , Morbilidad , Análisis de Supervivencia , Reacción a la Transfusión , Resultado del TratamientoRESUMEN
Hepatitis G virus (HGV) is a recently described, parenterally spread, positive-strand RNA virus of the Flaviviridae family. There is a high rate of HGV coinfection in patients with hepatitis C virus (HCV). Whether HGV can cause or is pathogenetically related to clinically apparent chronic liver disease, or whether HGV alters the course of hepatitis C in patients who are coinfected with both viruses is unknown. We studied 13 biopsy specimens from 11 patients coinfected with HGV and HCV and compared them with 15 biopsy specimens from a group of patients infected only with HCV who were matched for age, sex, disease duration, and transmission mode to characterize the histologic features of coinfected liver biopsy specimens and to look for any histologic features that might allow identification of coinfected patients. Three of the biopsy specimens from coinfected patients had a modified histologic activity index score of minimal chronic hepatitis, three of mild, two of mild/moderate, and five of moderate chronic hepatitis. Bile duct injury was absent in seven specimens, minimal in five, and mild in one. The biopsy specimens from patients who were coinfected with HGV and HCV had similar histologic features to the biopsy specimens of patients infected with HCV alone. There were no detectable histologic differences between the biopsy specimens from the two patient groups. The P values for the statistical comparisons confirmed this impression. In addition, no group of histologic features distinguished the coinfected patient group from the control group. Any suspicion that a clinician might have about the presence of HGV requires confirmation by reverse transcriptase-polymerase chain reaction testing of serum samples. Our results suggest that HGV most likely does not actively participate in the cytotoxic effects of chronic hepatitis or does so by a mechanism as yet undefined. Although HGV can cause chronic infection, the present study provides no evidence that it causes or contributes to chronic hepatitis.
Asunto(s)
Hepatitis C/patología , Hepatitis Crónica/patología , Hepatitis/patología , Hepatitis/virología , Biopsia , Hepatitis Crónica/virología , Humanos , Hígado/patología , Cirrosis Hepática/patología , Estudios RetrospectivosRESUMEN
OBJECTIVES: Alfa interferon therapy is conventionally offered only to chronic hepatitis C patients with abnormal serum alanine aminotransferase (ALT) values. Therapeutic response is traditionally gauged by normalization of liver enzymes. Treatment of patients with persistently normal serum aminotransferases is not routinely done. The purpose of this study was to determine whether standard therapy with alfa interferon can eradicate hepatitis C virus in viremic patients with persistently normal or near-normal serum aminotransferases. METHODS: Between 1990 and 1996 we evaluated 565 patients with chronic hepatitis C. Of these, 49 patients (8.7%) (15 men, 34 women) had normal or near-normal ALT levels (less than 1.5 times upper limit of normal) for at least 3 consecutive months. Of these, 15 patients were studied. Treatment consisted of interferon alfa-2b 3 million units thrice weekly for 6 months. RESULTS: Normal or near normal ALT levels are more common in women than men. All patients completed 6 months of therapy, and 12 patients completed 6 months of posttreatment follow-up. Only one patient lost hepatitis C virus RNA during treatment and viremia reappeared in this patient immediately after cessation of therapy. CONCLUSIONS: Standard antiviral therapy of patients with normal or near-normal ALT levels does not result in sustained viral eradication in most patients.