[Peripapillary lipomas "in cluster"].
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Biomedical subjects
Publications and source records attributed to L García Buey.
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Modification of the pharmacokinetic profile of interferon-alfa (IFNalfa) through pegylation (addition of a polyethylenglicol molecul) has resulted in a marked improvement of drug efficacy for the treatment of infection due to hepatitis C virus. Two pegylated derivatives of IFNalfa are available: PEG-IFNalfa-2a, with a 40 kDa polyethylenglicol molecule of branched structure, and PEG- IFNalfa- 2b, with a 12kDa linear PEG. Both compounds have slower absorption, more reduced distribution and lower elimination rate than the respective non- pegylated IFNalfa, which assures that concentrations appropriate to inhibit viral replication are maintained during longer periods of time, thus a allowing administration once a week, In addition to archieving greater therapeutic efficacy, the adverse effects related to excessive Cmax are reduced, the risk of therapeutic failure is decreased by eliminating the intervals of inefficient plasma levels, and the uncomfortable thrice weekly injection regimens are avoided. The current recommendations include the use of a combination therapy with pegylated IFNalfa and ribavirin as the standard treatment. However, further research is required to archieve dosage optimization of pegylated IFN and rebavirin according to the patientś characteristics and to evaluate the efficacy and safety of this combined theraphy for difficult- to- treat patients.
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We present a mesenteric desmoid tumor in a man without associated diseases. Characteristics of this tumor are reviewed and the need to perform total exeresis of the mass for diagnosis is emphasized. Although surgery is the treatment of choice, alternative treatments are recommended when surgery cannot be performed, has been incomplete, or in cases of repeated recurrence.
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Serum iron studies have high values in 30% of patients with virus C (HCV) chronic hepatitis even in hemochromatosis range. These indices do not represent hepatic iron storage which has a low to moderate intensity. Heterozygosity for hereditary hemochromatosis could be responsible of the iron liver storage in some patients. Nowadays the relationship between hepatic iron loading and HCV infection is unknown. It has been suggested that iron storage could allow HCV infection or, by other way, it may be caused by the infection. Iron, per se, has hepatolesive effect and acts synergistically with HCV worsening liver injury. Also, iron storage reduces the interferon response rate, and iron depletion with phlebotomies improves transaminases level. However, it is discussed if the association: iron removal-interferon treatment improves interferon alone treatment response. In this work all these points are reviewed.
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OBJECTIVE: To analyze the expression of different HLA class I antigens and cell adhesion molecules on frozen liver sections from patients with chronic active hepatitis, types B and C. EXPERIMENTAL DESIGN: Liver biopsy samples were divided into two parts, one for routine histological examination and another, after snap-freezing and storing at -80 degrees C, for immunohistochemical analysis. To carry out immunoperoxidase and immunofluorescence stainings, a panel of monoclonal antibodies specific for HLA class I light (beta 2-microglobulin) and heavy chain determinants, and for adhesion molecules such as intercellular adhesion molecule-1 and lymphocyte function associate antigen-3 was used. PATIENTS: Immunohistochemistry was performed in frozen liver biopsy sections from 25 patients with viral chronic active hepatitis, 10 type B and 15 type C. As controls, normal liver samples and liver specimens from patients with cholestasis or steatosis were also studied. RESULTS: HLA class I light and heavy chain determinants were expressed on hepatocytes, biliary duct epithelium, sinusoidal lining cells and lymphocytes from patients and controls; however, the beta 2-microglobulin conformational epitope was undetectable on hepatocytes from normal livers or with cholestasis or steatosis, but clearly positive on hepatocytes from patients with hepatitis. In addition, in liver sections from controls no adhesion molecules positivity was detected on hepatocytes; by contrast, hepatocytes from patients with hepatitis showed markedly enhanced membranous reactivity for both adhesion molecules in areas of piecemeal and lobular necrosis. CONCLUSIONS: Virus B and C infections could induce an increased hepatocellular expression of HLA-class I determinants, including the conformational epitope adequate for antigen presentation, and cell-cell adhesion molecules. These findings underline the role of cell mediated immune reactions in the pathogenesis of hepatic injury in viral chronic hepatitis.
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The rate of HBeAg clearance and the outcome were analyzed in 46 patients with asymptomatic chronic hepatitis B virus (HBV) infection whose condition was followed for 1-4 yr (mean 2.4). Mean age was 32.5 yr (range 10-68), and 28 (61%) were males. All had chronic hepatitis, on biopsy, and were positive for HBcAg on hepatocytes. Alcoholics, homosexuals, drug abusers, immunocompromised patients, and those with advanced liver disease were excluded. During the follow-up, 25 patients (54%) cleared HBeAg and became seronegative for HBV-DNAp. The estimated annual rate of seroconversion was 26%. One patient cleared HBsAg. After seroconversion, 18 patients had no evidence of ongoing liver disease, proved by biopsy in eight and by clinical follow-up in 10 that refused biopsy. A second liver biopsy was available in 15 patients, and HBcAg was negative in all; histology was normal in eight, unchanged in one, and compatible with cirrhosis in six. All six had clinical and/or biochemical evidence of advanced liver disease. These were significantly older at the start of the study, and had chronic active hepatitis with bridging necrosis on initial biopsy. Early identification of patients with silent chronic HBV infection and high levels of viral replication for antiviral therapy could prevent transmission of the infection and stop progression to liver cirrhosis and hepatocellular carcinoma.
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