A study was performed in 10 European health care centers in which 914 patients coinfected with hepatitis C virus (HCV) and human immunodeficiency virus (HIV) who had elevated serum alanine aminotransferase (ALT) levels underwent liver biopsy during the period of 1992 through 2002. Overall, the METAVIR liver fibrosis stage was F0 in 10% of patients, F1 in 33%, F2 in 22%, F3 in 22%, and F4 in 13%. Predictors of severe liver fibrosis (METAVIR stage, F3 or F4) in multivariate analysis were age of >35 years (odds ratio [OR], 2.95; 95% confidence interval [CI], 2.08-4.18), alcohol consumption of >50 g/day (OR, 1.61; 95% CI, 1.1-2.35), and CD4+ T cell count of <500 cells/mm3 (OR, 1.43; 95% CI, 1.03-1.98). Forty-six percent of patients aged >40 years had severe liver fibrosis, compared with 15% of subjects aged <30 years. The use of antiretroviral therapy was not associated with the severity of liver fibrosis. In summary, severe liver fibrosis is frequently found in HCV-HIV-coinfected patients with elevated serum ALT levels, and its severity increases significantly with age. The rate of complications due to end-stage liver disease will inevitably increase in this population, for whom anti-HCV therapy should be considered a priority.
PBMC with interleukin-2 (IL-2) was observed in ALC, itChronic alcohol intake is associated with an increased did not reach the levels observed in healthy subjects. incidence of certain neoplasms. Natural killer (NK) cells Overall, our results show that the behavior of PB NKhave been considered to be involved in control tumor cell population in chronic alcoholism is different acdevelopment and growth. The goal of the present study cording to both the moment of EtOH consumption and was to contribute to a better understanding of the effects the existence or not of ALC. Alcohol by itself induced an of ethanol (EtOH) per se on the NK-cell population. Both increase in the number and lytic activity of NK-cells. By patients with chronic alcoholism without liver disease contrast, the NK cytolytic activity is constantly de-(AWLD) and subjects with alcohol-induced cirrhosis pressed in the stage of alcoholic cirrhosis, supporting (ALC) were carefully selected for this study. Immunothe notion that immunosurveillance mechanisms may phenotypical and functional studies of peripheral blood be affected in these patients. (HEPATOLOGY 1997;25:1096-(PB) NK-cells were performed during active EtOH in-1100.) take and after 3 months of a withdrawal period. In the AWLD group a significant increase in number of NKcells (CD30/CD56/) (P õ .05) associated with a parallel Chronic alcohol intake is associated with an increased inciincrease in NK-cell lytic activity (P õ .01) was observed.dence of larynx, esophageal, liver, and pancreas neoplasms. 1 In addition, the number of cytotoxic T cells displayingThis feature has been related, at least partially, to an ethanol the CD3//CD56/ phenotype as well as CD80/CD57/ NK-(EtOH)-induced enzymatic activation of the conversion of cell subset was also increased (P õ .01 and P õ .001, procarcinogens into carcinogens. 2,3 In addition, previous rerespectively). By contrast, in ALC patients with active ports suggest that an alteration of the immunosurveillance EtOH intake (ALCET group), although a significant incould also contribute to the higher incidence of neoplasms crease in the number of NK PB lymphocytes was obobserved in these patients. 4 Natural killer (NK) cells have served (P õ .05), NK lytic activity was depressed (P õ been classically considered to be involved in control of tumor .05), suggesting the existence of a decreased lytic activdevelopment and growth. 5 ity/NK-cell. After 3 months of EtOH withdrawal, PBThe study of NK-cells in chronic alcoholism has provided mononuclear cells (PBMC) from the AWLD group paconflicting results in the literature. 6 Several variables can tients still displayed an increased NK cytolytic activity;contribute to these discrepancies: 1) the time-point at which in addition, the number of PB NK-cells (CD30/CD56/ the study was performed (active alcoholism vs. withdrawal and CD80/CD57/) and CD3//CD56/ PB T cells continperiod), 2) the criteria used for patient selection (alcoholic ued to be increased. Independently of the duration of liver disease vs. alcoholism withou...
Metastatic pulmonary calcifications, unlike dystrophic calcifications, occur in the normal healthy lung. The radiological pattern is quite specific. The disease is commonly described in chronic renal failure with calcium disorders. The prognosis is totally unpredictable.In 1992, a 50 yr old man underwent a successful renal transplantation during the final stage of chronic renal failure. He subsequently developed asymptomatic diffuse nodular opacities, that were discovered in 1995. An open lung biopsy confirmed the diagnosis of metastatic pulmonary calcification. There was no calcium disorder in this patient.In contrast to the benign course of pulmonary calcification in most patients, some fulminant pulmonary calcifications complicating renal transplantation or hypercalcaemia have been described. Radiographic identification of such entities is important to permit correction of calcium disorders. Otherwise, the condition is a potentially progressive and fatal cause of respiratory failure.
Central-nervous-system toxoplasmosis developed in 7 of 269 patients with the acquired immunodeficiency syndrome reported to the New York City Health Department through July 1982. Focal neurologic abnormalities, mass lesions on computed-tomographic brain scans, lymphocytic cerebrospinal fluid pleocytosis, and detectable IgG antibody to Toxoplasma gondii were common; but IgG titers of 1:1024 or more, IgM antibody to T. gondii, and positive open brain biopsies were uncommon. Serologic findings suggested that the disease resulted from recrudescent rather than primary infection. Four of five patients improved when treated with sulfonamides and pyrimethamine, but 2 had relapses. An aggressive diagnostic approach and sometimes even empiric therapy are warranted when central-nervous-system toxoplasmosis is suspected in a seropositive patient with the acquired immunodeficiency syndrome.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.