Subject(s)
Acquired Immunodeficiency Syndrome/complications , Anti-Infective Agents/adverse effects , Aryl Hydrocarbon Hydroxylases/genetics , Drug Hypersensitivity/genetics , Glutathione S-Transferase pi/genetics , Polymorphism, Genetic , Sulfonamides/adverse effects , Acquired Immunodeficiency Syndrome/enzymology , Acquired Immunodeficiency Syndrome/genetics , Adult , Cytochrome P-450 CYP2C9 , Drug Hypersensitivity/etiology , Female , Humans , Inactivation, Metabolic/genetics , Male , Skin/immunologyABSTRACT
BACKGROUND AND OBJECTIVES: Guidelines for conducting studies and reading medical literature on diagnostic tests have been published: Requirements for the selection of cases and controls, and for ensuring a correct reference standard are now clarified. Our objective was to provide tables for sample size determination in this context. STUDY DESIGN AND SETTING: In the usual situation, where the prevalence Prev of the disease of interest is <0.50, one first determines the minimal number Ncases of cases required to ensure a given precision of the sensitivity estimate. Computations are based on the binomial distribution, for user-specified type I and type II error levels. The minimal number N(controls) of controls is then derived so as to allow for representativeness of the study population, according to Ncontrols=Ncases [(1-Prev)/Prev]. RESULTS: Tables give the values of Ncases corresponding to expected sensitivities from 0.60 to 0.99, acceptable lower 95% confidence limits from 0.50 to 0.98, and 5% probability of the estimated lower confidence limit being lower than the acceptable level. CONCLUSION: When designing diagnostic test studies, sample size calculations should be performed in order to guarantee the design accuracy.
Subject(s)
Diagnostic Tests, Routine/standards , Sample Size , Biomedical Research/methods , Humans , Research Design , Sensitivity and SpecificityABSTRACT
Immortalization of B cells by Epstein-Barr virus (EBV) and their subsequent proliferation leads to B-cell non-Hodgkin's lymphoma in immunocompromised patients. The role of hepatitis C virus (HCV) in B-cell non-Hodgkin's lymphoma has recently been raised, and an interaction between HCV and EBV is supported by recent in vitro experiments. The aim of this study was to investigate in vivo interactions between HCV and EBV in patients with AIDS, i.e., patients exposed to the risk of EBV-related B-cell non-Hodgkin's lymphoma. A total of 135 patients were prospectively studied. Serological and molecular markers of HCV, EBV, and human immunodeficiency virus (HIV) infection were sought. All the patients harbored latent EBV infection, and 20% had detectable HCV RNA in serum. No significant relationship was found between HIV, HCV, and EBV viral load in peripheral blood mononuclear cells or plasma. There was no difference between anti-HCV-positive and -negative patients or between HCV RNA-positive and -negative patients with regard to the prevalence of EBV markers, especially EBV replication markers. The presence of EBV replication markers was not related to HCV RNA seropositivity or to HCV viral load. Five patients subsequently developed B-cell non-Hodgkin's lymphoma, none of whom had markers of EBV or HCV replication. These results argue against an in vivo interaction between HCV and EBV in patients with AIDS, and against a role of HCV infection in the occurrence of B-cell non-Hodgkin's lymphoma in these patients.
