The impact of taste and smell alterations on quality of life in head and neck cancer patients.

PURPOSE: Taste and smell alterations (TSAs) are among the most frequent and troublesome symptoms reported by head and neck cancer (HNC) patients after treatment. Little is known about the relationship between TSAs and quality of life (QoL) among HNC patients. The aim of this study was to determine the effect of TSAs on overall QoL among tube-fed and orally fed HNC patients before treatment, at end of treatment and at 2.5-month follow-up. METHODS: Data were collected in a longitudinal study prior to treatment (n = 126), at end of treatment (n = 100) and at 2.5-month follow-up (n = 85). Chemosensory Complaint Score (CCS) and the University of Washington Quality of Life Questionnaire version 3 were used to assess TSAs and QoL, respectively. Generalized estimated equation modeling was used to estimate the effect of CCS on QoL. RESULTS: At end of treatment, QoL and CCS had declined for both tube-fed and orally fed patients and thereafter improved, but not to pre-treatment levels. Neither QoL nor CCS mean scores were different between the two groups at any time point. CCS was a significant predictor of overall QoL (ß = -1.82, p < 0.0001), social-emotional (ß = -1.76, p < 0.0001), physical (ß = -1.12, p < 0.0001) and overall functions (ß = -1.15, p < 0.0001) at a multivariate level. Taste was reported as an important symptom for both tube-fed and orally fed groups at end of treatment and follow-up. CONCLUSIONS: TSAs are an important symptom and an independent predictor of QoL for both tube-fed and orally fed HNC patients. HNC patients need support to manage TSAs, regardless of the method of nutritional intake.

Induction of IFN-alpha in peripheral blood mononuclear cells by HIV-infected monocytes. Restricted antiviral activity of the HIV-induced IFN.

PBMC cocultured with HIV-infected monocytes for 12 to 48 h released high levels of IFN activity. IFN titers were directly dependent upon time after virus infection and level of HIV replication in infected cells. IFN induction in PBMC was evident with HIV-infected monocytes and PBMC and with myeloid and lymphoblastoid cell lines with at least three different HIV strains. In HIV-infected cell line pairs in which virus infection occurs in both productive and restricted forms, IFN induction in PBMC occurred only with productive infection. IFN activity was acid stable and completely neutralized by antibodies against IFN-alpha. Induction of IFN required cell-cell contact between HIV-infected cells and PBMC, but was independent of MHC compatibility. With PBMC co-cultured with autologous HIV-infected monocytes, IFN induction was highly selective: IL-1 beta, IL-6, or TNF-alpha activity and mRNA were not detected. Cell surface determinants on HIV-infected monocytes that induced IFN in PBMC remained active after fixation in 4% paraformaldehyde. Both adherent and nonadherent PBMC produced IFN after coculture with HIV-infected monocytes. Ability to produce IFN by PBMC was not affected by depletion of T cell, NK cell, B cell, or monocyte subpopulations. The IFN activity produced by PBMC cocultured with HIV-infected cells was about 20-fold less active than equal quantities of rIFN-alpha 2b for inhibition of HIV replication in monocytes and at low concentrations enhanced virus growth. Clinical studies with HIV-infected patients and parallel findings in animal lentivirus disease suggest an adverse role for IFN in disease progression. Conditions for induction of IFN in the culture system described in this report may mimic those in the HIV-infected patient. Defining the molecular basis for IFN induction, the cells that produce IFN, and the altered biologic activity of this important cytokine may provide insight into the pathogenesis of HIV disease.