Symptoms predicting health-related quality of life in prostate cancer patients treated with localized radiation therapy

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Abstract

Objective Patient-reported health-related quality-of-life (HRQOL) measures can provide guidance for treatment decision making, symptom management, and discharge planning. HRQOL is often influenced by the distress experienced by patients from disease or treatment-related symptoms. This study aimed to identify symptoms that can predict changes in HRQOL in men undergoing external beam radiation therapy (EBRT) for nonmetastatic prostate cancer (NMPC). Methods Fifty-one men with NMPC scheduled for EBRT were assessed at the baseline, at the midpoint of EBRT, and at the end of EBRT. All participants received 38–42 daily doses of EBRT (five times a week), depending on the stage of their disease. Validated questionnaires were administered to evaluate depressive symptoms, urinary and sexual functions, bowel issues, symptom-related distress, fatigue, and HRQOL. Pearson correlations, repeated-measures ANOVA, and multiple regressions examined the relationships among variables. Results Intensification of symptoms and increased symptom-related distress, with a corresponding decline in HRQOL, were observed during EBRT in men with NMPC. Changes in symptoms and symptom distress were associated with changes in HRQOL at the midpoint of EBRT (r=−0.37 to −0.6, P=0.05) and at the end of EBRT (r=−0.3 to −0.47, P=0.01) compared with the baseline. The regression model comprising age, body mass index, Gleason score, T category, androgen-deprivation therapy use, radiation dose received, symptoms (urinary/sexual/bowel problems, fatigue), and overall symptom distress explained 70% of the variance in predicting HRQOL. Urinary problems and fatigue significantly predicted the decline in HRQOL during EBRT. Conclusion Identifying specific symptoms that can influence HRQOL during EBRT for NMPC can provide feasible interventional targets to improve treatment outcomes.

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Estimating clinically meaningful changes for the Functional Assessment of Cancer Therapy--Prostate: results from a clinical trial of patients with metastatic hormone-refractory prostate cancer.

David Cella, Michael B Nichol, David Eton … (2015)

To determine clinically meaningful changes (CMCs) for the Functional Assessment of Cancer Therapy-Prostate (FACT-P). We obtained data from a Phase III trial of atrasentan in metastatic hormone-refractory prostate cancer patients (n = 809). We determined anchor-based differences using Karnofsky Performance Status (KPS), bone alkaline phosphatase (BAP), hemoglobin, time to disease progression (TTP), adverse events (AE), and survival. One-third and one-half standard deviation and standard error of measurement (SEM) were used as distribution-based criteria for CMCs. Comparison across baseline FACT-P domains and derived scales [FACT-P total score, Trial Outcome Index (TOI) score, prostate cancer subscale (PCS) score, pain-related score, and FACT Advanced Prostate Symptom Index (FAPSI)] were conducted for KPS, BAP, and hemoglobin using Student's t tests. Twelve-week change scores were compared for TTP, AE, and survival using ANCOVA. CMCs were estimated as 6 to 10 for FACT-P total score, 5 to 9 for FACT-P TOI score, 2 to 3 for FACT-P PCS, 1 to 2 for the 4 PCS pain-related questions, and 2 to 3 for FAPSI. CMCs were also estimated using distribution-based criteria. Kappa statistics were computed to determine the degree of correspondence between the recommended guideline of 1.0 SEM and empirically derived standards. Most of the kappas for health-related quality of life domains and SEM standards had "substantial" to "almost perfect" concordance. The significant relationship between clinical and quality of life data provides support for the use of CMCs to increase interpretability of FACT-P scores.

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Oxidative phosphorylation and aging.

Charles Hoppel, E Lesnefsky (2006)

This review addresses the data that support the presence and contribution of decreased mitochondrial oxidative phosphorylation during aging to impaired cellular metabolism. Aging impairs substrate oxidation, decreases cellular energy production and increases the production of reactive intermediates that are toxic to the cell. First, the basic principles of mitochondrial oxidative physiology are briefly reviewed. Second, the focus on the relationship of altered mitochondrial respiration to the increased production of reactive oxygen species that are employed by the "rate of living" and the "uncoupling to survive" theories of aging are discussed. Third, the impairment of function of respiration in aging is reviewed using an organ-based approach in mammalian systems. Fourth, the current state of knowledge regarding aging-induced alterations in the composition and function of key mitochondrial constituents is addressed. Model organisms, including C. elegans and D. melanogaster are included where pertinent. Fifth, these defects are related to knowledge regarding the production of reactive oxygen species from specific sites of the electron transport chain.

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Missense mutations in the BCS1L gene as a cause of the Björnstad syndrome.

Pankaj Sharma, N Breivik, Larry Seidman … (2007)

The Björnstad syndrome, an autosomal recessive disorder associated with sensorineural hearing loss and pili torti, is caused by mutation of a previously unidentified gene on chromosome 2q34-36. Refined genetic mapping and DNA sequencing of 44 genes between D2S2210 and D2S2244 revealed BCS1L mutations. Functional analyses elucidated how BCS1L mutations cause the Björnstad syndrome. BCS1L encodes a member of the AAA family of ATPases that is necessary for the assembly of complex III in the mitochondria. In addition to the Björnstad syndrome, BCS1L mutations cause complex III deficiency and the GRACILE syndrome, which in neonates are lethal conditions that have multisystem and neurologic manifestations typifying severe mitochondrial disorders. Patients with the Björnstad syndrome have mutations that alter residues involved in protein-protein interactions, whereas mutations in patients with complex III deficiency alter ATP-binding residues, as deduced from the crystal structure of a related AAA-family ATPase. Biochemical studies provided evidence to support this model: complex III deficiency mutations prevented ATP-dependent assembly of BCS1L-associated complexes. All mutant BCS1L proteins disrupted the assembly of complex III, reduced the activity of the mitochondrial electron-transport chain, and increased the production of reactive oxygen species. However, only mutations associated with complex III deficiency increased mitochondrial content, which further increased the production of reactive oxygen species. BCS1L mutations cause disease phenotypes ranging from highly restricted pili torti and sensorineural hearing loss (the Björnstad syndrome) to profound multisystem organ failure (complex III deficiency and the GRACILE syndrome). All BCS1L mutations disrupted the assembly of mitochondrial respirasomes (the basic unit for respiration in human mitochondria), but the clinical expression of the mutations was correlated with the production of reactive oxygen species. Mutations that cause the Björnstad syndrome illustrate the exquisite sensitivity of ear and hair tissues to mitochondrial function, particularly to the production of reactive oxygen species. Copyright 2007 Massachusetts Medical Society.