ABSTRACT
OBJECTIVE: This prospective study aimed to estimate the prevalence and course of depression during chemotherapy in women with Stage I-III breast cancer, identify potential risk factors for depression and determine which treatments for depression were being used and which were most preferred. METHOD: Thirty-two women were followed over consecutive chemotherapy infusions, with 289 assessments conducted altogether (mean, 9.0 assessments/subject). Current depression, anxiety, physical symptoms and mental health service use were recorded during each assessment. A linear mixed effects model was used to identify factors associated with depression. Patients also ranked depression treatment preferences. We referred patients with more severe depression for treatment. RESULTS: Clinically significant depression was identified in 37.5% of patients. Depression severity tended to peak at 12-14 weeks and 32 or more weeks of chemotherapy. Depression severity was associated with anxiety severity, physical symptom burden, non-White race, receiving one's first chemotherapy regimen, Adriamycin-Cytoxan chemotherapy and chemotherapy duration. Most (65.5%) patients preferred evidence-based treatments for depression, and 66.7% of depressed patients were using such treatments. CONCLUSIONS: Depression is common in women receiving chemotherapy for breast cancer. Most patients prefer evidence-based depression treatments. We recommend regular screening for depression during chemotherapy to ensure adequate detection and patient-centered treatment.
Subject(s)
Breast Neoplasms/psychology , Depressive Disorder/psychology , Patient Preference , Adult , Antidepressive Agents/therapeutic use , Antineoplastic Agents/therapeutic use , Anxiety Disorders/complications , Anxiety Disorders/psychology , Breast Neoplasms/complications , Breast Neoplasms/drug therapy , Cohort Studies , Depressive Disorder/complications , Depressive Disorder/therapy , Disease Progression , Fatigue/complications , Fatigue/psychology , Female , Humans , Mental Health Services/statistics & numerical data , Middle Aged , Prospective Studies , Psychotherapy , Severity of Illness IndexABSTRACT
Fibroblast growth factor-2 (FGF2, bFGF) has been proposed to regulate wound healing and angiogenesis, but skin wound healing in FGF2-knockout (FGF2-KO) animals is only slightly delayed. To determine the role of FGF2 in myocardial infarct repair, we studied the evolution of left ventricular geometry, cell proliferation, matrix content, and cardiac function in mice lacking or overexpressing (FGF2-Tg) FGF2. Despite having no effect on initial infarct size, deletion of FGF2 resulted in reduced fibroblast proliferation and interstitial collagen deposition, decreased endothelial proliferation and vascular density, and decreased cardiomyocyte hypertrophy. Furthermore, FGF2-KO mice demonstrated a complete absence of scar contraction, resulting in increased final infarct size and marked increases in chamber size and infarct expansion. These deficits ultimately impaired left ventricular dP/dt compared with wild-type infarcted mice. Conversely, overexpression of FGF2 increased fibroblast proliferation and collagen deposition, accelerated endothelial proliferation, and enhanced cardiomyocyte hypertrophy after infarction. These changes curbed infarct expansion and preserved left ventricular function. Thus, FGF2 is an important regulator of cell proliferation, angiogenesis, collagen synthesis, myocyte hypertrophy, scar contraction, and, ultimately, left ventricular contractile function during infarct repair. FGF2 may be more important in healing of infarcts compared with skin wounds because of the mechanical stress under which infarcts heal.
