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Objective: This study investigated whether cancer patients with and without major depression exhibit immune system abnormalities similar to those reported in medically healthy, depressed subjects without cancer. Method: The study subjects consisted of patients diagnosed with pancreatic, esophageal, or breast cancer. Other groups consisted of subjects with major depression (without cancer) and healthy comparison subjects. Subjects’ diagnoses were made with the Structured Clinical Interview for DSM-III-R. Severity of depression was measured with the Hamilton Depression Rating Scale. Plasma concentrations of interleukin-6 (IL-6) and postdexamethasone cortisol were measured. Results: Cancer patients with depression had markedly higher plasma concentrations of IL-6 than healthy comparison subjects and cancer patients without depression. Although significant correlations were found between Hamilton depression scale scores and plasma concentrations of postdexamethasone cortisol, no significant correlations were found between plasma IL-6 and postdexamethasone cortisol concentrations. Conclusions: Higher than normal plasma IL-6 concentrations were associated with a diagnosis of major depression in cancer patients. IL-6 may contribute to sickness behavior that has overlapping symptoms with major depression. (Am J Psychiatry 2001; 158:1252–1257) Cancer patients, who experience marked physiologic, economic, and psychological stressors, have long been observed to have elevated prevalence rates of major depression, compared with the general population (1). Among cancer patients, the highest prevalence rates are exhibited by patients with either oropharyngeal cancer (2–4) or pancreatic cancer (5–7). Prospective or crosssectional studies of patients with pancreatic cancer have documented a remarkable point prevalence rate of depression of 50% (5–8). Although a number of neurochemical, neuroendocrine, neuroanatomical, and neuroimmune alterations have been associated with unipolar depression, few of these psychobiologic alterations have been systematically investigated in cancer patients with depression.

Objective: This study iizvestigated whether depressed patients exhibit exaggerated platelet reactivity. Method: In vivo platelet activatioiz, secretioz, and dose-response aggregation were measured in 12 depressed patients and eight normal comparison subjects after overizight bed rest aizd following orthostatic challenge. Results: The depressed patients exhibited increased platelet activation at baseli,ze, demonstrated by increased binding of monoclonal antibody (moAb) annexin V protein reacting with prothrombinase complex binding sites. Followizg orthostatic challeizge, the depressed patients exhibited increases in binding of moAbs PACI a,zd anti-LIBS1 agaiizst actii'atedglycoprotein Jib/lila and GEI2 against P-selecti,z expressed 111)01? secretion. The normal comparison subjects exhibited increases in platelet activatioz only with GE I 2. Conclusions: Depressed patients exhibit enhazced baseline platelet activation and respozsiveness in comparisoz with normal subjects. Heightened susceptibility to platelet acti- vation flltlV he a mechanism b�' which depression is a significant risk factor for ischemic heart azd cerebrovascular disease and/or mortality after myocardial infarction. (AmJ Psychiatry 1996; 153:1313-1317)