A Pilot Study of Nonpharmacological Interventions for Hospice Patients With Behavioral and Psychological Symptoms in Dementia.

Agitation is a common, treatable symptom that profoundly impacts quality of life and exacerbates caregiver fatigue in the hospice setting for patients with dementia. The objective of this study was to analyze the efficacy of tailored nonpharmacological interventions for mitigation of unwanted behaviors in the population of patients with behavioral and psychological symptoms in dementia while receiving hospice care. The 4-domain Pittsburgh Agitation Scale (PAS; Motor, Verbal, Aggressive, Resistance to Care) was used for multiple baseline and posttest measurements of agitation. Effectiveness of nonpharmacological interventions was evaluated using analysis of variance for repeated measures for the total PAS score. Motor agitation was the presenting problem with highest-rated severity compared with Verbal, Aggression, and Resistance to Care domains. Analysis of variance demonstrated no difference between baseline referral and pretest total PAS measures (P = .8), but a significant drop in total PAS agitation after intervention (P < .001). The best outcomes, however, were with patients receiving both nonpharmacological and standard pharmacological interventions as opposed to nonpharmacological interventions alone (P = .034). For patients with dementia presenting with behavioral and psychological symptoms, selected nonpharmacological interventions provide significant mitigation of agitation.

Plasma alpha2-HS glycoprotein concentrations in patients with acute myocardial infarction quantified by a modified ELISA.

BACKGROUND: Human alpha2-HS glycoprotein (alpha2-HSG) is synthesized and secreted by the liver into circulation. Plasma concentrations of alpha2-HSG decrease significantly following infection, inflammation and malignancy. Since increased plasma concentrations of C-reactive protein are observed in patients with acute myocardial infarction (AMI), we hypothesized that plasma concentrations of alpha2-HSG would decrease during the initial phase of AMI and begin to increase in the recovery phase. METHODS: Twenty patients diagnosed with AMI were recruited for the study. A sensitive and specific ELISA was developed to assay alpha2-HSG concentrations in plasma. RESULTS: In AMI patients, plasma alpha2-HSG concentrations were decreased (281.3+/-25.8 mg/l, ranging from 132 to 489 mg/l on admission) compared to healthy individuals (312.3+/-9.9 mg/l, ranging from 210 to 450 mg/l) (P= 0.142). Interestingly, 40% of AMI patients demonstrated alpha2-HSG concentrations below 200 mg/l compared to none in the healthy control group. During the recovery period, alpha2-HSG concentrations begin to increase, with a mean+/-SEM of 290.1+/-22.1 mg/l. Regression analysis comparing plasma alpha2-HSG concentrations on admission to concentrations on discharge showed a significant positive correlation in matched-pair patient samples (P<0.01, r=0.45). CONCLUSIONS: We conclude that, in contrast to C-reactive protein, alpha2-HSG functions as a negative acute phase protein in AMI patients. Plasma alpha2-HSG concentrations start to decrease within a few hours after the onset of AMI and return to near normal concentrations during the recovery period (5-7 days after AMI).