Post-discharge hospital utilization among adult medical inpatients with depressive symptoms.

BACKGROUND: Little evidence exists to determine whether depression predicts hospital utilization following discharge among adult inpatients on a general medical service. OBJECTIVE: We aimed to determine whether a positive depression screen during hospitalization is significantly associated with an increased rate of returning for hospital services. DESIGN: A secondary analysis was performed using data from 738 English-speaking, hospitalized adults from the Project RED randomized controlled trial (clinicaltrials.gov Identifier: NCT00252057) conducted at an urban academic safety-net hospital. MEASUREMENTS: We used the nine-item Patient Health Questionnaire (PHQ-9) depression screening tool to identify patients with depressive symptoms. The primary endpoint was hospital utilization, defined as the number of emergency department (ED) visits plus readmissions within 30 days of discharge. Poisson regression was used to control for confounding variables. RESULTS: Of the 738 subjects included in the analysis, 238 (32%) screened positive for depressive symptoms. The unadjusted hospital utilization within 30 days of discharge was 56 utilizations per 100 depressed patients compared with 30 utilizations per 100 non-depressed patients, incident rate ratio (IRR) (confidence interval [CI]), 1.90 (1.51-2.40). After controlling for potential confounders, a higher rate of post-discharge hospital utilization was observed in patients with depressive symptoms compared to patients without depressive symptoms (IRR [CI], 1.73 [1.27-2.36]). CONCLUSIONS: A positive screen for depressive symptoms during an inpatient hospital stay is associated with an increased rate of readmission within 30 days of discharge in an urban, academic, safety-net hospital population.

A reengineered hospital discharge program to decrease rehospitalization: a randomized trial.

BACKGROUND: Emergency department visits and rehospitalization are common after hospital discharge. OBJECTIVE: To test the effects of an intervention designed to minimize hospital utilization after discharge. DESIGN: Randomized trial using block randomization of 6 and 8. Randomly arranged index cards were placed in opaque envelopes labeled consecutively with study numbers, and participants were assigned a study group by revealing the index card. SETTING: General medical service at an urban, academic, safety-net hospital. PATIENTS: 749 English-speaking hospitalized adults (mean age, 49.9 years). INTERVENTION: A nurse discharge advocate worked with patients during their hospital stay to arrange follow-up appointments, confirm medication reconciliation, and conduct patient education with an individualized instruction booklet that was sent to their primary care provider. A clinical pharmacist called patients 2 to 4 days after discharge to reinforce the discharge plan and review medications. Participants and providers were not blinded to treatment assignment. MEASUREMENTS: Primary outcomes were emergency department visits and hospitalizations within 30 days of discharge. Secondary outcomes were self-reported preparedness for discharge and frequency of primary care providers' follow-up within 30 days of discharge. Research staff doing follow-up were blinded to study group assignment. RESULTS: Participants in the intervention group (n = 370) had a lower rate of hospital utilization than those receiving usual care (n = 368) (0.314 vs. 0.451 visit per person per month; incidence rate ratio, 0.695 [95% CI, 0.515 to 0.937]; P = 0.009). The intervention was most effective among participants with hospital utilization in the 6 months before index admission (P = 0.014). Adverse events were not assessed; these data were collected but are still being analyzed. LIMITATION: This was a single-center study in which not all potentially eligible patients could be enrolled, and outcome assessment sometimes relied on participant report. CONCLUSION: A package of discharge services reduced hospital utilization within 30 days of discharge. FUNDING: Agency for Healthcare Research and Quality and National Heart, Lung, and Blood Institute, National Institutes of Health.

Parathyroid hormone stimulates expression of the Notch ligand Jagged1 in osteoblastic cells.

We previously demonstrated that activation of the Parathyroid Hormone Receptor (PTH1R) in osteoblastic cells increases the Notch ligand Jagged1 and expands hematopoietic stem cells (HSC) through Notch signaling. However, regulation of Jagged1 by PTH in osteoblasts is poorly understood. The present study demonstrates that PTH treatment increases Jagged1 levels in a subpopulation of osteoblastic cells in vivo and in UMR106 osteoblastic cells in vitro. Since PTH(1-34) activates both Adenylate Cyclase/Protein Kinase A (AC/PKA) and Protein Kinase C (PKC) downstream of the PTH1R in osteoblastic cells, we independently determined the effect of either pathway on Jagged1. Activation of AC with Forskolin or PKA with PTH(1-31) or cell-permeable cAMP analogues increased osteoblastic Jagged1. This PTH-dependent Jagged1 increase was blocked by H89 and PKI, specific PKA inhibitors. In contrast, PKC activation with phorbol ester (PMA) or PTH(13-34) did not stimulate Jagged1 expression, and PTH-dependent Jagged1 stimulation was not blocked by Gö6976, a conventional PKC inhibitor. Therefore, PTH treatment stimulates osteoblastic Jagged1 mainly through the AC/PKA signaling pathway downstream of the PTH1R. Since Jagged1/Notch signaling has been implicated not only in stromal-HSC interactions but also in osteoblastic differentiation, Jagged1 may play a critical role in mediating the PTH-dependent expansion of HSC, as well as the anabolic effect of PTH in bone.