Prevalence of Anticholinergic Medication Use in the Program of All-Inclusive Care for the Elderly.

OBJECTIVES: Evaluate the prevalence of anticholinergic medication use in the Program of All-Inclusive Care for the Elderly (PACE). DESIGN: Cross-sectional, retrospective chart review. SETTING: The Basics at Jan Werner PACE, Amarillo, Texas. PARTICIPANTS: PACE participants (n = 128) and long-term care residents (n = 105) 65 years of age and older. MAIN OUTCOME MEASURE: The primary outcome was percentage of prescribed medications with anticholinergic properties and risk factors associated with prescribing: study site, gender, race, age, and creatinine clearance. RESULTS: Anticholinergic medication prescribing was significantly lower in the PACE program (2.3% of total medications vs. 3.9%; P < 0.05) as well as total medication use (12.1 medications per subject vs. 20.8; P < 0.05 in the long-term care environment). Only the long-term care study site had a significant association with anticholinergic prescribing (odds ratio = 5.04, confidence interval 2.71-9.38). PACE participants also had lower Anticholinergic Risk Scale scores (score of 0, 60.2% PACE vs. 16.2%), reduced fall rates (23.8 per month PACE vs. 66.9), and similar hospitalization rates (5.4 per month PACE vs. 5.7). CONCLUSION: PACE participants were prescribed fewer medications and had lower anticholinergic burden, which potentially lowers their risk of adverse effects. These data support the PACE interdisciplinary model by demonstrating the benefit of team care in appropriate use of medications. It provides a potential blueprint to organizations aimed at reducing potentially inappropriate medication prescribing in older adults.

The influence of metastatic site on the expression of CEA and cellular localization of ß-catenin in colorectal cancer.

BACKGROUND AND AIM: The usefulness of carcinoembryonic antigen (CEA) in the diagnosis and prognosis of colorectal cancer (CRC) is unclear. The aim was to analyze changes in the expression of CEA during CRC progression and metastasis, so as to determine the influence of tumor metastatic organ on the CEA expression by CRC cells. METHODS: The human biopsies of adenocarcinomas in colon and CRC liver and lung metastases were analyzed by immunohistochemistry for the expression of CEA. Expression of E-cadherin and ß-catenin was also analyzed to localize the CRC neoplastic glands in metastatic tissues. RESULTS: The CRC neoplastic glands in colon and liver expressed significantly higher amount of CEA compared with crypts in normal colon. In contrast, CRC neoplastic glands formed in lung expressed low CEA level. However, CEA expression was high in areas of tumor necrosis in lung. E-cadherin and ß-catenin were cell membrane-bound in normal crypts and CRC neoplastic glands in colon and liver. Although these two proteins were also cell membrane-bound in a majority of CRC neoplastic glands in lungs, a significant proportion of these expressed ß-catenin in the nucleus, which lacked either E-cadherin or ß-catenin at the cell membrane. CONCLUSION: Our findings indicate that lung microenvironment is unique in that it suppresses the expression of CEA by CRC cells forming neoplastic glands. In addition, lung microenvironment promotes nuclear localization of ß-catenin, suggesting that the Wnt signaling pathway is relatively active highly in CRC metastasized to lung, when compared with liver or colon.