[Association between lymphopenia of elderly patients and intrahospital mortality in a geriatric acute care unit]. / Association entre lymphopénie et mortalité chez les sujets âgés admis en unité de médecine aiguë gériatrique.

UNLABELLED: Age-related immune impairment may be one of the factors influencing successful and pathological aging, being strongly tied to nutritional status. Several long term cohort studies suggest that a lower total lymphocyte count is associated with higher mortality. Nevertheless, prevalence, incidence and impact of lymphopenia on frailty and prediction of pathological events have not been described extensively. The principal aim of this study was to examine the relation of lymphopenia and intra-hospital mortality in the elderly. MATERIALS AND METHOD: This cohort study has been carried out in a geriatric acute care unit of the Grenoble University hospital in France. Clinical and biological data have been retrospectively retrieved from the electronic medical record of each patient. All patients aged 75 or older admitted in the unit from May to October 2011 were eligible for inclusion. A lymphocyte count was obtained within 48h hours before or after admission. RESULTS: 239 patients were included. Mean age (SD) was 87.04(5.50) years, 82(34.3%) patients were men, median ADL (activities of daily living) score prior to hospitalization was 4 (Q1:2; Q3:6). 31(13%) patients died during their admission. A lympocyte's threshold of 1,100cells/µL establishes a sensitivity of 79.3%, a specificity of 57.2%, a positive predictive value (PV+) of 21.7%, as well as a negative predictive value (PV-) of 94.9%. The OR was 3.44(IC95%, [(1.54-8.10]). The AL's threshold was found to be 3g/dL, establishing a sensitivity of 79.3%, a specificity of 62.0%, a PV+ of 22.8%, PV- of 95.5%. The OR was 4.90(IC 95%, [(2.17-11.87]). In multivariate analysis, LC and AL were significantly predicting in hospital death (OR=2.80 IC95% [(1.18-7.02] p=0.02, OR=3.34 (IC95%, [(1.41 -8.36]) p=0.007 respectively). CONCLUSION: This observational study carried out with malnourished, functionally impaired older inpatients with multiple comorbidities shows that lymphopenia independentely predicts intra-hospital mortality. In multivariate analysis lymphocyte count and albumin level independently predict intra-hospital mortality in with a similar predictive performance. Low albumin levels have previously been shown to be an independent risk factor for all-cause mortality in community-dwelling older persons as well as to predict intra-hospital mortality. However in our study we included patients with an acute condition and multiple comorbidities, potentially confounding the relation between lymphopenia and mortality. Lymphopenia may be an interesting marker of frailty and prognosis in very elderly people presenting an acute condition.

Finances in the older patient with cognitive impairment: "He didn't want me to take over".

Financial capacity can be defined as the ability to independently manage one's financial affairs in a manner consistent with personal self-interest. Financial capacity is essential for an individual to function independently in society; however, Alzheimer disease and other progressive dementias eventually lead to a complete loss of financial capacity. Many patients with cognitive impairment and their families seek guidance from their primary care clinician for help with financial impairment, yet most clinicians do not understand their role or know how to help. We review the prevalence and impact of diminished financial capacity in older adults with cognitive impairment. We also articulate the role of the primary care clinician, which includes (1) educating older adult patients and their families about the need for advance financial planning; (2) recognizing signs of possible impaired financial capacity; (3) assessing financial impairments in cognitively impaired adults; (4) recommending interventions to help patients maintain financial independence; and (5) knowing when and to whom to make medical and legal referrals. Clearly delineating the clinician's role regarding identification of financial impairment could establish for patients and families effective financial protections and limit the economic, psychological, and legal hardships of financial incapacity on patients with dementia and their families.

Comparison of signalling mechanisms involved in rat mesenteric microvessel contraction by noradrenaline and sphingosylphosphorylcholine.

1 We have compared the signalling mechanisms involved in the pertussis toxin-sensitive and -insensitive contraction of rat isolated mesenteric microvessels elicited by sphingosylphosphorylcholine (SPC) and noradrenaline (NA), respectively. 2 The phospholipase D inhibitor butan-1-ol (0.3%), the store-operated Ca(2+) channel inhibitor SK>F 96,365 (10 microM), the tyrosine kinase inhibitor genistein (10 microM), and the src inhibitor PP2 (10 microM) as well as the negative controls (0.3% butan-2-ol and 10 microM diadzein and PP3) had only little effect against either agonist. 3 Inhibitors of phosphatidylinositol-3-kinase (wortmannin and LY 294,002, 10 microM each) or of mitogen-activated protein kinase kinase (PD 98,059 and U 126, 10 microM each) did not consistently attenuate NA- and SPC-induced contraction as compared to their vehicles or negative controls (LY 303,511 or U 124). 4 The phospholipase C inhibitor U 73,122 (10 microM) markedly inhibited the SPC- and NA-induced contraction (70% and 88% inhibition of the response to the highest NA and SPC concentration, respectively), whereas its negative control U 73,343 (10 microM) caused only less than 30% inhibition. 5 The rho-kinase inhibitors Y 27,632 (10 microM) and fasudil (30 microM) caused a rightward-shift of the NA concentration-response curve by 0.7-0.8 log units and reduced the response to 10 microM SPC by 88% and 83%, respectively. 6 These data suggest that SPC and NA, while acting on different receptors coupling to different G-protein classes, elicit contraction of rat mesenteric microvessels by similar signalling pathways including phospholipase C and rho-kinase.