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In the current healthcare environment, there is an increasing consensus for a holistic approach to the patient by means of a bio-psychosocial and spiritual model. The first part of this article describes how, in the context of a laic healthcare environment, physicians, nurses and spiritual caregivers are asked to change their way to communicate and to take into account this spiritual dimension. In the second part we will discuss some of the challenges of this interdisciplinary approach of the spiritual dimension in the hospital and the community. We will describe potential benefits for the patients, their family members and the caregivers. At the end, taking into account the spiritual dimension of the patient without proselytism will depend on the capacity of each caregiver to speak about it and to share this information in multidisciplinary team.

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Trust is essential to foster and preserve a long-term relationship between primary care physicians and their patients suffering from chronic diseases. However, this relation remains insufficient to successfully manage more complex situations, such as those of older patients with multiple diseases and disability. For the primary care physician, a significant limitation is the time required to plan and coordinate interventions supplied by different health and social care providers. This article describes a structured approach to support primary care physicians in this difficult task and help them to identify vulnerable older patients requiring to mobilize and coordinate health and social care resources. Current and future resources available to family physicians to complete this challenging task are further described.

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As population ages, a growing number of older patients present the constellation of diabetes and dementia. Numerous recent studies highlight that diabetes may increase the risk for Alzheimer and vascular dementia. Among patients with previous severe hypoglycemia, that risk may even double. Inversely demented patients have about three times higher risk of hypoglycemia. Given that spiral link between hypoglycemia and dementia, the latter should be considered as a possible complication of diabetes and consistently be screened for among older diabetic patients. Furthermore, the American Diabetes Association and American Geriatric Society consensus recommends a more flexible glycemic treatment goal of AIC among demented patients, with a target range between 8 and 9%.

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Age-related physiological changes and comorbidities affect older patients' tolerance to surgery. Pre-operative assessment in these patients requires, beside the usual physical evaluation, the systematic screening of common geriatric syndromes. Cognitive, gait and balance, nutritional, and functional impairments, all flag patients at higher risk for per- and postoperative complications. Preoperative assessment is an opportunity to detect these syndromes and propose preventative interventions (physical therapy, nutritional and cognitive support measures) likely to reduce the incidence of postoperative morbidity.

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2012 brought additional evidence regarding the benefits of exercise in older persons in showing morbidity compression in those most active. Several studies invite to revise therapeutic targets in older diabetics, especially those with cognitive impairment or dementia where a value of 8 to 9% for HbAlc might be a good compromise. On the dementia side, a study suggests that biological and structural abnormalities associated with Alzheimer's disease might occur as early as 25 years before its first clinical manifestations. On the therapeutic side, ginkgo and the double therapy with memantine and donepezil did not make it in RCTs, and two studies about treatments for behavioral symptoms of dementia showed that interruption could be deleterious.

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In 2011, new tools to evaluate life expectancy are available. Controversy about PSA-based screening for prostate cancer is still going on, with new data from the US Preventive services task force. A brief behavioral treatment for insomnia can be efficient and durable. Gliptines are be useful to avoid treatment-induced hypoglycemia in diabetic patients. New Alzheimer diagnostic criteria, including biomarkers, have been published.

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In gram-negative bacteria, the outer membrane lipopolysaccharide is the main component triggering cytokine release from peripheral blood mononuclear cells (PBMCs). In gram-positive bacteria, purified walls also induce cytokine release, but stimulation requires 100 times more material. Gram-positive walls are complex megamolecules reassembling distinct structures. Only some of them might be inflammatory, whereas others are not. Teichoic acids (TA) are an important portion (> or =50%) of gram-positive walls. TA directly interact with C3b of complement and the cellular receptor for platelet-activating factor. However, their contribution to wall-induced cytokine-release by PBMCs has not been studied in much detail. In contrast, their membrane-bound lipoteichoic acids (LTA) counterparts were shown to trigger inflammation and synergize with peptidoglycan (PGN) for releasing nitric oxide (NO). This raised the question as to whether TA are also inflammatory. We determined the release of tumor necrosis factor (TNF) by PBMCs exposed to a variety of TA-rich and TA-free wall fragments from Streptococcus pneumoniae and Staphylococcus aureus. TA-rich walls from both organisms induced measurable TNF release at concentrations of 1 microg/ml. Removal of wall-attached TA did not alter this activity. Moreover, purified pneumococcal and staphylococcal TA did not trigger TNF release at concentrations as high as > or =100 microg/ml. In contrast, purified LTA triggered TNF release at 1 microg/ml. PGN-stem peptide oligomers lacking TA or amino-sugars were highly active and triggered TNF release at concentrations as low as 0.01 microg/ml (P. A. Majcherczyk, H. Langen, et al., J. Biol. Chem. 274:12537-12543,1999). Thus, although TA is an important part of gram-positive walls, it did not participate to the TNF-releasing activity of PGN.

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We investigated prospectively 9 adult patients with the syndrome of jaundice complicating severe extrahepatic infection both clinically and by quantitative liver function tests. Five patients having severe extrahepatic infection without jaundice were used for comparison. Intraperitoneal infection was found to be a major risk factor for development of jaundice. Jaundice was mainly associated with gram-negative infection, but did not influence survival. Duration of jaundice was dependent on control of the underlying infection. Liver function tests showed a severely deranged organic anion transport, whereas synthetic, cytosolic, and microsomal functions remained preserved. Our study shows that (a) the syndrome of jaundice associated with extrahepatic infection is a functional disorder that is reversible upon control of infection, and that (b) cytosolic, synthetic, and microsomal function is preserved. This may have consequences for both assessing prognosis and clinical management.

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Fifty-two patients with postoperative sepsis were studied by abdominal and pelvic computerized tomography (CT) for the presence and location of septic foci. CT mapping of infected fluid collections had direct therapeutic consequences as it allowed the selection of patients for percutaneous drainage, local operative drainage or relaparotomy. As soon as sepsis is suspected, an abdominal and pelvic CT study should be performed so that therapeutic procedures may be carried out at a stage at which no organ is yet failing, that is, in a period of lowest mortality.

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Plasma fibronectin has been postulated to be an essential mediator of normal reticuloendothelial system (RES) function. The acute depletion of fibronectin is thought to impair RES function, whereas its repletion in states of deficiency has been reported to improve RES function. In vitro studies have documented fibronectin's ability to bind to some nonbacterial microaggregates and to promote the phagocytosis of bound targets by the RES. These properties may, however, be influenced by the in vivo milieu. There is substantial evidence for a parallelism between RES function and plasma fibronectin levels following blunt trauma in animal models; however, this association is not seen in experimentally induced intravascular coagulation, acute inflammation, and sepsis. Clinically, subnormal fibronectin levels are clearly associated with the triad of intravascular coagulation, organ failure and sepsis. Fibronectin is, however, not the only plasma protein reduced in these patients, nor is it an outstanding predictor of such complications. The therapeutic efficacy of fibronectin administration remains controversial. Whereas initial reports suggested therapeutic benefits of fibronectin-enriched cryoprecipitates, subsequent studies have produced negative results. Prospective, randomized, controlled clinical trials with purified fibronectin are needed before fibronectin should be recommended as an adjunct to the established principles of intensive care.

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Plasma Fibronectin (Fn) has been viewed as an essential opsonic mediator of the clearance function of the reticuloendothelial system (RES). An acute depletion of Fn would thus weaken the RES defense potential, which could be restored by Fn repletion. This concept, which was developed by Saba, has attracted considerable attention. Upon closer inspection, however, it turns out to be more complex and less clear cut than is commonly appreciated. The recent interest of acute care physicians is focussed on the behaviour of Fn during intravascular coagulation, organ failure, and sepsis. However, the informative content of plasma Fn levels in this setting is limited, too. The behaviour of Fn is only one part of a broader plasma protein "depletion and recovery syndrome" and therapeutic effects of Fn repletion have as yet not been adequately documented by controlled clinical trials. The use of plasma fibronectin as a part of intensive care is therefore premature, and the concept underlying its use requires further investigation.

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Subnormal plasma fibronectin (Fn) levels are found in patients with severe abdominal infections (SAI). The repletion of Fn has been postulated to have therapeutic benefit by virtue of its opsonic, reticuloendothelial system (RES) stimulating effects. A controlled, prospective trial of Fn administration was performed in patients with SAI to assess its use as an adjunct to standard procedures of intensive care. Thirty-three SAI patients were given daily doses of 0.8 g of purified Fn on days 1-5 following admission to the ICU, whereas 34 control patients received no Fn. All patients received the clinical care, antibiotics, and pharmacologic agents appropriate to their individual needs. The admission status and laboratory profiles of the two patient groups (+ and -Fn) were comparable on admission to the study. No side effects of the Fn preparation were observed. As judged by subgroup averages, the Fn replacement regimen was effective in elevating Fn levels to within normal range from day 2 onwards, as measured by immunological and functional assays. The estimated intravascular recovery of Fn averaged 82% in those patients who survived, yet only 52% in the nonsurvivors. Ultimate hospital mortality was 9/33 (27.3%) in the +Fn group versus 13/34 (38.2%) in the -Fn group (p = 0.244, Fisher's exact test). Although ultimate mortality was not significantly changed by the administration of Fn, the Fn treated patients appeared to survive longer than did the control patients. This trend was confirmed through the analysis of expected survival curves (D = 3.12, 0.1 greater than p greater than 0.05). When compared to the survivors, the ultimate nonsurvivors entered the study with statistically higher group averages of bilirubin and creatinine concomitant with lower averages of Fn, antithrombin III, C4, C3, C3b-INH, and transferrin. These differences persisted throughout the 11-day monitoring period; differences between survivors and nonsurvivors with respect to platelets, plasminogen, B-1-H, alpha-2-macroglobulin, and prealbumin appeared during the same period. Dramatic differences between the +Fn and -Fn treatment groups were not seen. Other than Fn, the Fn recipients only developed higher levels of the acute phase reactants C4, C3b-INH, B-1-H and alpha-1-antitrypsin (p less than 0.05) than did their non-Fn treated counterparts. In the present study, we again found a highly significant pattern of correlations between the absolute levels as well as the changes of Fn and other plasma proteins.(ABSTRACT TRUNCATED AT 400 WORDS)

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An acute depletion of plasma fibronectin or FN has been observed in critically ill, surgical, or trauma patients, but there is little information on the relationships between FN levels and the final outcome in such cases, and on the simultaneous behaviour of other serum proteins. The daily values of FN, antithrombin III, IgG, C3, prealbumin, and transferrin were monitored in 98 intensive care patients after major elective surgery or trauma. According to their clinical course, they were divided retrospectively into three groups. Group A (33 patients) had sepsis. Group B (31 patients) had nonseptic complications, and group C (34 patients) had no complications in the ICU. The individual, nadir levels of FN, AT III, prealbumin, and transferrin were lower (p less than 0.01) in the septic group A than in B and C. Within the septic group, the nadir levels of AT III, but not those of FN, were lower (p less than 0.01) in the 14 nonsurvivors than in the 19 survivors. The FN and AT III levels had returned at least temporarily to the normal range in the six ultimate fatalities from sepsis who survived for more than two weeks. In the septic group, transferrin showed the highest percentages of actually subnormal levels and differed from FN in this respect with p less than 0.05. Furthermore, all six proteins showed a significant overall pattern (p less than 0.01) of parallel variations. The results confirm other reports on the behavior of fibronectin in septic patients as a group, but it was not informative as to the individual outcome, and its reduction might be viewed as part of a general plasma protein depletion associated with acute septic disease. This pattern is probably attributable to a combination of intravascular consumption and an overall excess of protein catabolism over synthesis.

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