Braden scale for pressure ulcer risk predicts rehabilitation placement after pancreatic resection

BackgroundPatients undergoing pancreatic resection frequently require rehabilitation facilities after hospital discharge. We evaluated the predictive role of validated markers of frailty on rehabilitation facility placement to identify patients who may require this service.MethodsSingle-center retrospective cohort study of patients who underwent pancreatic resection from 2010 to 2015. 90-day morbidity and mortality were calculated. Postoperative validated markers of frailty (Activities of Daily Living scale, Braden scale [assesses pressure ulcer risk, lower scores = higher risk] and Morse fall scale) were evaluated via multivariate regression to identify predictors of discharge to rehabilitation facility.Results470 patients with complete data were included. Mean age was 62 and 49.2% were male. Postoperative median length of stay (LOS) was 8 (IQR 7–10). 92 (19.66%) patients were discharged to rehabilitation facilities and 138 (29.49%) patients were readmitted within 90 days. On multivariate analysis, age, sex, LOS > 8 days, inpatient Comprehensive Complication Index (CCI) and initial Braden scale were predictive of rehabilitation placement.ConclusionA marker of frailty routinely collected daily by nursing staff, the Braden scale, is available to help surgeons predict the need for postoperative rehabilitation placement after pancreatic resection. Engaging discharge planning services for at-risk patients may help prevent delayed hospital discharge and should be further evaluated.     

HSP60 overexpression increases the protein levels of the p110α subunit of phosphoinositide 3‐kinase and c‐Myc

Heat shock protein 60 (HSP60) is a chaperone protein which plays an essential role in facilitating the folding of many newly synthesized proteins to reach their native forms. Increased HSP60 expression is observed in various types of human cancers. However, proteins induced by HSP60 to mediate transformation remain largely unknown. Here we show that HSP60 overexpression increases the protein levels of the p110α subunit of phosphoinositide 3‐kinase (PI3K). The amino acid domain 288‐383 of HSP60 is used to increase the protein levels. Overexpression of HSP60 also induces the levels of phosphorylated Akt. In addition, the amino acid domain 288‐383 of HSP60 is used to induce c‐Myc expression. Finally, a mono‐ubiquitinated form of β‐catenin has a higher activity to activate β‐catenin downstream targets compared to wild‐type β‐catenin. These results indicate that HSP60 overexpression induces the levels or activity of multiple oncogenic proteins to mediate transformation.     

Association of arterial calcification with chronic limb ischemia in patients with peripheral artery disease

Objective

Arterial calcification is associated with an increased risk of limb events, including amputation. The association between calcification in lower extremity arteries and the severity of ischemia, however, has not been assessed. We thus sought to determine whether the extent of peripheral artery calcification (PAC) was correlated with Rutherford chronic ischemia categories and hypothesized that it could independently contribute to worsening limb status.

Malignant lymphoma and erythrophagocytosis simulating malignant histiocytosis

Six patients with malignant lymphoma are described, in whom a syndrome that mimicked malignant histiocytosis clinically and pathologically developed as a terminal event. The clinical course was characterized by hepatosplenomegaly, fever, and a rapid fall in all hematologic counts. Survival from onset of this syndrome was less than six weeks. Pathologically, activation of benign histiocytes with marked erythrophagocytosis was seen throughout the reticuloendothelial system. Disseminated lymphoma was also evident but was grossly and microscopically segregated from the erythrophagocytic process. Immunologic and cytochemical studies in two cases indicated the lymphomas to be of peripheral T cell origin, whereas the phagocytic cells had markers characteristic of histiocytes. A likely mechanism for this syndrome is the production of lymphokines (macrophage-activating factors) by neoplastic T lymphocytes.     

Diagnosis and treatment of tuberculous pleural effusion in 2006

Tuberculous (TB) pleural effusion occurs in approximately 5% of patients with Mycobacterium tuberculosis infection. The HIV pandemic has been associated with a doubling of the incidence of extrapulmonary TB, which has resulted in increased recognition of TB pleural effusions even in developed nations. Recent studies have provided insights into the immunopathogenesis of pleural TB, including memory T-cell homing and chemokine activation. The definitive diagnosis of TB pleural effusions depends on the demonstration of acid-fast bacilli in the sputum, pleural fluid, or pleural biopsy specimens. The diagnosis can be established in a majority of patients from the clinical features, pleural fluid examination, including cytology, biochemistry, and bacteriology, and pleural biopsy. Measurement of adenosine deaminase and interferon-gamma in the pleural fluid and polymerase chain reaction for M tuberculosis has gained wide acceptance in the diagnosis of TB pleural effusions. Although promising, these tests require further evaluation before their routine use can be recommended. The treatment of TB pleural effusions in patients with HIV/AIDS is essentially similar to that in HIV-negative patients. At present, evidence regarding the use of corticosteroids in the treatment of TB pleural effusion is not clear-cut.     

Inhibition of BTK and PI3Kδ impairs the development of human JMML stem and progenitor cells

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Long-term effects of nasal continuous positive airway pressure therapy on cardiovascular outcomes in sleep apnea syndrome

BACKGROUND: Obstructive sleep apnea syndrome (OSAS) has been associated with increased morbidity and mortality, principally from cardiovascular disease, but the impact of nasal continuous positive airway pressure (CPAP) therapy is unclear. METHODS: We performed a long-term follow-up study of 168 patients with OSAS who had begun receiving CPAP therapy at least 5 years previously, most of whom had been prospectively followed up, having been the subject of an earlier report on cardiovascular risk factors in OSAS patients. The average follow-up period was 7.5 years. We compared the cardiovascular outcomes of those patients who were intolerant of CPAP (untreated group, 61 patients) with those continuing CPAP therapy (107 patients). RESULTS: CPAP-treated patients had a higher median apnea-hypopnea index score than the untreated group (48.3 [interquartile range (IQR), 33.6 to 66.4] vs 36.7 [IQR, 27.4 to 55], respectively; p = 0.02), but age, body mass index, and time since diagnosis were similar. Deaths from cardiovascular disease were more common in the untreated group than in the CPAP-treated group during follow-up (14.8% vs 1.9%, respectively; p = 0.009 [log rank test]), but no significant differences were found in the development of new cases of hypertension, cardiac disorder, or stroke. Total cardiovascular events (ie, death and new cardiovascular disease combined) were more common in the untreated group than in the CPAP-treated group (31% vs 18%, respectively; p < 0.05). CONCLUSIONS: The data support a protective effect of CPAP therapy against death from cardiovascular disease in patients with OSAS.