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1.

Objective

The objective of this study is to identify factors predicting intensive care unit (ICU) mortality in cancer patients admitted to a medical ICU.

Patients and methods

We conducted a retrospective study in 162 consecutive cancer patients admitted to the medical ICU of a 1000-bed university hospital between January 2009 and June 2012. Medical history, physical and laboratory findings on admission, and therapeutic interventions during ICU stay were recorded. The study end point was ICU mortality. Logistic regression analysis was performed to identify independent risk factors for ICU mortality.

Results

The study cohort consisted of 104 (64.2%) patients with solid tumors and 58 patients (35.8%) with hematological malignancies. The major causes of ICU admission were sepsis/septic shock (66.7%) and respiratory failure (63.6%), respectively. Overall ICU mortality rate was 55 % (n = 89). The ICU mortality rates were similar in patients with hematological malignancies and solid tumors (57% vs 53.8%; P = .744). Four variables were independent predictors for ICU mortality in cancer patients: the remission status of the underlying cancer on ICU admission (odds ratio [OR], 0.113; 95% confidence interval [CI], 0.027-0.48; P = .003), Acute Physiology and Chronic Health Evaluation II score (OR, 1.12; 95% CI, 1.032-1.215; P = .007), sepsis/septic shock during ICU stay (OR, 8.94; 95% CI, 2.28-35; P = .002), and vasopressor requirement (OR 16.84; 95% CI, 3.98-71.24; P = .0001). Although Acute Physiology and Chronic Health Evaluation II score (OR, 1.30; 95% CI, 1.054-1.61; P = .014), admission through emergency service (OR, 0.005; 95% CI, 0.00-0.69; P = .035), and vasopressor requirement during ICU stay (OR, 140.64; 95% CI, 3.59-5505.5; P = .008) were independent predictors for ICU mortality in patients with hematological malignancies, Sequential Organ Failure Assessment score (OR, 1.83; 95% CI, 1.29-2.6; P = .001), lactate dehydrogenase level on admission (OR, 1.002; 95% CI, 1-1.005; P = .028), sepsis/septic shock during ICU stay (OR, 138.4; 95% CI, 12.54-1528.4; P = .0001), and complete or partial remission of the underlying cancer (OR, 0.026; 95% CI, 0.002-0.3; P = .004) were the independent risk factors in patients with solid tumors.

Conclusion

Intensive care unit mortality rate was 55% in our cancer patients, which suggests that patients with cancer can benefit from ICU admission. We also found that ICU mortality rates of patients with hematological malignancies and solid tumors were similar.  相似文献   
2.
Our aim was to determine whether N-terminal pro-B-type natriuretic peptide (NT-pro-BNP) and cardiac troponin I (cTnI) levels are valuable for predicting prognosis in patients with infective endocarditis (IE). We analyzed measured plasma NT-pro-BNP levels at admission in 45 patients with definite IE. The primary end point was early surgery or in-hospital death. The other data recorded were baseline clinical, echocardiographic, and laboratory parameters. Thirty patients underwent early surgery, and 9 died in hospital. Univariate analysis revealed that log NT-pro-BNP, cTnI > or =0.03 ng/ml, New York Heart Association functional class III to IV symptoms, left atrial diameter, left ventricular end-diastolic diameter, left ventricular end-systolic diameter, and severe valvular regurgitation were associated with increased risk of reaching the primary end point. Cox proportional hazard regression analysis identified log NT-pro-BNP (hazard ratio 1.5; 95% confidence interval 1.2 to 1.9, p <0.001) as the only independent predictor of the primary end point. The log NT-pro-BNP cut-off value with the highest sensitivity (97%) and specificity (92%) for predicting primary end point was 7.2 (1,500 pg/ml). Patients with NT-pro-BNP level > or =1,500 pg/ml had significantly lower event-free survival than others. In conclusion, admission NT-pro-BNP is of prognostic value in patients with IE. The combination of admission NT-pro-BNP and cTnI levels appears to have even greater value for risk stratification in this patient group.  相似文献   
3.
4.
BACKGROUND/AIMS: Apoptotic and anti-proliferative effects of heparin on a number of cancers have been described. There have been no studies analyzing the effect of heparin on human hepatoma cells. The aim of this study was to investigate the effect of heparin on human hepatoma cell line, HepG2. METHODOLOGY: HepG2 cell line was cultured with different concentrations of heparin. Colony count, viability assay, percentage of the apoptosis and proliferative index were assessed at the end of the 7th day. Trypan blue was used to assess viability. Apoptosis and proliferative indexes were assessed by flow-cytometry. RESULTS: Hepatoma cells were arrested at the G0/G1 phase with heparin incubation and proliferative indexes decreased significantly in 20, 40 and 80 U/mL of heparin concentrations in comparison with the control (36 +/- 1%, 30 +/- 5% and 29 +/- 8% vs. 44 +/- 1%, p < 0.01). Flow cytometry revealed a statistically significant increase in apoptosis in groups incubated with 40 and 80 U/mL of heparin in comparison with the control (39 +/- 26% and 58 +/- 18% vs. 0.83 +/- 1.3%, p < 0.01). Colony counts per well and viable cells per microL decreased significantly in 80 U/mL of heparin. CONCLUSIONS: Heparin leads to a significant anti-proliferative and an apoptotic effect on human hepatoma cells in vitro.  相似文献   
5.
Neural regeneration research is designed in part to develop strategies for therapy after nerve damage due to injury or disease. In this study, a new gelatine‐based biomimetic scaffold was fabricated for brain tissue engineering applications. A technique combining thermally induced phase separation and porogen leaching was used to create interconnected macropores and nanofibrous structure. To promote tissue regeneration processes, the scaffolds were integrated with nerve growth factor (NGF)‐loaded alginate microspheres. The results showed that nanofibrous matrix could only be obtained when gelatine concentration was at least 7.5% (w/v). The scaffold with a modulus value (1.2 kPa) similar to that of brain tissue (0.5–1 kPa) was obtained by optimizing the heat treatment time, macropore size and gelatine concentration. The encapsulation efficiencies of NGF into 0.1% and 1% alginate microspheres were 85% and 100%, respectively. The release rate of NGF from the microspheres was controlled by the alginate concentration and the poly(L‐lysine) coating. The immobilization of the microspheres in the scaffold reduced burst release and significantly extended the release period. The nanofibrous architecture and controlled release of NGF from the microspheres induced neurite extension of PC12 cells, demonstrating that the released NGF was in an active form. The results suggest that the scaffolds prepared in this study may have potential applications in brain tissue engineering due to topologic and mechanical properties similar to brain tissue and pore structure suitable for cell growth and differentiation. Copyright © 2016 John Wiley & Sons, Ltd.  相似文献   
6.
Some automated systems used in clinical microbiology laboratories are able to detect products responsible for antimicrobial resistance. In this study, 626 isolates (436 Escherichia coli, 134 Klebsiella pneumoniae and 56 Klebsiella oxytoca strains) were examined for the presumptive detection of extended-spectrum beta-lactamase (ESBL) production by 2 methods: the Sceptor system (BD, Sparks, MD, USA) and the E-test. ESBL production was detected in 26 E. coli strains (5.96%), 60 K. pneumoniae strains (44.77%) and 15 K. oxytoca strains (26.78%) by ceftazidime/ceftazidime-clavulanate E-test. Using the E-test, ESBL production was detected in 25 of 201 E. coli strains (12.43%), 55 of 75 K. pneumoniae (73.33%) and 14 of 27 K. oxytoca strains (51.85%) that were alerted as ESBL-producing strains by the Sceptor system. ESBL positivity was detected in 1 E. coli, 5 K. pneumoniae and 1 K. oxytoca strains, that were not warned as being ESBL producers by the Sceptor system. These data suggest that clinical microbiology laboratories should not only rely on these rapid automated systems but also use another method for screening ESBL producers, such as the E-test. The rates of these ESBL-producing isolates in this study were lower than those in other studies reported from other parts of Turkey, but higher than those reported from the USA and Europe.  相似文献   
7.
8.
Previous studies showed a link between systemic lupus erythematosus (SLE) and Epstein-Barr virus (EBV) infection. We sought to determine the features of serologic response to EBV in SLE patients and whether this response differs from those of systemic sclerosis (SSc) and primary antiphospholipid syndrome (PAPS) patients as well as healthy individuals. Sera from 198 consecutive SLE patients have been tested to detect IgG antibodies to EA/D, EBNA-1, VCA P18 and for comparison, cytomegalovirus (CMV) using commercially available ELISA kits (Trinity Biotech, USA). Forty-six SSc patients and 38 PAPS patients were enrolled as diseased control groups and sixty-five individuals as healthy controls. Significantly more SLE (54%, P?=?0.001, OR 5.77, 95% CI 2.8?C11.6), SSc (41.3%, P?=?0.005, OR 3.4, 95% CI 1.4?C8.2) and PAPS sera (36.8%, P?=?0.023, OR 2.86, 95% CI 1.14?C7.22) reacted against EA/D than healthy controls (16.9%). The mean age of anti-EA/D-positive SLE patients was significantly higher, and their disease duration was longer compared to anti-EA/D-negative SLE patients (41 ± 14 vs. 33.8 ± 10.8?years, P?<?0.001 and 100 ± 73 vs. 71 ± 62?months, P?=?0.003). In SLE patients, EA/D reactivity was associated with Raynaud??s phenomenon and the presence of any anti-ENA antibodies. Although it did not reach a statistical significance, anti-EBNA-1 reactivity was slightly lower in patients with SLE. The frequency of anti-CMV Ig G positivity was found significantly higher in SLE patients (100%) when compared to patients with SSc (95.7%), PAPS (94.7%) and healthy controls (95.4%) (P?=?0.035, P?=?0.025 and P?=?0.015 respectively). Our results support the proposed link between EBV and SLE. The finding that SSc and PAPS patients also have increased frequency of anti-EA/D response has revealed that this immune interaction may not be unique to patients with SLE, and there may be a common mechanism involving EBV in these autoimmune diseases.  相似文献   
9.
Familial Mediterranean fever is an autosomal recessive disease characterized by recurrent self-limited attacks of fever accompanied by peritonitis, pleuritis, and arthritis. Approximately 5% of individuals with familial Mediterranean fever have been reported to have Henoch–Schonlein purpura and about 1% to have polyarteritis nodosa. A 7-year-old girl presenting with complaints of purpuric rash, abdominal pain, arthritis, hematuria, and proteinuria and having IgA depositions on renal biopsy was diagnosed as Henoch–Schönlein nephritis. She had a history of recurrent fever, abdominal and joint pain and M694 V compound homozygote mutation. Colchicine treatment was started for the diagnosis of FMF. When constitutional symptoms such as myalgia, weight loss, fatigue, fever, and hypertension were added to the clinical picture, the diagnosis of polyarteritis nodosa HSP was thought and confirmed by the demonstration of microaneurisms on renal arteries. There was no response to corticosteroid and cyclophosphamide treatments; however, the symptoms were rapidly and dramatically reduced after the administration of intravenous immunoglobulin. In conclusion, polyarteritis nodosa and Henoch–Schonlein purpura can be seen together with familial Mediterranean fever. It is also suggested that IVIG might be an important adjunct therapy in selected patients with polyarteritis nodosa, especially in the lack of response to steroids and immunsuppressive drugs.  相似文献   
10.

OBJECTIVES:

Acute ST-elevation myocardial infarction is associated with ventricular dysfunction due to ischemia-induced progressive myocardial damage. The decrease in ventricular compliance causes left atrial dilatation and stretching of the atrial myocardium, which are the main stimuli for the secretion of atrial natriuretic peptide. The aim of this study was to evaluate left atrial dimensions and atrial natriuretic peptide levels in patients early after their first acute ST-elevation myocardial infarction and assess the probable interaction between coronary lesions and these measurements.

METHODS:

A total of 110 patients with acute myocardial infarction and 50 controls were studied. Plasma atrial natriuretic peptide was measured at admission. Left ventricular function, diameter, and volume index were evaluated using transthoracic echocardiography. Gensini and vessel scores of the patients who underwent coronary angiography were calculated.

RESULTS:

Plasma atrial natriuretic peptide in the patients with myocardial infarction was increased compared with that in controls (3.90±3.75 vs. 1.35±0.72 nmol/L, p<0.001). Although the left atrial diameter was comparable in patients and controls, the left atrial volume index was increased in patients with acute myocardial infarction (26.5±7.1 vs. 21.3±4.9 mL/m2, p<0.01). Multivariate regression analysis showed a strong independent correlation between the left atrial volume index and the plasma atrial natriuretic peptide level (β = 0.23, p = 0.03).

CONCLUSIONS:

The left atrial volume index and plasma atrial natriuretic peptide level were correlated in patients with acute myocardial infarction.  相似文献   
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