scholarly journals Independent risk factors predicting acute graft rejection in cardiac transplant recipients treated by triple drug immunosuppression

1989 ◽  
Vol 98 (6) ◽  
pp. 1113-1121 ◽  
Author(s):  
Günther Laufer ◽  
Johannes Miholic ◽  
Axel Laczkovics ◽  
Gregor Wollenek ◽  
Christoph Holzinger ◽  
...  
2020 ◽  
Vol 30 (2) ◽  
pp. 111-116
Author(s):  
Shimon Izhakian ◽  
Walter G. Wasser ◽  
Baruch Vainshelboim ◽  
Avraham Unterman ◽  
Moshe Heching ◽  
...  

Background: Leukocytosis (white blood cell count >12 000/µL) in the delayed postoperative period (4-7 days) after lung transplantation is due to diverse etiologies. We aimed to describe the etiologies of delayed postoperative leukocytosis in lung transplant recipients and to evaluate the association of leukocytosis causes with short-term survival. Methods: A retrospective chart review of 274 lung transplantations performed in our institution during 2006 to 2013. Results: Delayed postoperative leukocytosis was seen in 159 (58.0%) of lung transplant recipients. In 57 (35.8%) of them, the etiology of the leukocytosis was not identified. The etiologies of leukocytosis that were identified were infection (n = 39), second surgery, acute rejection (n = 12), primary graft dysfunction (n = 3), multiple etiologies (n = 17), and other causes (n = 10). On multivariate analysis, delayed postoperative leukocytosis was one of the variables that most significantly associated with decreased survival in the entire sample (hazard ratio [HR] = 1.52, 95% confidence interval [CI]: 1.01-2.29, P = .040). On additional analysis for mortality assessing each leukocytosis subgroup, the data were acute graft rejection (HR = 8.21, 95% CI: 4.09-16.49, P < .001), second surgery (HR = 2.05, 95% CI: 1.08-3.90, P = .020), primary graft dysfunction (HR = 2.72, 95% CI: 0.65-11.33, P = .169), other causes (HR = 1.30, 95% CI: 0.47-3.62, P = .620), and unknown etiology (HR = 0.94, 95% CI: 0.54-1.62, P = .800). Conclusions: Delayed post-lung transplant leukocytosis is a poor prognostic sign, especially when attributed to acute graft rejection, infection, and multiple etiologies. In the absence of an identifiable etiology, it can be attributed to postoperative reactive stress, is not associated with increased mortality, and likely does not warrant further diagnostic investigation.


2010 ◽  
Vol 51 (2) ◽  
pp. 163-170 ◽  
Author(s):  
P. M. Soccal ◽  
J.‐D. Aubert ◽  
P.‐O. Bridevaux ◽  
J. Garbino ◽  
Y. Thomas ◽  
...  

2010 ◽  
Vol 32 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Christina M. Phelps ◽  
Cecile Tissot ◽  
Shannon Buckvold ◽  
Jane Gralla ◽  
D. Dunbar Ivy ◽  
...  

2013 ◽  
Vol 43 (1) ◽  
pp. 69-85 ◽  
Author(s):  
Mohammad Hossein Karimi ◽  
Sara Hejr ◽  
Bita Geramizadeh ◽  
Saman Nikeghbalian ◽  
Eskandar Kamali-Sarvestani ◽  
...  

2018 ◽  
Vol 69 (7) ◽  
pp. 1192-1197 ◽  
Author(s):  
Maddalena Peghin ◽  
Ibai Los-Arcos ◽  
Hans H Hirsch ◽  
Gemma Codina ◽  
Víctor Monforte ◽  
...  

Abstract Background The relationship between community-acquired respiratory viruses (CARVs) and chronic lung allograft dysfunction (CLAD) in lung transplant recipients is still controversial. Methods We performed a prospective cohort study (2009–2014) in all consecutive adult patients (≥18 years) undergoing lung transplantation in the Hospital Universitari Vall d’Hebron (Barcelona, Spain). We systematically collected nasopharyngeal swabs from asymptomatic patients during seasonal changes, from patients with upper respiratory tract infectious disease, lower respiratory tract infectious disease (LRTID), or acute rejection. Nasopharyngeal swabs were analyzed by multiplex polymerase chain reaction. Primary outcome was to evaluate the potential association of CARVs and development of CLAD. Time-dependent Cox regression models were performed to identify the independent risk factors for CLAD. Results Overall, 98 patients (67 bilateral lung transplant recipients; 63.3% male; mean age, 49.9 years) were included. Mean postoperative follow-up was 3.4 years (interquartile range [IQR], 2.5–4.0 years). Thirty-eight lung transplant recipients (38.8%) developed CLAD, in a median time of 20.4 months (IQR, 12–30.4 months). In time-controlled multivariate analysis, CARV-LRTID (hazard ratio [HR], 3.00 [95% confidence interval {CI}, 1.52–5.91]; P = .002), acute rejection (HR, 2.97 [95% CI, 1.51–5.83]; P = .002), and cytomegalovirus pneumonitis (HR, 3.76 [95% CI, 1.23–11.49]; P = .02) were independent risk factors associated with developing CLAD. Conclusions Lung transplant recipients with CARVs in the lower respiratory tract are at increased risk to develop CLAD.


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