Journal of Critical Care 41 (2017) 161–165

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Journal of Critical Care

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Serum lactate dehydrogenase is predictive of persistent organ failure in

acute pancreatitis
Jing Cui ⁎,1, Jiongxin Xiong 1, Yushun Zhang ⁎, Tao Peng, Min Huang, Yan Lin, Yao Guo,
Heshui Wu, Chunyou Wang
Department of Pancreatic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China

a r t i c l e i n f o a b s t r a c t

Keywords: Purpose: Elevated serum lactate dehydrogenase (LDH) has been reported in a serious of clinical diseases. Howev-
Lactate dehydrogenase er, the relationship between LDH and the incidence of persistent organ failure (POF) in acute pancreatitis (AP)
Acute pancreatitis has not been characterized.
Persistent organ failure Materials and methods: A total of 105 patients with AP who presented within 72 h from symptom onset between
2014 and 2015 were included in this retrospective study. Demographic parameters and laboratory data on ad-
mission were compared between patients with and without POF. Multivariable logistic regression analyses
were utilized to evaluate the prognostic value of LDH for predicting POF.
Results: 21 patients were diagnosed with POF. Compared to non-POF, patients with POF showed a significantly
higher value of serum LDH on admission (741.57 ± 331.72 vs. 296.08 ± 135.73 U/L, P b 0.001). After multivariate
logistic analysis, LDH remained an independent risk factor for POF (Hazard ratio 4.38, 95%CI: 1.42–13.47; P =
0.010). A LDH value of 647 U/L predicted POF with an area under the curve (AUC) of 0.876, a sensitivity with
76.2% and specificity with 98.8%, respectively.
Conclusions: Our results indicate that serum LDH on admission is independently associated with POF in AP and
may serve as a potential prognostic factor.
© 2017 Elsevier Inc. All rights reserved.

1. Introduction
Acute pancreatitis (AP) is an inflammatory disorder characterized by
local and systemic immuno-inflammation, which is observed clinically
as a spectrum ranging from local pancreatitis to systemic inflammatory
response, organ failure (OF) and death. Most patients suffer from a mild,
self-limiting inflammatory derangement, but the remaining will devel-
op a severe disease associated with local or systemic complications and/
or OF [1]. According to 2012 revised Atlanta classification for AP, severe
AP (SAP) has been redefined as AP with persistent OF (OF lasts N48 h)
with a lethality rate of 20–60% [2-6].
Early assessment of disease severity is pivotal for the determination
of therapeutic strategy since effective treatment could significantly de-
crease mortality of patients with severe pancreatitis [7,8]. Lactate dehy-
drogenase (LDH) is a cytoplasmic enzyme that is widely expressed in
tissues. The enzyme converts pyruvate, which is the final product of gly-
colysis, to lactate when oxygen is in short supply [9]. Elevated LDH is ob-
served in disease conditions such as tissue injury, necrosis, hypoxia,
hemolysis or malignancies [10-12]. LDH is clarified as a prognostic
⁎ Corresponding authors.
E-mail addresses: cuijingjj@aliyun.com (J. Cui), zhyshun@hust.edu.cn (Y. Zhang).
1
Jing Cui and Jiongxin Xiong contributed equally to this paper.
factor for severe type of AP (1992 Atlanta criteria), pancreatic necrosis
(PNec), infection and mortality in AP [13-15]. However, the association
underlying LDH and POF in the AP pathophysiology has not been eluci-
dated yet.
2. Materials and methods
2.1. Patients
Consecutive adults (aged 18 years and above) admitted to the Pan-
creatic Disease Institute of Wuhan Union Hospital with a confirmed di-
agnosis of AP between January 2014 and January 2015 were included in
this study. Diagnosis of AP was based on the presence of two or more of
the following three criteria: 1) abdominal pain consistent with AP;
2) serum amylase and/or lipase elevation ≥ three times the upper
limit of normal; and/or 3) computed tomography (CT) findings charac-
teristic of AP [2]. The exclusion criteria included any of the following:
the time from abdominal pain onset to hospital admission ≥ 72 h, age
younger than 18 years, pancreatitis induced by trauma, chronic pancre-
atitis, and unavailable laboratory measurements or medical records.
Laboratory data were obtained from the blood screening test at hospi-
talization. Blood samples were collected within 2 h after hospitalization
and analyzed using an automated clinical chemical analyzer within 6 h

http://dx.doi.org/10.1016/j.jcrc.2017.05.001
0883-9441/© 2017 Elsevier Inc. All rights reserved.
162 J. Cui et al. / Journal of Critical Care 41 (2017) 161–165

of sampling in the same core clinical laboratory in Union Hospital Table 1

(Wuhan, China). LDH levels were measured enzymatically using kits Basic characteristic of AP patients according to LDH level (normal range b 245 U/L).

(Roche Diagnostics, Basel, Switzerland). The reference values of LDH LDH b 245 U/L LDH ≥ 245 U/L P-value
levels with this assay are 109 to 245 U/L. Patients' electronic medical re- No. 39 66
cords and paper charts were reviewed by one independent physician for Age, years 50.92 ± 13.30 47.82 ± 13.37 0.252
information on demographics, physiologic variable, and disease severi- Male gender 22 (56.4%) 40 (60.6%) 0.673
ty. The study was conducted according to the principles of the Declara- Daily drinker 17 (43.6%) 30 (45.5%) 0.853
Current smoker 18 (46.2%) 34 (51.5%) 0.595
tion of Helsinki. Informed consent for individual patient was not
Etiology 0.629
obtained since all data were retrieved retrospectively from the laborato- Biliary 24 (61.5%) 33 (50.0%)
ry test information system without additional blood samples or labora- Alcoholic 8 (20.5%) 20 (30.3%)
tory analysis. The ethics review board of Wuhan Union Hospital Hyperlipidemia 6 (15.4%) 10 (15.2%)
approved this study. Idiopathic 1 (2.6%) 3 (4.5%)
Outcomes
POF 2 (5.1%) 19 (28.8%) 0.003
2.2. Definitions PNec 8 (20.5%) 35 (35.0%) 0.001
In-hospital mortality 0 (0.0%) 6 (9.1%) 0.052

Disease severity was determined according to the revised 2012 At- Abbreviations: AP, acute pancreatitis; ICU, intensive care unit; LDH, lactate dehydroge-
lanta classification [2]. OF was diagnosed when the following cutoffs nase; PNec, pancreatic necrosis; POF, persistent organ failure.
were exceeded: 1) cardiovascular failure if systolic blood pressure was
b90 mm Hg despite fluid replacement; 2) respiratory failure if the
ratio of PaO2/FiO2 was b 300 mm Hg; and 3) renal failure if serum cre- 0.001) and higher (but not significant) in-hospital mortality (9.1% vs.
atinine was ≥ 170 umol/L (1.9 mg/dL). POF was identified if OF lasts 0.0%; P = 0.052).
for N 48 h. PNec was defined as appearance of pancreatic parenchymal
and/or peripancreatic necrosis on CECT images [2].
3.3. Comparison between patients with and without POF
2.3. Statistical analysis
Compared to patients without POF, patients with POF were much
older, had elevated rates of pancreatic necrosis, and in-hospital mortal-
Statistical analysis was performed using SPSS 20.0 (SPSS Inc., Chica-
ity (Table 1). Conventional severity scores such as Ranson and SIRS were
go IL, USA). Continuous data are presented as means and standard der-
significantly higher in POF ones. The level of serum LDH was significant-
ivation (SD). Categorical variables are reported as number (frequency).
ly lower, while the levels of white blood count, glucose, urea and creat-
Student's t-test and Mann-Whitney U test were used to evaluate the dif-
inine were statistically higher in patients with POF (Table 3).
ferences of baseline characteristics between the study cohort and the
control group. Multiple group comparisons were performed using the
Chi-square test for categorical variables and the Kruskal-Wallis test for
3.4. Admission serum LDH as an independent prognostic factor for POF
continuous data. Univariate analysis was performed using log-rank
test. All variables with statistically significant prognostic value in uni-
In order to further investigate the association between serum LDH
variate analysis were selected for further multivariate analysis. Multi-
and incidence of POF, we used multivariate Cox regression model. Uni-
variate analysis was undertaken with a Cox regression model. Hazard
variate analysis suggested serum glucose, albumin, urea, creatinine, cal-
ratios (HRs) and 95% confidence intervals (95% CIs) are presented.
cium, LDH, SIRS score and Ranson score correlated significantly with the
Receiver-operator curves (ROC) were constructed to evaluate the sensi-
incidence of POF. Multivariate analysis was performed using the charac-
tivity, specificity, positive predictive value (PPV) and negative predic-
teristics shown to have statistical significance (P b 0.05) by univariate
tive value (NPV) of the parameters in predicting persistent organ
analysis.
failure. A P value b 0.05 was considered a statistically significant
On multivariate analysis, only serum LDH ≥ 647 U/L was identified as
difference.
an independent prognostic factor (HR: 4.38, 95%CI 1.42–13.47; P =
0.010) (Table 4). As shown in Table 5 and Fig. 1, serum LDH on admis-
3. Results sion had an area under curve of the receiver operating characteristic
of (AUC) of 0.876 (95%CI: 0.767–0.985) for prediction of POF, with a
3.1. Patients sensitivity of 76.2%, specificity of 98.8%, PPV of 94.1%, and NPV of
94.3%. The optimal threshold was 647 U/L. The AUC of SIRS score and
A total of 105 patients with confirmed AP admitted to Union hospital Ranson score for predicting POF were 0.749 (95%CI: 0.643–0.855) and
(Wuhan, China) during the period were included in this study. Baseline 0.768 (95%CI: 0.663–0.872), respectively.
characteristics of these patients according to LDH levels (elevated or
normal) are presented in Table 1. The mean age was 48.97 years and
62 (59%) of the patients were male. Overall, 21 (20%) patients were
identified with POF. There were 14 patients developing solitary POF
(all of respiratory system). Multiple POF was observed in 7 patients (5 Table 2
Types of POF and the corresponding in-hospital mortality.
of lung and kidney, 1 of lung and heart, and 1 of lung, kidney and
heart). During hospitalization, 6 patients with POF died with an overall POF In-hospital mortality
mortality of 5.7%. No death was observed in patients without POF Solitary POF 14 2 (14.3%)
(Table 2). Respiratory 14 (100.0%) 2 (14.3%)
Renal 0 (0.0%) 0 (0.0%)
Cardiovascular 0 (0.0%) 0 (0.0%)
3.2. Comparison between patients with different LDH levels Multiple POF 7 4 (57.1%)
Respiratory + renal 5 (71.4%) 2 (40.0%)
Compared to patients with normal or low LDH (n = 39), patients Respiratory + cardiovascular 1 (14.3%) 1 (100.0%)
with high LDH (n = 66) show significantly higher incidences of devel- Respiratory + cardiovascular + renal 1 (14.3%) 1 (100.0%)

oping POF (28.8% vs. 5.1%; P = 0.003), PNec (35.0% vs. 20.5%; P = Abbreviations: POF, persistent organ failure.
 J. Cui et al. / Journal of Critical Care 41 (2017) 161–165 163

Table 3 Table 5
Clinical data of the patients with and without POF. Receiving operator curve analysis of LDH, SIRS and Ranson scores in predicting POF.

All patients Non-POF POF P-value AUC (95%CI) Cut-off Sensitivity Specificity PPV NPV
No. 105 84 21
LDH, U/L 0.876 647 0.762 0.988 0.941 0.943
Age, years 48.97 49.63 46.33 0.314 (0.767–0.985)
± 13.37 ± 13.41 ± 13.19 SIRS score 0.749 3 0.714 0.643 0.333 0.900
Male gender 62 (59.0%) 49 (58.3%) 13 (61.9%) 0.766 (0.643–0.855)
Daily drinker 47 (44.8%) 35 (41.7%) 12 (57.1%) 0.202 Ranson 0.768 4 0.857 0.548 0.321 0.939
Etiology 0.270 score (0.663–0.872)
Biliary 57 (54.3%) 49 (58.3%) 8 (38.1%)
Abbreviations: AUC: area under the curve; CI: confidence intervals; LDH, lactate dehydro-
Alcoholic 27 (25.7%) 19 (22.6%) 9 (42.9%)
genase; NPV: negative predictive value; POF, persistent organ failure; PPV: positive pre-
Hyperlipidemia 16 (15.2%) 13 (15.5%) 3 (14.3%)
dictive value; ROC, receiver operating curve.
Idiopathic 4 (3.8%) 3 (3.6%) 1 (4.7%)
Laboratory data
White blood count, 12.90 13.03 12.37 0.494
×109/L ± 3.93 ± 3.87 ± 4.24 grade of care and for designing appropriate medical treatment and
Hematocrit, % 41.73 41.46 42.80 0.357 intervention.
± 5.95 ± 5.43 ± 7.76 A lot of invasive or non-invasive methods, including biochemical pa-
Platelet count, ×109/L 196.92 198.54 190.48 0.652
rameters, radiological imaging modalities and severity scores have been
± 72.65 ± 64.53 ± 100.55
Serum glucose, mmol/L 9.34 ± 4.73 8.26 ± 3.44 13.68 b0.001 utilized for predicting POF in patients with AP [16]. Some studies com-
± 6.52 pared several existing clinical scoring systems (such as Ranson, Glas-
Total bilirubin, μmol/L 29.20 27.90 34.40 0.262 gow, APACHE II and the Bedside Index of Severity in Acute Pancreatitis
± 23.63 ± 24.27 ± 20.61 (BISAP) scoring systems) to predict POF in patients with AP [17-19].
Aspartate 93.19 96.32 80.67 0.658
The authors figured out that these scores showed modest accuracy
aminostransferase, U/L ± 143.75 ± 156.20 ± 77.42
Albumin, g/L 35.41 36.97 29.34 b0.001 (AUC at admission of 0.6 to 0.8 in both the training and the validation
± 5.61 ± 4.51 ± 5.43 cohorts) and seemed to have reached their maximal efficacy.
Serum urea, mmol/L 5.66 ± 3.84 4.68 ± 1.84 9.57 ± 6.53 b0.001 Recently, we found that the reduction of peripheral blood CD4 + T
Serum creatinine, μmol/L 81.49 64.99 147.51 b0.001
lymphocytes is able to distinguish POF from transient OF among AP pa-
± 70.19 ± 19.47 ± 135.37
Serum calcium, mmol/L 1.99 ± 0.33 2.08 ± 0.25 1.63 ± 0.37 b0.001
tients with OF [20]. In another study, neutrophil to lymphocyte ratio on
LDH, U/L 385.18 296.08 741.57 b0.001 admission was identified as an independent risk factor for POF and mor-
± 260.62 ± 135.73 ± 331.72 tality in AP [21]. In addition, we also found that mean platelet volume
Severity scores and was predictive of POF in AP [22].
SIRS 2.34 ± 0.95 2.17 ± 0.90 3.05 ± 0.80 b0.001
The LDH has been reported as a predictor of disease severity in sev-
Ranson 3.62 ± 1.70 3.30 ± 1.62 4.90 ± 1.41 b0.001
Outcomes eral clinical conditions. Morello et al. [23] evaluated the LDH in patients
PNec 43 (40.9%) 23 (27.4%) 20 (95.2%) b0.001 with acute aortic syndromes. In their study, mortality was significantly
In-hospital mortality 6 (5.7%) 0(0.0%) 11 (28.6%) b0.001 higher in patients with LDH N 450 U/L compared to patients with LDH
Abbreviations: LDH, lactate dehydrogenase; PNec, pancreatic necrosis; POF, persistent b 450 U/L. Hu et al. [24] suggested that elevated level of serum LDH is
organ failure; SIRS, systemic inflammatory response syndrome. a significant predictor of adverse outcomes in patients with idiopathic
pulmonary arterial hypertension. Kim et al. [25] indicated that patients
4. Discussion with pectus excavatum showed abnormal and significantly elevated
LDH level measured before surgery.
In this study, we demonstrated that serum LDH detected upon pre- The association between serum LDH and severity of AP has also been
sentation was independently associated with the incidence of POF in pa- assessed. Chen et al. [13] implied that LDH isoenzymes (LDH-4) is more
tients with AP. The predictive value was superior to scores of SIRS and valuable than Ranson's criteria in the early assessment of severe AP (ac-
Ranson's criteria. cording to 1992 Atlanta criteria). In the pancreas, the predominant LDH
Although a majority of patients with AP have a mild course of the isoenzymes are LDH-2 and LDH-3. This implies that the pancreas is not
disease, severe forms of AP require more attention because of its high the major origin of the increase of LDH. Damage to the liver, lung or
morbidity and mortality. POF, the most widely seen cause of mortality renal in severe attacks may all contribute to the higher value of serum
within the first 2 weeks of disease onset, develops in 10%–20% of AP pa- LDH in AP. Moreover, serum LDH has been reported to be a sensitive in-
tients, with a mortality rate between 20% and 50% [2,3]. The ability to as- dicator of PNec [14]. This is in accordance with our finding that patients
sess AP patients at risk for developing persistent organ failure early in with elevated LDH (LDH over 245 U/L) showed a higher rate of develop-
hospitalization is critical, both for triaging patients to the appropriate ing PNec. In 2007, Ueda et al. [15] suggested LDH-max/lymphocyte-max
on day 14 (optimum cutoff level: 1.5) was a simple and useful parame-
Table 4 ter for predicting infection and mortality in AP patients with PNec.
Uni- and multi-variate logistic regression analyses of risk factors for POF. Based on these studies, we tried to assess whether LDH could be use-
ful to predict the incidence of POF in AP, and to find a cutoff value of
Univariate analysis P-value Multivariate P-value
analysis
LDH. In our study, the incidence of POF was 20% (21/105) among all
Hazard ratio Hazard ratio AP patients. Our results suggested that serum LDH was an independent
(95%CI) (95%CI) prognostic factor of POF in AP. Using LDH ≥ 647 U/L as a cutoff value, the
Glucose ≥ 7.1 mmol/L 5.85 (1.36, 25.10) 0.018 2.22 (0.50, 9.95) 0.297 AUC for the prediction of POF was 0.876, which was comparable with
Albumin b 35 g/L 8.96 (2.09, 38.48) 0.003 3.63 (0.74, 17.79) 0.112 the AUCs of severity scores of Ranson and SIRS. The LDH is a convenient
Calcium b 2 mmol/L 12.67 (2.95, 54.38) b0.001 2.42 (0.40, 14.73) 0.337 and cheap laboratory test that could be routinely utilized in clinical
LDH ≥ 647 U/L 9.72 (3.56, 26.54) b0.001 4.38 (1.42, 13.47) 0.010
setting.
SIRS score ≥ 3 3.33 (1.29, 8.59) 0.013 1.35 (0.51, 3.59) 0.630
Ranson score ≥ 4 5.04 (1.48, 17.10) 0.010 Several limitations are evident in our research. First, due to the small
number of our study population and its retrospective nature, selection
Abbreviations: CI, confidence interval; LDH, lactate dehydrogenase; SIRS, systemic inflam-
matory response syndrome.
bias may influence the generalization of our results. Second, as this is
*Because Ranson score is not independent of serum calcium, we choose to exclude Ranson an observational single-center study, the causality role of LDH and POF
score for multi-variate analysis. in AP, however, requires to be investigated further in prospective
164 J. Cui et al. / Journal of Critical Care 41 (2017) 161–165
Fig. 1. Receiving operator curve of serum LDH, SIRS and Ranson scores on admission in predicting POF.
multi-center validation researches. Besides, we only examined one time
measurements. Therefore, this study did not address the problem of
intra-individual variation in LDH value. Additional prospective data on
consecutive patients are urgently needed to confirm our findings.
The strengths of the present study are as follows: 1) To our knowl-
edge, this is the first detailed study exploring the relationship between
LDH and POF in AP patients. 2) Patients included were all admitted
within 72 h from AP symptom onset and without any treatment before
the blood samples were collected. It is possible that therapeutic manip-
ulations may rapidly influence the value of serum LDH. 3) Uni- and
multi-variate logistic analyses were utilized, and the predictive value
of LDH was compared with conventional severity scores such as SIRS
and Ranson's criteria.
5. Conclusion
In conclusion, our present study indicates that serum LDH on admis-
sion is independently associated with POF in AP. LDH may serve as a
valuable tool for a rapid assessment of POF in patients with AP.
Competing interests
The authors declare that there was no any financial or ethical conflict
of interest.
Acknowledgements
The authors thank the staff from Pancreatic Disease Institute of Wu-
han Union Hospital for their support during the study.
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