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Serum Bilirubin Concentrations in Patients With Takayasu Arteritis.

Takayasu arteritis (TA) is a chronic, recurrent, inflammatory vasculitis characterized by granulomatous inflammation in the vessel wall, and mainly affects young females. (1) The aortic arch and its primary branches, such as the ascending aorta, abdominal aorta, and thoracic descending aorta, are primarily implicated in patients with TA. (2) In the clinical laboratory, some inflammatory markers such as erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and tumor necrosis factor (TNF) have been associated with disease progression. (3,4) There is growing evidence that progression of inflammation involving arteries is a crucial activator in the pathogenesis of TA, which results in occlusion, dilatation, and segmental stenosis. Obviously, it is important to estimate inflammatory conditions for the management of patients with TA.

Antioxidative enzymes and antioxidative substances play important roles in the oxidative stress and inflammation defense system. Bilirubin, as a product generated by heme metabolism, is an effective scavenger of free radicals and strong endogenous antioxidants factors in the body. (5) In some oxidative stress-mediated diseases, serum bilirubin concentrations are inversely correlated with cardiovascular diseases. (6) Very recently, lower serum bilirubin concentrations have been also reported in patients with carbon monoxide poisoning, migraine, and pulmonary embolism. (7-9) Notably, several recent studies found bilirubin to be significantly related to several rheumatic diseases, including systemic lupus erythematosus, polymyositis, and rheumatoid arthritis. (10-12) These studies provide evidence that oxidative stress and inflammation may tend to alter serum bilirubin concentrations. It is known that inflammatory cells can infiltrate and localize in the adventitia in patients with TA, and few reliable clinical markers are available to reflect the progression and remission of TA patients. (13) Therefore, the goal of this study was to investigate the relationship between serum bilirubin and TA.

MATERIALS AND METHODS

Patient Selection

Our study involved 115 consecutive patients with TA from Affiliated Hospital of Youjiang Medical University for Nationalities (Baise, China) between January 2014 and July 2016. These patients with TA were diagnosed in accordance with the American College of Rheumatology classification criteria. (14) The present study excluded patients who had cardiovascular disease, hepatic or renal insufficiency, dyslipidemia, infectious disease, metabolic disease, malignancy, smoking, or other rheumatic diseases. The control groups consisted of 193 sex- and age-matched healthy subjects.

The study's protocol was approval by the Ethics Committee of Affiliated Hospital of Youjiang Medical University for Nationalities; all subjects signed informed consent forms.

Laboratory and Clinical Investigation

Laboratory parameters and clinical data were obtained from the medical records. Body mass index was calculated by dividing weight in kilograms by height in meters squared. Fasting blood samples were collected for these laboratory measurements. Values of serum alanine aminotransferase, aspartate aminotransferase, creatinine, total protein (TP), glucose, and bilirubin concentrations were measured on an identical automatic analyzer with standard assays. Serum total bilirubin was measured by using the diazo method (Roche Inc, Basel, Switzerland). The serum concentrations of CRP were determined with immunonephelometry, and ESR was measured using the traditional Westergren method. Clinical characteristics such as disease duration, hypertension, diabetes mellitus, and medication history were summarized in all patients.

Disease Activity Assessment

According to the National Institutes of Health criteria, (15) active patients with TA were defined by the following features: (1) typical clinical symptoms, (2) vascular insufficiency signs, (3) typical angiographic characteristics, and (4) increased ESR with no infection. According to the criteria, there were 54 patients in the active phase of the disease and 61 patients in the inactive phase at the outset of this study.

Follow-up of Active Patients

The patients who were diagnosed with the active phase of the disease were followed and received prednisone therapy (1 mg/kg per day). Concomitant medications were not used during the period of the study. Responders were defined by the following clinical remission criterion: (1) disappearance or decrease of clinical symptoms, (2) no significant disease progress in vascular imaging findings, and (3) ESR within normal values. Further, laboratory and clinical data were compared in active TA patients before and after treatment.

Statistical Analysis

Statistical analysis was performed with SPSS 16.0 statistical software (SPSS Inc, Chicago, Illinois). The Kolmogorov-Smirnov test was used to determine normal distribution. The Student t test or Mann-Whitney U test for continuous variables and [chi square] test for categorical variables were used, as appropriate. We used the Spearman approach to evaluate the correlations between serum bilirubin and demographics or laboratory parameters. Multiple logistic regression analysis was used to calculate the odds of serum bilirubin concentrations in patients with TA compared with controls, and multiple linear regression analysis was used with statistical adjustments for underlying confounders. The receiver operating characteristic curve was used to estimate the performance of serum bilirubin in identifying active patients in all patients with TA. Finally, laboratory measurements before and after prednisone treatment were compared with paired t test. Statistical significance was set at P < .05.

RESULTS

The demographic and laboratory data for TA patients and healthy individuals are shown in Table 1. Most of these patients were found to have a medication history (prednisone) and hypertension (77.4% and 55.7%, respectively). The mean disease duration was 4.1 [+ or -] 6.72 years. The mean values for serum bilirubin, CRP, and ESR were 0.6 [+ or -] 0.31 mg/dL, 11.1 [+ or -] 5.32 mg/L, and 22.8 [+ or -] 15.13 mm/h, respectively, in all patients with TA (to convert serum bilirubin concentration to millimoles per liter, multiply by 17.104). Of note, lower concentrations of serum bilirubin were detected in TA patients compared with healthy subjects (0.6 [+ or -] 0.31 versus 0.7 [+ or -] 0.22 mg/dL, P = .02).

All patients with TA were divided into active and inactive patients; clinical features and laboratory findings of these patients are reported in Table 2. At baseline, age, sex, body mass index, disease duration, medication history, diabetes mellitus, hypertension, alanine aminotransferase, aspartate aminotransferase, creatinine, TP, and fasting blood glucose did not differ between the 2 groups. Values of ESR and CRP in active patients with TA were significantly high as compared with those in inactive TA patients. Serum bilirubin concentrations in active TA patients were lower than those in inactive patients (0.5 [+ or -] 0.20 versus 0.8 [+ or -] 0.32 mg/dL, P < .001).

In all patients with TA, correlation analysis revealed that serum bilirubin correlated positively with TP (r = 0.193, P = .04), and negatively with CRP and ESR (r = -0.213, P = .03, and r = -0.532, P < .001, respectively). The correlation analysis was performed separately for active patients and inactive patients; the serum concentrations of bilirubin correlated negatively with ESR (r = -0.326, P = .02), and positively with TP (r = 0.348, P = .01) in active patients, whereas no correlations with ESR or CRP were found in inactive patients.

Multiple logistic regression analysis showed that each decrease of 1 mg/dL in serum bilirubin was found to be associated with a 1.10 times increase in the odds for TA compared with the controls (odds ratio = 0.913; 95% CI, 0.856-0.974; P = .006). Multiple linear regression analysis was used with serum bilirubin as an objective variable and age, sex, disease duration, medication history, diabetes mellitus, hypertension, alanine aminotransferase, aspartate aminotransferase, TP, CRP, and ESR as explanatory variables, indicating that serum bilirubin was correlated with ESR (b = -0.170, P < .001) independently of other parameters in multiple linear regression analysis (Table 3). The area under the curve for serum bilirubin in estimating active TA patients was 0.802 (95% CI, 0.723-0.88; P < .001). A threshold of 0.54 for predicting active versus inactive disease in patients with TA was determined by receiver operating characteristic curve analysis.

Among 54 patients with active-phase TA, a total of 50 patients received prednisone treatment. After treatment modification, 42 active patients were considered as responders with clinical remission. Serum bilirubin levels were found to be significantly increased (0.5 [+ or -] 0.20 mg/ dL versus 0.7 [+ or -] 0.15 mg/dL, P = .002), whereas ESR and CRP were reduced after prednisone treatment, as shown in Table 4.

DISCUSSION

Clinically, imaging examinations are important and indispensable for the diagnosis of TA, and the presence of clinical symptoms and signs such as ischemia, vascular murmur, hypertension, disappeared or weakened pulsation, and large-vessel inflammation contributes to help identify patients with TA. (16) In addition, CRP and ESR have distinct and complementary roles for establishing the diagnosis of TA. (17) In our study, the serum concentrations of bilirubin were associated with TA independently of CRP and ESR, and active patients with TA showed significantly lower serum bilirubin levels compared with patients with inactive disease. Moreover, serum bilirubin correlated negatively with ESR in all patents with TA in multiple linear regression analysis. Surprisingly, serum bilirubin levels of active patients were found to be increased after prednisone therapy.

Lower serum bilirubin concentrations have been associated with coronary atherosclerosis and cardiovascular disease. (18,19) It has also been shown that serum concentrations of bilirubin are related to chronic kidney disease, cardioembolic stroke, and severe sepsis. (20-22) Our study revealed the association between lower serum levels of bilirubin and TA. Bilirubin as a novel biochemical tool has been regarded as a potent antioxidant, and bilirubin has much stronger anti-inflammatory and antioxidative stress action than many other antioxidants. (23) A reverse relationship between low serum bilirubin levels and CRP has been reported in apparently healthy adults, indicating that bilirubin metabolism has antioxidant and antiinflammatory effects. (24) Current evidence has also demonstrated that serum bilirubin can provide important protection against inflammation. (25) Furthermore, serum bilirubin can suppress TNF-[alpha]-related induction in endothelial adhesion molecules, and presents a protective action against inflammatory progress. (26) Accumulating data have indicated that serum bilirubin positively correlates with the total antioxidant capacity in the human body. (27) In view of the above summary, the protective role of bilirubin against inflammation may be a potential mechanism to explain lower serum bilirubin levels in active patients with TA, because bilirubin may be destroyed by strong inflammation and oxidative stress, and excessive inflammatory response may result in primary consumption and deficit of bilirubin, which may be associated with lower serum bilirubin concentrations in TA patients in the active phase.

Compared with imaging examinations, serum bilirubin as a component of biochemical tests is an available and simple marker with no additional costs for patients in clinical practice, and serum bilirubin is more convenient for the assessment of inflammatory progression compared with angiography in patients with TA. An increase in serum bilirubin levels was observed after successful prednisone therapy in active patients with TA, suggesting that treatment with anti-inflammatory medication in active patients can influence bilirubin metabolism because of alleviated inflammation. Accordingly, the results indicated that serum bilirubin may be considered as a biomarker to estimate prednisone treatment outcome in TA patients in the active phase.

The main limitation of our study is a small sample for the relatively rare disease, especially for the active patients with prednisone therapy during the follow-up period. Second, several genes with gene coding for uridine diphosphate-glucuronosyltransferase are involved in the regulation of serum bilirubin levels by the heme catabolic pathway. (28) However, genomic DNA from patients with TA was not available in the current study. Third, a single measurement for all patients with TA did not estimate intraindividual variability. Finally, the correlation between serum bilirubin concentrations and disease classification of patients with TA was not analyzed. In summary, our study suggests lower serum bilirubin levels are associated with TA, and serum bilirubin may be influenced by prednisone therapy in active TA patients. Serum bilirubin levels in TA patients correlate negatively with ESR. Nevertheless, our results need confirmation with larger samples.

Please Note: Illustration(s) are not available due to copyright restrictions.

References

(1.) Keser G, Direskeneli H, Aksu K. Management of Takayasu arteritis: a systematic review. Rheumatology (Oxford). 2014; 53(5):793-801.

(2.) Bicakcigil M, Aksu K, Kamali S, et al. Takayasu's arteritis in Turkey--clinical and angiographic features of 248 patients. Clin Exp Rheumatol. 2009; 27(1)(suppl 52):S59-S64.

(3.) Serra R, Grande R, Buffone G, et al. Effects of glucocorticoids and tumor necrosis factor-alpha inhibitors on both clinical and molecular parameters in patients with Takayasu arteritis. J Pharmacol Pharmacother. 2014; 5(3):193-196.

(4.) Peng YF, Guo J, Deng YB. The role of mean platelet volume in patients with Takayasu arteritis [published online ahead of print June 20, 2016]. Ann Clin Biochem. pii:0004563216658312.

(5.) Stocker R, Yamamoto Y, McDonagh AF, Glazer AN, Ames BN. Bilirubin is an antioxidant of possible physiological importance. Science. 1987; 235:1043-1046.

(6.) Breimer LH, Spyropolous KA, Winder AF, Mikhailidis DP, Hamilton G. Is bilirubin protective against coronary artery disease? Clin Chem. 1994; 40(10): 1987-1988.

(7.) Cervellin G, Comelli I, Buonocore R, Picanza A, Rastelli G, Lippi G. Serum bilirubin value predicts hospital admission in carbon monoxide-poisoned patients: active player or simple bystander? Clinics (Sao Paulo, Brazil). 2015; 70(9):628-631.

(8.) Peng YF, Xie LQ, Xiang Y, Xu GD. Serum bilirubin and their association with C-reactive protein in patients with migraine [published online ahead of print March 21, 2016]. J Clin Lab Anal. doi:10.1002/jcla.21967.

(9.) Cervellin G, Buonocore R, Sanchis-Gomar F, Lippi G. Low serum bilirubin values are associated with pulmonary embolism in a case-control study. Clin Chem Lab Med. 2016; 54(8):e229-e230.

(10.) Vitek L, Muchova L, Janoeva E, et al. Association of systemic lupus erythematosus with low serum bilirubin levels. Scand J Rheumatol. 2010; 39(6): 480-484.

(11.) Peng YF, Zhang L, Pan GG, Wei YS. A potential clinical usefulness of measuring serum bilirubin levels in patients with polymyositis. Eur Rev Med Pharmacol Sci. 2016; 20(4):631-635.

(12.) Fischman D, Valluri A, Gorrepati VS, Murphy ME, Peters I, Cheriyath P. Bilirubin as a protective factor for rheumatoid arthritis: an NHANES study of 2003-2006 data. J Clin Med Res. 2010; 2(6):256-260.

(13.) Saadoun D, Garrido M, Comarmond C, et al. Th1 and Th17 cytokines drive inflammation in Takayasu arteritis. Arthritis Rheumatol. 2015; 67(5):1353-1360.

(14.) Arend WP, Michel BA, Bloch DA. The American College of Rheumatology 1990 criteria for the classification of Takayasu arteritis. Arthritis Rheum. 1990; 33: 1129-1134.

(15.) Kerr GS, Hallahan CW, Giordano J, et al. Takayasu arteritis. Ann Intern Med. 1994; 120:919-929.

(16.) Pipitone N, Vesrari A, Salvarani C. Role of imaging studies in the diagnosis and follow-up of large-vessel vasculitis: an update. Rheumatology. 2008; 47:403-408.

(17.) Keser G, Direskeneli H, Aksu K. Management of Takayasu arteritis: a systematic review. Rheumatology (Oxford). 2014; 53(5):793-801.

(18.) Akboga MK, Canpolat U, Sahinarslan A, et al. Association of serum total bilirubin level with severity of coronary atherosclerosis is linked to systemic inflammation. Atherosclerosis. 2015; 2400):110-114.

(19.) Tsai WN, Wang YY, Liang JT, Lin SY, Sheu WH, Chang WD. Serum total bilirubin concentrations are inversely associated with total white blood cell counts in an adult population. Ann Clin Biochem. 2015; 52(pt 2):251-258.

(20.) Sakoh T, Nakayama M, Tanaka S, et al. Association of serum total bilirubin with renal outcome in Japanese patients with stages 3-5 chronic kidney disease. Metabolism. 2015; 64(9):1096-1102.

(21.) Lin SP, Lin PY, Jiang HL, Long YM, Chen XH. Is serum total bilirubin useful to differentiate cardioembolic stroke from other stroke subtypes? Neurol Res. 2015; 37(8):727-731.

(22.) Patel JJ, Taneja A, Niccum D, Kumar G, Jacobs E, Nanchal R. The association of serum bilirubin levels on the outcomes of severe sepsis. J Intensive Care Med. 2015; 30(1):23-29.

(23.) Wu TW, Carey D, Wu J, et al. The cytoprotective effects of bilirubin and biliverdin on rat hepatocytes and human erythrocytes and the impact of albumin. Biochem Cell Biol. 1991; 69:828-834.

(24.) Hwang HJ, Lee SW, Kim SH. Relationship between bilirubin and Creactive protein. Clin Chem Lab Med. 2011; 49(11):1823-1828.

(25.) Zhou ZX, Chen JK, Hong YY, et al. Relationship between the serum total bilirubin and inflammation in patients with psoriasis vulgaris. J Clin Lab Anal. 2016; 30(5):768-775.

(26.) Vera T, Stec DE. Moderate hyperbilirubinemia improves renal hemodynamics in ANG II-dependent hypertension. Am J Physiol Regul Integr Comp Physiol. 2010; 299(4):10442-10490.

(27.) Belanger S, Lavoie JC, Chessex P. Influence of bilirubin on the antioxidant capacity of plasma in newborn infants. Biol Neonate. 1997; 71:233-238.

(28.) Vitek L, Schwertner HA. The heme catabolic pathway and its protective effects on oxidative stress-mediated diseases. Adv Clin Chem. 2007; 43:1-57.

You-Fan Peng, MD; Yi-Bin Deng, MD

Accepted for publication October 3, 2016.

Published as an Early Online Release April 18, 2017.

From the Department of Laboratory Medicine, Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, China.

The authors have no relevant financial interest in the products or companies described in this article.

Reprints: You-Fan Peng, MD, Department of Laboratory Medicine, Affiliated Hospital of Youjiang Medical University for Nationalities, No. 18 Zhongshan Er Rd, Baise, Guangxi 533000, China (email: youfanpeng7177@sina.com).
Table 1. Demographic and Laboratory Data for Takayasu
Arteritis (TA) Patients and Healthy Individuals

                                               TA Patients

Female, No. (%)                                    110
Age, y                                     27.9 [+ or -] 8.62
Body mass index, kg/[m.sup.2]              25.1 [+ or -] 3.25
Disease duration, y                         4.1 [+ or -] 6.72
Medication history (prednisone), No. (%)        89 (77.4)
Diabetes mellitus, No. (%)                       2 (1.7)
Hypertension, No. (%)                           64 (55.7)
C-reactive protein, mg/L                   11.1 [+ or -] 5.32
Erythrocyte sedimentation rate, mm/h       22.8 [+ or -] 15.13
Alanine aminotransferase, U/L              20.1 [+ or -] 10.56
Aspartate aminotransferase, U/L            18.7 [+ or -] 7.97
Creatinine, mg/dL                           0.7 [+ or -] 0.16
Total protein, g/dL                         6.8 [+ or -] 0.79
Fasting blood glucose, mg/dL               83.3 [+ or -] 21.27
Serum bilirubin, mg/dL                      0.6 [+ or -] 0.31

                                                Controls          P

Female, No. (%)                                   183            .74
Age, y                                     28.9 [+ or -] 4.42    .23
Body mass index, kg/[m.sup.2]              24.7 [+ or -] 3.59    .33
Disease duration, y                               ...           ...
Medication history (prednisone), No. (%)          ...           ...
Diabetes mellitus, No. (%)                        ...           ...
Hypertension, No. (%)                             ...           ...
C-reactive protein, mg/L                   1.6 [+ or -] 0.47    <.001
Erythrocyte sedimentation rate, mm/h       9.7 [+ or -] 4.70    <.001
Alanine aminotransferase, U/L              18.4 [+ or -] 7.15    .15
Aspartate aminotransferase, U/L            18.8 [+ or -] 3.89    .90
Creatinine, mg/dL                          0.6 [+ or -] 0.09     .04
Total protein, g/dL                        7.0 [+ or -] 0.65     .02
Fasting blood glucose, mg/dL               54.7 [+ or -] 8.38    .48
Serum bilirubin, mg/dL                     0.7 [+ or -] 0.22     .02

SI conversion factors: To convert creatinine concentration to
millimoles per liter, multiply by 88.4. To convert blood glucose
concentration to millimoles per liter, multiply by 0.0555. To convert
serum bilirubin concentration to millimoles per liter, multiply by
17.104.

Table 2. Clinical and Laboratory Features in Active and Inactive
Patients

                                             Active Patients

Female, No. (%)                                 53 (98.1)
Age, y                                     27.2 [+ or -] 8.42
Body mass index, kg/[m.sup.2]              25.5 [+ or -] 3.24
Disease duration, y                         4.5 [+ or -] 7.64
Medication history (prednisone), No. (%)        44 (81.5)
Diabetes mellitus, No. (%)                        0 (0)
Hypertension, No. (%)                           32 (59.3)
C-reactive protein, mg/L                   18.4 [+ or -] 21.28
Erythrocyte sedimentation rate, mm/h       34.9 [+ or -] 7.64
Alanine aminotransferase, U/L              21.9 [+ or -] 12.36
Aspartate aminotransferase, U/L            20.0 [+ or -] 9.89
Creatinine, mg/dL                           0.7 [+ or -] 0.17
Total protein, g/dL                         6.7 [+ or -] 0.97
Fasting blood glucose, mg/dL               86.3 [+ or -] 29.22
Serum bilirubin, mg/dL                      0.5 [+ or -] 0.20

                                           Inactive Patients      P

Female, No. (%)                                57 (93.4)         .44
Age, y                                     28.5 [+ or -] 8.82    .41
Body mass index, kg/[m.sup.2]              24.7 [+ or -] 3.24    .18
Disease duration, y                        3.7 [+ or -] 4.78     .51
Medication history (prednisone), No. (%)       45 (73.8)         .32
Diabetes mellitus, No. (%)                      2 (3.3)          .53
Hypertension, No. (%)                          32 (52.5)         .46
C-reactive protein, mg/L                   4.7 [+ or -] 3.93    <.001
Erythrocyte sedimentation rate, mm/h       12.1 [+ or -] 5.22   <.001
Alanine aminotransferase, U/L              18.4 [+ or -] 8.43    .08
Aspartate aminotransferase, U/L            17.5 [+ or -] 5.66    .11
Creatinine, mg/dL                          0.7 [+ or -] 0.15     .21
Total protein, g/dL                        6.9 [+ or -] 0.58     .11
Fasting blood glucose, mg/dL               80.6 [+ or -] 9.46    .17
Serum bilirubin, mg/dL                     0.8 [+ or -] 0.32    <.001

SI conversion factors: To convert creatinine concentration to
millimoles per liter, multiply by 88.4. To convert blood glucose
concentration to millimoles per liter, multiply by 0.0555. To convert
serum bilirubin concentration to millimoles per liter, multiply by
17.104.

Table 3. Impact of Multiple Factors on Serum Bilirubin
Concentrations in Patients With Takayasu Arteritis

                             Unstandardized
                             Coefficients

                             [beta]   SE      [beta]   t        P

Sex                          -2.498   3.612   -0.066   -0.692     .49
Age                          -0.015   0.109   -0.023   -0.134     .89
Disease duration              0.113   0.139    0.131    0.809     .42
Hypertension                  0.813   1.022    0.077    0.796     .43
Diabetes mellitus             4.613   5.105    0.087    0.904     .37
Medication history           -1.231   1.177   -0.097   -1.045     .30
C-reactive protein           -0.070   0.045   -0.210   -0.157     .12
Erythrocyte sedimentation    -0.170   0.046   -0.506   -3.732   <.001
  rate
Alanine aminotransferase      0.109   0.072    0.212    1.518     .13
Aspartate aminotransferase   -0.132   0.088   -0.208   -1.505     .14
Total protein                 0.161   0.071    0.251    2.264     .03

Table 4. Comparison of Laboratory Features in Active Patients
Before and After Prednisone Therapy

                                          Pretreatment

C-reactive protein, mg/L               17.1 [+ or -] 21.18
Erythrocyte sedimentation rate, mm/h   34.3 [+ or -] 13.67
Alanine aminotransferase, U/L          21.5 [+ or -] 12.38
Aspartate aminotransferase, U/L        18.6 [+ or -] 7.08
Creatinine, mg/dL                       0.7 [+ or -] 0.17
Total protein, g/dL                     6.8 [+ or -] 0.95
Fasting blood glucose, mg/dL           87.5 [+ or -] 25.95
Serum bilirubin, mg/dL                  0.5 [+ or -] 0.20

                                          Posttreatment      P

C-reactive protein, mg/L                5.0 [+ or -] 4.07     .007
Erythrocyte sedimentation rate, mm/h   12.3 [+ or -] 5.41    <.001
Alanine aminotransferase, U/L          16.9 [+ or -] 7.80     .07
Aspartate aminotransferase, U/L        16.5 [+ or -] 4.81     .15
Creatinine, mg/dL                       0.7 [+ or -] 0.15     .05
Total protein, g/dL                     6.8 [+ or -] 0.55     .76
Fasting blood glucose, mg/dL           80.7 [+ or -] 10.65    .13
Serum bilirubin, mg/dL                  0.7 [+ or -] 0.15     .002

SI conversion factors: To convert creatinine concentration to
millimoles per liter, multiply by 88.4. To convert blood glucose
concentration to millimoles per liter, multiply by 0.0555. To convert
serum bilirubin concentration to millimoles per liter, multiply by
17.104.
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Author:Peng, You-Fan; Deng, Yi-Bin
Publication:Archives of Pathology & Laboratory Medicine
Article Type:Report
Date:Jun 1, 2017
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