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 Table of Contents  
ORIGINAL ARTICLE
Year : 2021  |  Volume : 10  |  Issue : 1  |  Page : 55-58

Serum lactate dehydrogenase level in childhood acute lymphoblastic leukemia


1 Department of Hemato-Oncology, Child's Central Teaching Hospital, Baghdad, Iraq
2 Department of Nepherology, Al-Karama Teaching Hospital, Baghdad, Iraq

Date of Submission04-Jan-2021
Date of Acceptance10-Feb-2021
Date of Web Publication21-Jun-2021

Correspondence Address:
Dr. Entisar Hadi Al-Shammary
Department of Hemato-Oncology, Child's Central Teaching Hospital, Baghdad
Iraq
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijh.ijh_4_21

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  Abstract 


BACKGROUND: Acute lymphoblastic leukemia (ALL) is the most common malignancy in children. It accounts for one-fourth of all childhood cancers and 72% of all cases of childhood leukemia.
OBJECTIVE: The objective was to evaluate the significant increase in serum lactate dehydrogenase (LDH) enzyme levels in patients with ALL with respect to patients' characters, clinical presentation, and patients' induction outcome.
PATIENTS AND METHODS: A prospective study had been conducted during the period from November 1, 2017 to October 31, 2018, included 86 patients newly diagnosed ALL patients under the age of 15th years, admitted to the pediatric hemato-oncology unit in the Child's Central Teaching Hospital the data were collect from the patients, included, age, sex, clinical presentation, investigation and induction outcome of ALL patients to undergo analysis of study.
RESULTS: Of a total (86) ALL patients started induction therapy, only (75/86) of them completed induction phase of therapy and those were enrolled in analysis of this study, while (11/86) did not complete induction therapy and excluded from the study (because 10 died, and one patient loss follow-up during induction). The mean age was 4.7 years. The male-to-female ratio was 1.26:1. LDH level ranged from 100 to 1995 U/L. There was a significant association between LDH level at day 0 and each of age and ALL risk group and no association with gender, hepatomegaly, splenomegaly, lymphadenopathy, central nervous system status, and induction outcome (remission/no remission). The mean of LDH levels at diagnosis was highly elevated in patients with ALL (726 ± 422 U/L); the response to induction treatment was observed by the significant decrease in mean LDH level (324 ± 201 U/L) at day 28th of treatment P value (0.0001).
CONCLUSIONS: The serum LDH level was highly elevated at diagnosis in the majority of ALL patients and decreased significantly in response to chemotherapy. The estimation of serum LDH level is easy, and available, so it may be a helpful tool in evaluating the clinical aspect of the disease, the response to induction chemotherapy.

Keywords: Acute lymphoblastic leukemia, induction, lactate dehydrogenase


How to cite this article:
Zahra SS, Al-Shammary EH, Hameed IM. Serum lactate dehydrogenase level in childhood acute lymphoblastic leukemia. Iraqi J Hematol 2021;10:55-8

How to cite this URL:
Zahra SS, Al-Shammary EH, Hameed IM. Serum lactate dehydrogenase level in childhood acute lymphoblastic leukemia. Iraqi J Hematol [serial online] 2021 [cited 2021 Jul 30];10:55-8. Available from: https://www.ijhonline.org/text.asp?2021/10/1/55/318767




  Introduction Top


All is the most common malignancy in children. It accounts for one-fourth of all childhood cancers and 72% of all cases of childhood leukemia.[1] The peak incidence of ALL occurs between 2 and 5 years of age.[2],[3] The incidence of ALL is higher among boys than girls, and this difference is greatest among pubertal children.[4] There are geographic differences in the frequency and age distribution of ALL. This geographic variation may reflect in part the distribution of different immunologic and cytogenetic ALL subtypes.[5] LDH exists in many different cell systems and subsequent to tissue or cell damage, serum LDH levels may be elevated.[6] It is not clear whether the increased serum levels of LDH commonly found in cancer patients reflect greater production and release of the enzyme by malignant cells.[7] A relationship between neoplasia and increased LDH levels has been reported by many workers in both human and animal tumors.[6]

Markedly elevated level of LDH is recorded in the majority of patients with ALL and is suggestive of increase cell proliferation and turnover and number of white blood cell (WBC) during remissions or relapses of the disease.[6],[8] On the other hand, it was suggested that elevated serum LDH may relate to total leukemia cell mass.[9] Early measurement of serum LDH can be used in identifying a group of standard-risk ALL patients with a high relapse hazard.[10] Following induction therapy with archived complete remission, serum LDH level decreases, and when tumor growth recurrent as the patient relapse, serum LDH level rises again.[11]

Aim of the study

The aim was to evaluate the significant increase in serum lactate dehydrogenase (LDH) enzyme levels in patients with acute lymphoblastic leukemia (ALL) with respect to patients' characters, clinical presentation, and patients' induction outcome.


  Patients and Methods Top


A prospective study had been conducted during the period from November 1, 2017 to October 31, 2018, over a period of 1 year, included 86 patients newly diagnosed precursor B cell ALL patients under the age of 15th years (ALL-L3 and T-cell ALL were excluded from the study), who admitted to the pediatric hemato-oncology unit in the Child's Central Teaching Hospital. He data were collect from the patients, included, age, sex, clinical presentation, investigation and induction outcome of ALL patients to undergo analysis of study. Physical examination was performed, the liver and the spleen considered hepatomegaly and splenomegaly if enlargement ≥5 cm below the costal margin and axillary and cervical lymph nodes considered enlarge if >1 cm and inguinal lymph nodes >1.5 cm. Patients stratified into standard and higher risk group as follows standard risk, WBC <50,000/ml and age 1–9.9 years; high risk, WBC ≥50,000/ml or age ≥10 years.[12] The patients with complete remission (CR) have no evidence of leukemia when evaluated by physical examination and hematologic assessment of peripheral blood and bone marrow (lymphoblasts fewer than 5% in bone marrow).[13] Serum LDH levels were determined at the time of diagnosis (at day 0 before starting chemotherapy) and at end of induction (day 28 of induction). The range of serum LDH level was 90–190 U/L (the cutoff level of serum LDH was 200 U/L, levels above that were considered to be elevated).

Statistical analysis

Patients' data were analyzed by using (IBM SPSS Statistics for Windows, Version 24.0. Armonk, NY: IBM Corp) program, Database and statistics program for public health to estimated P value. Qualitative data are expressed as frequency and percentage, quantitative data as mean and median. P < 0.05 is considered statistically significant.


  Results Top


A total (86) ALL patients were enrolled in this study, 11 of them did not complete induction phase (10 of them died, and one patient lost follow-up during induction), the remaining (75) patients completed induction phase and achieved CR. The most common age group was 1.1–9.9 years; the male-to-female ratio was 1.26:1.

The gender, age and risk groups, clinical findings, and central nervous system (CNS) status of the patients are described in [Table 1].
Table 1: Descriptive data of 86 acute lymphoblastic leukemia patients at diagnosis

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This study demonstrates that there was a significant association between LDH level at day 0 and each of ALL risk groups and age (P value 0.0001, and 0.0001). There is no significant association between LDH level at day 0 and sex, hepatomegaly, splenomegaly, leukocyte alkaline phosphatase (LAP), and CNS status (P value not significant) as shown in [Table 2] and [Table 3].
Table 2: Correlation between serum lactate dehydrogenase level at day 0 and patient character

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Table 3: Correlation between serum lactate dehydrogenase level at day 0 and patient clinical finding

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The serum level of LDH at date of diagnosis (day 0 of induction therapy) and after completed induction phase of chemotherapy (day 28 of induction therapy) for (75/86) patients who complete induction therapy and achieved complete remission. The response to treatment was observed by the decrease in LDH level. This decrease was statistically highly significant (P value 0.0001), as described in [Table 4].
Table 4: Correlation between lactate dehydrogenase level according to induction time for 75 acute lymphoblastic leukemia patients

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  Discussion Top


A prospective study was involving a sample of 86 ALL patients. This study found that patients with high-risk group ALL had a higher LDH level at diagnosis than standard risk group ALL with a significant P value (0.0001) which was similar to Hiçsönmez et al.[14] study; this finding may be related to that the patients with high risk ALL had most likely greater bulk of the disease than standard-risk ALL. In the present study, females show higher LDH levels at diagnosis as compared to males which was statistically not significant P value (0.4), Pujari et al.,[15] agree with us while Pui et al.[10] disagree. In this study, we found a significant association between age and LDH level at diagnosis, patients with age group ≥10 years had higher LDH levels than other age groups with significant P value (0.0001), a finding similar to Pujari et al.,[15] who found there was a significant trend in LDH levels with respect to age P value (<0.001) while Pui et al.,[10] found that there was no association between LDH level and age. The current study found no significant association between LDH level at diagnosis and hepatomegaly, splenomegaly, LAP, and CNS status P value 0.4, 0.6, 0.1, and 0.9, respectively. The Pui et al. study shows no significant association between LDH level at diagnosis and hepatomegaly, while higher LDH level at diagnosis had a larger spleen size P value (0.04).[10]

This study found that the mean of LDH levels among ALL patients at diagnosis was highly elevated (726 ± 422 U/L); these results were consisted with results obtained from Pui et al.,[10] Pujari et al.,[15] Pandit et al.,[16] Kornberg and Polliack,[6] D'Angelo et al.,[17] Hiçsönmez et al.[14] and Ghosh et al.[18] The results could be explained as LDH levels will be elevated due to tissue damage, leukemic cell lysis, and rapid cell turnover. Furthermore, increased cellular LDH activity reflects a shift toward anaerobic metabolism and increased glycolysis in the cytoplasm of malignant cells. In the present study, the response to induction treatment was observed by the significant decrease in mean LDH level (324 ± 201 U/L) on day 28th of treatment which was a statistically significant P value (0.0001). All the patients in this study got a CR after induction of chemotherapy. These results regarding LDH level were similar to those obtained from Pandit et al.,[16] Hafiz and Mannan,[11] AL-Saadoon et al.[19] (P < 0.01), Hafiz et al.[20] (P < 0.001), and Bien and Balcerska.[21] These observations were explained in that the patients with ALL on presentation had high LDH levels and with the institution of induction therapy enzymatic activities dropped gradually till normalization this was coincidental with clinical and hematological remission.


  Conclusions Top


The serum LDH level was highly elevated at diagnosis in the majority of ALL patients decreased significantly in response to chemotherapy. There was a significant association between LDH level at diagnosis and each of ALL risk groups and age. The estimation of serum LDH level is easy, and available, so it may be a helpful tool in evaluating the clinical aspect of the disease, the response to induction chemotherapy.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

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2.
Hrusák O, Trka J, Zuna J, Poloucková A, Kalina T, Starý J, et al. Acute lymphoblastic leukemia incidence during socioeconomic transition: Selective increase in children from 1 to 4 years. Leukemia 2002;16:720-5.  Back to cited text no. 2
    
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Render A. Leukemias. In: Lanzkowsky P. Manual of pediatric Hematology and Oncology. 5th ed., Vol. 17. Academic Press, Elisevier, Inc; 2011. p. 518-35.  Back to cited text no. 3
    
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Pui CH, Relling MV, Downing JR. Acute lymphoblastic leukemia. N Engl J Med 2004;350:1535-48.  Back to cited text no. 4
    
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Ramot B, Magrath I. Hypothesis: The environment is a major determinant of the immunological sub-type of lymphoma and acute lymphoblastic leukaemia in children. Br J Haematol 1982;50:183-9.  Back to cited text no. 5
    
6.
Kornberg A, Polliack A. Serum lactic dehydrogenase (LDH) levels in acute leukemia: Marked elevations in lymphoblastic leukemia. Blood 1980;56:351-5.  Back to cited text no. 6
    
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Lehninger AL. Organ interrelationships in the metabolism of mammals. In: Lehninger Textbook of Biochemistry. New York: Worth; 2000. p. 829.  Back to cited text no. 7
    
8.
Blatt J, Spiegel RJ, Papadopoulos NM, Lazarou SA, Magrath IT, Poplack DG. Lactate dehydrogenase isoenzymes in normal and malignant human lymphoid cells. Blood 1982;60:491-4.  Back to cited text no. 8
    
9.
Rambotti P, Davis S. Lactic dehydrogenase in normal and leukemic lymphocyte sub-populations: Evidence for the presence of abnormal T and B cells in CLL. Blood 1981;57:324-7.  Back to cited text no. 9
    
10.
Pui CH, Dodge RK, Dahl GV, Rivera G, Look AT, Kalwinsky D, et al. Serum lactic dehydrogenase level has prognostic value in childhood acute lymphoblastic leukemia. Blood 1985;66:778-82.  Back to cited text no. 10
    
11.
Hafiz G, Mannan MA. Serum lactate dehydrogenase level in childhood acute lymphoblastic leukemia. Bangladesh Med Res Counc Bull 2007;33:88-91.  Back to cited text no. 11
    
12.
Judith FM, Karen RR, Steuber CP, Poplack GD. Acute lymphoblastic leukemia. In: Pizzo PA, Poplack DG, editors. Principles and Practice of Pediatric Oncology. 6th ed., Vol. 19. Philadelphia: Lippincott Williams and Wilkins; 2011. p. 518-65.  Back to cited text no. 12
    
13.
Pui CH, Campana D. New definition of remission in childhood acute lymphoblastic leukemia. Leukemia 2000;14:783-5.  Back to cited text no. 13
    
14.
Hiçsönmez G, Caglar K, Renda N. Prognostic value of the determination of serum lactic dehydrogenase and its isoenzymes in children with acute lymphoblastic leukaemia. Scand J Haematol 1985;34:256-60.  Back to cited text no. 14
    
15.
Pujari KN, Jadkar SP, Belwalkar GJ: Lactate dehydrogenase levels in leukemias. Int J Pharma Bio Sci 2012;3:B454-B9.  Back to cited text no. 15
    
16.
Pandit MK, Joshi BH, Patel PS, Chitnis KE, Balar DB. Efficacy of serum lactate dehydrogenase and its isozymes in monitoring the therapy in patients with acute leukemia. Indian J Pathol Microbiol 1990;33:41-7.  Back to cited text no. 16
    
17.
D'Angelo G, Giardini C, Calvano D. Clinical significance of the determination of lactate dehydrogenase in acute leukemia and non-Hodgkin's lymphoma. Minerva Med 1989;80:549-52.  Back to cited text no. 17
    
18.
Ghosh K, Malik K, Das KC. Serum and leukocyte lactate dehydrogenase activity in leukaemias. Haematologia (Budap) 1988;21:227-32.  Back to cited text no. 18
    
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Al-Saadoon EA, Al-Naama LM, Hassan JK. Serum lactate dehydrogenase (LDH) activity in children with malignant diseases. Bahrain Med Bull 2003;25:71-3.  Back to cited text no. 19
    
20.
Hafiz MG, Rahman MM, Mannan MA. Serum lactate dehydrogenase as a prognostic marker of childhood acute lymphoblastic leukemia. Mymensingh Med J 2008;17:169-73.  Back to cited text no. 20
    
21.
Bień E, Balcerska A. Clinical significance of erythrocyte sedimentation rate, C-reactive protein and serum lactate dehydrogenase levels in the diagnosis, prognosis and treatment monitoring of children suffering from cancer. Med Wieku Rozwoj 2004;8:1081-9.  Back to cited text no. 21
    



 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4]



 

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