This study was carried out with blood samples taken from 65 children, 32 NHL and 33 HD. The mean age was 11 years, while age range between 4 and 18 years. The mean age at disease onset was 7 ranging from 1 to 12 years. Patients came from the Department of Hematology, University Hospital Center of Beni Messous, Algeria. They had already a confirmed histologic diagnosis of lymphoma. The clinical data of age, gender, stage of disease and histologic subtype were recorded. Patients were treated for 14 weeks with LBM 2001 group B protocol (Prednisone, cyclophosphamide, vincristine, MTX) for non-Hodgkin's lymphoma and ABVD protocol (Adreamycien, bleomycin, vinblastine And dacarbazine) for hodgkin's disease. The patients received, according to their stage, two or three cures. The control group consisted of 75 unrelated healthy subjects, with no chronic or autoimmune disease and no personal or family history. The mean age was 13 years (Table 1). Serum LDH and other biochemical and hematological parameters were measured spectrophotometrically using biochemical analyzer. LDH level of > 470 U/L is considered high according to ILabTest TM LDH-P (Normal range is 235-470U/L). Statistical analysis was performed and results are expressed as mean±SD. Differences between lymphoma and control groups were assessed using the Student’s t test. Regression and correlation analyses between variables were performed by calculating Pearson’s correlation coefficients (r). P values of > 0.05 were considered not significant.

Among biochemical parameters, lactate dehydrogenase (LDH) represents a very valuable enzyme in patients with malignant lymphomas. The serum level has been considered as very important in the evaluation of disease extension in non- Hodgkin's lymphomas (NHL) and Hodgkin's disease (HD)13.

In this study, we have analazed the relation between serum LDH level, stage and response to treatment on 33 patients with HL and 32 patients with NHL. The LDH level was significantly elevated in lymphoma patients compared to control. This finding agrees with that, reported by other investigators1415.This intense LDH level observed in patients during cancerous conditions may be the result of high glycolytic rate16. In fact, the high glycolytic rate is important for rapidly proliferating cancers

Protein kinases, various hormones and growth factors have been shown to regulate LDH gene expression2021. In most cases, these factors induce a shift towards A-subunit containing isoenzymes which can derive more energy under anaerobic conditions. Furthermore, it has been shown that TNFα is capable of inducing LDH-A expression in cultured Sertoli cells22. Human lymphoma cells obtained from fresh tumor samples have been shown to produce TNF23. It is therefore possible that the serum LDH alterations observed in lymphoma patients may be due to the production of inflammatory cytokines. The importante of serum LDH as a direct indicator of tumor burden has already been pointed out in other clinical studies2425. Indeed, mechanisms for energy production involved in cell duplication require a high LDH cell content and renewal of NAD resynthesis, in support of a continuing glycolysis. For a given tumor bulk LDH production is conceived as being proportional to its metabolic and proliferative activity. Accordingly, high LDH production suggests either large tumor bulk or a fast proliferation in a smaller tumor, and this could explain an aggressive course and a poorer response to therapy2627.

In addition, the tumor cells may produce LDH enzyme to respond to the increase of lactic acid, resulting in oxidtive reductive reaction to become pyruvic acid. High LDH level describes high aggressiveness and proliferation of the tumor cells. Therefore, LDH level in NHL is a marker of cell turnover and correlated with tumor burden. Several studies showed correlation between LDH level and the result of therapy. High LDH level often provides less response to the result of therapy, often relapses, and has a potential of metastasis28.

Lactate efflux provokes a local inflammatory response that attracts immune cells such as macrophages, which secrete cytokines and growth factors that drive tumor cell growth and metastasis3031. Indeed, the inflammatory response is often necessary for tumor progression, and elevated numbers of inflammatory cells, such as tumor-associated macrophages, connote poor prognosis31. Furthermore, lactate in the tumor cell milieu impairs the adaptive immune response, disabling immune surveillance 323334. Thus, lactate also appears to promote tumorigenesis via non–tumor cell mediated effects on the inflammatory and immune responses.

Lactate dehydrogenase (LDH) plays an important role in tumor initiation and maintenance since its ability to function in anaerobic metabolism helps cancer cells grow even after their rapid proliferation leads to low-oxygen conditions in the tumor microenvironment. The elevated serum LDH could be used to select patients who will benefit from more intensified treatment.