|Year : 2019 | Volume
| Issue : 1 | Page : 19-21
Tuberculous pleural effusion: Modification of metabolome by the effect of common metabolic disease, diabetes mellitus
Pathum Sookaromdee1, Viroj Wiwanitkit2
1 TWS Medical Center, Bangkok, Thailand
2 Department of Biological Science, Joseph Ayobabalola University, Ikeji-Arakeii, Osun State, Nigeria
|Date of Submission||05-Jan-2019|
|Date of Decision||13-Feb-2019|
|Date of Acceptance||18-Feb-2019|
|Date of Web Publication||13-Mar-2019|
Dr. Pathum Sookaromdee
TWS Medical Center, Bangkok
Source of Support: None, Conflict of Interest: None
Background: Pleural effusion is an important problem in chest medicine. This problem might be seen in several conditions including tuberculosis and cancer. The differential diagnosis between tuberculous effusion and other effusions usually requires a good diagnostic test. The advance metabolomics approach is mentioned for the usefulness for differential diagnosis. The important consideration is on the effect of background metabolic alterations of the patients. Methods: The authors hereby assess the effect of background diabetes mellitus on the metabolome in tuberculous effusion. The common specific metabolome between tuberculous effusion and diabetes is searched for. The simulation to assess the confounding and overlapping effect of metabolome in diabetes to tuberculous effusion is done. Results: The only one identified common metabolome is citric acid. According to the simulation, there is a significant confounding and overlapping effect of citric acid in diabetes to tuberculous effusion. Conclusion: Diabetes might interfere with the use of citric acid as a metabolomic biomarker for tuberculous effusion.
Keywords: Citric acid, diabetes mellitus, effusion, metabolomics, tuberculosis
|How to cite this article:|
Sookaromdee P, Wiwanitkit V. Tuberculous pleural effusion: Modification of metabolome by the effect of common metabolic disease, diabetes mellitus. Biomed Biotechnol Res J 2019;3:19-21
|How to cite this URL:|
Sookaromdee P, Wiwanitkit V. Tuberculous pleural effusion: Modification of metabolome by the effect of common metabolic disease, diabetes mellitus. Biomed Biotechnol Res J [serial online] 2019 [cited 2019 May 21];3:19-21. Available from: http://www.bmbtrj.org/text.asp?2019/3/1/19/254102
| Introduction|| |
Pleural effusion is an important problem in clinical practice. This problem is an important clinical presentation in several conditions including tuberculosis and cancer. The differential diagnosis between tuberculous effusion and other effusions requires a good diagnostic test., The primary diagnostic approach is by classical laboratory medicine technique to differentiate between exudative effusion in tuberculous effusion and other exudative and transudative effusions.,
The difficulty in diagnostic approach is common. The advance metabolomics approach is mentioned for the advantage in differential diagnosis. This technique is based on the modern biochemioinformatics technique to identify specific metabolome for discrimination between different clinical disorders. It can also be applied for tuberculosis. Nevertheless, the important consideration is on the effect of background metabolic alterations of the patients. The metabolic disorder is a common clinical problem in the present day. Diabetes mellitus is a very common metabolic disorder seen worldwide. The metabolic alteration in diabetes is observable. The interesting research question is whether there is any effect of specific metabolic change due to diabetes on the specific metabolome in tuberculous effusion. In this study, the authors perform an analysis on this specific topic.
| Methods|| |
This is a bioinformatics study. The aim of this study is to assess the effect of background diabetes mellitus on the metabolome in tuberculous effusion. The common specific metabolome between tuberculous effusion and diabetes is searched for. The primary data from the previous metabolomics study for tuberculous effusion and diabetes are collected and used for further mathematical modeling study. The simulation to assess the confounding and overlapping effect of metabolome in diabetes to tuberculous effusion is done. For simulation study, the magnitude of identified metabolome changes in tuberculous effusion and diabetes is firstly calculated, and this magnitude is directly simulated to the healthy normal controls. The results after simulation for tuberculous effusion and diabetes are compared to assess possible overlapping or confounding phenomenon. Furthermore, a similar simulation for the scenario with both tuberculous effusion and diabetes is also done to assess the possible synergy phenomenon.
This research is not based on human subject, animal, or clinical sample but uses mathematical informatics technology. Hence, it does not require written informed consent of the patients and ethical approval.
| Results|| |
According to the literature search, specific reports on metabolomics for tuberculous effusion and diabetes can be derived. In each report, the specific metabolomes are available. For tuberculous effusion, the specific metabolomes are L-alanine, citric acid, and creatine. For diabetes mellitus, the specific metabolomes are glucose, fructose, cholesterol, tyrosine, phosphoric acid, lactic acid, glycine, alanine, glutamine, proline, and citric acid. From Venn diagram analysis, there is only one common specific metabolome, citric acid.
In referenced studies,, the level of citric acid in tuberculous effusion, diabetes, and controls can be derived. The result from the comparison of a specific level of citric acid to controls in both tuberculous effusion and diabetes is shown in [Table 1]. The decreasing level of citric acid comparing to controls is observable in both tuberculous effusion and diabetes. The magnitude of change is calculated and shown in [Table 1].
|Table 1: Comparison of observed level of citric acid to controls in both tuberculous effusion and diabetes|
Click here to view
From the simulation, there is no overlapping between citric acid level in tuberculous effusion and diabetes (0.42–1.34 vs. 1.45–2.34). For synergy in case with both tuberculous effusion and diabetes, the simulated magnitude of change of citric acid is 1.87–3.68 times.
| Discussion|| |
The biomarker for differential diagnosis of tuberculous effusion is interesting. There are different methods for diagnostic of pleural effusion. The modern DNA test is also applicable for differential diagnosis of pleural effusion, but it might not be available in several settings. The use of new biomarker will also be useful. The good example of a new biomarker is adenosine deaminase., Seeking for a new biomarker is the new issue of mycobacteriology research. The use of metabolomics approach for identification of new biomarker is possible. There are many reports on applied metabolomics researches for biomarker findings for several medical disorders including tuberculous effusion. According to the recent study by Wang et al., the specific metabolomes for tuberculous effusion can be detectable. Those metabolomes are specific for tuberculosis comparing to the other exudate and transudate effusions. Nevertheless, an important consideration is the possible effect of confounding metabolic disorder.
In general, metabolic problem is common and observed in any countries around the world. Diabetes is one of the most common metabolic diseases. For diabetes, there are also specific metabolomes in this medical disorder. Here, the authors can show that there are common metabolomes between the two medical disorders, tuberculous effusion and diabetes. The identified common metabolome is citric acid.
To use this metabolome in differentiate tuberculous effusion from other effusion, one has to beware of the interference from diabetes. Without diabetes, the decrease in citric acid might be observable in tuberculous effusion, and this might be helpful in differential diagnosis. Nevertheless, if there is additional underlying diabetes, there will be a synergy effect and there will be no decreased citric acid. In fact, without diabetes, there is still a chance that there might be no decreased citric acid in tuberculous effusion. Based on these findings, it might show that the citric acid might be useful for differential diagnosis in case that there is a reduction in its level. In case without reduction or increased level, there is a change of interference of diabetes that might result in false diagnosis as no tuberculous effusion.
To avoid interference effect from diabetes, the other remained specific metabolomes seen in tuberculous effusion including L-alanine and creatine should be considered as biomarkers for discrimination of pleural effusion.
| Conclusion|| |
According to this study, diabetes might interfere with the use of citric acid as a metabolomic biomarker for tuberculous effusion.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Marel M, Fila L, Červená M. The differential diagnosis of pleural effusions. Vnitr Lek Fall; 62:598-604.
Light RW. Pleural effusions. Med Clin North Am 2011;95:1055-70.
Preez ID, Luies L, Loots DT. Metabolomics biomarkers for tuberculosis diagnostics: Current status and future objectives. Biomark Med 2017;11:179-94.
Wang C, Peng J, Kuang Y, Zhang J, Dai L. Metabolomic analysis based on 1H-nuclear magnetic resonance spectroscopy metabolic profiles in tuberculous, malignant and transudative pleural effusion. Mol Med Rep 2017;16:1147-56.
Lou YB, Fan FX, Mu YC, Dong X. The implication of diabetes metabolomics in the early diagnosis and pathogenesis of pancreatic cancer. J Biol Regul Homeost Agents 2018;32:75-82.
Bayhan GI, Sayir F, Tanir G, Tuncer O. Pediatric pleural tuberculosis. Int J Mycobacteriol 2018;7:261-4.
] [Full text]
Amer S, Hefnawy AE, Wahab NA, Okasha H, Baz A. Evaluation of different laboratory methods for rapid diagnosis of tuberculous pleurisy. Int J Mycobacteriol 2016;5:437-45. [Full text]
Yanovich OO, Titov LP, Dyusmikeeva MI, Shpakovskaya NS. Evaluation of adenosine deaminase (ADA) and ADA1 and ADA2 isoenzyme activities in patients with pleurisy. Int J Mycobacteriol 2015;4:93-4. [Full text]