Decreased Serum Cholinesterase Activity- A Reliable Diagnostic Aid for Tuberculosis

Introduction: Siderophore, the low molecular weight ferric iron chelator, is secreted extracellularly by Mycobacterium tuberculosis, an obligate aerobe. The pathogenic mycobacteria need iron as co-factor for the extracellularly secreted enzyme Superoxide Dismutase (SOD) for its pathogenicity as well as it requires iron for its metabolic functions like reduction of oxygen for synthesis of Adenosine Triphosphate (ATP), etc. The termination of impulse conduction is endorsed by the rapid hydrolysis of Acetylcholine (ACh) by Acetylcholinesterase (AChE) in the central as well as peripheral nervous system (cholinergic pathway). The inhibitors to Cholinesterase (ChE) might lead to accumulation of ACh, hyper stimulation of nicotinic and muscarinic receptors and also disruption of neurotransmission. Possibility of an inhibitor substance for AChE in Tuberculosis (TB) patients interestingly correlates with the symptom of night sweating in those subjects. Aim: To assay the level of serum ChE in normal control, lung disease control and tubercular subjects;circumvent the serum ChE level as a diagnostic potential in TB at an early stage. Materials and Methods: The study was conducted on total 124 subjects, and were divided into three groups: Group 1: normal control (n=31), Group 2: lung disease control (n=31) and Group 3: patients suffering from TB {3A: pulmonary TB (n=31) and 3B: extrapulmonary TB (n=31)}. Serum ChE activity for all the subjects were measured according to the method of Hestrin S. Serum ChE level was assayed for group 3 subjects after additional one month’s anti-TB drug treatment and also for group 2 subjects after one month with usual treatment. The level of significance was assessed using Student’s t-test. Results: There was a significant inhibition of serum ChE activity in both pulmonary and extrapulmonary TB patients in comparison to that of in normal control as well as lung disease control subjects (p<0.01). With the anti-tubercular drug therapy for one month, there was significant recovery in the serum ChE activity in pulmonary as well as extrapulmonary tubercular subjects (p<0.01). Conclusion: It appears that the high level of hydroxamate type of siderophores (secreted by Mycobacterium tuberculosis for acquiring iron) might form ACh ferric hydroxamate complex binding more strongly with serum ChE resulting in inhibition of serum ChE activity in tubercular subjects. With anti-tubercular drug therapy, there was decrease in serum ACh ferric hydroxamate complex level resulting in recovery of serum ChE activity.