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Year : 2018  |  Volume : 43  |  Issue : 4  |  Page : 322-323

Infection-induced hyperglycemia in tuberculosis patients at selected health institutions in North India

1 Department of Community Medicine, ESIC Medical College and Hospital, Faridabad, Haryana, India
2 Department of Community Medicine, Dr. S Radhakrishnan Government Medical College, Hamirpur, Himachal Pradesh, India
3 Department of Community Medicine, Dr. Rajendra Prasad Government Medical College, Kangra, Himachal Pradesh, India

Date of Submission21-Mar-2018
Date of Acceptance29-Nov-2018
Date of Web Publication21-Dec-2018

Correspondence Address:
Dr. Dinesh Kumar
Department of Community Medicine, Dr. Rajendra Prasad Government Medical College, Tanda, Kangra - 176 001, Himachal Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijcm.IJCM_77_18

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How to cite this article:
Singh M, Bharadwaj AK, Kumar D. Infection-induced hyperglycemia in tuberculosis patients at selected health institutions in North India. Indian J Community Med 2018;43:322-3

How to cite this URL:
Singh M, Bharadwaj AK, Kumar D. Infection-induced hyperglycemia in tuberculosis patients at selected health institutions in North India. Indian J Community Med [serial online] 2018 [cited 2022 Jul 4];43:322-3. Available from: https://www.ijcm.org.in/text.asp?2018/43/4/322/248200


Chronic noncommunicable diseases proliferated at par with infectious diseases and their interaction is of public health significance.[1] With the rising prevalence of diabetes mellitus (DM), significant proportion of TB cases are accounted for DM in the future.[2] Tuberculosis (TB) associates with infection-induced hyperglycemia (IIH),[3] and the present study assessed change in random blood glucose (RBG) among TB patients on treatment, recruited from four designated microscopy centers (DMCs) of district Kangra, Himachal Pradesh, India. Sample size was estimated as 369, assuming an average 20% prevalence of DM in TB patients, at 95% confidence interval (CI), 80% study power, and design effect of 1.5. This prospective study, from April 2014 to March 2015, included 400 patients (age ≥20 years) with TB (sputum smear positive and negative) receiving treatment as per the Revised National Tuberculosis Control Programme (RNTCP) guidelines.[4] Cases already diagnosed with human immunodeficiency virus, Mycobacterium leprae infection, and multidrug-resistant TB patients were excluded from the study. Patients without telephonic details (four patients) indicative of difficulty in follow-up were also excluded. Written informed consent of all participants was obtained before gathering any information under the protocol approved by the institution's Ethics Committee. All diagnosed TB patients were assessed three times; at the time of diagnosis, at 2-month follow-up, and at the end of treatment, for RBG with recording for known or unknown case of DM. RBG was recorded using by glucometer (SD Codefree™ 2013).

During the course of study, 61 (15.3%) were censored; of which 21 (34.4%) died before treatment completion and 33 (7.0%) could not be contacted after three attempts due to wrong phone/switched off number.

Of all patients, the baseline RBG assessment showed that 12.8% (51) of patients had RBG value ≥200 mg/dl; however, 42 (10.5%) patients of these were already diagnosed for DM. The known diabetics (42) were excluded from the analysis; hence, the data for 358 TB patients were analyzed for RBG. The difference between baseline mean RBG and the second follow-up (at the end of TB treatment) was calculated, and it was observed that the difference of means was statistically significant for age, gender, residence, body mass index, smoking, alcohol consumption, and for different categories of bacterial load. The mean reduction of 30.2 mg/dl was observed for 358 patients and it was statistically significant (P = 0.00) [Table 1]. Proportion of patients with high RBG (≥200 mg/dl) also declined significantly from 12.8% to 6.2%. Only three prospective studies from Turkey, Nigeria, and India observed that either proportion of diabetics or mean blood glucose level has reduced at the end of 3 months.[5],[6],[7] DM among TB patients was also reported across various cross-sectional studies with range from 14% to 35.5%,[3],[8],[9],[10] probably due to cytokine-induced insulin resistance, decreased insulin production, and carbohydrate metabolism-induced state of relative insulin deficiency.[11],[12],[13]
Table 1: Change in the random blood glucose across age group, gender, place of residence, caste, body mass index, substance use, and bacterial load over period of follow-up in diagnosed tuberculosis patients, 2015, Himachal Pradesh

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General linear repeated-measures model was applied to account for confounding for decline in mean RBG. The dependent variable was RBG at the three points of contact, and the independent variables were bacterial load, age, sex, smoking, and alcohol intake history. The model estimated that the average RBS at the three points of contact was marginally lower than the original average RBG, but even the estimated mean RBG observed a decline from the baseline (123.7 mg/dl) to second follow-up (106.6 mg/dl) (P = 0.00). We ran a multiple linear regression model to account for mean RBG reduction across bacterial load from baseline to follow-up for variables such as age, sex, caste, residence, smoking, and alcohol. It was observed that the reduction in mean RBG stayed significant across bacterial load (P = 0.020) and caste (P = 0.001). There is evidence in favor of IIH among patients with TB, although long duration of follow-up for RBG, 6–12 months after treatment completion, is required to categorically assess the influence of declining bacterial load over RBG, the IIH.


We would like to thank Dr. RK Sood, District TB Officer, Kangra, Dr. MK Gupta, Medical Officer, RNTCP, Himachal Pradesh, and staff at the DMCs and peripheral health institutions for helping with the study. We would also thank Himachal Pradesh State Operational Research Committee for funding this research.

Financial support and sponsorship

Funding for the project was sought from State Task Force, Himachal Pradesh (RNTCP).

Conflicts of interest

There are no conflicts of interest.

   References Top

Goldhaber-Fiebert JD, Jeon CY, Cohen T, Murray MB. Diabetes mellitus and tuberculosis in countries with high tuberculosis burdens: Individual risks and social determinants. Int J Epidemiol 2011;40:417-28.  Back to cited text no. 1
Ruslami R, Aarnoutse RE, Alisjahbana B, van der Ven AJ, van Crevel R. Implications of the global increase of diabetes for tuberculosis control and patient care. Trop Med Int Health 2010;15:1289-99.  Back to cited text no. 2
Dooley KE, Tang T, Golub JE, Dorman SE, Cronin W. Impact of diabetes mellitus on treatment outcomes of patients with active tuberculosis. Am J Trop Med Hyg 2009;80:634-9.  Back to cited text no. 3
World Health Organization. TB/HIV: A Clinical Manual. 2nd ed. Geneva: World Health Organization; 2004.  Back to cited text no. 4
Başoğlu OK, Bacakoğlu F, Cok G, Sayiner A, Ateş M. The oral glucose tolerance test in patients with respiratory infections. Monaldi Arch Chest Dis 1999;54:307-10.  Back to cited text no. 5
Oluboyo PO, Erasmus RT. The significance of glucose intolerance in pulmonary tuberculosis. Tubercle 1990;71:135-8.  Back to cited text no. 6
Singh MM, Biswas SK, Shah A. Impaired glucose tolerance in active pulmonary tuberculosis. Indian J Tuberc 1984;31:118-21.  Back to cited text no. 7
Hsu AH, Lee JJ, Chiang CY, Li YH, Chen LK, Lin CB, et al. Diabetes is associated with drug-resistant tuberculosis in Eastern Taiwan. Int J Tuberc Lung Dis 2013;17:354-6.  Back to cited text no. 8
Chen HG, Liu M, Jiang SW, Gu FH, Huang SP, Gao TJ, et al. Impact of diabetes on diagnostic delay for pulmonary tuberculosis in Beijing. Int J Tuberc Lung Dis 2014;18:267-71.  Back to cited text no. 9
Kim SJ, Hong YP, Lew WJ, Yang SC, Lee EG. Incidence of pulmonary tuberculosis among diabetics. Tuber Lung Dis 1995;76:529-33.  Back to cited text no. 10
Young F, Critchley JA, Johnstone LK, Unwin NC. A review of co-morbidity between infectious and chronic disease in Sub Saharan Africa: TB and diabetes mellitus, HIV and metabolic syndrome, and the impact of globalization. Global Health 2009;5:9.  Back to cited text no. 11
Pickup JC. Inflammation and activated innate immunity in the pathogenesis of type 2 diabetes. Diabetes Care 2004;27:813-23.  Back to cited text no. 12
Broxmeyer L. Diabetes mellitus, tuberculosis and the mycobacteria: Two millennia of enigma. Med Hypotheses 2005;65:433-9.  Back to cited text no. 13


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