The Bidirectional Relationship between Tuberculosis and Diabetes

Tuberculosis Research and Treatment
Volume 2017 (2017), Article ID 1702578, 6 pages
https://doi.org/10.1155/2017/1702578

The Bidirectional Relationship between Tuberculosis and Diabetes

1Endocrine & Diabetes Unit, Department of Medicine and Therapeutics, School of Medicine and Dentistry, College of Health Sciences, University of Ghana, Legon, Accra, Ghana
TwoDirectorate of Medicine, Endocrine and Diabetes Unit, Komfo Anokye Teaching Hospital, Kumasi, Ghana
3Department of Medicine and Therapeutics, School of Medicine and Dentistry, College of Health Sciences, University of Ghana, Legon, Accra, Ghana

Received 11 August 2017; nonetheless 25 September 2017; Accepted 17 October 2017; Released 12 November 2017

Academic Editor: Tom Ottenhoff

Copyright © 2017 Ernest Yorke et al.. That is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

The burden of tuberculosis (TB) particularly in developing countries continues to stay high despite efforts to enhance preventive strategies. Known traditional risk factors for TB include malnutrition, poverty, overcrowding, and HIV/AIDS; however, diabetes, obesity, which causes immunosuppression, is increasingly being identified as an independent risk factor for tuberculosis, and both often coexist and affect each other. Diabetes can also result in acute illness, reactivation of dormant tuberculosis foci, and poor treatment results. Tuberculosis as a disease entity on the other hand and some commonly used antituberculous medications separately may cause impaired glucose tolerance. This review seeks to highlight the effect of comorbid TB and diabetes on each other. It is our expectation that this review will increase the awareness of clinicians and managers of both TB and diabetes program on the impact of the interaction between these two disease entities and how to better monitor and manage patients.

1. Introduction

TB infections are still a concern worldwide and it remains a deadly communicable disease. The World Health Organization (WHO) estimated that 10.4 million new cases of TB occurred and 1.4 million died from the illness in 2015 despite many preventative approaches to decrease the burden and affect [1]. Over 70 percent of these new cases occurred in developing countries, with the African American region experiencing the highest rate of death relative to population [1]. The International Diabetes Federation (IDF) quotes a current worldwide diabetes disorder burden of about 415 million, and this will be estimated to hit 642 million by 2040 (over 60% growth) [2]. Developing countries are expected to undergo the most gains driven mainly by type 2 diabetes [2]. This expected trend in both states would also increase the interaction between them [1, 2].

Aside from the traditional risk factors including malnutrition, poverty, overcrowding, and immunosuppression such as HIV/AIDS, diabetes is increasingly being acknowledged as an independent risk factor for tuberculosis, and both often coexist [3, 4]. Several studies around the world suggest that 5–30 percent of TB patients have concomitant diabetes mellitus [5].

This TB and diabetes institution was known by Avicenia in as early as 1000 AD, when he noticed that tuberculosis (called phthisis in Greek) was often associated with diabetes [6]. Additionally, an Indian saint, Yugimahamuni, clarified a bunch of symptoms for the TB/diabetes institution (which he predicted meganoikal). These symptoms include obesity, glycosuria, thirst, incontinence, respiratory symptoms, and unconsciousness [7]. Afterward, this interaction between TB and diabetes is increasingly being recognized and handled [3]. Diabetes and TB as different disease entities affect negatively each other [8]. Whilst diabetes can result in a more severe type of TB and affect its presentation, TB can result in impaired glucose tolerance and hamper glycemic control [9].

2. The Interplay between Diabetes and Tuberculosis

2.1. Diabetes as a Risk Factor for TB

Diabetes is a risk factor for lower respiratory infections such as TB. Regardless of the fact that TB is more associated with other immunosuppressive states like HIV infection, due to the larger amounts, diabetes remains a more important factor for TB infections in the population level [3]. A review by Stevenson et al. reported that diabetes increases TB risk 1.5 to 7.8 times [10], whilst some other meta-analysis by Jeon and Murray found that the relative risk for TB among diabetes patients had been 3.11 [11]. In the latter evaluation, among TB patients, diabetes incidence ranged from 1.9% to as large as 35% following screening; and the highest rates were among regions of the planet with the highest diabetes prevalence [11]. Again, an American study noted that the odds ratio of multidrug-resistant (MDR) TB associated with diabetes patients is 2.1 [12].

Although type 2 diabetes is much more prevalent worldwide, the probability of tuberculosis in type 1 diabetes is three to five times [13, 14] greater due to comparatively poorer controller, lower body weight, and youthful age of affected persons [14].

Whilst it isn’t clear whether diabetes impacts the presentation of TB, among diabetes patients, they tend to reveal more lower lobe involvement than their nondiabetic counterparts due to reactivation of older foci [8]. Again, some studies have reported lower rates of cavitation [12] whilst some reported greater prices [15–17]. TB associated with diabetes might also reveal higher rates of hemoptysis, fever, and atypical presentations compared with nondiabetics with TB [10, 12, 18].

Alisjahbana et al. reported in 2007 that TB patients who had diabetes experienced more symptoms, but with no signs of more severe illness, and a greater percent positive sputum for acid-fast bacilli after microscopic examination in two weeks compared with their nondiabetic counterparts (18.1% versus 10.0%). However, this was no longer statistically significant after adjustment for age, sex, BMI, study website, chest radiograph abnormalities, and sputum mycobacterial load before initiation of treatment. The study also reported that, after 6 weeks, 22.2% of the sputum of these diabetes sufferers climbed Mycobacterium tuberculosis compared with 6.9% among controls (adjusted odds ratio: 7.65; ) [12]. In a retrospective study between TB patients from South Texas (USA) and northeastern Mexico they found out that patients with diabetes (identified by self-reporting) were more likely to stay positive in the first month (Texas cohort) or second month (Mexico cohort) of treatment [15]. Other studies also have shown a tendency towards increased time to sputum conversion [19–22], although other have demonstrated no connection between diabetes and sputum conversion rate in the end of month two [21–24].

Diabetes increases the probability of failure and death combined, death, and relapse among patients with TB. A systematic review by Baker et al. reported patients with diabetes have a risk ratio (RR) for the combined outcome of failure and death of 1.69 (95% CI: 1.36 into 2.12), although the RR of death during tuberculosis treatment among 23 unadjusted research was 1.89 (95 percent CI: 1.52 into 2.36) [25]. Diabetes was also associated with a greater risk of relapse (RR: 3.89; 95 percent CI: 2.43 into 6.23) [25]. This review however failed to find evidence for an increased risk of tuberculosis recurrence with drug-resistant strains among individuals with diabetes [25]. In a Brazilian study that was aimed at assessing the sociodemographic and clinical factors that might affect different results of TB in patients with diabetes discovered in the Brazilian nationwide database from 2001 to 2011, it had been found out that the development of MDR TB was more related to alcoholism (OR = 9.60, 95 percent CI: 6.07–15.14), previous default (OR = 17.13, 95 percent CI: 9.58–30.63), and transfer of treatment centres (OR = 7.87, 95 percent CI: 4.74–13.07) [26].

Diabetes can affect the pharmacokinetics of anti-TB drugs, particularly rifampicin, by decreasing their plasma levels [4]. But, there are conflicting reports on whether this impacts the effectiveness of TB treatment [4, 8]. As a result, the routine for treatment of TB among both diabetics and nondiabetics remains the same in the moment [3, 4].

2.2. TB as a Risk Factor for Diabetes

Whilst the bidirectional connection between diabetes and TB continues to be proven, dedicated studies to evaluate if TB increases the risk of diabetes are few [27–29]. TB may result in impaired glucose tolerance (IGT) [29, 30] and new onset diabetes [9, 18, 29]. Normally, IGT normalizes following the TB has been successfully treated, however, it’s a substantial risk factor for developing type 2 diabetes later on [31].

It is often difficult to conclusively label TB as the risk factor for recently discovered hyperglycemia or diabetes among previously unscreened TB sufferers [28, 29, 32]. Basoglu et al. [29], in a study of active TB patients with no history of diabetes mellitus, discovered glucose intolerance among 10.4% and diabetes at 8.6% in his cohort; and compared with a matched control group of community-acquired pneumonia, 17.4% were found to have diabetes and none of them had sugar intolerance. There was no substantial difference between both groups (). Oral glucose tolerance test (OGTT) results returned to normal in both TB and pneumonia classes following treatment. In a Nigerian study, a sequential follow-up of oral glucose tolerance tests on 54 patients with active TB sufferers, 42.6% were found to have abnormal results, of whom 5.6% had diabetes and 37.0% had IGT [28]. Three weeks following the antituberculosis medication, just one of those eight patients with impaired glucose tolerance in the second oral glucose tolerance test remained intolerant of sugar whilst just one individual was frankly diabetic. Again, among a mostly white English population, a retrospective cohort analysis using information from two Oxford Record Linkage Study (ORLS) datasets from 1963 to 2005 was carried out by Young et al. [27]. They found out that although diabetes has been associated with two- to threefold greater risk of TB, there was no proof that TB increases the probability of DM.

This infection-related hyperglycemia and some commonly used antituberculosis drugs such as rifampicin and isoniazid can result in overdiagnosis of diabetes in previously unscreened TB sufferers [3, 33, 34] and worsen glycemic control in previously diagnosed diabetes sufferers [31]. The latter situation may therefore warrant adjustment in doses of antiglycemic agents or a comprehensive switch to insulin treatment.

3. The Underlying Pathophysiological Mechanisms

The increased risk of TB among diabetes patients is multifactorial [35–37] and many putative mechanisms are suggested (refer to Figure 1). There’s diminished cellular immunity due to reduced T-lymphocyte count in addition to function and a reduced neutrophil count [35]. Diabetics reveal a diminished T-helper 1 (TH 1) cytokine response level, tumor necrosis factor (TNF-alpha and TNF-beta), interleukin-1, and interleukin-6 production compared to their nondiabetic counterparts [35, 36]. The susceptibility of diabetes patients to TB is mainly due to reduced amounts and function of T-lymphocytes. Especially TH1 cytokine inhibition of Mycobacterium tuberculosis [35, 36]. There’s macrophage dysfunction in diabetes which causes impaired production of reactive oxygen species and phagocytic and chemotactic function [35, 36]. Chemotaxis of monocytes can also be diminished in patients with diabetes, a flaw which does not improve with insulin [38]. Hyperglycemia is thought to also inhibit the force of respiratory burst in expelling pathogens [35, 36]. Whilst these suggested mechanisms are plausible, it is necessary that additional mechanistic studies are done to confirm them otherwise.

Figure 1: Pathophysiological mechanisms underlying TB–diabetes discussion [3, 18, 28, 29, 31, 35–39]. TH1: T-helper 1; TNF: tumor necrosis factor; TB: tuberculosis.

The stress response to infection may also play a role in dysglycemia, a situation mediated by the impact of interleukin-1 (IL-1), interleukin-6 (IL-6), and TNF-alpha [3, 31, 39]. This temporal relationship has been demonstrated in some research where between 19 and 42.6% of active TB patients were discovered to have IGT or diabetes with a substantial reduction or complete regression at the rates following treatment [28, 29]. One of those research had a comparable rate of glucose intolerance in the control group who’d community-acquired pneumonia, further encouraging the possibility of a stress reaction to infection [29]. By comparison, in the analysis by Zack et al. [40], 41% of 256 patients admitted to the TB ward had glucose intolerance when oral glucose tolerance tests were conducted after a minumum of one month of hospitalization. A larger number of patients chose to have glucose intolerance with some developing diabetes. But, it is thought that the largely abnormal test results, acquired a month after treatment was started, may reflect underlying true glucose intolerance as opposed to a stress reaction to infection [40].

On the flip side, TB might lead to TB pancreatitis in addition to pancreatic endocrine hypofunction that might lead to IGT or new onset diabetes or interrupts its control [31, 39]. TB pancreatitis might become evident only after the person develops diabetes [31, 39]. Last, whilst malnutrition has been suggested as a risk factor for ailments and dysglycemia, body mass index hasn’t yet been associated with IGT or diabetes [18, 28, 29].

4. Management of Diabetes Comorbid Diabetes and TB

Despite hints that diabetes can result in more severe illness, death, and relapse, the dosage regimen and duration of anti-TB drugs among those with or without TB are not distinct [1, 25]. Traditionally, many centers treat TB for 2 months, comprising an initial intensive period of 2 months of rifampicin, isoniazid, pyrazinamide, and ethambutol and a further 4-month continuation period of rifampicin and isoniazid [1].

There’s a suggested pharmacokinetic and pharmacodynamic interaction between anti-TB drugs and antiglycemic agents. Rifampicin, which is vital among the cocktail of anti-TB drugs, through enzyme induction, accelerates the metabolism of sulphonylureas and biguanides, reducing their plasma levels and thus leading to hyperglycemia [3, 41]. One of nondiabetics, it enhances the intestinal absorption of sugar [41]. Isoniazid antagonizes the activity of sulphonylureas and worsens glycemic control [34]. In some scenarios, isoniazid decreases the metabolism of oral antiglycemic agents and increases their blood glucose levels, such as cytochrome P2C9 (CYP2C9) involved in the metabolism of sulphonylureas; however, it is thought that the inducing effect of rifampicin far outweighs this inhibitory effect [42]. Again, it may inhibit the release of insulin among nondiabetics inducing hyperglycemia [34]. Rifampicin and isoniazid are not known to affect the breakdown of insulin significantly since insulin is largely degraded from the hydrolysis of disulphide bonds throughout the activity of insulin degrading enzyme in the liver [43].

Theoretically, dipeptidyl peptidase (DPP) IV inhibitors can cause immune paresis and possibly worsen treatment results in TB direction [3, 44]. Thiazolidinediones may be substrates for the cytochrome P450 enzymes, which are triggered by rifampicin. Rosiglitazone is metabolized largely by CYP2C8, and rifampicin decreases levels of rosiglitazone from 54–65% and pioglitazone by 54 percent [21].

The treatment of diabetes with concomitant TB infection requires careful evaluation and decision of antiglycemic medicine. Again, the general method of management of diabetes doesn’t differ in the presence of TB or not, regardless of the potential drug–drug interactions described above [1, 3].

Appropriate diet advice is necessary, taking under consideration the need to balance glycemic control and the nutrient needs of largely underweight and malnourished individuals [45]. Metformin remains the first-line antiglycemic agent, a comparatively safe and cheap medication with reduced incidence of hypoglycemia [45]. Other agents to be considered include sulphonylureas, meglitinides, alpha-glucosidase inhibitors, dipeptidyl peptidase (DPP) IV inhibitors, glucagon-like peptide (GLP) 1 analogs, thiazolidinediones, and insulin [45]. The specific medication choice has to be based on patients’ characteristics, accessibility, and price as well side effects profile. Indeed, treatment has to be individualized [45]. Treatment could be escalated with regard to increasing dosages or frequency of a specific class or the inclusion of a couple of classes as the situation may merit to achieve adequate glycemic control or goals [45].

In many scenarios, insulin would be the preferred agent in type 2 diabetes where there is active TB infection [3]. The rationale for the selection of insulin comprises the acute TB infection, body tissue loss, the demand for greater anabolism, pancreatic hypofunction, interaction between oral antidiabetic agents and some antituberculous medications as indicated previously, and the possibility of associated liver disease which would preclude using oral agents [3, 33].

For the reasons previously, patients with preexisting diabetes on oral agents might be switched to insulin treatment in active TB after identification is made, or when on insulin already; adjustments may have to be made for worsening glycemic control. Once glucotoxicity improves and infection is controlled, insulin requirement may fall. However, requirement can grow again once appetite improves and food intake increases [3]. The alternative of insulin should be based on safety, effectiveness, cost, and individual characteristics. It has to be said, but that when the infection has been controlled, oral antidiabetic agents may be carefully considered [3]. Despite these advantages, insulin might not be easily available or costly to manage in some areas of the planet [46].

For optimal control, routine glucose monitoring is necessary. This helps in the early recognition of potential side effects such as hypoglycemia from some antiglycemic medications like sulphonylurea and insulin and also the spatial trend of sugar profiles that may need dose adjustments. Nonetheless, in many parts of the world such as in developing countries, individuals are required to pay for glucometers and sugar strips and there are no compensation schemes or reimbursement. This frees the ability to achieve goals and identify and confirm hypoglycemia.

Most importantly, patient education is key in understanding the disorder character (both TB and diabetes), length of treatment, side effects of drugs, and complications of illness in addition to the promotion of healthy lifestyle choices [45, 47, 48].

5. Limitations

The effect and connection between TB and diabetes may change across different regions of the planet based on the incidence and prevalence of each state. Diabetes is most widespread in the western developed world with comparatively lower incidence of TB [2]; it is expected that the incidence of TB among diabetes patients would be reduced whilst other respiratory ailments may be more significant [4]. In the developing world with the highest number of TB cases and projected growth in diabetes, the interaction and also the incidence of TB among diabetes would be far greater [2, 4]. Compared to developing countries, resources for the management of these two states will also be skewed in favor of the western and other more developed countries, a situation that might further compound this expected negative interaction of comorbid diabetes and TB on each other.

6. Conclusion

There’s a bidirectional connection between TB and diabetes, and they both affect the presentation of each other [3]. Diabetes has been increasingly acknowledged as a risk factor for TB and might affect its presentation, whilst TB may worsen glycemic control or contribute to IGT among TB patients [3]. This connection demands adjustment in treatment and the requirement to use insulin in the treatment of hyperglycemia during active TB infection when required. A review of the antiglycemic agent(s) can be warranted once TB treatment is over [3].

The expected rise in diabetes cases in developing countries (driven mainly by type 2 diabetes) which also bear the brunt of tuberculosis will increase the effect of diabetes on TB in the forthcoming future [1, 2].

It is estimated that this review will offer additional insights to whether regular screening for dysglycemia should be done for many TB patients, particularly at the time of diagnosis. Among patients with diabetes, there is a stronger case to be made for screening for TB regularly or in the least suspicion [48]. Diagnosed patients should promptly be referred to a TB center for treatment. Strategies for preventing TB must continually be highlighted [48]. These include improvements in housing and nutrition, poverty reduction, treatment of HIV/AIDS, and over all the availability of diagnostic instruments such as sputum smear microscopy, X-rays, and automatic molecular evaluations [1, 48].

The realization of these efforts and approaches for the prevention and management of comorbid diabetes are going to be a challenge in less developed areas of the world [1, 48]. These nations have the least healthcare resources which will hamper their ability to manage the expected negative effect of diabetes on TB and vice versa [3, 48].

Abbreviations

AIDS: Acquired immune deficiency syndrome
CI: Confidence interval
CYP: Cytochrome P
DPP IV: Dipeptidyl peptidase IV
HIV: Human immunodeficiency virus
IDF: International Diabetes Federation
IGT: Impaired glucose tolerance
IL: Interleukin
MDR: Multidrug-resistant tuberculosis
OGTT: Oral glucose tolerance test
OR: Opportunities ratio
ORLS: Oxford Record Linkage Study
RR: Relative risk
TB: Tuberculosis
TNF: Tumor necrosis factor
TH: T-helper
USA: United States of America
WHO: World Health Organization.

Disclosure

This analysis was financed by the lead writer.

Conflicts of Interest

The authors declare no conflicts of interest concerning the publication of this manuscript.

Authors’ Contributions

Ernest Yorke conceived the study, participated in its design and literature search, and drafted the manuscript and collation of all drafts. Yacoba Atiase, Josephine Akpalu, Osei Sarfo-Kantanka, Vincent Boima, and Ida Dzifa Dey led to the study design, literature search, and manuscript draft. All authors read and approved the last version of the manuscript.

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