Diabetes and tuberculosis, An Unholy Alliance
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This document discusses the relationship between diabetes (DM) and tuberculosis (TB). It notes that 347 million people worldwide have diabetes, and DM increases the risk of TB 3-fold. DM impairs immunity and lung function, aiding the growth of TB bacteria. Patients with both DM and TB may have atypical symptoms and lung abnormalities on imaging. The interaction between the two diseases can make their treatment more challenging.
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Diabetes and tuberculosis, An Unholy Alliance
- 1. Dr. MohammadTanvir Islam Assistant Professor, Medicine Bangabandhu Sheikh Mujib Medical University Dr. Shamim Ahmed Assistant Professor, RespiratoryMedicine Bangabandhu Sheikh Mujib Medical University
- 2. 347 million people worldwide have diabetes 80% diabetes deaths in low- and middle- income countries 7th leading cause of death in 2030 In Bangladesh between 2% and 21%
- 7. About 9 million people around the world A total of 1.5 million people died in 2013 The incidence ofTB in Bangladesh is 225 per 100,000
- 12. Big concern about twin epidemics Low to middle income countries DM increases the risk ofTB 3 fold TB causes glucose intolerance
- 13. Association between diabetes and active tuberculosis in studies stratifying by glucose control
- 14. 14.8% of PTB & 20.2% smear positive PTB cases are directly linked to DM TB causes glucose intolerance 50 % of which normalizes after ATT DM increases risk ofTB 3 times TB increases risk of DM 2 times
- 15. Since ancient times Susruta in 600 AD Avicenna (780-1027 AD) Roots 1950 Nicholas 1957 McCornick 2007
- 17. Four possible outcomes: Immediate clearance of the organism Latent infection The onset of active disease (primary disease) Active disease many years later (reactivation disease).
- 18. Persons with medical conditions that weaken the immune system HIV infection Diabetes mellitus Medical treatments such as corticosteroids or organ transplant Substance abuse Organ transplants Malignancy
- 19. Hyperglycemia favours growth , viability and propagation of tubercle bacilli and hamper resistance to infection & repair capacity Increased availability of glycerol and nitrogenous substances aid the growth of tubercle bacilli High level of insulin have been shown to promote a decrease inTh1 immunity through a reduction in theTh1 cell toTh2 cell ration and interferon gamma to IL-4 ratio
- 20. Abnormal chemotaxis Decreased peripheral monocytes with impaired phagocytosis Poor blast transformation of lymphocytes DefectiveC3 opsonic function Decrease inTh1 immunity
- 22. Diminished bronchial reactivity Reduced diffusion capacity Occult mucous plugging of airways Reduced ventilatory response to hypoxaemia
- 23. Microangiopathic change in pulmonary vasculature Non-enzymatic glycosylation of tissue protein Thickening of epithelial and caplillary BM Interference with clearance mechanism
- 24. Increased risk of tuberculosis Diabetes Neutrophil • Abnormal Chemotaxis • Phagocytosis • Microbicidal acitvity Reduction inTh1 cellsInterferon gamma Increased availability of Glycerol and nitrogenous substances Lung physiological and pathological dysfunction
- 25. Increased risk ofTuberculosis Impairment of Innate immunity Acquired immunity Diabetes Lung Physiologic dysfunction Lung Pathologic dysfunction
- 26. Relative and absolute overproduction of adrenocorticotropic hormone Increased supply of corticosteroids Corticosteroids are insulin antagonists resulting in insulin resistant diabetes.
- 27. More aggressive course Less clinical manifestations Typical features like cough, weight loss are less prominent Prolonged duration of fever
- 28. Features of one disease can mimic the other Might progress rapidly Flare up or spread of tuberculosis More complications Risk for Drug-resistantTB
- 29. Clinical feature DM &TB TB only Fever 64% 98% Night sweat 52% 85% Cough>3wks 71% 96% Weight loss 69% 94% Hossain D, Latif ZA, Mahtab H Clinical and radiological presentation of pulmonary Tuberculosis in diabetic and non-diabetic patients. J Soc Heart Chest Dis 2004;2:69-72
- 30. Frequently atypical Lower lobe opacity Multilobar Cavitary lesion Pleural effusion
- 31. Radiological feature DM +TB TB alone Upper lobe opacity 17% 56% Lower lobe opacity 19% 7% Multi lobe opacity 64% 36% Cavity 82% 59% C.Perez et.al. 2001
- 33. DM &TB prevalence is increasing They are epidemic in identical areas DM is a risk factor forTB TB causes glucose intolerance Clinical and radiological features in a diabetic TB patient may be atypical
Notes de l'éditeur
- Tuberculosis in diabetes mellitus: aggravation and its immunological mechanism: Kazuyoshi KAWAKAMI (Department of Internal Medicine, Division of Infectious Diseases, Graduate School and Faculty of Medicine, University of the Ryukyus). It has been well documented that diabetes mellitus (DM) is a major aggravating factor in tuberculosis. The onset of this disease is more frequent in DM patients than in individuals with any underlying diseases. However, the precise mechanism of this finding remains to be fully understood. Earlier studies reported that the migration, phagocytosis and bactericidal activity of neutrophils are all impaired in DM patients, which is related to their reduced host defense to infection with extracellular bacteria, such as S. aureus and E. colli. Host defense to mycobacterial infection is largely mediated by cellular immunity, and Th1-related cytokines, such as IFN-gamma and IL-12, play a central role in this response. It is reported that serum level of these cytokines and their production by peripheral blood mononuclear cells (PBMC) are reduced in tuberculosis patients with DM, and this is supposed to be involved in the high incidence of tuberculosis in DM. The increase of infections in patients with DM is known to depend upon an immunosuppressive condition which is brought about by impaired innate immunity and acquired immunity. For instance, functions of neutrophils such as phagocyte, chemotaxis and cytokine-production are decreased in DM model mouse and hyperglycemia and a Th2-axis shift which reduces Th1-dependent immunity are observed in DM patients. However, the majority of results concerning interaction of hyperglycemia and immune function are controversial and relevance of hyperglycemia and/or hyperinsulinemia to immunosuppressive mechanisms remains unclear.