Leading Article
47,3
TUBERCULOSIS AND DIABETES : AN APPRAISAL
Since ancient times, physicians have been aware
of the association between tuberculosis and diabetes
mellitus: perhaps the earliest to note it was the great
Indian physician Susruta, in 600 A.D, while
Avicenna (780-1027 A.D.) had commented that
phthisis frequently complicated diabetes.1 The global
burden of diabetes mellitus was estimated by the
World Health Organisation2 in 1998. It has been
projected that the prevalence of diabetes among
adults world wide will more than double, from 135
million (4%) to 300 million (5.4%), by the year 2025.
The major part of this tremendous increase will occur
in developing countries, like India and China,
wherein a 170% increase, from 84 million to 228
million is projected. With the revision of the criteria
for the diagnosis of diabetes (Appendix), by the
American Diabetes Association, in 19973, which are
simpler to apply compared with those proposed by
the National Diabetes Data Group of the National
Institute of Health, in 19794, the prevalence rates of
diabetes are expected to increase further.
Tuberculosis has already been declared a “global
emergency” by the WHO5 in 1992, with an estimated
one third of the world’s population infected with
Mycobacterium tuberculosis and tuberculosis
recognised as the single biggest killer. Now, with
diabetes assuming epidemic proportions in the first
quarter of the 21st century, it is imperative to take
measures for the prevention and control of this deadly
duo.
Diabetes mellitus is also recognised as an
independent risk factor for developing lower
respiratory tract infections6. Whereas infections with
Staphylococcus aureus, Gram-negative bacteria, and
fungi occur more frequently, those with organisms
like Streptococcus, Legionella, and Influenza cause
significantly more morbidity and mortality7.8.
Tuberculosis occurs with an increased frequency in
diabetics 9.10 and causes a significantly greater
mortality11.12. Increased reactivation of tuberculosis
lesions has also been recorded in diabetics13. At the
same time, tuberculosis appears to aggravate
diabetes, with patients requiring higher than before
doses of insulin. The incidence of diabetes as such
appears to be higher among tuberculosis patients14-16
as compared to the general population.
Ind. J. Tub., 2000.
Tuberculosis Complicating Diabetes Mellitus
In 1883, Windle autopsied 333 known diabetic
subjects and observed pulmonary tuberculosis in
more than 50% of them17. In a classic study, Root’’
reported that 2.8% of 1373 hospitalised diabetics
had pulmonary tuberculosis. Of the 750 juvenile
diabetics, 1.6% had tuberculosis as compared to
0.12% among school children. After studying the
association between diabetes and tuberculosis, he
made the following observations:
(i) The development of tuberculosis occurred
ten times more frequently in juvenile
diabetics.
(ii) In 85% of the patients, tuberculosis had
developed after the onset of diabetes.
(ii) The occurrence of pulmonary tuberculosis
increased with the duration of diabetes.
Hence, he concluded that a diabetic patient
appeared doomed to die of pulmonary tuberculosis
if he succeeded in escaping diabetic coma. Root,
however, postulated that the association between the
two diseases was one sided i.e., diabetic patients
tended to contract tuberculosis but the reverse was
rare.
The Philadelphia survey revealed that 8.4% of
the 3,106 diabetics had pulmonary tuberculosis as
compared to 4.3% of the 71,767 presumably healthy
industrial workers10. Tuberculosis was present in
17% of the diabetics who had had the disease for
more than 10 years compared to 5% in the diabetics
with less than 10 years of the disease. A higher
prevalence of tuberculosis was found in diabetics
requiring more than 40 units of insulin per day.
Diabetes mellitus was present in 8.3% of the cases
of reactivation tuberculosis in New York city1’, the
second most common association after alcoholism.
A Korean study18 found that pulmonary tuberculosis
had developed in 170 patients among 8,015 diabetics
(2.1%) as compared to 4,935 patients among
806,698 control subjects (0.6%). Estimated annual
incidence rates of bacteriologically confirmed cases
of tuberculosis in diabetics and non-diabetics were
281 and 55 per 10,000 respectively. The study
concluded that the relative risk of developing
pulmonary tuberculosis, bacteriologically confirmed,
 3 AMRIT GUPTAN AND ASHOK SHAH

was 5.15 times higher in diabetics than in matched glycated haemoglobin, tuberculosis follows a more
controls. destructive course and is associated with higher
Some of the later studies, done in developed mortality. Multiple pulmonary physiologic
countries have failed to demonstrate an abnormalities have also been documented in
epidemiological association between tuberculosis diabetics that contribute to delayed clearance of and
and diabetes19, 20. Perhaps, this is largely due to the spread of infection in the host.22 Infection with
low prevalence of tuberculosis in these areas. tubercle bacilli leads to further alterations in
However, in countries like India, diabetes remains cytokines, monocyte-macrophages and CD4/CD8 T
one of the most important risk factors disposing cell populations.25. 26 The balance of the T lymphocyte
towards tuberculosis, along with malnutrition, subsets CD4 and CD8 plays a central role in the
alcoholism and HIV infection. The prevalence of modulation of host defenses against mycobacteria
pulmonary tuberculosis in diabetics in India varies and has a profound influence on the rate of regression
from 3.3% to 8.3%, about 4 times that of general of active pulmonary tuberculosis.27
population.
Glucose Intolerance in Tuberculosis
Is Immune Dysfunction in Diabetics a
Predisposing Factor ? In the early part of this century, the prevailing
view, as suggested by Root9 was that “tuberculous
A probable cause of increased incidence of patients do not develop diabetes with any greater
pulmonary tuberculosis in diabetics could be defects frequency than the non-tuberculous". However,
in host defenses and immune cell functions Nichols14, in 1957, changed this view when he
(Table 1) 2 1 . 2 2 . The immune derangements described 178 tuberculous patients of whom 5% had
predominantly involve the cell-mediated arm of the diabetes and a further 22% had an abnormal
immune system. Also, the degree of hyperglycemia screening test. In India16, a multicentric study done
has been found to have a distinct influence on the in 1987 found the prevalence of unsuspected diabetes
microbicidal function of macrophages, with even in tuberculous patients to be of the order of 9.7%: In
brief exposures to blood sugar level of 200 mg% males above 40 years, the rate was 17.8% compared
significantly depressing the respiratory burst of these with 5.1% in those below 40 years. And in females,
cells.23.24 This is borne out by the observation that in the respective rates were 23.5% and 4.0%, the
poorly controlled diabetics, with high levels of overall rates for males and females being 10% and
8.7% respectively. Various other Indian studies have
Table 1. List of defects in diabetics’ immunologic make- estimated the prevalence of glucose intolerance in
up and physiologic pulmonary functions tuberculosis to be between 1.5% to 14%.
Immunologic abnormalities Pulmonary physiologic Two recent studies conducted in Africa also had
in diabetics dysfunctions in diabetics
similar findings. In the Tanzanian study,28 done as
Abnormal chemotaxis, Diminished bronchial per WHO criteria, in 506 consecutive patients
adherence, phagocytosis reactivity
admitted w i t h sputum positive pulmonary
and microbicidal function
of polymorphonuclear tuberculosis, 9 of whom were known diabetics,
Decreased peripheral Reduced elastic recoil and
diabetes was diagnosed by the consecutive oral
monocytes with impaired lung volumes. glucose tolerance tests (OGTTs), in 11 additional
phagocytosis. patients giving a crude diabetes prevalence rate of
Poor blast transformation Reduced diffusion capacity 4%. Impaired glucose tolerance (IGT) was present
of lymphocytes. in 82 patients (16.2%). In comparison, a similar
Defective C3 opsonic Occult mucus plugging of OGTT survey, carried out by the authors in a
function airways community, revealed prevalence of 0.9% in respect
Reduced ventilatory of diabetes and 8.8% for IGT. The Nigerian study29,
response to hypoxaemia done on 54 patients with active pulmonary
and tuberculosis found that 3 patients had OGTT values
Adapted from: Infections in Diabetes Mellitus21-22 in the diabetic range and 20 had IGT.
 TUBERCULOSIS AND DIABETES : AN APPRAISAL
An 8 year study, done in Japan30 from 1987 to
1994, revealed that in 2,659 patients the prevalence
of diabetes in cases of active tuberculosis was 13.2%:
In males above 40 and 50 years of age, the rates
were 22% and 21.3% respectively. The prevalence
in males was significantly higher than in females.
Moreover, the prevalence of diabetes among patients
with active pulmonary tuberculosis was significantly
higher during 1991-1994 compared with during
1987-1990.
Impaired glucose tolerance in tuberculosis is much
higher than overt diabetes. Although IGT reverts to
normal in a large number of cases with effective
chemotherapy, the higher percentage with IGT is
significant because, according to the National
Diabetes Data Group of NIH, one to five per cent of
patients with IGT may progress to overt diabetes,
annually.
Causes of Glucose Intolerance in Tuberculosis
Acute severe stress is an important cause of the
development of impaired glucose tolerance. Fever,
protracted inactivity and malnutrition stimulate the
stress hormones epinephrine, glucagon, cortisol and
growth hormone, which acting synergistically raise
the blood sugar level in excess of 200 mg%.31 Plasma
levels of IL-1 and TNF alpha are also raised in severe
illness which can stimulate the anti-insulin
hormones32. Age, co-existent illnesses and alcoholism
also influence the host response. Tempting though it
may be to ascribe the metabolic derangements in
tuberculosis to stress, the complex host parasite
relationship suggests otherwise. Serum levels of
adrenocortico-tropin hormone, cortisol and T3 have
been found to be decreased in patients with
tuberculosis.33 Clinical and sub-clinical
hypoadrenalism has been described frequently in these
patients.34 These abnormalities make the patient’s
ability for a stress response doubtful. The endocrine
function of pancreas has also been found to be
adversely affected in severe tuberculosis,” and a
higher incidence of chronic calcific pancreatitis occurs
in patients w i t h concomitant diabetes and
tuberculosis35 leading to an absolute orrelative insulin
deficiency state. A family of fatty-acid-transporter
proteins in the tubercle bacillus may cause
dysregulation of energy homeostasis in the disease.36
The fatty acid transporter protein gene of myco-
bacterium when expressed in mammalian
5
hepatocytes increases preferentially the uptake of
long chain fatty acids (LCFAs). The LCFAs are an
important source of energy for most organisms and
also function as blood hormones regulating key
functions such as hepatic glucose metabolism.36
Derangements of lipid metabolism have been
described in patients with tuberculosis.37
Effect of Anti-tuberculosis Drugs on Blood
Sugar Level
Rifampicin is a powerful inducer of the hepatic
microsomal enzyme system and frequently interacts
with other drugs. It lowers the serum levels of
sulphonyl ureas and biguanides.38 Hence, patients
with co-existing diseases should have their doses of
oyal anti-diabetic dnigs adjusted upwards according
to plasma glucose concentration.
Takayasu et al39 observed that Rifampicin induced
an early phase hyperglycemia which he attributed to
augmented intestinal absorption. However, no case
of overt diabetes was observed and it was felt that
Rifampicin was not diabetogenic. Rifabutin, a newer
rifamycin, also induces hepatic metabolism but is
not as potent an inducer as is Rifampicin.40 Although
its interactions with Zidovudine, Fluconazole and
Clarithromycin have been studied extensively, the
effects of concomitant administration of oral
hypoglycemics have still to be clarified.
Other anti-tuberculosis drugs interfere very rarely
with blood sugar level. An overdose of INH41 may
cause hyperglycemia while in rare circumstances,
diabetes may become difficult to control in patients
on Pyrazinamide.42 Hypoglycemia may rarely be seen
in patients on Ethionannde.43
Clinical Aspects of Concomitant Tuberculosis
and Diabetes
Symptoms of one disease often mimic those of
the other. Loss of weight, loss of appetite and
lassitude are common to both the diseases. The
association is more common among those above 40
years of age and males appear to be at a somewhat
greater risk compared with females. Holden and
Hiltz43 described 106 patients with tuberculosis and
diabetes in which diabetes appeared first in 48, while
tuberculosis appeared first in 40 and the two
conditions were diagnosed simultaneously in 18
patients, as did Sumrova come to similar findings.17
6 AMRIT GUPTAN AND ASHOK SHAH
Patients of tuberculosis who develop diabetes
have greater clinical severity at the onset, a greater
degree of lung involvement and residual changes.
The diabetics who develop pulmonary tuberculosis
have higher blood sugar levels and develop complica-
tions like coma and diabetic microangiopathies.17
Radiological Aspects of Concomitant
Tuberculosis and Diabetes
The radiological aspects of concomitant tuber-
culosis and diabetes were first described by Sosman
and Steidl 4 4 . They reported that “diabetic
tuberculosis” has a special radiological pattern
consisting of confluent, cavitary, wedge shaped
lesions spreading from the hilum towards the
periphery, predominantly in lower zones, to the extent
of around 20%.I4-4S
Marias46 observed lower lung field tuberculosis
in 29% of patients with diabetes, as compared to
4.5% in the non-diabetic patients. However, in other
studies 47 , cavitary disease and multi-lobe
involvement was found to be more common in
patients with pulmonary tuberculosis and diabetes.
A study48 to evaluate the CT features of pulmonary
tuberculosis in immunocompromised and diabetic
patients compared with patients with no underlying
disease was done in Japan. Diabetics and immuno-
compromised patients had a higherprevalence of non-
segmental distribution (30%) and multiple small
cavities (44%). Unusual localisation of the disease
including basal segment of lower lobe, anterior
segment of upper lobe or right middle lobe occurred
equally in both the groups (17% and 18%). Earlier
studies17-43 had also noted that these patients have a
greater extent of lesion and more frequent cavitation.
Besides, there is more frequent tuberculous pleural
effusion 49,51.52 Since the association of diabetes only
and none of the other factors was found to be statisli-
cally significant, such radiographic presentations
should be first investigated for the presence of
diabetes.
Principles of Management of Co-existent
Tuberculosis and Diabetes53,54
1. Proper care.
2. Patients with poor diabetic control should be
hospitalised for stabilizing their blood sugar
level.
3. Ideally, insulin should be used to control blood
sugar levels.
4. Oral hypoglycemics should be used only in cases
of mild diabetes. Drug interaction with
Rifampicin should be kept in mind.
5. Glycaemic equilibrium is essential for the
success of anti-tuberculosis therapy and must
be achieved in every patient with co-existent
disease. The goals of therapy are: fasting plasma
glucose < 120 mg% and glycated Hb <7%.
6. Vigorous and good chemotherapy is essential.
Monitoring for adverse effects, particularly of
hepatic and nervous systems should be done. Use
of potentially neuropathic agents (INH) in
patients with peripheral neuropathy demands
special consideration with mandatory
administration of pyridoxine.
7. Duration of chemotherapy is entirely dependent
upon the control of diabetes and response of the
patient to treatment. A longer treatment course
may be needed.
8. Supportive therapy for diabetes must be actively
pursued.
9. Management of co-existent illnesses,
malnutrition and rehabilitation of the alcoholic
diabetic remain of prime concern.
PROPHYLAXIS
All diabetics require regular medical examination
and bi-annual chest radiograph. This should be
followed more rigorously in patients who are more
than 40 years of age or with weight less than 10% of
the ideal body weight. Any diabetic- who suddenly
develops cough, loss of weight, abnormal chest
radiograph or needs increasing doses of insulin to
control blood glucose should be investigated for
presence of tuberculosis.
The American Thoracic Society recommended,
in 198656, that diabetics, particularly poorly
controlled IDDM patients, should be given INH
chemoprophylaxis. Although, primary chemopro-
phylaxis may be useful in certain communities with
high prevalence rates of diabetes and tuberculosis,
like the Oglala Sioux natives of North America, there
seems to be no reason for using primary chemo-
 TUBERCULOSIS AND DIABETES : AN APPRAISAL
prophylaxis in well controlled diabetic patients, in
general. Secondary chemoprophylaxis in tuberculin
positive diabetic patients is generally recommended,
although some investigators have questioned the
actual benefit to the diabetic patient.56
Amrit Guptan & Ashok Shah
Department of Respiratory Medicine,
Vallabhabhai Patel Chest Institute,
University of Delhi, Delhi
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APPENDIX
Criteria for the Diagnosis of Diabetes Mellitus*
1. Symptoms’ of diabetes plus casual2 plasma glucose of
> 11.1 mmol/L(200mg/dL)
or
2. Fasting 3 plasma glucose of > 7.0 mmol/L (126 mg/dL)
or
3. 2h plasma glucose of > 1 1.1 mmol/L (200 mg/dL)
during an OGTT with 75 g anhydrous glucose
* Adapted from the report of the Expert Committee on the
Diagnosis and Classification of Diabetes Mellitus, l997.
1. The classic’ symptoms of diabetes include polyuna.
polydipsia and unexplained weight loss.
2 Casual is defined asalany time of the day without rcgaid to
time since last meal
3 Fasting is defined as no caloric intake for at least 8 hours.
In the absence of unequivocal hypcrglycaemia with
acute metabolic decompensation, these c r i l e n a
should be confirmed In repeat testing on a di Herein day.
The third measure is not lecommendcd for routine clinical
use.