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85]

Review Article

Use of Corticosteroids in Tuberculosis

Saurabh K. Singh, Kamlesh K. Tiwari

Department of Pulmonary Tuberculosis (TB) is considered as a lethal disease in the present era. Effective

ABSTRACT
Medicine, Gajra Raja antituberculous therapy is available, which has reduced significantly the morbidity
Medical College and
Jayarogya Group of
and mortality due to TB. Literature advocates the use of corticosteroids in TB. Use of
Hospitals, Gwalior, Madhya corticosteroids in conjunction with antituberculous therapy showed a reduction in
Pradesh, India mortality and morbidity in pericardial and central nervous system TB. Signs and
symptoms in pleural and severe pulmonary TB improve rapidly with the addition of
corticosteroids. Corticosteroid should be used cautiously with antituberculous therapy
in view of drug interaction seen between them.
Received: November 2016
Accepted: March 2017 KEYWORDS: Central nervous system, corticosteroids, pericardial, tuberculosis

INTRODUCTION years of therapy. There was no evidence of active TB in any

W orldwide, about 1.5 million peoples are dieing
annually due to tuberculosis (TB); hence, it is
considered as a lethal infectious disease in the present
era.[1] However, around 43 million lives were saved
through TB diagnosis and treatment between 2000 and
2014, and the TB death rate dropped 47% between 1990
and 2015.
Tissue damage caused by inflammatory reaction to
Mycobacterium may cause edema leading to organ
dysfunction. This may result in atelectasis or fluid
blockage.[2] Treatment of TB due to drug-susceptible
disease requires at least 6 months of therapy, whereas
the multidrug resistance TB requires treatment of 24
months. To counter these inflammatory reactions, we
require add-on corticosteroids treatment. On the
contrary, steroids can make people vulnerable to other
infections.[3] Earlier, animal models showed that
corticosteroids can markedly increase the virulence of
TB if used with and without antituberculous therapy.[4,5]
However, in humans, it was shown that at-risk patients
who were receiving low-dose corticosteroid for rheumatic
diseases do not develop reactivation of TB.[6] This study
also showed that chemoprophylaxis with isoniazid (INH)
is unnecessary in those receiving corticosteroids.
In another study, the prevalence of active TB and positive
tuberculin skin tests (TST) was assessed in 132
corticosteroid-treated patients having asthma for an
evaluation period that represented the 620 corticosteroid-
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of these patients. This study also concluded that INH is not
indicated for corticosteroid-treated patients having asthma
regardless of their tuberculin status. It may worsen the
clinical course of TB itself if corticosteroids are used
alone without antituberculous therapy. However, the
American Thoracic Society recommends the use of INH
prophylaxis in steroid-treated patients with TST positive.[7]
Pharmacokinetic interactions have been shown between
rifampicin and steroids to cause a decrease in efficacy of
both the drugs.
The use of corticosteroid in patients with TB is quite a
controversial topic. It has been used for all forms of TB
since a very long time. However, its effect and benefit in
various forms of TB are quite different. Its effect and
benefit in TB are entirely organ specific. With this, we try
to review the use of corticosteroids in various forms of TB.
MENINGITIS
Without treatment, tuberculous meningitis (TBM) is
uniformly a fatal disease, and, at times, it leads to a
neurological deficit. Corticosteroids are being in use
along with antitubercular treatment for the management
of tuberculous meningitis for the last 60 years.[8] In a
review of five studies by Prasad et al.,[9] steroids were
Address for correspondence: Dr. Saurabh Kumar Singh, Assistant
Professor, Department of Pulmonary Medicine, Gajra Raja Medical
College and Jayarogya Group of Hospitals, Gwalior - 474 009,
Madhya Pradesh, India.
E-mail: doctorsaurabhsingh@gmail.com
This is an open access article distributed under the terms of the Creative Commons
Attribution-NonCommercial-ShareAlike 3.0 License, which allows others to remix,
tweak, and build upon the work noncommercially, as long as the author is
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For reprints contact: reprints@medknow.com

DOI:
10.4103/jacp.jacp_40_16 How to cite this article: Singh SK, Tiwari KK. Use of corticosteroids in
tuberculosis. J Assoc Chest Physicians 2017;5:70-5.

70 © 2017 The Journal of Association of Chest Physicians | Published by Wolters Kluwer - Medknow
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Singh and Tiwari: Use of corticosteroids in tuberculosis
associated with fewer deaths (relative risk [RR] 0.79; 95%
confidence interval [CI] 0.65–0.97) and a reduced
incidence of death and severe residual disability (RR
0.58, 95% CI 0.38–0.88). Prasad et al. again reviewed
the effect of steroid in tubercular meningitis by including
two more studies and found that corticosteroids reduced
the risk of death (RR 0.78, 95% CI 0.67–0.91). Disabling
neurological deficit was also reduced in the corticosteroid-
treated group (RR 0.82, 95% CI 0.70–0.97; 720
participants, three trials).[10] Further extending the
research, Prasad et al.[11] in 2016 concluded that
corticosteroid could reduce mortality caused by
tuberculous meningitis in the short term in human
immunodeficiency virus (HIV)-negative children and
adults, but its effect in an HIV-positive person was
uncertain. They further added that corticosteroid had no
effect on the number of people who survived tuberculous
meningitis with disabling neurological deficit.
In a randomized, double-blind, placebo-controlled trial[12] in
Vietnam, the inpatients over 14 years of age who had
tuberculous meningitis, with or without HIV infection,
were assigned to receive dexamethasone and placebo.
Dexamethasone was given in a tapering dose for 8 weeks.
A reduced risk of death (RR 0.69; 95% CI 0.52–0.92;
P = 0.01) was seen in the dexamethasone-treated group. It
was not associated with a significant reduction in the
proportion of patients with severely disabled condition
among survivors in the dexamethasone group versus in
the placebo group or in the proportion of patients who
had either died or were severely disabled after 9 months
(odds ratio, 0.81; 95% CI 0.58–1.13; P = 0.22). Usage of
adjunctive dexamethasone for up to 2 years of follow-up also
showed improvement in the probability of survival in
patients with TBM.[13]
No trial has been performed to compare the efficacy of
different corticosteroid regimen. Therefore, the choice of
corticosteroid depends upon the regimen used in different
trials.[14] Dexamethasone in the doses of 0.4 mg/kg/day is
recommended in adults (>14 years) in conjugation with
antitubercular drugs. The dose should be reduced over 6–8
weeks, while in children (<14 years), prednisolone 4 mg/
kg/24 h (or equivalent dexamethasone 0.6 mg/kg/24 h) is
given for 4 weeks followed by a reducing dose over 4
weeks.[14] In adults, it has been recommended that the
effect of corticosteroid should be assessed within a month
of starting the treatment. Tapering of the dose should be
initiated, once it seems to be safe.[14]
PLEURAL EFFUSION
Studies have shown that the use of corticosteroid in TB is
conflicting. In the study, performed by Mathur et al.,[15] an
intra-pleural instillation of hydrocortisone in the cases of
tubercular pleural effusion showed dramatic response in the
The Journal of Association of Chest Physicians ¦ Volume 5 ¦ Issue 2 ¦ July-December 2017
general condition of the patients in comparison to the control
group. Disappearance of the pleural fluid was also faster in
the hydrocortisone group as compared to the control group.
Similarly, favorable outcomes were shown by other studies
that used intrapleural corticosteroids[16,17] for tuberculous
pleural effusion.
In another study by Grewal et al.,[18] 102 patients with pleural
TB were treated with either chemotherapy (INH and
streptomycin), chemotherapy plus systemic corticosteroids,
chemotherapy plus repeated thoracocentesis, or chemotherapy
plus repeated thoracocentesis and intrapleural corticosteroids.
In this study, a treatment with prednisolone, in a dose of 20 mg/
day followed by a tapering off along with an antituberculous
drug, was significantly better than the treatment with
intrapleural instillation of steroid.
Lee et al.[19] demonstrated that administration of
corticosteroid in parallel with antituberculous drug
would resolve the clinical symptoms more quickly and
would hasten the absorption of tuberculous pleural
effusion. However, no influence was seen on pleural
adhesion by the addition of corticosteroid in a small
cohort. Galarza et al.[20] used oral corticosteroid along
with antituberculous treatment and found that addition
of steroid had no effect on the clinical outcome or the
development of long-term pleural sequelae in tuberculous
effusion.
Wyser et al.[21] conducted the first double-blind, placebo-
controlled, randomized study by using corticosteroid in
tuberculous pleural effusion. They used three-drug
chemotherapy and performed thoracocentesis in all
cases. At the end of the study, they found a significant
improvement in symptoms in the prednisolone group as
compared to the placebo group. Residual thickening was
seen in 53.3% of the patients on prednisolone as compared
to 605 patients in the placebo group, and this difference
was not significant. Lung function test was also
comparable at the end of the study in both the groups.
These studies concluded that standard antituberculous
therapy and early complete drainage could be
considered adequate for the treatment of tuberculous
effusion. Similarly, Bang et al.[22] showed a more rapid
improvement in clinical features in the corticosteroid
group, but absorption of pleural effusion and occurrence
of pleural adhesion was not significant.
Elliott et al.[23] conducted a randomized, double-blind,
placebo-controlled trial of prednisolone as an adjunct to
TB treatment in adults with HIV-1-associated tuberculous
pleural effusion. They showed use of prednisolone was
associated with more rapid improvement in all the
principal signs and symptoms of pleural effusion. There
was a more rapid improvement in the prednisolone group.
However, prednisolone was associated with a significantly
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Singh and Tiwari: Use of corticosteroids in tuberculosis
higher incidence of Kaposi sarcoma. This study did not
recommend the use of prednisolone in HIV-associated
tuberculous pleurisy due to lack of survival benefit and
the increased risk of Kaposi sarcoma.
Cochrane review performed by Engel et al.[24] found that
there were insufficient data to support evidence-based
recommendations regarding the use of adjunctive
corticosteroids in people with pleural effusion due to
TB. However, the addition of corticosteroid hastens the
absorption of pleural fluid, and there occurs a faster
recovery from sign and symptoms of tuberculous
pleural effusion.
Corticosteroids can be in conjunction with antituberculous
chemotherapy in the severely ill patients with pleural TB.
This could be administered as prednisolone 0.75 mg/kg/
day initially and then tapered off, when improvement of
the chest X-ray is seen.[2]
PULMONARY TUBERCULOSIS
Eighteen trials, including 3816 participants, were
reviewed[25] to know the role of adjunctive steroid
therapy for managing pulmonary TB. When compared
to taking placebo or no steroid, corticosteroid use was
not shown to reduce the all-cause mortality, or result in
higher sputum conversion at 2 months or at 6 months.
However, corticosteroid use was found to increase weight
gain, decrease length of hospital stay (data not pooled,
three trials, 379 participants, and very low quality of
evidence), and increase clinical improvement within 1
month.
The study using meta-regression analysis to examine the
relationship between corticosteroid dose and sputum
culture conversion, using published data from controlled
clinical trials including 1806 corticosteroid-treated TB
patients, found that adjunctive corticosteroids accelerate
sputum culture conversion in pulmonary TB.[26] The study
raised concerns that the doses required are unlikely to
support a favorable benefit risk balance for individual
patients with TB.
In one of the earlier systematic reviews, it has been
concluded that a systemic corticosteroid therapy in
conjunction with antitubercular drug can safely provide
significant early and prolonged clinical and radiographic
benefits in selected patients with advanced pulmonary
TB.[27]
Role of steroid in miliary TB is still controversial. Very
few studies had been performed to know the role of
corticosteroids in military TB. In a study, performed by
Sun et al.[28] on 55 patients with miliary TB, the effect of
corticosteroid was evaluated. They found that an addition
of corticosteroid to the chemotherapy helped in the control
of infection and lessened toxic symptoms.
72 The Journal of Association of Chest Physicians ¦ Volume 5 ¦ Issue 2 ¦ July-December 2017
ENDOBRONCHIAL TUBERCULOSIS
It is a type of pulmonary TB. The role of steroid in
endobronchial TB is quite controversial. Nemir et al.[29]
conducted a double-blind study to know the effectiveness of
corticosteroid. They found that patients receiving adjunct
steroid therapy before the fourth month of tuberculous
infection had a 76% chance of improvement as compared
to a 36% chance of improvement in a placebo group
suggesting the value of prednisone in an early stage.
Because of the anti-inflammatory properties, the use of
corticosteroids reduces inflammation and, thus, reduces
the local pressure.[30] Another study, performed in
childhood endobronchial TB, concludes that whenever
severe bronchial compression had been demonstrated,
steroids remained beneficial and should be added.[31]
In a study, performed by Park et al.[32] in adults, they
showed that after treatment, the healing rate of
bronchoscopic findings and the changes in pulmonary
function were equal in both the non-corticosteroid
and the corticosteroid groups and concluded that
prompt treatment with early diagnosis, before the
formation of fibrosis would be necessary to prevent
the complications of endobronchial TB. Prednisolone
at the dose of 1 mg/kg was prescribed for 4–6 weeks
followed by slow taper for the same for the edematous-
hyperemic, actively caseating and tumorous types, as
these tend to progress to tracheobronchial stenosis.
Um et al.[33] found that oral corticosteroids
(prednisolone equivalent ≥30 mg/day) did not reduce
the frequency of persistent airway stenosis in adults.
PERICARDIAL EFFUSION
In a study, performed by Strang et al.,[34] they conducted a
placebo-controlled, double-blind trial in the patients of
tuberculous pericarditis. Their patients were randomly
allocated to receive, in addition to chemotherapy, either
prednisolone or placebo for the first 11 weeks. They found
a more rapid improvement in the signs and symptoms in
the prednisolone group. Mortality in the prednisolone
group was 4% as compared to 11% in the placebo
group. The need for pericardiectomy was also more in
the placebo group. This trial concluded that unless
contraindicated, antituberculous drug should be
supplemented with steroids in pericarditis.
In another study, performed by Strang et al.,[35] the 240
cases of active tuberculous effusion were randomly
allocated to prednisolone or matching placebo for the
first 11 weeks, on a double-blind basis. In the
comparison between the prednisolone and placebo
groups, prednisolone reduced the risk of death and the
need for repeat pericardiocentesis during the 24 months of
follow-up. It also reduced the need for open surgical
drainage because of the rapid re-accumulation of
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Singh and Tiwari: Use of corticosteroids in tuberculosis
pericardial fluid despite repeated pericardiocentesis (4%
vs. 9% for placebo). There was a low incidence of
pericarditis in the prednisolone group during 2 years of
follow-up.
Later on, these patients with pericardial effusion and
pericarditis were followed up for 10 years by Strang
et al.[36] In a multivariate survival analysis (stratified by
type of pericarditis), prednisolone reduced the overall
death rate after adjusting for age and sex, and
substantially reduced the risk of death from pericarditis.
In another study by Hakim et al.,[37] performed to know the
effect of adjunctive prednisolone on morbidity, pericardial
fluid resolution, and mortality in patients with HIV
seropositive with effusive tuberculous pericarditis, they
found that adjunctive prednisolone produced a marked
reduction in mortality in the patient of effusion. In the
prednisolone-treated group, there was a significantly rapid
resolution of raised jugular venous pressure, hepatomegaly,
and ascitis. Improvement in physical activity was also more in
the prednisolone group. However, Reuter et al.[38] found that
intrapericardial and systemic corticosteroids were well
tolerated but did not improve the clinical outcome in the
patients with tuberculous pericarditis.
The result of the Investigation of the Management of
Pericarditis (IMPI) trial[39] is still awaited. The IMPI
trial is a multicenter, international, randomized, double-
blind placebo-controlled, 2 × 2 factorial study. In this
study, eligible patients were randomly assigned to
receive oral prednisolone or placebo for 6 weeks and
Mycobacterium w immunotherapy or placebo for 3
months. The patients were followed up at weeks 2, 4,
and 6 and months 3 and 6 during the intervention
period and 6-monthly, thereafter, for up to 4 years.
IMPI is the largest trial conducted so far comparing an
adjunctive immunotherapy in pericarditis. Its results
will define the role of adjunctive corticosteroids and
M. w immunotherapy in patients with TB pericardial
effusion.
The recommended prednisolone dose for tuberculous
pericarditis is 1 mg/kg/day in the acute phase tapered
off during the next 3 months.[2]
ADRENAL INSUFFICIENCY
Adrenal gland involvement due to TB causes the adrenal
gland destruction leading to adrenal insufficiency.[40]
Rifampicin is the well-known hepatic enzyme inducer
and, thus, may unmask subclinical adrenal insufficiency,
which may lead to addisonian crisis.[41] Brooke and
Monson[42] suggested that glucocorticoid replacement
should be given three times daily, with the largest dose
(10–20 mg) before getting out of bed to mimic the
physiological peak just before waking, followed by
The Journal of Association of Chest Physicians ¦ Volume 5 ¦ Issue 2 ¦ July-December 2017
5 mg at midday and 5 mg at 6 PM. They also suggested
that a treatment with fludrocortisone was to achieve
normal sodium homeostasis in a dose of 50–100 mg
twice daily.
ABDOMINAL TUBERCULOSIS
The role of steroid in the management of abdominal TB
is not well established, and, thus, the corticosteroids
have not been used routinely in abdominal TB.
Suggestion had been made to use the steroid to reduce
the late adhesive complications. In a small group of
patients, the use of corticosteroid in combination of
antituberculous drugs found to reduce the frequency
of morbidity and complications in patients with
peritoneal TB.[43] However, to implement the use of
corticosteroids for abdominal TB, a double-blind
study in a larger cohort is needed.
UPPER RESPIRATORY TRACT TUBERCULOSIS
The use of antituberculous drugs is considered sufficient
for the treatment of upper respiratory tract TB. Patients
having difficulty in eating and swallowing the
antituberculous medication due to laryngeal ulcers,
pharyngitis, and oral ulcers may get relief by using a
short course of prednisolone 40–60 mg with a rapid
tapering within 2–3 weeks. This should be used in
adjunct with antituberculous medication.[44]
HYPERSENSITIVITY TO ANTITUBERCULOUS
DRUGS
Any offending drug is supposed to be stopped in the
cases of hypersensitivity reactions occurring due to
antituberculous drug. In the case of multidrug resistance
or the drug cannot be replaced, desensitization therapy for
the antituberculous drug has shown effective results.[45]
The cases of severe or generalized erythematous rash or
rashes with angioedema should be treated with systemic
steroids.[46]
OCULAR TUBERCULOSIS
Topical and/or systemic steroid is used in ocular TB along
with antituberculous drugs. Prednisolone acetate eyedrops
are used in the treatment of phlyctenular
keratoconjunctivitis, episcleritis, scleritis, interstitial
keratitis, and uveitis.[47] Systemic steroids are used for
the first few weeks with an antituberculous treatment to
decrease damage caused to the ocular tissues. A systemic
corticosteroid use without the addition of antituberculous
drug may worsen the clinical process of tuberculous
choroiditis.[48] Periocular steroids are also advocated in
moderate-to-severe chronic uveitis, posterior scleritis, or
recalcitrant anterior uveitis.[47]
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Singh and Tiwari: Use of corticosteroids in tuberculosis
TUBERCULOSIS IMMUNE RECONSTITUTION
INFLAMMATORY SYNDROME
Most of the cases of HIV-associated tuberculosis immune
reconstitution inflammatory syndrome (TB-IRIS) are
transient and do not require any treatment.
Occasionally, the inflammation may be worst and may
lead to death of the patient.[49] In such life-threatening
manifestations, a temporary stoppage of antiretroviral
therapy is recommended followed by the use of short
course of corticosteroids with 1 mg/kg/day of
prednisolone for 1–2 weeks with a gradual reduction,
thereafter.[50] In a double-blind, placebo-controlled trial,
it was found that in the patients with TB-IRIS, prednisone
reduced the need for hospitalization and therapeutic
procedures, and hastened improvements in symptoms,
performance, and quality of life.[51] Proposed
mechanism of prednisolone is the suppression of
predominantly proinflammatory cytokine responses of
innate immune origin.[52] At times, TB-IRIS can
develop in a non-HIV infected person. Such paradoxical
reactions can be managed by a continuation of
antituberculous therapy. Corticosteroids are needed for
severe pleural and central nervous system edema in the
doses that are described in the previous sections.[50]
CONCLUSION
The use of corticosteroid is recommended in treating
tuberculous meningitis and pericarditis.[53] In tuberculous
pleural effusion, it causes the faster recovery of clinical
symptoms, but final outcomes remain the same. Similarly,
in pulmonary TB, corticosteroids relieve the morbidity in
a severe disease, but the final outcome remains the same
with and without corticosteroids. In abdominal TB,
corticosteroids lead to a rapid improvement in the
condition of patients in a small trial, but its use in
peritoneal TB needs more studies. Upper respiratory
tract TB showed a rapid relief in difficulty in swallowing,
when corticosteroids were used along with antituberculous
therapy. For ocular TB, topical and systemic corticosteroids
can be used. Severe hypersensitivity reactions due to
antituberculous drug required corticosteroids therapy. In
cases of adrenal crisis, a corticosteroid replacement
becomes mandatory.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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