Central Nervous
System Tuberculosis
Mimicking
Neuropsychiatric Systemic
Lupus Erythematosus
To the Editor:
W
e read with interest the report in the
Journal of Clinical Rheumatology
that tuberculosis (TB) is not uncommon
even in patients with systemic lupus ery-
thematosus (SLE) being followed up in a
county hospital in the United States.
1
We
present a patient with SLE who developed
an uncommon form of TB. This 42-year-
old man presented with intermittent fe-
ver, joint pains, weight loss (7 kg) since
9 months and oral ulcers and a rash on
the face for the past 20 days. He had a
malar rash, oral ulcers, and hepatomegaly
of 3 cm below the costal margin. Investiga-
tions revealed transaminitis, mild thrombo-
cytopenia, positive result in the antinuclear
antibody test, low complements, and ele-
vated double-stranded DNA (Table 1 avail-
able online). He was diagnosed with SLE
with lupus hepatitis and started on pred-
nisolone 1 mg/kg per day and azathioprine
2 mg/kg per day. At 6 months of follow-
up, he was much better, and his pred-
nisolone treatment had been tapered to a
maintenance dose of 7.5 mg.
One year after diagnosis, he pres-
ented to the emergency services with fever
lasting 6 weeks and altered sensorium for
3 days. There was no history of headache,
vomiting, or seizures. He was agitated and
was moving all his limbs. There was no
neck rigidity or papilledema. Bilateral re-
flexes were exaggerated, and plantars were
up-going. Results from respiratory, car-
diovascular, and abdominal examinations
were normal. The differential included con-
ditions related or unrelated to lupus. Un-
related causes included infections like
meningitis (partially treated bacterial, tu-
bercular, or fungal), viral encephalitis, en-
teric encephalopathy, cerebral malaria, and
disseminated brain parenchymal infec-
tions. Increased activity of SLE could also
present with neuropsychiatric involvement
and fever.
Investigations revealed bicytopenia
but normal electrolytes and blood glucose
levels. Chest radiography revealed doubt-
ful basal infiltrates. Result from the cere-
brospinal fluid (CSF) examination was
normal. Serum complement revealed a
low level of C4 (see Table 1, SDC 1, http://
links.lww.com/RHU/A17). Considering the
normal result from the CSF examination,
the absence of focal deficits, bicytopenia,
and the low C4, a possibility of neuro-
psychiatric SLE seemed likely. However,
imaging clinched the diagnosis. The mag-
netic resonance image showed multiple
ring-enhancing lesions in the cerebral
hemispheres and brainstem (see Figure 1,
SDC 2, http://links.lww.com/RHU/A18),
and the high-resolution computed tomo-
graphic scan of the chest showed mil-
iary shadows (see Figure 2, SDC 3,
http://links.lww.com/RHU/A19). A bone
marrow biopsy showed ill-formed granu-
lomas and necrosis of marrow tissue but
was negative for acid-fast bacilli (not
shown). AntiYtubercular therapy (AAT)
was started, and prednisolone dosage was
increased to 40 mg/d. The dosage of
prednisolone was gradually tapered later.
After 1 year of treatment, a second mag-
netic resonance image showed resolution
of most tuberculomas (see Figure 3, SDC
4, http://links.lww.com/RHU/A20). AntiY
tubercular treatment was subsequently con-
tinued for another year, after which a third
magnetic resonance image showed com-
plete clearance of tuberculomas (not shown).
One year later, he remains well except for
some forgetfulness.
Since the recognition of an in-
creased risk of TB in lupus in the 1980s,
it has come to rank among the most
common infections in lupus patients.
2
Important risk factors for TB in SLE in-
clude a recent diagnosis of lupus (1Y2 y),
active disease, and a high dose of steroids
(cumulative or concurrent).
3Y9
The lungs
remain the commonest site of involve-
ment by TB in SLE (see Table 2, SDC 5,
http://links.lww.com/RHU/A21). However,
many studies have found a higher propor-
tion of extrapulmonary and disseminated
forms to occur in patients with lupus.
3Y5
Among these extrapulmonary sites, central
nervous system TB (CNS TB) is not un-
common and accounts for up to 10% of all
cases of TB in SLE (see Table 2, SDC 5,
http://links.lww.com/RHU/A21). Tubercular
meningitis remains the commonest form
of CNS involvement in SLE. Parenchymal
tuberculomas or ‘‘small abscesses’’ like in
our case are reported less frequently.
10
The presence of headache, vomiting,
altered sensorium, or a focal deficit can be
a clue to CNS TB. The CSF level is in-
variably abnormal in meningitis; however,
in tuberculomas, the CSF level may be
normal (raised protein in 50%). Tubercu-
lomas are recognized on magnetic reso-
nance or computed tomographic scans as
ring-enhancing lesions but cannot be re-
liably differentiated from toxoplasmosis,
neurocysticercosis, fungal infections, and
metastatic neoplasia.
11
The presence of
disseminated TB, specifically concomi-
tant lung involvement, can be a clue to
tubercular etiology as in our case. Cur-
rent guidelines recommend 1 year of ATT;
however, intracranial tuberculomas often
take a long period to resolve. One study
found two thirds of patients (without SLE)
to have residual lesions after 1.5 years of
ATT, necessitating prolonged therapy
11,12
Steroids have a definite role in tubercular
meningitis and a possible role in intracra-
nial tuberculomas; the recommended dos-
age varies from 12 mg/d dexamethasone to
4 mg/kg per day prednisolone for 4 weeks.
11
In the setting of SLE, CNS TB can be fatal
in a matter of days, so early treatment is
recommended.
10
Varun Dhir, MD, DM
Yogesh Preet Singh, MD, DM
Ramnath Misra, MD, FRCP
Amita Aggarwal, MD, DM
Department of Immunology
Sanjay Gandhi Post Graduate
Institute of Medical Sciences
Lucknow, India
aa.amita@gmail.com
REFERENCES
1. Chu AD, Polesky AH, Bhatia G, et al.
Active and latent tuberculosis in patients with
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226Y229.
2. Alarcon GS. Infections in systemic
connective tissue diseases: systemic lupus
erythematosus, scleroderma and
polymyositis/dermatomyositis. Infect Dis
Clin North Am. 2006;20:849Y875.
3. Hernandez-Cruz B, Sifuentes Osornio J,
Ponce de Leon Rosales S, et al.
Mycobacterium tuberculosis infection in
patients with systemic rheumatic diseases.
A case-series. Clin Exp Rheumatol.
1999;17:289Y296.
The authors declare no conflicts of interest.
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114 www.jclinrheum.com JCR: Journal of Clinical Rheumatology & Volume 18, Number 2, March 2012
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