DISCUSSION:
Tuberculosis continues to remain one of the leading causes of death due
to infectious diseases with a global total of 10 million cases diagnosed
in 2020 [8].
Intracranial tuberculomas account for 0.15–4% of space-occupying
lesions in developed countries. However, in developing countries, they
account for 30-34% of intracranial space-occupying lesions [9,11].
Among these, calvarial involvement is seen in 0.2-1.3% of the affected
individuals with skeletal TB [10]. There have been many case reports
showing an increased incidence of tuberculoma in patients with CKD and
patients on hemodialysis [12]. CKD is associated with various
comorbidities and has been identified as one of the independent risk
factors for active tuberculosis. The incidence of TB in patients with
End Stage Kidney Disease has been observed to be 10-15 times higher than
that in healthy population [13]. This can be attributed to the
immunocompromised state of individuals with CKD. Oxidative stress,
inflammation,25-hydroxyvitamin D deficiency, malnutrition associated
with advanced CKD may act as predisposing factors. Changes in the immune
system begin in Stage 3 of CKD with progressive worsening in later
stages, presenting with functional abnormalities in B and T cells, white
blood cells (predominantly neutrophils and monocytes) and natural killer
cells [14].
Patients undergoing hemodialysis are at a higher risk of developing TB.
Numerous studies have confirmed a higher incidence of TB in patients
with CKD on dialysis [13-17]. Studies indicate 3-to-25-fold higher
risk in these patients compared to healthy individuals [17].
Impaired cell-mediated immunity in dialysis predisposes patients to
infections and their complications [14].
Our patient is a known case of CKD for the past10 years and is
undergoing hemodialysis. CKD being an independent risk factor for TB and
hemodialysis being a predisposing factor may have contributed as
etiological factors for tuberculoma in this case. Tuberculomas occur
secondary to a primary infection, the focus usually being lungs or lymph
nodes. The mode of spread is through the hematogenous route. It can
occur from granuloma in the parenchyma or through the spread of foci
from the meninges to the brain parenchyma. Lesions affecting the skull
are more common in the frontal and parietal regions. The granulation
tissue replaces the bony trabeculae and the capillary is seen.
Concentrically placed proliferating fibroblasts contain the spread of
infection to either table [10]. A history of tubercular meningitis
isn’t a necessity for the diagnosis of tuberculoma.
Tuberculomas are slow-growing lesions, that can be single or multiple
with a thicker wall compared to a pyogenic abscess [18,19]. They can
have varied clinical presentations. Seizures, headache, vomiting,
giddiness, sensory and motor deficits, and cranial nerve palsies are
some of the symptoms observed in previous case reports [20]. Our
patient had 4 episodes of seizures with a past history of similar
episode of GTCS managed in a tertiary care center. Presentation of a
soft, painless, fluctuant swelling over the scalp has also been observed
in many cases.
Radiological diagnosis, supported by microbiological and histological
evidence, serves as the diagnostic modality for tuberculomas. PCR
detection of mycobacterial DNA in paraffin-embedded tissue has also been
used successfully in recent publications though the definitive diagnosis
still remains to be biopsied material showing granulomas complemented by
acid-fast staining and culture [12].
CT is one of the radiological diagnostic tests performed on these
patients. Tuberculoma lesions are seen as isodense or hyperdense lesions
surrounded by peripheral edema. They may be disc-shaped or calcified. In
the initial stages, they can appear as non-enhanced hypodense lesions,
but mature granulomas are seen as mixed or combined forms with nodular
or ring enhancement. A ring lesion with a central hyperdensity is the
pathognomonic finding of tuberculoma which is also called the target
sign [21]. The CT scan of our patient showed punched out cystic
ring-enhancing lesion with surrounding edema in the left frontal lobe.
The diagnosis was confirmed by the histopathological report and the
acid-fast bacilli seen on Ziehl Neelsen staining.
Management strategies include surgery and anti-tubercular therapy.
Hemodialysis and other symptomatic management of CKD was carried out
[22]. Recent reports indicate that a combination of surgery and
chemotherapy shows better results compared to chemotherapy alone
[12,23,24]. In our case, a similar treatment strategy was followed.