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.