| Abstract|| |
Tuberculosis can be an opportunistic infection complicating the course of patients receiving prolonged immunosuppression. In these patients, the tuberculosis can involve the central nervous system and can cause diagnostic difficulty due to atypical features. Often, the diagnosis of central nervous system tuberculosis in resource limited settings is indirect, like imaging. But anti-tubercular drugs, given even on empirical basis can be life saving. A case of a young female systemic lupus erythematosus patient (on prolonged steroids) with intracranial tuberculoma is presented here. She presented with blindness and headache and her computed tomography scan showed a calcified mass in the suprasellar location. However, she responded well to anti-tubercular drugs. The differential diagnoses of such lesions are also discussed.
Keywords: Lupus, Suprasellar calcification, Tuberculosis
|How to cite this article:|
Paul R, Banerjee AK, Bandyopadhyay R. Suprasellar tuberculoma presenting as sudden onset blindness in a patient of lupus. J Global Infect Dis 2012;4:75-8
|How to cite this URL:|
Paul R, Banerjee AK, Bandyopadhyay R. Suprasellar tuberculoma presenting as sudden onset blindness in a patient of lupus. J Global Infect Dis [serial online] 2012 [cited 2020 Jul 4];4:75-8. Available from: http://www.jgid.org/text.asp?2012/4/1/75/93766
| Introduction|| |
Systemic lupus erythematosus needs prolonged immunosuppressive therapy for control of symptoms. However, this immunosuppressed condition can predispose the patient to opportunistic infections like tuberculosis. In these patients, tuberculosis can affect different systems and can have uncommon clinical presentations. A case of a young female of lupus (on steroids) with suprasellar tuberculoma is described here. She presented with blindness and intense headache.
| Case Report|| |
A 22-year-old female was admitted through emergency with sudden onset severe headache, vomiting, and dimness of vision (6/60) in both eyes. She was diagnosed with systemic lupus erythematosus one year ago by clinical and laboratory criteria (ACR) with nephropathy grade three. She had been given pulse cyclophosphamide 1 year earlier (6 doses, 21 days apart each). After that, she was put on oral steroids (prednisolone, 7.5 mg/day oral) and she continued the drug in the intervening period. At the time of admission she was still on oral steroids (7.5 mg/day). She had no other manifestations of lupus and her mental status was normal. She also had no prior visual problems.
After admission, the patient developed low grade fever and her dimness of vision progressed. By third day, she had no perception of light in either eye. Local examination of the eyes showed pupils to be dilated and non-reactive. Ophthalmoscopy showed mild papilledema bilaterally. No neck rigidity was elicited. There was bilateral sixth cranial nerve weakness; but no other neurological signs. Ophthalmologists opined that the pathology was not intra-ocular; neurologists were of the opinion that there was a vascular event in cranium. Immediate imaging was advised.
Routine laboratory tests showed mild anemia and thrombocytopenia. Her blood glucose was raised (fasting=144 mg/dL), probably due to long intake of steroids. Due to the presence of papilledema, we did a CT scan of brain [Figure 1] which showed a calcified mass in suprasellar region with perilesional edema (black arrow) with obstructive hydrocephalous. There was also mild cerebral atrophy. The Mantoux test of the patient was negative (she was on steroids), sputum did not show any acid-fast bacilli and chest X-Ray was also normal. She had contact with a sputum positive case of tuberculosis 3 months ago. Her hormonal profile was normal. We could not attempt a spinal tap due to hydrocephalous. The Magnetic resonance imaging scan could not be done due to cost factor. In view of the emergent nature of the illness, we started her on oral anti tubercular drugs with an increased dose of oral steroids. Her headache decreased, but vision improved only mildly. Subsequently, after 1 month, a brain biopsy was done and the lesion was found to be calcified granuloma with aggregates of epitheloid cells, calcifications, necrosis, blood vessel destructions, and few scattered caseations [Figure 2]. The lesion did not show any acid fast bacilli, but overall features were suggestive of tuberculosis. A CSF sample collected at time of brain biopsy showed increased cells (45/μL), increased protein (102 mg/dL). AFB stain of CSF was negative; a PCR from CSF was positive for mycobacterium tuberculosis. Repeat CT scan [Figure 3] showed only a mild decrease in the size of the edema; calcified mass size was the same. She was put on anti-tubercular drugs for 1 year. At present her vision is finger counting at three feet.
|Figure 1: The CT scan of the patient showing suprasellar calcified mass (upper left and upper right panels, perilesional edema (black arrow), and hydrocephalous (white arrow, right lower panel)|
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|Figure 3: Repeat CT scan of the patient after 5 months, showing only decrease of edema, calcification size same|
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| Discussion|| |
Tuberculomas are an important cause of space occupying lesions in brain in developing countries like India. In cases like ours, with no extra cranial manifestations of tuberculosis, diagnosis can be difficult and only suggested by CT scans. For confirmation, a stereotactic brain biopsy can be attempted.  However, non-invasive methods like PET scan can be useful; if CSF study can be done, PCR or ELISA for Mycobacterium tuberculosis from the fluid can be attempted. Tuberculosis of central nervous system can have different forms like meningitis, abscess, tuberculoma, subdural collection or miliary form.  The abscess or tuberculoma may heal with calcification. These parenchymal lesions can also cause obstructive hydrocephalous.  Suprasellar tuberculoma can present with diabetes insipidus, visual loss, or hypothyroidism. In resource-limited settings, and when the patient is severely ill, often diagnosis is not possible and empirical treatment is needed. Steroids are usually indicated in these cases. Surgery may also be needed. Calcified mass in brain seen in CT scan can have many etiologies.  The following chart [Table 1] shows the different common etiologies of cerebral calcification and their differentiation with special reference to suprasellar lesions:
|Table 1: Table Showing the characteristics of different lesions with cerebral calcification|
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Suprasellar lesions can present with hypogonadism, features of raised intracranial pressure and hemianopia. But sudden visual loss is quite rare. Also, lesions with an infective cause should be differentiated from calcified tumors and aneurysms because drug treatment is helpful in tuberculoma, whereas in other cases prompt surgery is the only option. The idea of presenting this case is to draw attention on the catastrophic effects of long-term steroids. Although tuberculosis is a known complication of long-term immunosuppression, tuberculomas are rare and suprasellar tuberculoma causing visual impairment is indeed very rare. A case like ours was reported from India by Sharma et al in 2003.  Their patient had permanent visual loss. Very rarely, tuberculomas are found near optic chiasm, but when they occur, they can cause these catastrophic consequences.  Another similar case was recently reported.  In that case, adalimumab treatment resulted in tuberculoma and the patient presented with dyspraxia. However, fortunately, that case was diagnosed before the calcification stage and the patient responded favorably to drugs.
Also, intracranial calcification is a vexing problem in a resource limited settings. Proper differentiation of the lesions in CT scan is important to the treating physician. In a resource limited setting, anti-tubercular drug, even on empirical basis can be life saving and should be used without delay. Newer diagnostic methods like PET scan can also help in distinguishing these lesions (tuberculosis has lower FDG uptake than lymphoma).  MR spectroscopy can also help in this regard; tuberculoma shows prominent lipid peak at 1.3 ppm. 
The lesion of tuberculosis will show significant change in subsequent imaging following therapy although the radiological resolution may not match with the clinical improvement, especially in central nervous system lesions. Specially calcified lesions often indicate irreversible damage. These patients should be followed up for development of epilepsy.
| Conclusion|| |
This case shows the importance of brain imaging in suspected infective disorders and the need to interpret the images quickly for maximum benefit of the patients. Especially in the background of the immunosuppressed state, any infection (like tuberculosis) can present with a catastrophe like blindness and timely therapy can prevent subsequent morbidity to a large extent. At times, empirical therapy can also be used, provided clinical suspicion is strong and diagnostic tests are unavailable or impractical. Also, clinicians need to be well versed with the differential diagnoses of intra cranial calcification, which, though a common finding, can be a diagnostic dilemma at times.
| References|| |
|1.||Haddadian K, Rezaei O, Samadian M. Multiple brain tuberculomas and role of open brain biopsy: A case report and review. The Internet Journal of Infectious Diseases. 2005;4: [about 1 p]. Available from: http://www.ispub.com/journal/..../multiple_brain_tuberculomas_and_role_of_open_brain_biopsy_a_case_report_and_review.html [Last cited on 2010, Dec 23]. |
|2.||Garg RK. Tuberculosis of the central nervous system. Postgrad Med J 1999;75:133-40. |
|3.||Khoo JL, Lau KY, Cheung CM, Tsoi TH. Central nervous system tuberculosis. J HK Coll Radiol 2003;6:217-28. |
|4.||Kýroglu Y, Çallý C, Karabulut N, Öncel C. Intracranial calcifications on CT. Diagn Interv Radiol 2009;16:263-9. |
|5.||Ketonen L, Koskiniemi ML. Gyriform calcification after herpes simplex virus encephalitis. J Comput Assist Tomogr 1983;7:1070-2. |
|6.||Khan AN, Turnball I, Al-Okaili R, Macdonald S. Imaging in CNS Toxoplasmosis: Imaging. WebMD; 2010 Available from: http://emedicine.medscape.com/article/344706-imaging. [Last Cited on 2010 Dec 24]. |
|7.||Hwang T, Valdivieso JG, Yang CH, Wolin MJ. Calcified brain metastasis. Neurosurgery 1993;32:451-4. |
|8.||Sinha VD, Dharker SR, Pandey CL. Congenital intracranial teratoma of the lateral ventricle. Neurol India 2001;49:170. |
|9.||Anderson JR. Intracerebral calcification in a case of systemic lupus erythematosus with neurological manifestations. Neuropathol Appl Neurobiol 1981;7:161-6. |
|10.||Iwaski Y, Kinoshita M, Takamiya K. Rapid development of basal ganglia calcification caused by anoxia. J Neurol Neurosurg Psychiatry 1988;51:449-50. |
|11.||Kotan D, Aygul R. Familial Fahr disease in a Turkish family. South Med J 2009;102:85-6. |
|12.||Lee KF, Sub JH. CT evidence of grey matter calcification secondary to radiation therapy. Comput Tomogr 1977;1:103-10. |
|13.||Kieslich M, Errázuriz G, Posselt HG, Moeller-Hartmann W, Zanella F, Boehles H. Brain white-matter lesions in celiac disease: A prospective study of 75 diet-treated patients. Pediatrics 2001;108:E21. |
|14.||Sharma K, Pradhan S, Varma A, Rathi B. Irreversible blindness due to multiple tuberculomas in the suprasellar cistern. J Neuroophthalmol 2003;23:211-2. |
|15.||Lesoin F, Dubois F, Rousseaux M, Pasquier F, Petit H, Jomin M. Chiasmatic tuberculoma. 2 cases. Semin Hop Paris 1984;60:1185-8. |
|16.||Lynch K, Farrell M. Cerebral tuberculoma in a patient receiving anti-TNF alpha adalimumab treatment. Clin Rheumatol 2010;29:1201-4. |
|17.||Villringer K, Jäger H, Dichgans M, Ziegler S, Poppinger J, Herz M, et al. Differential diagnosis of CNS lesions in AIDS patients by FDG-PET. J Comput Assist Tomogr 1995;19:532-6. |
|18.||Saini KS, Patel AL, Shaikh WA, Magar LN, Pungaonkar SA. Magnetic resonance spectroscopy in pituitary tuberculoma. Singapore Med J 2007;48:783. |
Department of Medicine, Medical College Kolkata, 88 College street, Kolkata, West Bengal
Source of Support: None, Conflict of Interest: None
[Figure 1], [Figure 2], [Figure 3]