|Year : 2021 | Volume
| Issue : 3 | Page : 324-326
Tuberculous peritonitis complicated by immunologic cerebral vasculitis
Mansoor C Abdulla
Department of General Medicine, M.E.S. Medical College, Perinthalmanna, Kerala, India
|Date of Submission||16-May-2021|
|Date of Acceptance||13-Jun-2021|
|Date of Web Publication||03-Sep-2021|
Mansoor C Abdulla
Department of General Medicine, M.E.S. Medical College, Perinthalmanna - 679 338, Kerala
Source of Support: None, Conflict of Interest: None
A 53-year-old female was admitted with ascites for 3 weeks, decreased response, and weakness of right upper and lower limbs for 1 day. Peritoneal biopsy showed necrotizing granulomatous inflammation, and cartridge-based nucleic acid amplification test for tuberculosis (TB) of biopsy was positive without rifampicin resistance. Magnetic resonance imaging brain showed multiple foci of diffusion restriction in bilateral cerebral hemisphere and cerebellum, suggestive of acute infarcts. After ruling out the secondary causes of cerebral infarction by appropriate tests and demonstrating that there was no evidence for tuberculous meningitis or direct injury, it was concluded that the reason for multiple cerebral infarctions in this patient is likely to be immunologic injury secondary to TB. Multiple cerebral infarctions secondary to immunologic injury in TB were reported only once previously.
Keywords: Cerebral vasculitis, extrapulmonary tuberculosis, tuberculous peritonitis
|How to cite this article:|
Abdulla MC. Tuberculous peritonitis complicated by immunologic cerebral vasculitis. Int J Mycobacteriol 2021;10:324-6
| Introduction|| |
Infection can cause vasculitis in several ways including direct invasion of the vessel wall, immune complex deposition, or through secondary cryoglobulinemia. Tuberculosis (TB) can cause cerebral vasculitis by two different mechanisms. It can be either secondary to direct invasion (the basal exudates causing inflammatory changes in the vessels predominantly involving the circle of Willis) or by immunologic injury (the deposition of tuberculoprotein immune complexes in the small vessel walls resulting in inflammatory changes of small cerebral vessels). We present a patient with tuberculous peritonitis (TBP) who developed immunologic cerebral vasculitis.
| Case Report|| |
A 53-year-old female was admitted with abdominal pain and distention for 3 weeks, decreased response, and weakness of right upper and lower limbs for 1 day. She had no history of previous medical illness and had no addictions. She denied a history of high-risk behavior and had no sick contacts. Initial examination showed soft and distended abdomen, bilateral flank dullness, and right-sided hemiparesis. Rest of the examination was unremarkable.
Hemoglobin was 10.5 g/dl, total leucocyte count 4850/ml, platelet count 2,78,000/μL, and erythrocyte sedimentation rate 82 mm in 1 h. Blood chemistries were normal. Chest X-ray was normal. Purified protein derivative test showed 14-mm induration. Ultrasonography of the abdomen showed ascites, mild grade fatty liver, and diffuse peritoneal thickening. Ascitic fluid analysis was done which showed lymphocytic predominant exudative effusion with high ADA (36.38IU/L). Ascitic fluid Gram stain, cartridge-based nucleic acid amplification test for TB, and bacterial culture were negative. Peritoneal biopsy showed necrotizing granulomatous inflammation [Figure 1], and cartridge-based nucleic acid amplification test of biopsy was positive without rifampicin resistance. Magnetic resonance imaging brain showed multiple foci of diffusion restriction in bilateral cerebral hemisphere and cerebellum, suggestive of acute infarcts. Magnetic resonance angiogram, carotid vertebral Doppler, and transthoracic echocardiogram were normal. Cerebrospinal fluid analysis was normal. The procoagulant workup showed negative IgG and IgM anticardiolipin antibody, IgG and IgM beta-2 glycoprotein, and lupus anticoagulant tests. Factor V Leiden, methylenetetrahydrofolate reductase polymorphism, and prothrombin G20210A were not detected. Her serum levels of homocysteine, protein C, and protein S were normal. Her blood coagulation profile was also normal. Her autoantibody profiles including antinuclear antibody profile, rheumatoid factor test, c and P antineutrophil cytoplasmic antibodies, and cryoglobulins were all negative. HIV, hepatitis B, and hepatitis C serologies were negative. She was diagnosed to have TBP with immunologic cerebral vasculitis and was started on antitubercular drugs with steroids. She was continued on antitubercular drugs for 6 months, and steroids were tapered and discontinued.
|Figure 1: Peritoneal biopsy showing necrotizing granulomatous inflammation (a and b). Magnetic resonance imaging of the brain showing multiple foci of diffusion restriction in bilateral cerebral hemisphere and cerebellum, suggestive of acute infarcts (c and d)|
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| Discussion|| |
Tuberculous vasculitis accounts for 12.5% of secondary cerebral vasculitis. It can be either secondary to direct invasion or by immunologic injury. The vasculitis secondary to direct invasion is a major complication of tuberculous meningitis. Cerebral infarction occurs in 15%–57% of tuberculous meningitis patients, mainly during Stage 3 of the illness. According to previous studies, 75% of infarcts occurred in the areas supplied by the medial lenticulostriate and thalamoperforating arteries, whereas only 11% occurred in the regions supplied by the lateral lenticulostriate, anterior choroidal, and thalamogeniculate arteries. Magnetic resonance angiogram in such patients shows enhancement of the basal meninges, narrowing of the basal cerebral or cortical vessels, and possible multiple small infarctions from the resultant vasculitis. Tuberculous vasculitis secondary to immunologic injury is considered to be secondary to the deposition of tuberculoprotein immune complexes in the small vessel. Other infections including hepatitis B and Epstein–Barr virus can also cause vasculitis by a similar mechanism. Magnetic resonance imaging can show stroke-like lesions from spasm or occlusion in such cases.
Abdominal TB usually involves the gastrointestinal tract, peritoneum, omentum, mesentery, and its lymph nodes. TBP is an extrapulmonary manifestation of TB which often presents with symptoms of ascites, abdominal pain, night sweats, and fever. The involvement of peritoneum in TB can have various manifestations including ascites, peritoneal thickening, enhancement, omental fat stranding, nodules, caking, mesenteric masses, and adhesions. Laparoscopic visualization allows a diagnosis to be achieved in 92.7% of TBP cases, and histology is 93% sensitive.
The patient described here was diagnosed to have peritoneal TB which was complicated by multiple cerebral infarctions (infarcts in the left posterior frontal lobe, left frontal white matter, and right occipital lobe). She was a 53-year-old female with no premorbid illness or habits and had no risk factors for developing a multi-infarct state (normal echocardiogram, normal procoagulant workup, and a negative autoantibody profile). Her cerebrospinal fluid analysis was normal, and the brain imaging did not show any evidence for direct injury (enhancement of the basal meninges and narrowing of the basal cerebral or cortical vessels). Hence, after ruling out the secondary causes of cerebral infarction by appropriate tests and demonstrating that there was no evidence for tuberculous meningitis or direct injury, it was concluded that the reason for multiple cerebral infarctions in this patient is likely to be immunologic injury secondary to TB.
We describe a patient who developed multiple cerebral infarctions secondary to immunologic injury which was reported only once previously.
All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki Declaration and its later amendments or comparable ethical standards.
Informed signed written consent was taken from the patient involved.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.
I would like to thank Dr. Asik Siddik of pathology whose comments and suggestions were immensely valuable for improving this case report.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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