| Abstract|| |
A 26-year-old women diagnosed as having lupus nephritis was managed with immunosuppressive therapy, which included cycles of Inj. Cyclophosphomide along with Inj. Mesna and Inj. Leprolide. After 1-month therapy, the patient developed moderate- to high-grade fever associated with cough and expectoration.
Sputum examination was positive for acid-fast bacilli by modified Ziehl - Neelsen (ZN) staining technique. Chest skiagram Posterioanterior (PA) view and Computed tomography (CT) scan thorax depicted thick-walled cavity in right upper zone of lung with air-fluid level. Patient was managed with second-line antituberculosis drugs during hospitalization and was followed.
Keywords: Cavitary lesion, immunosuppressive therapy, pulmonary tuberculosis, systemic lupus erythrematosus
|How to cite this article:|
Mishra A, Shilpa, Agarwal S. Pulmonary tubercular cavitory lesion: An unusual presentation in systemic lupus erythematosus. Ann Trop Med Public Health 2017;10:444-6
|How to cite this URL:|
Mishra A, Shilpa, Agarwal S. Pulmonary tubercular cavitory lesion: An unusual presentation in systemic lupus erythematosus. Ann Trop Med Public Health [serial online] 2017 [cited 2019 Jun 26];10:444-6. Available from: http://www.atmph.org/text.asp?2017/10/2/444/208719
| Introduction|| |
Systemic lupus erythrematosus (SLE) is an autoimmune collagen vascular disease, and apart from various features, systemic involvement is also characterized by variety of pulmonary manifestations. Notably, development of a cavitary pulmonary lesion is highly uncommon in SLE but can happen secondarily due to either infection, pulmonary embolism, or vasculitis. Among the list of infections, pulmonary tuberculosis is reported infrequently in SLE. In available sparse reports, observed pulmonary manifestations that included miliary involvement, segmental or lobar consolidation and pleuritis with or without effusion, and others., However, occurrence of cavitary lesion is extremely rare as observed in many case series of SLE with pulmonary tuberculosis. Extra pulmonary lesions reported in SLE happen due to wide-spread dissemination.
Here we present a case of SLE being treated as nephritis developing a large thick-walled cavity due to superimposed pulmonary tuberculosis infection. Immune suppressed state due to treatment with steroids and cyclophosphamide appeared to be cause for occurrence of this finding.
| Case Report|| |
A 26-year-old women presented in our emergency department with complaints of on and off fever, polyathralgia, facial puffiness, and loss of hair. There was no history of any drug intake or any systemic illness in the past.
On arrival, her oral temperature was 38.2°C, pulse rate 102/min, respiratory rate 22/min, and blood pressure 126/70 mm Hg in right arm supine position.
General examination revealed mild-to-moderate anemia and bilateral pedal edema. On systemic examination, cardiovascular, abdominal, and neurological systems did not reveal any positive findings.
Laboratory values revealed Hb 6.7 g/dL, white blood cell count of 5.6 × 109/L with neutrophils 78%, platelet 66 × 109/L, total serum bilirubin 0.13 mg/dL, serum glutamic oxaloacetate transminase 20.4 IU/L, serum glutamic pyruvate transminase 8.7 IU/L, random blood glucose 82 mg/dL, albumin 1.07g/dL, urine examination showed protein 100 mg%, 1 to 2 pus cells/ High power field (HPF), 4 to 5 Red blood cells (RBC)/HPF. Twenty-four-hour urinary protein was 3020.3 mg%. Anti-dsDNA and Smith antigen were positive. Ultrasound abdomen showed bilateral grade II echogenic kidney with attenuated corticomedullary differentiation. Biopsy could not be done due to denial by the patient. Patient met the SLE collaborating clinical criteria and was then diagnosed as a case of SLE presented with features of nephritis.
Patient was kept on Inj. methylprednisolone 1g i.v. once daily for 3 days, followed by pulse therapy of Inj. Cyclosphosphamide 7 mg/kg/month given in infusion along with Inj. Mesna and Inj. Leuprolide to prevent hemorrhagic adverse effects and ovarian failure, respectively. The patient was then discharged and followed up monthly for clinical evaluation and urine albumin levels. At each follow-up visit, for the next 4 months, the patient was regularly administered the above mentioned pulse therapy. On her fourth follow-up the patient complained of fever with cough and expectoration for 15 days. She was admitted and was screened for the present complaints. Laboratory values revealed white cell counts of 4.6 × 109/L, Hb 9.3 mg/dL, platelet counts 2.2 lakhs, S. bilirubin total 0.2 mg/dL, serum glutamic oxaloacetate transminase 18.5 IU/L, serum glutamic pyruvate transaminase 24.2 IU/L, blood culture was sterile, chest x-ray posterior anterior view showed bilateral upper zone infiltration with a well-defined cavitary lesion is right upper zone [Figure 1]. Sputum for acid-fast bacilli by modified ZN staining method showed grade 4 positivity. High resolution computed tomography (HRCT) thorax revealed a large thick-walled cavitary lesion in right upper lobe [Figure 2]. Patient was stated on Antitubercular therapy after these reports.
|Figure 1: Sputum for acid-fast bacilli by modified ZN staining method showed grade 4 positivity. HRCT thorax revealed a large thick-walled cavitary lesion in right upper lobe.|
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|Figure 2: Patient was stated on antituberuclar therapy after these reports.|
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| Discussion|| |
Cavitary lung lesions are extremely rarely reported in SLE itself as primary lesion. Available reports citing secondary causes leading to cavitary lesions are also very rare. These include various infections, embolism, or underlying vasculitis. Variety of infections reported leading to cavity formation are bacterial (75%), fungal (7%), and viral (5%) agents. Bacterial infection usually presents with pneumonia with cavitation or may manifest as lung abscess. Organisms reported mostly are Staphylococcus, Serratia, Pseudomonas aeruginosa, mixed gram-positive cocci, and gram-negative bacilli.
Fungal organisms in patients with SLE also can present as cavitary pulmonary nodules and common organisms are Aspergillus, Coccidioidomycosis, Nocardia, Cryptococcus, and Candida., Among viruses, Cytomegalovirus is reported to be responsible for cavitary lesion in patients on corticosteroid treatment.
Among other causes, Wegener granulomatosis, rheumatoid nodule, pulmonary infarct, septic embolism, localized bronchiectasis, and other secondary causes are also reported sparsely in different case reports.
Mycobacterium tuberculosis infection is chiefly responsible for disseminated extrapulmonary spread. Pulmonary manifestations are observed as miliary, segmented or lobar consolidation, unifocal patchy consolidation, nodular opacities, and pleuritis with or without effusion. This description is not having a mention of cavitary lesion in the lung parenchyma valuing it as a very rare occurrence among reported pulmonary manifestations.
Globally association of pulmonary tuberculosis with SLE is considered to be uncommon. However, in India, prevalence of pulmonary tuberculosis in patients with SLE is reported in a range of 5% to 11.6%.
It is interesting to note that though almost all clinicopathalogical manifestations of pulmonary and extrapulmonary tuberculosis are observed in patients of SLE, but occurrence of a cavity is rarely reported in available literature. In our case, pulmonary tuberculosis appears to be developing secondary to immunosuppressive therapy, which included steroids and inj. Cyclophosphamide exacerbating already existing immunodeficiency state in SLE. Resultant destruction of lung parenchyma lead to development of the cavity as observed in this case.
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Conflicts of interest
There are no conflicts of interest.
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Department of Medicine, King George's Medical University, Lucknow, Uttar Pradesh
Source of Support: None, Conflict of Interest: None
[Figure 1], [Figure 2]