A 26-year-old man had endobronchial...

A 26-year-old man had endobronchial tuberculosis diagnosed in succession bronchoscopy. He was treated with standard antituberculosis physics but the endobronchial lesions deteriorated bronchoscopically. This is believed to be a hypersensitivity reaction to tuberculoprotein. The lesions improved rapidly with addition of corticosteroids.

Endobronchial tuberculosis is an important complication of pulmonary tuberculosis. However, its pathogenesis is not established and its clinical course is variable. Corticosteroid treatment has been advocated by means of some authors but others claimed no benefit.[1,2]

We report a patient whose endobronchial tuberculosis deteriorated initially during standard antituberculosis chemotherapy. Prednisone was introduced and rapid clinical, radiologic and bronchoscopic improvement ensu As far as we are aware, this is the first photographically documented case of endobronchial tuberculosis which deteriorated during chemotherapy and improved after addition of steroids.

CASE REPORT

A 26-year-old man was admitted to the hospital because of ferment and dry cough for ten days. Physical examination was normal. No satisfactory sputum specimens could be produc for examination. Tuberculin ordeal was positive. A chest radiograph showed consolidation in the RLL (Fig 1 left) Bronchoscopy revealed inflammation of the carina and right main bronchus with small pale mucosal nodules forward its medial wall. The anterior basal portion of the RLL was occlud on necrotic material (Fig 2, a and b) Biopsy showed several granulomas consisting of epithelioid small cavitys lymphocytes and plasma cells. Ziehl Neelsen staining for AFB was negative. Bronchial aspirate was also negative for AFB (but civilization was positive six weeks later).

Antituberculosis treatment with rifampicin, isoniazid, pyrazinamide and streptomycin was started. The patient's febrile affection subsided in three days and he was subsequently discharged from the hospital. However, cough persisted and a chest x-ray film six weeks later showed no improvement. Repeat bronchoscopy showed progression of the endobronchial lesions. The right main bronchus contained exuberant tissue upon its medial wall where small, pale nodules had been observ previously, and the anterior basal section of the RLL was completely hindered (Fig 2, c and d) Biopsy of the right main bronchus showed granuloma formation with no caseous material or demonstrable AFB. In view of the rapid enlargement of the endobronchial lesions, prednisone, 30 mg daily, was started. His cough resolv pair days later. A repeat chest x-ray examination four weeks later showed partial resolution of the RLL consolidation (Fig 1 b) A third bronchoscopy was performed. There was a great deal improvement and shrinkage of the lesions in the right main bronchus and the anterior basal section was no longer occluded (Fig 2 e and f) Biopsy of the residual lesions in the right main bronchus again showed granulomas which were negative for AFB. The dose of prednisone was gradually reduc through the whole extent of six weeks.

DISCUSSION

Endobronchial tuberculosis has an incidence ranging from 60 percent in autopsy findings to 10 percent in succession routine bronchoscopy of tuberculosis patients.[3] Its pathogenesis is uncertain. There appear to be three major factors, namely: the consequence of mycobacteria, host immunity, and antituberculosis treatment. The interaction between these three factors is mingled and any variation in these three factors may terminate in an altered clinical course. It is an oversimplification to view all cases of endobronchial tuberculosis as a homogeneous group

Granuloma formation is regarded as the body's defense to capture and devour the mycobacteria. The key-note factor in the body's defense is the macrophage, on the other hand T and B lymphocytes and lymphokines also are involved.[4,5] The introduction of antituberculosis treatment would end in hastened killing of the mycobacteria and release of lonely dwelling wall material (tuberculoprotein), but this may elicit a delayed hypersensitive reply from the patient. This replication is not considered essential for disclosure of immunity,[6] and under a circumstances may even be detrimental.[6,7] Possible examples are the enlargement of lymph nodes in tuberculous adenitis and the disclosure of intracranial tuberculoma[8] on antituberculosis treatment.

Hypersensitivity to tuberculoprotein released during treatment with antituberculosis physics probably accounted for the initial deterioration in our patient. Corticosteroids suppres the hypersensitivity answer and this was the likely mechanism for the rapid resolution of the lesions.

Williams et al[9] also described three patients with endobronchial tuberculosis developing during antituberculosis treatment. However, solely one of these patients was bronchoscop before treatment, and biopsy did not reveal any evidence of endobronchial tuberculosis. We believe that our patient is the first photographically and histologically documented case of existing endobronchial lesions deteriorating while forward anti-tuberculosis treatment and resolving rapidly when corticosteroids were added. The inconsistent accrues of corticosteroids reported previously may be related to the pathogenesis of the endobronchial lesions: steroids are likely to be beneficial when hypersensitivity is the predominant mechanism, nevertheless are unlikely to be helpful in more advanced cases when extensive fibrosis is present