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Grantham Hospital Hong Kong, China
Correspondence to: Wing Wai Yew, MD, FCCP, Tuberculosis and Chest Unit, Grantham Hospital, 125 Wong Chuk Hand Road, Hong Kong, China.
To the Editor:
The article by Pietinalho et al,1
reporting the use
of inhaled budesonide in pulmonary sarcoidosis, has prompted us to
share our experience in the use of inhaled corticosteroid as adjunctive
therapy in tuberculous pyrexia. Similar mechanisms of cytokine
production and release through activation of lung T-lymphocytes, in
patients with sarcoidosis and in those with tuberculous alveolitis,
have been described.2
In the latter setting, cytokines
like TNF
, IL-1, and other interleukins might
be responsible for the pyrexia that occurs in some patients with
tuberculosis (TB).3
Modulation of cytokine release by
systemic corticosteroid, along with the administration of
antituberculosis drugs, can logically control the unremitting
pyrexia.3
The duration of such therapy is usually 4 to 10
weeks.3
4
Inhaled corticosteroid, if demonstrated to be
efficacious, may be the preferred alternative because of the following
advantages, namely, (1) circumvention of interaction with
antituberculosis drugs, especially rifampin,5
and (2) much
lower risk of systemic side effects, and suppression of the
hypothalamo-pituitary-adrenal axis.6
Thus, the inhaled
route might allow safe deployment of steroid treatment in TB patients
with relative contraindications to systemic corticosteroid therapy,
such as diabetes mellitus, hepatitis B/hepatitis C-related liver
diseases, and HIV coinfection.
Previously, we reported somewhat favorable experience with 9 HIV-negative patients with tuberculous pyrexia, who were treated for 2 weeks with inhaled budesonide at a dosage of 800 µg tid, via the dry powder inhaler.7 After this, we studied another 5 HIV-negative patients. When the results of all 14 patients were analyzed together, 9 of the 14 patients (64.3%) achieved defervescence (mean time required, 3.8 days; range, 2–6 days). When the mean maximum oral temperatures, for 7 days before and after starting inhaled corticosteroids, for all 14 patients were compared using the Wilcoxon signed ranks test (SPSS Software; SPSS, Inc; Chicago, IL), the decrease was significant: mean ± SD = 0.9 ± 0.5°C (p = 0.001; z = 3.238). Of these nine patients, two developed transient recrudescence or fever. Both conditions were resolved without recourse to systemic corticosteroid. Acceptance and tolerance by patients of inhaled budesonide was good. Two patients had hypothalamo-pituitary-adrenal axis function assessed and were found to be normal.
Our preliminary experience suggests that inhaled corticosteroid is efficacious in some patients with tuberculous pyrexia. The exact accountable mechanism is not clear. Inhaled budesonide, having high topical potency, may work via local-regional distribution through the ramifying bronchial vascular meshwork in the airways, partially anastomosing with the pulmonary microcirculation of the alveoli. Drugs absorbed gastrointestinally, following swallowing, are largely inactivated by first-pass metabolism and do not contribute much to systemic bioavailability.6 Systemic bioavailability secondary to lung bioavailability definitely occurs, but the contribution is insignificant.8 It is vitally important to delineate the possible characteristics of both patient and disease that are associated with favorable response. A randomized study comparing the efficacy of systemic and inhaled corticosteroids in patients with tuberculous pyrexia appears warranted. Finally, studies of the blood, or preferably of the bronchoalveolar-lavage-fluid cytokine profiles, before and after treatment with inhaled or systemic corticosteroid would further our understanding of the immunopathogenesis of tuberculous pyrexia and of the impact of different modes of steroid treatment.
References
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