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Pulmonary Tuberculosis and Steroids
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11111
Communications for this section will be published as space and priorities permit. The comments should not exceed 350 words in length, with a maximum of five references; one figure or table can be printed. Exceptions may occur under particular circumstances. Contributions may include comments on articles published in this periodical, or they may be reports of unique educational character. Specific permission to publish should be cited in a covering letter or appended as a postscript.
Pulmonary Tuberculosis and Steroids To the Editor: We read with interest the recent editorial (CHEST 1995; 107:1486-87) accompanying the article (CHEST 1995; 107:162130) on corticosteroids in pulmonary tuberculosis (TB), and we wish to highlight a few additional points on the use of corticosteroids in the management ofTB. 1 A small number of patients with post primary TB may also have true Addison's disease due to tuberculous destruction of the adrenal gland. 2 With the "stress" of the infection and the use of rifampicin, which increases steroid metabolism some two to three fold, 3 patients can develop adrenal failure. 4 This may be one explanation for the early mortality that occurs with TB, in spite of patients receiving appropriate therapy. 5 Identification of such patients and use of steroids as replacement therapy is one area that should always be considered and was not discussed in the editorial. Additionally, steroids have a major use in the management of pleural disease beyond "patients with extensive primary tuberculosis with a large pleural effusion" (CHEST 1995; 107:1486-87). Several studies have confirmed the advantage of systemic steroids in limiting the pleural fibrosis that may occur;6·8 intrapleural steroids confer no advantage. 9 In one study10 where steroids were not used in the management of pleural disease, an unacceptable 23 of 44 patients developed this complication despite effective chemotherapy. Furthermore, tuberculous pleural effusions may be a greater . . o f preVJous . disease. II · 12 problem in o lder patients WI'th reactivation These patients, like those with a primary disease producing pleural effusions should not be denied the benefit of steroids, which not only impro~e their constitutional symptoms but also limit the development of pleural flbrosis.
Paul Clarke, MD, and Martin B. Allen, MD; St. Luke's Hospital, Bradford, United Kingdom REFERENCES
1 Allen MB, Cooke NJ. Corticosteroids and tuberculosis. BMJ 1991; 303:871-72 2 Ellis ME, Tayoub F. Adre nal function in tuberculosis. Br J Dis Chest 1986; 80:7-12 3 McAllister WA, Thompson PJ, Al-Habet SM, et al. Rifampicin reduces effectiveness and bioavailability of prednisolone. BMJ 1983; 286:923-25
582
4 Wilkins EGL, Hnizdo E, Cope A. Addisonian crisis induced by treatment with rifampicin. Tubercle 1989; 70:69-73 5 Ellis ME, Webb AK. Cause of death in patients admitted to hospital for pulmonary tuberculosis. Lancet 1983; 1:665-67 6 Fleishman SJ, Coetzee AM, Mindel S, et al. Antituberculosis therapy combined with adrenal steroids in the treatment of pleural effusions a theraputic trial. Lancet 1960; 1:199-201 7 LeeCH, Wang WJ, Lan RS, et al. Corticosteroids in the treatment of tuberculous pleurisy: a double-blind, placebo controlled, randomized study. Chest 1988; 94:1256-59 8 Paley SS, Mihaly JP, MaisEL, et al. Prednisolone in the treatment of tuberculous pleural effusions. Am RevTuberc 1959; 79:307-14 9 Menon NK. Steroid therapy in tuberculous effusion. Tubercle 1964; 45:17-20 10 Barbas CSV, Ctilier A, de Varvalho CRR, et al. The relationship between pleural fluid findings and the development of pleural thickening in patients with pleural tuberculosis. Chest 1991; 100:1264-67 ll Epstein DM, Kline LR, Albelda SM, et al. Tuberculous pleural effusions. Chest 1987; 91:106-09 12 Moudgil H, Sridhar G, Leitch AG. Reactivation disease: the commonest form of tuberculous pleural effusion in Edinburgh, 1980-1991. Respir Med 1994; 88:301-04
Hazards of Ultraviolet Lighting Used for Tuberculosis Control To the Editor: Germicidal lamps using ultraviolet (UV) radiation are recommended to prevent transmission of tuberculosis. 1•2 The National Institute for Occupational Safety and Health recommends that exposure to UV radiation be limited to less than 0.2 pW/cm 2 (based on 8 h of exposure per day). More exposure may cause dermatosis or photokeratitis.3 Such problems have not yet been reported in the hospital setting. We report on five health-care workers who developed dermatosis or photokeratitis after exposure to an improperly maintained germicidal lamp in an emergency department (ED). No alternative explanation for the victims' symptoms was found in any case. One of the persons involved was a 35-year-old female nurse; the others were male physicians ranging in age from 27 to 35 years. All patients had redness, tenderness, and later desquamation on the exposed skin of their faces. Two persons had red, gritty eyes with blurry vision, and one person had severe ocular discomfort with redness, watering, and blurred vision that lasted 8 h. An investigation determined that one of the germicidal lamps in the ED was unshielded. A note in the ED log book confirmed that this light had been unshielded during the time when the cases occurred. This light was tested and found to be emitting UV-C radiation (200 to 300 nm) at levels up to 60 pW/cm2 . The National Institute for Occupational Safety and Health recommends less than 1 min of exposure to UV radiation at this level. The light was repaired and no further cases have occurred. Germicidal lamps are considered to be an effective method of reducing transmission of tuberculosis, and we do not intend to discourage their use. Health-care workers should be aware of the potential danger of exposure to UV radiation from these lamps. These Communications to the Edttor
-----~S- -:_Lc_o_m_m_un_ic_a_tio_n_s_ to_t_he_e_d_ito_r_ _ _ _ __
11111
Communications for this section will be published as space and priorities permit. The comments should not exceed 350 words in length, with a maximum of five references; one figure or table can be printed. Exceptions may occur under particular circumstances. Contributions may include comments on articles published in this periodical, or they may be reports of unique educational character. Specific permission to publish should be cited in a covering letter or appended as a postscript.
Pulmonary Tuberculosis and Steroids To the Editor: We read with interest the recent editorial (CHEST 1995; 107:1486-87) accompanying the article (CHEST 1995; 107:162130) on corticosteroids in pulmonary tuberculosis (TB), and we wish to highlight a few additional points on the use of corticosteroids in the management ofTB. 1 A small number of patients with post primary TB may also have true Addison's disease due to tuberculous destruction of the adrenal gland. 2 With the "stress" of the infection and the use of rifampicin, which increases steroid metabolism some two to three fold, 3 patients can develop adrenal failure. 4 This may be one explanation for the early mortality that occurs with TB, in spite of patients receiving appropriate therapy. 5 Identification of such patients and use of steroids as replacement therapy is one area that should always be considered and was not discussed in the editorial. Additionally, steroids have a major use in the management of pleural disease beyond "patients with extensive primary tuberculosis with a large pleural effusion" (CHEST 1995; 107:1486-87). Several studies have confirmed the advantage of systemic steroids in limiting the pleural fibrosis that may occur;6·8 intrapleural steroids confer no advantage. 9 In one study10 where steroids were not used in the management of pleural disease, an unacceptable 23 of 44 patients developed this complication despite effective chemotherapy. Furthermore, tuberculous pleural effusions may be a greater . . o f preVJous . disease. II · 12 problem in o lder patients WI'th reactivation These patients, like those with a primary disease producing pleural effusions should not be denied the benefit of steroids, which not only impro~e their constitutional symptoms but also limit the development of pleural flbrosis.
Paul Clarke, MD, and Martin B. Allen, MD; St. Luke's Hospital, Bradford, United Kingdom REFERENCES
1 Allen MB, Cooke NJ. Corticosteroids and tuberculosis. BMJ 1991; 303:871-72 2 Ellis ME, Tayoub F. Adre nal function in tuberculosis. Br J Dis Chest 1986; 80:7-12 3 McAllister WA, Thompson PJ, Al-Habet SM, et al. Rifampicin reduces effectiveness and bioavailability of prednisolone. BMJ 1983; 286:923-25
582
4 Wilkins EGL, Hnizdo E, Cope A. Addisonian crisis induced by treatment with rifampicin. Tubercle 1989; 70:69-73 5 Ellis ME, Webb AK. Cause of death in patients admitted to hospital for pulmonary tuberculosis. Lancet 1983; 1:665-67 6 Fleishman SJ, Coetzee AM, Mindel S, et al. Antituberculosis therapy combined with adrenal steroids in the treatment of pleural effusions a theraputic trial. Lancet 1960; 1:199-201 7 LeeCH, Wang WJ, Lan RS, et al. Corticosteroids in the treatment of tuberculous pleurisy: a double-blind, placebo controlled, randomized study. Chest 1988; 94:1256-59 8 Paley SS, Mihaly JP, MaisEL, et al. Prednisolone in the treatment of tuberculous pleural effusions. Am RevTuberc 1959; 79:307-14 9 Menon NK. Steroid therapy in tuberculous effusion. Tubercle 1964; 45:17-20 10 Barbas CSV, Ctilier A, de Varvalho CRR, et al. The relationship between pleural fluid findings and the development of pleural thickening in patients with pleural tuberculosis. Chest 1991; 100:1264-67 ll Epstein DM, Kline LR, Albelda SM, et al. Tuberculous pleural effusions. Chest 1987; 91:106-09 12 Moudgil H, Sridhar G, Leitch AG. Reactivation disease: the commonest form of tuberculous pleural effusion in Edinburgh, 1980-1991. Respir Med 1994; 88:301-04
Hazards of Ultraviolet Lighting Used for Tuberculosis Control To the Editor: Germicidal lamps using ultraviolet (UV) radiation are recommended to prevent transmission of tuberculosis. 1•2 The National Institute for Occupational Safety and Health recommends that exposure to UV radiation be limited to less than 0.2 pW/cm 2 (based on 8 h of exposure per day). More exposure may cause dermatosis or photokeratitis.3 Such problems have not yet been reported in the hospital setting. We report on five health-care workers who developed dermatosis or photokeratitis after exposure to an improperly maintained germicidal lamp in an emergency department (ED). No alternative explanation for the victims' symptoms was found in any case. One of the persons involved was a 35-year-old female nurse; the others were male physicians ranging in age from 27 to 35 years. All patients had redness, tenderness, and later desquamation on the exposed skin of their faces. Two persons had red, gritty eyes with blurry vision, and one person had severe ocular discomfort with redness, watering, and blurred vision that lasted 8 h. An investigation determined that one of the germicidal lamps in the ED was unshielded. A note in the ED log book confirmed that this light had been unshielded during the time when the cases occurred. This light was tested and found to be emitting UV-C radiation (200 to 300 nm) at levels up to 60 pW/cm2 . The National Institute for Occupational Safety and Health recommends less than 1 min of exposure to UV radiation at this level. The light was repaired and no further cases have occurred. Germicidal lamps are considered to be an effective method of reducing transmission of tuberculosis, and we do not intend to discourage their use. Health-care workers should be aware of the potential danger of exposure to UV radiation from these lamps. These Communications to the Edttor