eISSN: 2299-0046
ISSN: 1642-395X
Advances in Dermatology and Allergology/Postępy Dermatologii i Alergologii
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vol. 35
Letter to the Editor

Mycobacterium tuberculosis and pemphigus vulgaris

Katarzyna Osipowicz, Cezary Kowalewski, Katarzyna Woźniak

Adv Dermatol Allergol 2018; XXXV (5): 532-534
Online publish date: 2018/07/19
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Tuberculosis (TB) is a disease caused by Mycobacterium tuberculosis (M. tuberculosis) affecting principally the lungs. Recently, it has been postulated that M. tuberculosis causes more deaths than any other infectious disease [1]. Patients with smear-positive sputum for M. tuberculosis are the main source of infection. Normally, the therapy takes 6 to 9 months using isoniazid (INH), rifampicin (RMP), ethambutol (EMB), and pyrazinamide (PZA). For the drug-resistant forms of TB, treatment consists of a combination of fluoroquinolones with other injectable medications, such as kanamycin, capreomycin or amikacin [2].
Pemphigus vulgaris (PV) belongs to a group of acantholytic bullous dermatoses, with a potentially fatal outcome. The disease is characterized by flaccid bullae formation observed within the epidermis, being a result of IgG autoantibody production directed against desmoglein 1 and 3, expressed in the epidermis and, particularly, the mucosal epithelia.
In most patients, PV develops spontaneously [3]. Inducing or triggering factors, i.e. viral infections, physical agents, contact allergens, stress, dietary factors, and drug intake have also been reported. The PV may be induced by three groups of drugs, containing a sulfhydryl group, a phenol group and, finally, a non-phenol group [3].
We present the case of a patient with PV provoked by rifampicin taken due to pulmonary TB.
A 48-year-old male with a 2-year history of pulmonary TB treated with INH and RMP, and 1-year history of an active PV persistently treated with prednisone at a dose of 80 mg (1 mg/kg) and azathioprine at a dose of 100 mg. Despite that therapy, he still presented erosions located in the oral mucosa and on the trunk and extremities (Figure 1 A–C). The activity of PV was confirmed by direct and indirect immunofluorescence (Figure 2) study showing in vivo bound and circulating intercellular IgG antibodies at a titer of 1280. The increase in the dose of azathioprine to 150 mg/day did not lead to the improvement. After pulmonary consultation, antituberculotic medicines, were discontinued. One month later, we observed a significant improvement of the patient and a decreased level of pemphigus antibodies. Currently, the patient is in clinical remission of PV (Figures 1 D–F) and takes 30 mg/day of prednisone and 100 mg/day of azathioprine. The remission of TB has been confirmed by chest radiography.
Mycobacterium tuberculosis infection is one of the...

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