Start acitretin.

The transmission of tuberculosis (TB) is by inhalation of aerosolized Mycobacterium tuberculosis. If the inhaled bacilli are not cleared by pulmonary host defenses, latent or active infection can be established. In the United States, a total of 9421 tuberculosis cases (rate of 2.96 cases per 100,000 persons) were reported in 2014 (CDC 2015). Carriers with untreated tuberculosis of the respiratory tract are the most common source of infection (Getahun et al. 2015). The majority of patients with latent TB infection (LTBI) are asymptomatic. LTBI occurs when M. tuberculosis bacilli are contained within macrophages and granulomas, thereby limiting replication and spread of infection (Getahun et al. 2015). Reactivation of M. tuberculosis can result in hematologic dissemination and involve any tissue. Common sites of extrapulmonary disease include the meninges, cervical lymph nodes, kidneys, and lumbar vertebrae. The reactivation and progression of latent infection to active disease is dependent on multiple factors such as age, initial bacterial load, and suppression of immunity (e.g., HIV infection, systemic corticosteroid, tumor necrosis factor inhibitors, organ or hematologic transplantation) (Getahun et al. 2015). Tumor necrosis factor (TNF)-alpha is a critical component in the prevention of M. tuberculosis dissemination. TNF-alpha increases the phagocytic capacity of macrophages and the formation of granulomas to restrict infections (Ehlers 2005). This provides a possible explanation as to why TNF inhibitor use is associated with increased TB infections (Keane 2005).

Before initiating a TNF inhibitor or other immunosuppressive medication indicated for psoriasis, the prescribing physician should obtain a thorough history to screen for TB exposure and risk factors. Additionally, a baseline and annual purified protein derivative (PPD) skin test or interferon-gamma release assay (IGRA) must be obtained (Mazurek et al. 2010). For patients with a positive PPD or IGRA, a chest x-ray should be performed to rule out active tuberculosis. Those with normal findings on chest radiograph should receive treatment for LTBI. The preferred treatment for most patients with LTBI is isoniazid (INH) with vitamin B6 (pyridoxine) for 9 months (Cohn et al. 2000). For patients with LTBI who are initiating biologic therapy, the CDC recommends completing the full 9-month course of treatment prior to starting a biologic agent. However, some psoriasis experts believe 1–2 months of INH prophylaxis before starting biologic therapy is sufficient (Doherty et al. 2008). Those with active TB must defer psoriasis treatment and be referred to a specialist for standard multidrug antituberculosis drug therapy (RIPE).

Narrowband ultraviolet B (NB-UVB) phototherapy is not immunosuppressive and is not associated with the reactivation of TB (Doherty et al. 2008) Therefore, NB-UVB phototherapy is an ideal treatment option for patients with LTBI and psoriasis affecting more than 10% of body surface area (BSA). Screening for LTBI is not necessary before initiating UVB phototherapy.

Unlike many systemic medications used in the treatment of psoriasis, acitretin does not suppress the immune system or increase the risk for TB reactivation. Similarly, apremilast’s mechanism of action is primarily anti-inflammatory and has yet to have shown clinical signs of immunosuppression or increased incidence of TB (Chimenti et al. 2015). Therefore, both acitretin and apremilast are safe for use in patients with coexisting psoriasis and LTBI.

Topical corticosteroids have not been associated with the reactivation of TB. Other topical treatments such as vitamin D analogs (calcipotriene and calcitriol) and topical calcineurin inhibitors (pimecrolimus and tacrolimus) do not cause systemic immunosuppression and are also considered to be safe (Doherty et al. 2008). However, an alternative option should be considered for patients with more than 10% of BSA affected, as in the case of our patient.