Development of miliary tuberculosis related to anti‐tumor necrosis factor‐alpha inhibitor therapy for pustular psoriasis

Abstract

TNF-a agents and the anti-inflammatory effect of TNF-a blocking agents is not mediated by adiponectin, 1 the alteration of serum adipokines would not be the specific action of TNF-a blocking agents but rather be the result of decreased serum TNF-a levels by the successful psoriasis treatments including ustekinumab and NB-UVB.In conclusion, we demonstrated that improvements of serum levels of adiponectin, leptin and resistin are linked to successful treatment of psoriasis. Because these adipokines are significantly involved in "psoriatic march", adequate control of psoriasis may contribute to the decreased development of metabolic syndrome including cardiovascular disease. REFERENCES1 Peter MJ, Watt P, Cherry L et al. Lack of effect of TNF-alpfa blockade therapy on circulating adiponectin levels in patients with autoimmune disease: results from two independent prospective studies. Ann Rhem Dis 2010; 69: 1687-1690. 2 Karmiris K, Koutroubakis IE, Xidakis C et al. The effect of infliximab on circulating levels of leptin, adiponectin and resistin in patients with inflammatory bowel diease. Eur J Gastroenterol Hepatol 2007; 19: 789-794. 3 Shibata S, Saeki H, Tada Y et al. Serum high molecular weight adiponectin levels are decreased in psoriasis patients. J Dermatol Sci 2009; 55: 62-63. 4 Peters MJ, Watt P, Cherry L et al. Lack of effect of TNF-alpfa blockade therapy on circulating adiponectin levels in patients with autoimmune disease: results from two independent prospective studies. Ann Rhem Dis 2010; 69: 1-687.

Complexity and Controversies over the Cytokine Profiles of T Helper Cell Subpopulations in Tuberculosis

“…In fact, TNF- α acts synergistically with IFN- γ to stimulate the production of NO by macrophages and influences the expression of chemokines, such as CCL5, CCL9, CXCL10, and CCL2, which induce migration to and maintenance of immune cells in the infection site [ 82 ]. Blocking TNF- α , for example, in the treatment of rheumatoid arthritis, leads to a loss of granuloma structure and reactivation of the disease [ 45 – 48 ]. Conversely, M. tuberculosis -specific stimulation of IFN- γ (but not TNF- α ) and IFN- γ R signaling are significantly depressed in active TB, which correlates with TB disease severity and activity.…”

Psoriasis: Behind the scenes

“…Mucocutaneous candidiasis and invasive salmonellosis may occur in patients with IL12RB1 or IL12B deficiencies, probably due to impaired IL‐23‐dependent IL‐17A immunity . Therefore, careful monitoring is mandatory to prevent severe infection, especially with Mycobacterium , Candida or Salmonella , during the course of biologic therapy targeting the TNF‐α/IL‐23/IL‐17 axis . The risk of herpes zoster is also increased in psoriatic patients undergoing biologic treatment .…”

“…37,38 Therefore, careful monitoring is mandatory to prevent severe infection, especially with Mycobacterium, Candida or Salmonella, during the course of biologic therapy targeting the TNF-a/IL-23/IL-17 axis. 37,38,83,84 The risk of herpes zoster is also increased in psoriatic patients undergoing biologic treatment. 85 Various paradoxical reactions caused by biologics are also problematic and mysterious, but aberrant activation of the TNF-a/IL-23/IL-17 axis with IL-36c may indicate its pathomechanism.…”