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Current Drug Safety

Editor-in-Chief

ISSN (Print): 1574-8863
ISSN (Online): 2212-3911

Case Report

Double Infection in a Patient with Psoriatic Arthritis Under TNF-alpha Blockers Therapy: A Case Report

Author(s): Benedetto Caroleo, Alberto Migliore, Erika Cione, Stefania Zampogna, Francesco Perticone, Giovambattista De Sarro and Luca Gallelli*

Volume 14, Issue 2, 2019

Page: [147 - 150] Pages: 4

DOI: 10.2174/1574886314666190114124625

Price: $65

Abstract

Background: Either direct or indirect tumor necrosis factor (TNF)-alpha blockers are usually used to treat psoriatic arthritis (PA), but their use can increase susceptibility to infectious diseases.

Case Presentation: We report a rare case of double skin-knee wound and lung non-tubercular infection in a patient with PA under TNF-alpha blockers therapy. About 1 year after the beginning of adalimumab, a 48-year-old smoker suffering of PA was hospitalized for the skin-knee wound.

Results: Clinical evaluation and biochemical markers excluded the presence of a systemic disease, and a skin infection sustained by leishmaniasis probably related to adalimumab was diagnosed (Naranjo score: 6). Adalimumab was discontinued and oral treatment with apremilast and topical treatment with meglumine antimoniate was started with a complete remission of skin wound in 2 weeks. About 7 months later when the patient was under apremilast treatment, he presented to our observation for dyspnea, cough and fever. High-Resolution Computer Tomography (HRCT) chest highlighted alveolar involvement with centrilobular small nodules, branching linear and nodular opacities. Microbiological culture of both broncho-alveolar lavage fluid and sputum documented an infection sustained by nontuberculous mycobacteria. Even if apremilast treatment probably-induced lung infection, we can’t exclude that it worsened a clinical condition induced by adalimumab. Apremilast was stopped and an empirical antitubercular treatment was started. Patient's breathlessness and cough improved as confirmed also by HRCT chest.

Conclusion: This case highlights the importance to consider the possibility to develop leishmaniasis and/or non-tubercular mycobacterial infection in patients treated with TNF-alpha inhibitors.

Keywords: TNF-alpha inhibitors, skin-knees ulcer, lung infection, bDMARD, Psoriatic arthriatis, HR-CT.

[1]
Gossec L, Smolen JS, Ramiro S, et al. European League against Rheumatism (EULAR) recommendations for the management of psoriatic arthritis with pharmacological therapies: 2015 update. Ann Rheum Dis 2016; 75(3): 499-510.
[2]
Ramiro S, Smolen JS, Landewe R, et al. Pharmacological treatment of psoriatic arthritis: A systematic literature review for the 2015 update of the EULAR recommendations for the management of psoriatic arthritis. Ann Rheum Dis 2016; 75(3): 490-8.
[3]
Schemoul J, Poulain C, Claudepierre P. Treatment strategies for psoriatic arthritis. Joint Bone Spine 2018; 85(5): 537-44.
[4]
Roach DR, Bean AG, Demangel C, France MP, Briscoe H, Britton WJ. TNF regulates chemokine induction essential for cell recruitment, granuloma formation, and clearance of mycobacterial infection. J Immunol 2002; 168(9): 4620-7.
[5]
Bruns H, Meinken C, Schauenberg P, et al. Anti-TNF immunotherapy reduces CD8+ T cell-mediated antimicrobial activity against Mycobacterium tuberculosis in humans. J Clin Invest 2009; 119(5): 1167-77.
[6]
Ellerin T, Rubin RH, Weinblatt ME. Infections and anti-tumor necrosis factor alpha therapy. Arthritis Rheum 2003; 48(11): 3013-22.
[7]
Naranjo CA, Busto U, Sellers EM, et al. A method for estimating the probability of adverse drug reactions. Clin Pharmacol Ther 1981; 30(2): 239-45.
[8]
Wallis RS. Infectious complications of tumor necrosis factor blockade. Curr Opin Infect Dis 2009; 22(4): 403-9.
[9]
Wallis RS, Schluger NW. Pulmonary infectious complications of tumor necrosis factor blockade. Infect Dis Clin North Am 2010; 24(3): 681-92.
[10]
Fraser AD, van Kuijk AW, Westhovens R, et al. A randomised, double blind, placebo controlled multicentre trial of combination therapy with methotrexate plus ciclosporin in patients with active psoriatic arthritis. Ann Rheum Dis 2005; 64(6): 859-64.
[11]
Marchesoni A, Olivieri I, Salvarani C, et al. Recommendations for the use of biologics and other novel drugs in the treatment of psoriatic arthritis: 2017 update from the Italian Society of Rheumatology. Clin Exp Rheumatol 2017; 35(6): 991-1010.
[12]
Stiff KM, Glines KR, Porter CL, Cline A, Feldman SR. Current pharmacological treatment guidelines for psoriasis and psoriatic arthritis. Expert Rev Clin Pharmacol 2018; 11(12): 1209-18.
[13]
Sester M, van Leth F, Bruchfeld J, et al. Risk assessment of tuberculosis in immunocompromised patients. A TBNET study. Am J Respir Crit Care Med 2014; 190(10): 1168-76.
[14]
Diel R, Hauer B, Loddenkemper R, Manger B, Kruger K. Recommendations for tuberculosis screening before initiation of TNF-alpha-inhibitor treatment in rheumatic diseases. Pneumologie 2009; 63(6): 329-34.
[15]
Gallelli L, Guadagnino V, Caroleo B, Marigliano N, De Sarro G. Cutaneous ulceration induced by interferon alfa. Ann Pharmacother 2004; 38(1): 173-4.
[16]
Xie T, Ye J, Rerkasem K, Mani R. The venous ulcer continues to be a clinical challenge: An update. Burns Trauma 2018; 6: 18.
[17]
Babic V, Petitpain N, Guy C, et al. Nicorandil-induced ulcerations: A 10-year observational study of all cases spontaneously reported to the French pharmacovigilance network. Int Wound J 2018; 15: 508-18.
[18]
Song H, Gong Y, Yan X, Zhang J. A rare case of cutaneous diffuse large b-cell lymphoma presenting as a chronic “Infectious” skin ulcer. Ostomy Wound Manage 2018; 64(4): 44-7.
[19]
Mumoli L, Gambardella A, Labate A, et al. Rosacea-like facial rash related to metformin administration in a young woman. BMC Pharmacol Toxicol 2014; 15: 3.
[20]
De Vuono A, Palleria C, Scicchitano F, Squillace A, De Sarro G, Gallelli L. Skin rash during treatment with generic itraconazole. J Pharmacol Pharmacother 2014; 5(2): 158-60.
[21]
Gallelli L, Ferreri G, Colosimo M, et al. Adverse drug reactions to antibiotics observed in two pulmonology divisions of catanzaro, Italy: A six-year retrospective study. Pharmacol Res 2002; 46(5): 395-400.
[22]
Gallelli L, Ferreri G, Colosimo M, et al. Retrospective analysis of adverse drug reactions to bronchodilators observed in two pulmonary divisions of Catanzaro, Italy. Pharmacol Res 2003; 47(6): 493-9.
[23]
Gareri P, De Fazio P, Gallelli L, et al. Venlafaxine-propafenone interaction resulting in hallucinations and psychomotor agitation. Ann Pharmacother 2008; 42(3): 434-8.
[24]
Guedes-Barbosa LS, Pereira da Costa I, Fernandes V, Henrique da Mota LM, de Menezes I, Aaron SM. Leishmaniasis during anti-tumor necrosis factor therapy: Report of 4 cases and review of the literature (additional 28 cases). Semin Arthritis Rheum 2013; 43(2): 152-7.
[25]
Marcoval J, Penin RM, Sabe N, Valenti-Medina F, Bonfill-Orti M, Martinez-Molina L. Cutaneous leishmaniasis associated with anti-tumour necrosis factor-alpha drugs: An emerging disease. Clin Exp Dermatol 2017; 42(3): 331-4.
[26]
Ceccarelli F, Lucchetti R, Spinelli FR, et al. Early response to apremilast treatment in psoriatic arthritis: A real-life ultrasonographic follow-up study. Rheumatology (Oxford) 2018; 57(8): 1490-1.
[27]
Wells AF, Edwards CJ, Kivitz AJ, et al. Apremilast monotherapy in DMARD-naive psoriatic arthritis patients: Results of the randomized, placebo-controlled PALACE 4 trial. Rheumatology (Oxford) 2018.
[http://dx.doi.org/10.1093/rheumatology/key032]
[28]
Arvers P. Alcohol consumption and lung damage: Dangerous relationships. Rev Mal Respir 2018; 35(10): 1039-49.
[29]
Pincelli C, Schafer PH, French LE, Augustin M, Krueger JG. Mechanisms underlying the clinical effects of apremilast for psoriasis. J Drugs Dermatol 2018; 17(8): 835-40.
[30]
Crowley J, Thaci D, Joly P, et al. Long-term safety and tolerability of apremilast in patients with psoriasis: Pooled safety analysis for >/=156 weeks from 2 phase 3, randomized, controlled trials (ESTEEM 1 and 2). J Am Acad Dermatol 2017; 77(2): 310-7.
[31]
Chinnapaiyan S, Dutta R, Bala J, et al. Cigarette smoke promotes HIV infection of primary bronchial epithelium and additively suppresses CFTR function. Sci Rep 2018; 8(1): 7984.
[32]
Amatngalim GD, Schrumpf JA, Dishchekenian F, et al. Aberrant epithelial differentiation by cigarette smoke dysregulates respiratory host defence. Eur Respir J 2018; 51(4): pii 1701009.
[33]
Sfriso P, Ghirardello A, Botsios C, et al. Infections and autoimmunity: The multifaceted relationship. J Leukoc Biol 2010; 87(3): 385-95.
[34]
Strzelak A, Ratajczak A, Adamiec A, Feleszko W. Tobacco smoke induces and alters immune responses in the lung triggering inflammation, allergy, asthma and other lung diseases: A Mechanistic review. Int J Environ Res Public Health 2018; 15(5): pii E1033.
[35]
Kearley J, Silver JS, Sanden C, et al. Cigarette smoke silences innate lymphoid cell function and facilitates an exacerbated type I interleukin-33-dependent response to infection. Immunity 2015; 42(3): 566-79.
[36]
Atzeni F, Boiardi L, Salli S, Benucci M, Sarzi-Puttini P. Lung involvement and drug-induced lung disease in patients with rheumatoid arthritis. Expert Rev Clin Immunol 2013; 9(7): 649-57.
[37]
Paulin F, Mercado JF, Fernandez ME, Caro FM, Alberti ML, Fassola LA. Correlation between lung and joint involvement in patients with rheumatoid arthritis and interstitial lung disease: A cross-sectional study. Rev Invest Clin 2018; 70(2): 76-81.

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