• NITIKA SINDHU Department of Pharmacology, Kalpana Chawla Government Medical College, Karnal



Psoriasiform rash, Hyperproliferation, ATT, WHO-UMC scale


Objective: Psoriasiform drug eruptions can be induced by several drugs. Psoriasis is a chronic inflammatory disease characterized by T-cell-mediated cytokine production that drives the hyperproliferation and abnormal differentiation of keratinocytes. Drugs can cause new lesions when there is no prior history or family history of psoriasis. Based on the psoriatic drug eruption probability score, β‐blockers, synthetic anti‐malarial drugs, non‐steroidal anti‐inflammatory drugs (NSAIDs), lithium, digoxin and tetracycline antibiotics are relevant in psoriasis.

Methods: A 58-year-old male was admitted to the Department of Respiratory Medicine at B. P. S G. M. C, Khanpur Kalan, Sonepat as a case of pulmonary tuberculosis and was put on anti-tubercular drugs CAT-I (according to RNTCP guidelines). The patient had a history of diabetes mellitus and hypertension for the past six years. On the third day of initiation of ATT, the patient started developing a psoriasiform rash. The psoriasiform rash began to improve within a few days after discontinuing the ATT. A causality assessment was done as per the WHO-UMC scale, which showed that the adverse events were likely caused due to the ATT.

Results: Psoriasiform rash is a severe adverse drug reaction characterized by widespread lesions. Among all the various adverse drug reactions, lichenoid drug eruption is commonly associated with anti-tuberculosis medication and needs to be differentiated from psoriasiform eruption. The underlying pathomechanism of drug-induced psoriasiform eruptions remains uncertain, although several immunological interactions have been hypothesized.

Conclusion: ATT has been reported to cause psoriasiform rash, and its drug component needs to be reconsidered in view of safer alternatives available.


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Kasper, Fauci, Hauser, Longo, Jameson. Harrison’s principles of internal medicine. 19th ed. Vol; 2017. p. 347-8.

de Gannes GC, Ghoreishi M, Pope J, Russell A, Bell D, Adams S. Psoriasis and pustular dermatitis triggered by TNF-{alpha} inhibitors in patients with rheumatologic conditions. Arch Dermatol. 2007;143(2):223-31. doi: 10.1001/archderm.143.2.223, PMID 17310002.

Park JJ, Choi YD, Lee JB, Kim SJ, Lee SC, Won YH. Psoriasiform drug eruption induced by anti-tuberculosis medication: potential role of plasmacytoid dendritic cells. Acta Derm Venereol. 2010 May;90(3):305-6. doi: 10.2340/00015555-0827, PMID 20526555.

Vieira DE, Gomes M. Adverse effects of tuberculosis treatment: experience at an outpatient clinic of a teaching hospital in the city of São Paulo, Brazil. J Bras Pneumol. 2008;34(12):1049-55. doi: 10.1590/s1806-37132008001200010, PMID 19180340.

Kurokawa I, Nakahigashi Y, Teramachi M. Erythema multiforme-type drug eruption due to ethambutol with eosinophilia and liver dysfunction. Int J Antimicrob Agents. 2003;21(6):596-7. doi: 10.1016/s0924-8579(03)00091-8, PMID 12791479.

Grossman ME, Warren K, Mady A, Satra KH. Lichenoid eruption associated with ethambutol. J Am Acad Dermatol. 1995;33(4):675-6. doi: 10.1016/0190-9622(95)91307-6, PMID 7673504.

Nestle FO, Conrad C, Tun‐Kyi A, Homey B, Gombert M, Boyman O. Plasmacytoid predendritic cells initiate psoriasis through interferon‐alpha production. J Exp Med. 2005;202(1):135-43. doi: 10.1084/jem.20050500, PMID 15998792.

Collamer AN, Guerrero KT, Henning JS, Battafarano DF. Psoriatic skin lesions induced by tumor necrosis factor antagonist therapy: a literature review and potential mechanisms of action. Arthritis Rheum. 2008;59(7):996-1001. doi: 10.1002/art.23835, PMID 18576309.



How to Cite

SINDHU, N. “PSORIASIFORM DRUG ERUPTION INDUCED BY ANTI-TUBERCULOSIS MEDICATION: A CASE REPORT”. International Journal of Current Pharmaceutical Research, vol. 15, no. 1, Jan. 2023, pp. 68-69, doi:10.22159/ijcpr.2023v15i1.2075.



Case Study(s)