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2022, Number 2

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Rev Hematol Mex 2022; 23 (2)

Azathioprine-induced myelosuppression in Sjogren’s syndrome

Gómez-Piña JJ, Trujillo-Alonso J, Morales-Hernández AE
Full text How to cite this article

Language: English
References: 6
Page: 107-110
PDF size: 246.56 Kb.


Key words:

Azathioprine, Pancytopenia, Sjogren’s syndrome, Autoimmune disease.

ABSTRACT

Background: Sjogren’s syndrome is an autoimmune disease, which affects exocrine glands, presenting oral and ocular dryness, moreover, it’s considered a rheumatic disease, manifesting pain and swelling in joints. This disease is commonly treated with artificial tears, but can be prescribed some drugs, such as muscarinic agonists, ophthalmic cyclosporine, hydroxychloroquine, azathioprine, and methotrexate (arthralgias and cutaneous manifestations). Azathioprine is associated with several adverse events; myelosuppression, hepatotoxicity and tremors are the most harmful clinical outcomes. These adverse events depend on the duration of treatment, but some genetic conditions lead a faster develop of these events. The measure of thiopurine methyltransferase (TPMT) activity is recommended by Food and Drug Administration (FDA) in patients with azathioprine treatment, although it is poorly accessible in most hospitals.
Clinical case: A 53-year-old female patient with azathioprine-induced myelosuppression after being treated a short period due to Sjogren’s syndrome. This is a common drug prescribed in several rheumatology diseases, and these clinical outcomes need to be taken into consideration.
Conclusions: Nowadays Sjogren’s disease is treated with some different drugs including azathioprine, although cytopenia or myelosuppression are the main severe adverse effects, literature reported a 15.2% of hepatotoxicity, and 9.1% of myelosuppression, of which 17.3% reported pancytopenia.


REFERENCES

  1. Jack K, Koopman W, Hulley D, Nicolle MW. A review ofazathioprine-associated hepatotoxicity and myelosuppressionin myasthenia gravis. J Clin Neuromuscul Dis 2016; 18(1): 12-20. doi: 10.1097/CND.0000000000000133.

  2. Hung CM, Chen YF, Ko WC, Tsai TF, Chu CY. Azathioprineinducedsevere bone marrow toxicity. Dermatologica Sinica2009; 27: 44-51.

  3. Pruijt JF, Haanen JB, Hollander AA, Den Ottolander GJ.Azathioprine-induced pure red-cell aplasia. Nephrol DialTransplant 1996; 11: 1371-1373. https://doi.org/10.1093/ndt/11.7.1371.

  4. Boonsrirat U, Angsuthum S, Vannaprasaht S, KongpunvijitJ, et al. Azathioprine-induced fatal myelosuppressionin systemic lupus erythematosus patient carryingTPMT*3C polymorphism. Lupus 2008; 17: 132-4. doi:10.1177/0961203307085255.

  5. Choughule KV, Barnaba C, Joswig-Jones CA, Jones JP. Invitro oxidative metabolism of 6-mercaptopurine in humanliver: insights into the role of the molybdoflavoenzymesaldehyde oxidase, xanthine oxidase, and xanthine dehydrogenase.Drug Metab Dispos 2014; 42: 1334-1340. doi:10.1124/dmd.114.058107.

  6. Torkamani A. Azathioprine metabolism and thiopurinemethyltransferase (TPMT) deficiency [Internet]. Medscape;updated October 15, 2015; accessed Jan 18, 2021]. https://emedicine.medscape.com/article/1829596-overview#a2.




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Rev Hematol Mex. 2022;23