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Endocrine Abstracts (2018) 56 P993 | DOI: 10.1530/endoabs.56.P993

1Libre University, Cali, Colombia; 2Santiago de Cali University, Cali, Colombia; 3Javeriana University, Cali, Colombia.


Introduction: Rituximab is indicated in patients with active rheumatoid arthritis (RA), which through the Fab domain, binds to the CD20 antigen on the surface of B lymphocytes, generating lysis of B cells, present in the thyroid, by cytotoxicity dependent on complement, as a result of the binding of C1q, mediated by the Fc domain, destroying the thyroid follicles, by infiltration of inflammatory cells (1) (2).

Objective: Describe the characteristics of patients with RA who presented thyroiditis, after treatment with rituximab.

Methods: Descriptive study case series. We reviewed 4 clinical histories of patients with RA with therapeutic failure to DMARDs and anti TNF, without previous autoimmune thyroiditis, from a high complexity clinic in Cali, Colombia.

Results: Three patients were women, median age was 50 years (37–61), DAS28 3 (3–5), CRP 15.5 (8–28), ESR 78 (55–120), TSH 0.095 (0.01–0.2), T4L 2 (2–4), thyroid antiperoxidase antibodies 235 (92–800), and thyroiditis evolution time of 2.5 months (1–4). All had diffuse goiter by ultrasound and the scintigraphy was hypocaptant, none had a history of respiratory tract infection; they reported odynophagia and malaise. The 4 patients received management with steroid and 2 with beta-blockers. At 8 months they presented symptom improvement and complete resolution (DAS28 1 (1–3), TSH 0.9 (0.6–1.2), T4L 1.095 (1–1.3)).

Discussion: Biological agents can induce autoimmune phenomena, the evidence so far with rituximab is limited (3). Hyperthyroidism can be explained by an increased activation of thyroid peroxidase (TPO), enzyme that catalyzes reactions for the synthesis of T3 and FT4. A plausible explanation for the elevated TPO activity is a drop in the level of antibodies against TPO by rituximab-induced depletion of plasma cell precursors has been described in the literature and differs from Graves’ disease by lowering uptake in the scintigraphy (4). We observed in our patients complete resolution with tests of normal thyroid function at 8 months, probably due to recovery of B cells. It has been described that the B cell count in peripheral blood, begins to increase from week 24 and evidence of repopulation is observed in most patients, at week 40 (5).

Conclusions: Treatment with rituximab could be related to the presentation of thyroiditis in patients with active RA.

Bibliography:

1. DOI: 10.1007/s12020-015-0551-8.

2. DOI: https://doi.org/10.4049/jimmunol.180.11.7706

3. DOI: 10.1002/jcla.21674.

4. DOI: 10.1001/archinternmed.2009.116.

5. DOI: 10.1089/thy.2012.0489.

Volume 56

20th European Congress of Endocrinology

Barcelona, Spain
19 May 2018 - 22 May 2018

European Society of Endocrinology 

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