ArticleJournal of medical case reports2024
Azathioprine and hydroxychloroquine overdose in Sjögren's syndrome patient with hypocalcemia: a case report.
Article in Journal of medical case reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 4 citations in OpenAlex.
- Cognitive impairment in Sjogren's syndrome: Interplay between BACE1 activity, inflammatory blood biomarkers and neurocognitive testing.PloS one · 2025Article
- Comparative Analysis of Glandular and Extraglandular Manifestations in Primary and Secondary Sjögren's Syndrome: A Study in Two Academic Centers in North-East Romania.Diagnostics (Basel, Switzerland) · 2024Article
- Uncovering the Therapeutic Target and Molecular Mechanism of Upadacitinib on Sjogren's Syndrome.Biomedical engineering and computational biology · 2024Article
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Authors and funding
3 authors at 2 institutions in 2 countries.
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Abstract
introductionHydroxychloroquine and azathioprine have been routinely used to control and treat primary and secondary Sjögren's syndrome, which potentially triggered some overdoses by these drugs. Toxicity from hydroxychloroquine and azathioprine manifests in the form of cardiac conduction abnormalities, nausea, vomiting, and muscle weakness. Recognizing these unique drug overdoses and management of these toxicities is important. This case report aims to expand our current understanding of these drug overdoses and their management and also underscores the importance of anticipating and identifying fewer common complications, such as hypocalcemia. CASE REPORT: A 34-year-old Persian woman with a history of Sjögren's syndrome presented to the emergency department 3.5-4 hours after an intentional overdose of hydroxychloroquine and azathioprine and severe hypotension and loss of consciousness. Although the patient was regularly taking other medications, such as fluoxetine, naproxen, and prednisolone, she explicitly clarified that these were not the substances involved in her overdose. Early investigations showed hypokalemia (2.4 mEq/L), hypocalcemia (7.5 mg/dL), and hypoglycemia (65 mg/dL). She was also diagnosed with metabolic acidosis and respiratory alkalosis. The electrocardiogram showed changes in favor of hypokalemia; other lab tests were run on the patient. Supportive treatments were applied, including rapid intravenous fluid dextrose 5%, normal saline, potassium chloride 30 mEq, and calcium gluconate 100 mg. The patient was managed and monitored overnight in the emergency room and recovered without residual side effects.
conclusionHydroxychloroquine and azathioprine toxicity are considered rare, but it is likely to increase in frequency given the prevalence and increase in autoimmune diseases and the increasing usage of these drugs in treating such diseases. We found hypocalcemia as the presentation to this patient, which needs further investigation into the probable mechanism. Clinicians need to consider the unique effects of hydroxychloroquine and azathioprine poisoning and initiate appropriate emergency interventions to improve the outcomes in similar patients.
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