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Hemodynamic Collapse Following Therapeutic Plasma Exchange in a Patient Receiving an Angiotensin Receptor Blocker
Therapeutic plasma exchange (TPE) is a procedure for removal of plasma and its components while leaving behind cellular elements via an apheresis device. It is used in multiple conditions one among which is systemic lupus erythematosus (SLE). Adverse reactions from TPE range from mild hypotension an...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Cureus
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7081960/ https://www.ncbi.nlm.nih.gov/pubmed/32211262 http://dx.doi.org/10.7759/cureus.7028 |
Sumario: | Therapeutic plasma exchange (TPE) is a procedure for removal of plasma and its components while leaving behind cellular elements via an apheresis device. It is used in multiple conditions one among which is systemic lupus erythematosus (SLE). Adverse reactions from TPE range from mild hypotension and fever to life-threatening cardiovascular compromise. We report the case of sudden hemodynamic collapse following TPE for a neuropsychiatric lupus flare in a patient on losartan. A 62-year-old Caucasian female with a history of drug-induced lupus presented to the hospital with symptoms of a neuropsychiatric lupus flare. She was initiated on TPE with 5% albumin based on recommendations by her rheumatologist. Shortly after TPE, she became hypotensive with poor response to fluid boluses, requiring pressor support and intubation. These symptoms resolved within 24 hours on supportive measures. This was believed to be due to losartan use on the day of TPE. The medication was discontinued and she had further sessions of TPE with no complications. Angiotensin-converting enzyme (ACE) inhibitors have previously been associated with flushing and hypotension in patients undergoing TPE. Patients undergoing TPE have an activation of the prekallikrein and bradykinin system on contact with the extracorporeal membranes. ACE inhibitors potentiate this reaction by inhibiting bradykinin catabolism. Angiotensin receptor blockers (ARBs) have also been postulated to cause elevated bradykinin levels although data pertaining to the use of ARBs in TPE is limited. We hope to highlight this rare interaction in our case and emphasize the need for further data with regard to the same. |
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