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Human In Vitro Suppression as Screening Tool for the Recognition of an Early State of Immune Imbalance
Published on: July 22, 2011
Possible concentration-dependent suppression of immune response by verapamil
1University of Kentucky Medical Center, Lexington, USA.
Insights
Calcium channel blockers like verapamil may suppress immune function, leading to prolonged viral infections. Reducing verapamil dosage or switching to clonidine restored normal immune responses in a patient.
Area of Science:
- Immunology
- Pharmacology
Background:
- Calcium channel blockers (CCBs) are known to inhibit lymphocyte responses in vitro.
- Inhibition includes T-cell and natural killer cell activity.
Observation:
- A patient on verapamil hydrochloride experienced recurrent, prolonged viral infections.
- The patient exhibited suppressed lymphocyte responses to mitogens (phytohemagglutinin, pokeweed) and tetanus antigen.
- Mononuclear cell response to soluble tetanus was diminished, and there was no response to influenza vaccination.
Findings:
- Reducing verapamil dosage or switching to clonidine hydrochloride normalized immune functions.
- Immune function recovery included a positive response to influenza vaccination after therapy change.
- These observations suggest verapamil may suppress the immune system, contributing to prolonged infections.
Implications:
- Verapamil's potential immunosuppressive effects warrant further investigation.
- Clinical studies are needed to confirm the link between verapamil and impaired immune response.
- Understanding CCB effects on immunity could inform patient management and therapeutic choices.
Abstract:
Calcium channel blockers inhibit in vitro the lymphocyte response to mitogens and the generation of cytotoxic T-cell and natural killer cell activity. We report on a patient taking verapamil hydrochloride who experienced repeated, prolonged viral infections. His lymphocyte response to phytohemagglutinin, pokeweed mitogen, and tetanus antigen were suppressed; the mononuclear response to soluble tetanus was markedly diminished; and there was no response to influenza vaccination. On lowering the verapamil dose, or changing therapy to clonidine hydrochloride, all the above-mentioned functions returned to normal and a response to influenza vaccination was observed. We speculate that the prolonged viral infection observed in this patient may have been caused by suppression of the immune response by verapamil and we encourage further boad-based studies.
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