Thank you for your inquiry.
In my opinion, there would be no need for a dosage adjustment in your patient. The reason for this opinion is that cyclosporine primarily affects the T cell response rather than the antibody response to immunization (see abstract copied below). And the antibody response, particularly in venom allergy, is a strong determinant of its effect (see abstracts copied below).
Thank you again for your inquiry and we hope this response is helpful to you.
The effect of cyclosporine on immunization with tetanus and keyhole limpet hemocyanin (KLH) in humans
The Journal of Clinical Immunology
March 1985, Volume 5, Issue 2, pp 115-121
A. G. Palestine et al
Eleven patients with chronic uveitis treated with Cyclosporine were immunized with keyhole limpet hemocyanin (KLH) and tetanus toxoid. Delayed cutaneous hypersensitivity responses, lymphocyte blastogenic responses, and antibody production were compared with those of similarly immunized control individuals. A significant decrease in delayed cutaneous hypersensitivity (P<0.001 for KLH andP<0.01 for tetanus toxoid) was observed. No significant differences in blastogenic or antibody responses were noted. These findings demonstrate that the majority of the Cyclosporine-treated patients had intact T cell-dependent antigen responses as measured by both proliferative response and antibody production to primary and secondary antigenic challenges but that other immune functions such as delayed cutaneous hypersensitivity are affected by therapeutic doses of systemic Cyclosporine.
Khan et al: Bee venom anti-idiotypic antibody is associated with protection in beekeepers and bee sting-sensitive patients receiving immunotherapy against allergic reactions
The Journal of Allergy and Clinical Immunology
Volume 88, Issue 2, August 1991, Pages 199–208
Bee venom (BV) anti-idiotypic (anti-Id) antibodies (Abs) were studied in nonreactive beekeepers, patients receiving BV immunotherapy (IT), and in patients with bee-sting hypersensitivity. Detection of serum anti-BV was determined either by the Phadebas RAST test for IgE and IgG concentrations or by isoelectric focusing followed by capillary blotting onto nitrocellulose membranes. Clonotypic analyses of Ab were made with specific probes for BV or BV anti-Id; nonreactive multiple-sting beekeepers (93%; p = 0.00006) and patients receiving BV IT (100%; p = 0.0026) had detectable amounts of BV anti-Id in serum, whereas five BV-sensitive patients (0%) and four ragweed-sensitive control patients (0%) did not. Beekeeper's serum containing BV anti-Id was found to recognize and bind to IgE anti-BV idiotype from two different patient sources and inhibit their reactions in a Phadebas RAST test in a dose-dependent manner. Nonreactive beekeepers generally had BV-specific IgE levels <0.35 PRU/ml in serum with detectable BV anti-Id. BV-allergic patients before IT had elevated BV-specific serum IgE levels, even in the presence of BV-spceific IgG >136 U/ml with no BV anti-Id present. These findings provide strong support for a protective role of BV anti-Id against bee sting-allergic reactions.
Johns Hopkins Med J. 1978 Jan;142(1):1-7.
Effects of passive antibody in bee venom anaphylaxis.
Lessof MH, Sobotka AK, Lichtenstein LM.
Twelve patients allergic to honeybees were challenged by injections of bee venom; five responded systemically to the venom, with symptoms ranging from angioedema to respiratory distress. These patients were given intramuscular or intravenous infusions of gamma-globulin obtained from the plasma of hyperimmune beekeepers who had high levels of antibody to an allergen (phospholipase A) in the venom. Post-infusion, all five patients tolerated 1.5 to 5 times the venom dose that previously elicited adverse reactions. The quantity of passive IgG antibody infused did not impair the patient's own immune response to venom. These results represent the best available evidence for a direct role for IgG blocking antibodies in clinical protection against anaphylaxis occurring as a result of parenteral antigenic challenge as may be observed in penicillin and insect hypersensitivity.
Phil Lieberman, M.D.