Young Hee Rho, Jin-Hyun Woo, Seong Jae Choi, Young Ho Lee, Jong Dae Ji, and Gwan Gyu Song
Lupus is a systemic autoimmune disease of an unknown origin, and systemic lupus erythematosus (SLE) can be triggered by numerous stimuli. Bee venom therapy is an alternative therapy that is believed to be effective for various kinds of arthritis. We present here a case of a 49-year-old female who experienced a new onset lupus after undergoing bee venom therapy, and this looked like a case of angioedema. The patient was successfully treated with high dose steroids and antimalarial drugs. We discuss the possibility of bee venom contributing to the development of SLE, and we suggest that such treatment should be avoided in patients with lupus.
Lupus is a systemic autoimmune disease of an unknown origin, and systemic lupus erythematosus (SLE) is known to be under the immunological influence of Th2. Bee venom therapy is an alternative therapy that is believed to be effective for various kinds of arthritis. We present here a case of a new onset SLE after the patient underwent bee venom therapy, and the clinical picture resembled that of angioedema.
The idea of using bee venom as a treatment for arthritic symptoms is not a new one, and it is thought to have originated during ancient times. Bee venom is effective in murine arthritic models and it has also shown effectiveness in human trials. Its effectiveness is thought to be mediated through inhibition of macrophages and lymphocytes, which leads to decreased IL-1/IL-2 production and inhibition of NF-κb.
In addition, bee venom's anti-nociceptive effects were found to be mediated though alpha-2 adrenoceptors. At the same time, it is also well known that bee venom can inflict severe complications such as anaphylaxis. We cannot be entirely sure of the role of bee venom in our patient because rechallenge experiments could not be done. Also, the possibility of having an underlying infection as a precipitating factor cannot be totally refuted.
However, considering the temporal sequence of the patient's clinical history, it is likely that a mild subclinical level of lupus activity must have been ongoing, and it seems very likely that the venom triggered the borderline disease into a full-blown onset of overt lupus.
As there was no microbial evidence except oral candidiasis and no response to antimicrobial therapy, the influence of infection (if any) seems to be small. There are very few reports of lupus triggered by bee stings, with only one report of subacute cutaneous lupus that was triggered by a wasp sting. Our case is noteworthy for this as well.
It should be noted that the patient's IgE levels were high. As mentioned above, lupus is traditionally thought to be related to Th2 immunity, which is also associated with allergic diseases. There is evidence that the IgE levels correlate with lupus activity, so it may be postulated that the bee venom induced an immune response that most likely involved Th2, and this tipped the balance to the full development of lupus. Since no venom-specific antibodies were detected, the precise mechanism could not be clearly defined.
In conclusion, although bee venom therapy may be effective, taking a careful pre-treatment history and clinical evaluation must be done before starting treatment. It also should be noted that bee venom therapy may cause a flare-up of lupus, and this can happen in previously diagnosed patients, so prudence is needed before treating such patients.