Thank you for your recent inquiry.
I believe that the phrase "allergy to herself" refers to a condition known as "autoimmune urticaria." The term "autoimmune" in this instance does not imply a classic autoimmune inflammatory disorder such as one would see in systemic lupus erythematosus, rheumatoid arthritis, or the other "classic" autoimmune disorders.
The term is used to describe a phenomenon that described in the literature several years ago. It was noted that certain patients with urticaria have a positive allergy skin test when their own serum in injected into their skin. It was found that this skin test was due to an antibody against the alpha chain of the receptor for IgE or, in a minority of cases, IgE itself. It was hypothesized that this antibody resulted in mast cell and/or basophil histamine release. It was later confirmed that the mechanism also could involve complement fixation.
From a practical standpoint, it is only important in that it offers the patient at least some conception of the pathogenesis of their urticaria. As you know, the vast majority of cases of urticaria are idiopathic (only a small minority of acute urticaria is related to food allergy). The fact that the condition is idiopathic is frustrating both to patients and physicians. The demonstration of a positive skin test to one's own serum sometimes gives solace to the patient in that they are aware that the physician knows the mechanism underlying the hives.
However, the finding that a case of urticaria is "autoimmune" in nature has no practical importance regarding either treatment or prognosis. It is still managed as a case of idiopathic urticaria since there is no specific therapy for the autoimmune variety. The prognosis is also quite similar to that of patients with chronic idiopathic urticaria who do not demonstrate the presence of this autoantibody.
In addition to the skin test, there is also a blood test which can be used to assess for the presence of this autoantibody against the FC receptor. It is likely that the allergist who saw your patient either performed the skin test or the blood test, and found evidence for the presence of this antibody and described the condition by stating to the patient that she was "allergic to yourself."
It is important to make the distinction between this form of "autoimmunity" and that associated with the "classic autoimmune disorders." Autoimmune urticaria is non-inflammatory, does not carry with it a poor prognosis, does not cause to our knowledge any permanent damage, and in the majority of instances subsides spontaneously, as do cases of chronic idiopathic urticaria.
Thank you again for your inquiry and we hope this response is helpful to you.
Indian J Dermatol. 2009 Jul;54(3):269-74.
Chronic autoimmune urticaria: where we stand?
Goh CL, Tan KT.
Department of Dermatology, National Skin Center, Singapore.
It is well-recognized that 30-40% of chronic idiopathic urticaria is autoimmune in nature. Chronic autoimmune urticaria is caused by anti-FcepsilonRI and less frequently, by anti-IgE autoantibodies that lead to mast cell and basophil activation, thereby giving rise to the release of histamine and other proinflammatory mediators. Activation of the classical complement pathway and formation of C5a are important in dermal mast cell activation. C5a is also a neutrophil and eosinophil chemoattractant. Chronic autoimmune urticaria has been found to be associated with autoimmune thyroid disease. The autologous serum skin test is used as a screening test for chronic autoimmune urticaria and has a sensitivity and specificity of about 70 and 80%, respectively. The current gold standard diagnostic test is the basophil histamine release assay. The treatment of chronic autoimmune urticaria, as in chronic idiopathic urticaria, is with H1 antihistamines. Oral corticosteroids may be used during acute flares. Refractory cases have been shown to respond to cyclosporine and other immunomodulators. The prevalence of chronic autoimmune urticaria in Singapore is similar to that reported in Western countries at about 42%. The presence of thyroid autoimmunity appears to be higher than reported, with 22.5% of patients with chronic idiopathic urticaria here, exhibiting presence of thyroid autoantibodies.
Clin Exp Allergy. 2009 Jun;39(6):777-87. Epub 2009 Apr 22.
Pathogenesis of chronic urticaria.
Kaplan AP, Greaves M.
Department of Medicine, Division of Pulmonary and Critical Care Medicine, Allergy and Clinical Immunology, Medical University of South Carolina, Charleston, SC, USA. firstname.lastname@example.org
Chronic urticaria is defined as the presence of urticaria (hives) for at least 6 weeks with the assumption that it occurs daily or close to it. If we eliminate physical urticarias and urticarial vasculitis from consideration, the remainder can be divided into autoimmune chronic urticaria (45%) and idiopathic chronic urticaria (55%). The autoimmune subgroup is associated with the IgG anti-IgE receptor alpha subunit in 35-40% of patients and IgG anti-IgE in an additional 5-10%. These autoantibodies have been shown to activate blood basophils and cutaneous mast cells in vitro with augmentation of basophil activation by complement and release of C5a, in particular. Binding methods (immunoblot and ELISA) yield positives in many autoimmune diseases as well as occasional normal subjects or patients with other forms of urticaria but most such sera are non-functional. Activation of basophils or mast cells causing histamine release is quite specific for chronic urticaria and defines the autoimmune subgroup. Although pathogenicity is not formally proven, the antibodies cause wealing upon intradermal injection, and removal of the autoantibody leads to remission. A cellular infiltrate is seen to be characterized by mast cell degranulation and infiltration of CD4+ T lymphocytes, monocytes, neutrophils, eosinophils, and basophils. The intensity of the infiltrate and clinical severity of the disease (including accompanying angio-oedema) is more severe in the autoimmune subpopulation. This latter group also has a higher evidence of human leucocyte antigen DR alleles associated with autoimmunity and a 25% incidence of antithyroid antibodies with diagnosed hypothyroidism in some. Hypo-responsiveness of patients' basophils to anti-IgE and hyperresponsiveness to serum defines another subpopulation (at least 50%) that overlaps the idiopathic and autoimmune subgroups. Hypo-responsiveness to anti-IgE has been shown to be associated with elevated levels of cytoplasmic phosphatases that inhibit degranulation. Reversal of the abnormality is seen with disease remission. Further work will be needed to distinguish whether this is a cause or a consequence of persistent urticaria and to further assess the relationship (or lack thereof) of altered responsiveness (decreased or increased) with the presence or absence of activating autoantibodies.
Clin Rev Allergy Immunol. 2002 Oct;23(2):171-83.
That a subset of patients with chronic idiopathic urticaria possesses functional autoantibodies against the high affinity IgE receptor, or less commonly, IgE, is widely accepted. That these same autoantibodies are causative of chronic urticaria is highly probable, but not entirely proven, since no animal model of chronic urticaria has been devised using these autoantibodies. However we know that intradermal injection of anti-FceR1 IgG in healthy volunteers does cause an urticarial reaction. The concept of chronic urticaria as a disease caused by autoantibodies activating the normal function of target cells (mast cells) by combination with a receptor epitope is intriguing, although not entirely unique, since a similar mechanism appears to underlie some types of autoimmune hyperthyroidism. The detection of patients with these antibodies is usually not possible by clinical assessment alone. Unfortunately no convenient or reliable immunoassays have been developed to detect the autoantibodies, and the gold standard remains the basophil mediator release assay, using normal human donor basophils or a basophil leukemia cell line. The autologous serum skin test has proved to be a useful screening test for autoimmune urticaria. Identification of patients with autoimmune urticaria is of some importance because, apart from obviating the necessity for irrelevant tests, immunotherapy, using cyclosporin, intravenous immunoglobulin or even plasmapheresis can be contemplated in severely affected treatment-resistant patients.
Phil Lieberman, M.D.