Thank you for your inquiry.
Unfortunately, you are dealing with a patient who presents with two not uncommon problems, both of which in many instances defy a specific diagnosis. And there are very few conditions that present with both manifestations without a rash. I am assuming of course that your patient does not have a rash (atopic dermatitis for example), but is suffering from pruritus without rash. There are, however, some key references which I can point you to which should at least guide you in your evaluation.
We have many entries on our Ask the Expert website that deal with the causes of elevated IgE, and there is an excellent, very helpful, and easy to read review of pruritus itself in a recent New England Journal of Medicine article.
You may access entries on our website which list the causes of elevated IgE by going to the Ask the Expert website and entering "elevated IgE" into the search box. There are many entries, but the most pertinent for you will be the one posted on 4/24/13, entitled "Causes of elevated IgE."
You should have easy access to the New England Journal article which is: Yosipobitch G and Bernhard D. Chronic pruritus. N Engl J Med 2013; 368:1625-1634.
Unfortunately scanning the differential diagnoses of these entities, one does not come across a ready explanation for the concomitant existence of pruritus without rash and elevated IgE. However, there are two instances of which I am aware where these two findings coexist. I have copied below a reference (anisakis) and an abstract (scabies) of articles describing these. The Anisakis abstract is of particular interest because pruritus was the sole manifestation of this infection. Scabies is of course far more common, but usually, when there is a significant elevation of IgE, the scabies is severe and has cutaneous manifestations. Nonetheless, I believe both of these causes are worth investigating.
Also, since we know that parasitic infections can produce asymptomatic pruritus, it would be wise to evaluate the other infectious causes of an elevated IgE as outlined in the entry on our website mentioned above.
Unfortunately, as noted above, in the evaluation of these disorders it is not uncommon never to find an etiology. Hopefully, however, you will be successful, and we would greatly appreciate a follow-up if this is the case.
Thank you again for your inquiry.
J Am Acad Dermatol. 2012 Dec;67(6):e261. doi: 10.1016/j.jaad.2012.03.026.
Intractable chronic pruritus as the only manifestation of IgE hypersensitivity to Anisakis.
Gallo R, Cecchi F, Parodi A.
Clin Vaccine Immunol. 2010 Sep;17(9):1428-38. doi: 10.1128/CVI.00195-10. Epub 2010 Jul 14.
Increased allergic immune response to Sarcoptes scabiei antigens in crusted versus ordinary scabies.
Walton SF, Pizzutto S, Slender A, Viberg L, Holt D, Hales BJ, Kemp DJ, Currie BJ, Rolland JM, O'Hehir R.
School of Health and Sport Sciences, University of the Sunshine Coast, Maroochydore DC, QLD 4558, Australia.
Scabies, a parasitic skin infestation by the burrowing "itch" mite Sarcoptes scabiei, causes significant health problems for children and adults worldwide. Crusted scabies is a particularly severe form of scabies in which mites multiply into the millions, causing extensive skin crusting. The symptoms and signs of scabies suggest host immunity to the scabies mite, but the specific resistant response in humans remains largely uncharacterized. We used 4 scabies mite recombinant proteins with sequence homology to extensively studied house dust mite allergens to investigate a differential immune response between ordinary scabies and the debilitating crusted form of the disease. Subjects with either disease form showed serum IgE against recombinant S. scabiei cysteine and serine proteases and apolipoprotein, whereas naive subjects showed minimal IgE reactivity. Significantly (P < 0.05) greater serum IgE and IgG4 binding to mite apolipoprotein occurred in subjects with crusted scabies than in those with ordinary scabies. Both subject groups showed strong proliferative responses (peripheral blood mononuclear cells) to the scabies antigens, but the crusted scabies group showed increased secretion of the Th2 cytokines interleukin 5 (IL-5) and IL-13 and decreased Th1 cytokine gamma interferon (IFN-gamma) in response to the active cysteine protease. These data confirm that a nonprotective allergic response occurs in the crusted disease form and demonstrate that clinical severity is associated with differences in the type and magnitude of the antibody and cellular responses to scabies proteins. A quantitative IgE inhibition assay identified IgE immunoreactivity of scabies mite antigens distinct from that of house dust mite antigens, which is potentially important for specific scabies diagnosis and therapy.
Phil Lieberman, M.D.