Letters / Ann Allergy Asthma Immunol 114 (2015) 417e432
apoptosis that is parallel to the increasing density of Demodex mites. This is likely a result of the Demodex mites causing local immunosuppression, which thus enhances their survival in the human host.1 In healthy or immunocompromised patients, 5% permethrin cream, 1% lindane cream, selenium sulfide, topical retinoids, metronidazole cream, erythromycin, and oral ivermectin have all been used to varying degrees of success in the treatment of demodicidosis.2,9,10 Invariably, successful eradication of the infectious agent will depend on a normal host response and appropriate antiorganism therapy. In a reported case of a 56-year-old HIVseropositive man who developed facial demodicidosis 2 months after initiating highly active antiretroviral therapy, there was successful treatment with oral ivermectin and 5% permethrin cream.9 The absence of immunocompetence or treatment may result in a persistent or recurrent infection, which may lead to the clinical suspicion of an immunocompromised state. This case represents a unique presentation of recurrent demodicidosis in an adult that led to the diagnosis of chronic lymphocytic leukemia before the initiation of chemotherapy. Monica Sandhu, DO* Devi Jhaveri, DO* Haig Tcheurekdjian, MD*,y Robert W. Hostoffer, Jr, DO*,y
427 *University Hospitals Allergy/Immunology Associates Cleveland, Ohio [email protected] y
References [1] Akilov OE, Mumcuoglu KY. Immune response in demodicosis. J Eur Acad Dermatol Venereol. 2004;18:440e444. [2] Karincaoglu Y, Bayram N, Aycan O, Esrefoglu M. The clinical importance of Demodex follicularium presenting with nonspecific facial signs and symptoms. J Dermatol. 2004;31:618e626. [3] Patrizi A, Neri B, Chleregato C, Misciali M. Demodicidosis in immunocompetent young children: report of eight cases. Dermatology. 1997;195:239e242. [4] Sahn EE, Sheridan DM. Demodicidosis in a child with leukemia. J Am Acad Dermatol. 1992;27:799e801. [5] Castanet J, Monpoux F, Mariani R, Ortonne JP, Lacour J. Demodicidosis in an immunodeficient child. Pediatr Dermatol. 1997;14:219e220. [6] Ashack RJ, Frost ML, Norins AL. Papular pruritic eruption of Demodex folliculitis in patients with acquired immunodeficiency syndrome. J Am Acad Dermatol. 1989;21:306e307. [7] Delfos N, Collen A, Kroon F. Demodex folliculitis: a skin manifestation of immune reconstitution disease. AIDS. 2004;18:701e702. [8] Cotliar J, Frankfurt O. Demodex folliculitis mimicking acute graft-vs-host disease. JAMA Dermatol. 2013;149:1407e1409. [9] Aquilina C, Viraben R, Sire S. Ivermectin-responsive Demodex infestation during human immunodeficiency virus infection: a case report and literature review. Dermatology. 2002;205:394e397. lu Y, Bayram N, Aycan O, Kuku I. Density of Demodex [10] Seyhan ME, Karincaog follicularium in haematoligical malignancies. J Int Med Res. 2004;32:411e415.
Management of pollen food and oral allergy syndrome by health care professionals in the United Kingdom The term oral allergy syndrome (OAS) was first proposed in 1987 and referred to conventional IgE-mediated allergic reactions in which oral symptoms were observed before progression to other, systemic manifestations.1 It was only in 1988 that the term was used to describe oral symptoms to fruit and vegetables in pollen allergic patients.2 Valenta and Kraft3 proposed the term pollen food allergy syndrome (PFAS) to describe the latter, but since then both terms have been used synonymously. The resulting confusion is important. Many (if not most) patients with primary food allergy will exhibit oral symptoms to low doses of allergen and can thus progress to systemic symptoms and anaphylaxis with further allergen exposure.4 If such patients are diagnosed as having OAS, this may imply a very low risk of systemic reaction and anaphylaxis and thus no need for a management strategy that might require provision of epinephrine autoinjector (EAI) devices. It is for this reason that Ma et al5 conducted a survey of US allergists in 2003. They found that patients with primary food sensitization were frequently diagnosed as having OAS, which might result in patients with potentially severe allergies being managed inappropriately.5 Despite this, international guidelines continue to favor the entity OAS to describe food allergy due to secondary sensitization to cross-reactive pollens.6 A decade later, we sought to assess whether this situation exists among health care professionals (HCPs) in the United Kingdom. We conducted a web-based survey based on the survey published by Ma et al5 to allow for comparisons. The survey asked about general management strategies for PFAS and OAS and included 4 case vignettes (eTable 1). Pilot studies were performed with focus groups of HCPs. HCPs subscribing to the e-mail lists of
Disclosure: Dr Turner is funded by a Clinician Scientist Award from the UK Medical Research Council (grant no. MR/K010468/1).
the Allergy Academy at King’s College London and the British Society for Allergy and Clinical Immunology were invited to participate. We were advised by our local research ethics committee that approval was not required. Data were analyzed using Prism 6 software (GraphPad Software Inc, La Jolla, California); responses were analyzed using the c2 test (or the Fisher exact test when cell counts were
apoptosis that is parallel to the increasing density of Demodex mites. This is likely a result of the Demodex mites causing local immunosuppression, which thus enhances their survival in the human host.1 In healthy or immunocompromised patients, 5% permethrin cream, 1% lindane cream, selenium sulfide, topical retinoids, metronidazole cream, erythromycin, and oral ivermectin have all been used to varying degrees of success in the treatment of demodicidosis.2,9,10 Invariably, successful eradication of the infectious agent will depend on a normal host response and appropriate antiorganism therapy. In a reported case of a 56-year-old HIVseropositive man who developed facial demodicidosis 2 months after initiating highly active antiretroviral therapy, there was successful treatment with oral ivermectin and 5% permethrin cream.9 The absence of immunocompetence or treatment may result in a persistent or recurrent infection, which may lead to the clinical suspicion of an immunocompromised state. This case represents a unique presentation of recurrent demodicidosis in an adult that led to the diagnosis of chronic lymphocytic leukemia before the initiation of chemotherapy. Monica Sandhu, DO* Devi Jhaveri, DO* Haig Tcheurekdjian, MD*,y Robert W. Hostoffer, Jr, DO*,y
427 *University Hospitals Allergy/Immunology Associates Cleveland, Ohio [email protected] y
References [1] Akilov OE, Mumcuoglu KY. Immune response in demodicosis. J Eur Acad Dermatol Venereol. 2004;18:440e444. [2] Karincaoglu Y, Bayram N, Aycan O, Esrefoglu M. The clinical importance of Demodex follicularium presenting with nonspecific facial signs and symptoms. J Dermatol. 2004;31:618e626. [3] Patrizi A, Neri B, Chleregato C, Misciali M. Demodicidosis in immunocompetent young children: report of eight cases. Dermatology. 1997;195:239e242. [4] Sahn EE, Sheridan DM. Demodicidosis in a child with leukemia. J Am Acad Dermatol. 1992;27:799e801. [5] Castanet J, Monpoux F, Mariani R, Ortonne JP, Lacour J. Demodicidosis in an immunodeficient child. Pediatr Dermatol. 1997;14:219e220. [6] Ashack RJ, Frost ML, Norins AL. Papular pruritic eruption of Demodex folliculitis in patients with acquired immunodeficiency syndrome. J Am Acad Dermatol. 1989;21:306e307. [7] Delfos N, Collen A, Kroon F. Demodex folliculitis: a skin manifestation of immune reconstitution disease. AIDS. 2004;18:701e702. [8] Cotliar J, Frankfurt O. Demodex folliculitis mimicking acute graft-vs-host disease. JAMA Dermatol. 2013;149:1407e1409. [9] Aquilina C, Viraben R, Sire S. Ivermectin-responsive Demodex infestation during human immunodeficiency virus infection: a case report and literature review. Dermatology. 2002;205:394e397. lu Y, Bayram N, Aycan O, Kuku I. Density of Demodex [10] Seyhan ME, Karincaog follicularium in haematoligical malignancies. J Int Med Res. 2004;32:411e415.
Management of pollen food and oral allergy syndrome by health care professionals in the United Kingdom The term oral allergy syndrome (OAS) was first proposed in 1987 and referred to conventional IgE-mediated allergic reactions in which oral symptoms were observed before progression to other, systemic manifestations.1 It was only in 1988 that the term was used to describe oral symptoms to fruit and vegetables in pollen allergic patients.2 Valenta and Kraft3 proposed the term pollen food allergy syndrome (PFAS) to describe the latter, but since then both terms have been used synonymously. The resulting confusion is important. Many (if not most) patients with primary food allergy will exhibit oral symptoms to low doses of allergen and can thus progress to systemic symptoms and anaphylaxis with further allergen exposure.4 If such patients are diagnosed as having OAS, this may imply a very low risk of systemic reaction and anaphylaxis and thus no need for a management strategy that might require provision of epinephrine autoinjector (EAI) devices. It is for this reason that Ma et al5 conducted a survey of US allergists in 2003. They found that patients with primary food sensitization were frequently diagnosed as having OAS, which might result in patients with potentially severe allergies being managed inappropriately.5 Despite this, international guidelines continue to favor the entity OAS to describe food allergy due to secondary sensitization to cross-reactive pollens.6 A decade later, we sought to assess whether this situation exists among health care professionals (HCPs) in the United Kingdom. We conducted a web-based survey based on the survey published by Ma et al5 to allow for comparisons. The survey asked about general management strategies for PFAS and OAS and included 4 case vignettes (eTable 1). Pilot studies were performed with focus groups of HCPs. HCPs subscribing to the e-mail lists of
Disclosure: Dr Turner is funded by a Clinician Scientist Award from the UK Medical Research Council (grant no. MR/K010468/1).
the Allergy Academy at King’s College London and the British Society for Allergy and Clinical Immunology were invited to participate. We were advised by our local research ethics committee that approval was not required. Data were analyzed using Prism 6 software (GraphPad Software Inc, La Jolla, California); responses were analyzed using the c2 test (or the Fisher exact test when cell counts were
