IgE Mediated Autoallergy against Thyroid Peroxidase – A Novel Pathomechanism of Chronic Spontaneous Urticaria?

Altrichter, Sabine; Peter, H.; Pisarevskaja, Dina; Metz, Martin; Martus, Peter; Maurer, Marcus

doi:10.1371/journal.pone.0014794

Cited by 238 publications

(232 citation statements)

References 28 publications

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“…These autoantibodies, when they bound to and activate mast cells, could cause "autoallergic" mast cell degranulation, a novel pathogenic pathway of CU induction. The patients with positive IgG -anti-TPO are more likely to potentially express urticaria-inducing IgE -anti-TPO [32]. The authors also speculate that IgE antibodies directed against other autoantigens also may exist and act as mast cell activators.…”

Section: Tpo-anti-thyroid Peroxidase Antibodies Tsh-thyroid-stimulatmentioning

confidence: 92%

Chronic urticaria and thyroid autoimmunity markers

Chomičienė¹,

Jurgauskienė²,

Blažienė³

2012

Open Medicine

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Section: Tpo-anti-thyroid Peroxidase Antibodies Tsh-thyroid-stimulatmentioning

confidence: 92%

Chronic urticaria and thyroid autoimmunity markers

Chomičienė¹,

Jurgauskienė²,

Blažienė³

2012

Open Medicine

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“…At the beginning of the treatment, the quality of life index of our patients was in the range of [11][12][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27] (very large to extremely large effect), using the Dermatology Life Quality Index (DLQI), and the urticaria activity score for the preceding 7 days (UAS7) was in the range of 35-42 (severe activity). In all patients, skin biopsies of urticarial lesions were taken, and histological analyses were performed to exclude urticarial vasculitis.…”

Section: Patientsmentioning

confidence: 99%

Effective treatment of different phenotypes of chronic urticaria with omalizumab: Case reports and review of literature

Kasperska−Zając

Jarząb

Żerdzińska

et al. 2016

Int J Immunopathol Pharmacol

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Despite the excellent efficacy and safety profile of omalizumab in chronic spontaneous urticaria (CSU), there are scarce data concerning its role in the treatment of refractory cases with different phenotypes of urticaria. We describe our experience with the therapy of nine patients with CSU co-existing with delayed pressure urticaria (DPU) or angioedema or both and refractory to treatment with high-dose antihistamines. The first patient, with severe CSU and recurrent angioedema, did not respond well to cyclosporine A or corticosteroids and suffered from numerous side effects of longterm corticosteroid therapy. The second patient presented with severe symptoms of DPU, which first of all prevented any daily activities of the professional routines. Both patients showed a complete remission of urticaria after the first injection of omalizumab. The third patient with CSU and severe DPU had been ineffectively treated for more than 20 years with various medications. Following the administration of omalizumab, the symptoms of CSU subsided but those of DPU intensified, and the drug was withdrawn after two cycles. In another four patients with refractory CSU and angioedema, the symptoms subsided after the first administration of omalizumab, and the patients have been in remission for about 5 weeks. In the remaining two patients, the symptoms did not resolve despite four 300 mg doses of omalizumab. It is important to establish a therapeutic regimen with omalizumab (150-300 mg; every 4-8 weeks) tailored to individual patient's needs and dependent on the type of urticaria; this may minimize unnecessary the medication exposure, adverse drug effects, and healthcare costs.

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“…Recent studies have pointed to an autoimmune etiology of chronic spontaneous urticaria through the action of IgE isotype antibodies to thyroid peroxidase which cross-react with the high-affinity mast cell IgE receptor FCεRI [10]. A similar mechanism has been thought to be responsible in ncMCAS.…”

mentioning

confidence: 99%

Selective Response to Omalizumab in a Patient With Concomitant ncMCAS and POTS: What Does it Teach us About the Underlying Disease?

Kačar¹,

Denman²,

Savic³

2018

J Investig Allergol Clin Immunol

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261Investigations at the time showed no evidence of an allergic disorder. However, serum mast cell tryptase levels were periodically elevated, ranging from 10 mg/mL to 20 ng/mL between attacks, but increasing to >100 ng/mL following episodes of anaphylaxis. Subsequent investigations to exclude a clonal mast cell disorder were performed in another center. This included a complete bone marrow study to assess the number of mast cells and typical histological lesions of systemic mastocytosis, such as multifocal dense, sharply demarcated mast cell infiltrates [5]. Furthermore, bone marrow aspirate was examined for the number of mast cells and their morphological features, and immunophenotyping studies were performed to assess expression of CD2 and CD25, which are typically found on mast cells from patients with systemic mastocytosis [5]. Lastly, cKIT mutation analysis yielded negative results; however, we do not know if this was performed from purified mast cells, as currently recommended [6]. Altogether, these investigations showed no evidence of clonal mast cell proliferation.Blood tests including measurements of plasma levels of epinephrine, aldosterone, rennin, 5-hydroxyindoleacetic acid (5-HIAA), and gut hormones were all normal. An extensive autoantibody screen for POTS-related autoantibodies was negative. This included anti-α-1 adrenergic, anti-α-2 adrenergic, anti-β-1 adrenergic, and anti-β-2 adrenergic receptor antibodies, as well as antimuscarinic cholinergic receptor 1, 2, 3, 4, and 5 antibodies. The patient and close family members (mother, father, and a brother) underwent further genetic tests. Although there was no family history of ncMCAS/POTS, the severity and early onset of the patient's illness led us to consider a monogenic cause of this rare clinical phenotype. However, whole exome sequencing carried out on the patient's DNA failed to reveal an obvious genetic cause.The patient received numerous treatments for ncMCASrelated symptoms, including high-dose H 1 nonsedating antihistamines, H 2 antihistamines, montelukast, sodium cromoglycate, and the tyrosine kinase receptor inhibitor imatinib, which is an effective inhibitor of wild-type KIT; however, it is currently indicated for treatment of systemic mastocytosis with imatinib-sensitive KIT mutations only [7]. Considering that imatinib might cause potentially dangerous adverse effects, it is not recommended for routine use in ncMCAS. In this case, the permission to use imatinib was obtained from the hospital's Drugs and Therapeutics Committee, and appropriate consent was obtained from the patient prior to commencing the treatment. Unfortunately, none of the medications were fully effective, resulting in only partial improvement of the patient's condition. He also tried several medications to control his POTS-related symptoms. These included moxonidine and amlodipine for hypertension, pyridostigmine for orthostatic hypotension, pregabalin for erythromelalgia, and propantheline for hyperhidrosis. These drugs were discontinued owing to lack of effect (...

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IgE Mediated Autoallergy against Thyroid Peroxidase – A Novel Pathomechanism of Chronic Spontaneous Urticaria?

Cited by 238 publications

References 28 publications

Chronic urticaria and thyroid autoimmunity markers

Chronic urticaria and thyroid autoimmunity markers

Effective treatment of different phenotypes of chronic urticaria with omalizumab: Case reports and review of literature

Selective Response to Omalizumab in a Patient With Concomitant ncMCAS and POTS: What Does it Teach us About the Underlying Disease?

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