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Abstract
Urticaria has many known etiologies. An association with autoimmune thyroid disease is described. One individual had the triad of urticaria, Hashimoto's thyroiditis, and rheumatoid arthritis, whereas the other individual had urticaria preceding Graves' disease by over 1 year.
Graves' disease (GD) is an autoimmune disease that is characterized by the presence of antibodies targeting the thyroid gland. Commonly, the disease presents with symptoms of thyrotoxicosis such as sweating, tremors, and weight loss; less frequently, patients with GD might also have urticaria. Urticaria is clinically defined as the presence of wheals, angioedema, or both. While its pathophysiology is not completely understood, urticaria is believed to be an immune-mediated response activating mast cells, leading to the release of histamine and cytokines. Although the association between urticaria and GD is well established, it is uncommon for GD patients to present with urticaria as their sole complaint. In this paper, we present a case of a previously healthy patient who originally presented to the dermatology clinic with urticaria alone; however, she developed thyrotoxic symptoms soon after. Furthermore, her treatment was complicated by developing an allergic reaction to carbimazole.
Nel 75% dei casi la causa dell’orticaria cronica rimane ignota (orticaria cronica idiopatica, OCI). LOCI può associarsi a malattie autoimmuni o a positività per autoanticorpi. In questo articolo tratteremo dell’associazione dell’OCI con la patologia tiroidea autoimmune e le relative possibili conseguenze sul piano clinico-terapeutico.
Many patients present with symptoms suspected to be allergic in origin that ultimately turn out to be illnesses unrelated to allergic disease. As there are a number of upper and lower respiratory manifestations of endocrinopathies that may cause confusion with allergic diseases, a review of these illnesses is helpful for the clinician (Table 1). Hypothyroidism is the most common masquerader, causing nonallergic rhinitis, upper airway obstruction, or even a decline in central respiratory drive.6 An increase in central respiratory drive associated with thyrotoxicosis can present with dyspnea as its major clinical manifestation. Although the emphasis of this article is on thyroid diseases, other afflictions of the endocrine system that present as impostors are included. Acute hypoparathyroidism following thyroid surgery may lead to symptoms of laryngeal stridor and muscle weakness. Diabetes mellitus, the most prevalent of the metabolic diseases, is frequently complicated by infections that may pose as allergic disease of either the upper or lower respiratory tract.
Chronic urticaria is a common condition characterized by recurrent episodes of mast cell-driven wheal and flare-type skin reactions lasting for more than 6 weeks. In about 75% of cases, the underlying causes remain unknown, and the term chronic idiopathic urticaria (CIU) is used to emphasize that wheals develop independently of identified external stimuli. Although CIU affects about 1.0% of the general population, its etiopathogenesis is not yet well understood. It is now widely accepted that in many cases CIU should be regarded as an autoimmune disorder caused by circulating and functionally active IgG autoantibodies specific for the IgE receptor (FceRI) present on mast cells and basophils or for IgE itself. The well-known association of CIU with other autoimmune processes/diseases represents further indirect evidence of its autoimmune origin. Autoimmune thyroid diseases, especially autoimmune thyroiditis, represent the most frequently investigated diseases in association with CIU. Here we review this topic with particular regard to the association between Graves' disease and CIU. The possible pathogenetic mechanisms and the clinical implications of such an association are discussed.
Chronic urticaria is a common clinical condition whose etiology, in about 75% of cases, is unknown and is therefore called chronic idiopathic urticaria (CIU). A link between CIU and autoimmune thyroid diseases was proposed several decades ago. Here we review this topic.
Several studies have been performed to determine if and to what degree there is an association between CIU and autoimmune thyroid diseases, particularly autoimmune thyroiditis. Many of these studies were not well controlled, however. Approximately one-fourth of CIU patients have serological evidence of thyroid autoimmunity, suggesting that these two disorders are associated. The mechanisms for the apparent association between CIU and serological evidence of thyroid autoimmunity are not clear. There are no data regarding the correlations between CIU and histological features of autoimmune thyroiditis or hypothyroidism. Despite this, there are anecdotal reports regarding L-thyroxine administration in patients with CIU.
Screening for thyroid autoimmunity is probably useful in patients with CIU. More solid evidence, based on still lacking well-conducted controlled studies, is desirable to determine if there is a therapeutic role for L-thyroxine treatment in ameliorating the skin manifestations of urticaria.
A 60 year old woman affected by Hashimoto's thyroiditis presented with a history of recurring episodes of urticaria and angio-oedema. Clinical and laboratory evaluation of the patient excluded allergy to external agents, hereditary angio-oedema, and occult infections. A pathogenic relation between Hashimoto's thyroiditis and chronic urticaria/angio-oedema was suspected. However, treatment with L-thyroxine had no influence on the frequency and severity of the cutaneous and mucosal manifestations, which occurred almost daily and required repeated administration of steroids. The patient therefore underwent total thyroidectomy. Cytometric analysis of intrathyroidal lymphocyte subsets showed unusual abnormalities. Urticaria and angio-oedema completely remitted after surgery; 18 months postoperatively the patient was still asymptomatic.
Cutaneous manifestations of thyroid disease are protean in nature and affect all age groups. This review focuses on normal thyroid gland physiology, specific cutaneous/thyroid lesions such as the thyroglossal duct cyst and metastatic thyroid malignancies, nonspecific cutaneous alterations of the hyperthyroid and hypothyroid states, and the numerous associations of thyroid disease with other cutaneous and/or systemic disorders.
Thyroid autoimmunity has been increasingly reported to be associated with chronic urticaria and angioedema. The administration of thyroid hormone may alleviate chronic urticaria and/or angioedema in selected patients. This review focuses on the association of thyroid autoimmunity with chronic urticaria and/or angioedema. Recommendations for the therapeutic use of thyroid hormone in such patients are presented.
The coincidence of Hashimoto thyroiditis (HT) and chronic idiopathic urticaria (CIU) is a commonly observed phenomenon in western New York. Previous literature suggested that there may be a direct relationship between them. We undertook these studies to determine whether humoral or cell-mediated mechanisms might link HT and CIU. Skin biopsies from patients with CIU, with or without HT, were indistinguishable by light microscopy. No immune complex deposition was observed, although only the skin from patients with CIU and HT contained perivascular fibrin deposits. Similarly, immunohistochemical studies evaluating cellular expression of CD3, CD4, CD8, CD20, and CD68 failed to differentiate between CIU with or without HT. Analysis of Vbeta restriction in thyroid tissue of patients with HT and the skin of patients with CIU and HT by in situ polymerase chain reaction failed to reveal any oligoclonal T-lymphocyte subpopulations. In contrast, only patients with CIU and HT had anti-FcepsilonRI antibodies in their sera that could induce degranulation of normal basophils. Some sera from patients with CIU and HT caused degranulation of normal basophils in the absence of anti-FceRI. The factor causing basophil degranulation in these sera was not determined. Patients with CIU and HT failed to improve clinically with thyroid replacement therapy. All CIU patients were equally well managed with symptomatic therapies. In conclusion, HT likely represents a marker of other autoimmunity, rather than being a direct causative agent in CIU. Management of CIU, with or without HT and with or without anti-FceRI antibodies, should be the same. Future studies will have to examine whether cell-mediated responses participate in CIU, especially in association with HT.
The causes of chronic urticaria are numerous but are not always authenticated, the idiopathic forms remainder majority. In the literature of these ten last years, the causes leading to a specific treatment remain very few. They are primarily thyroid disease or Helicobacter pylori infection. The association between chronic urticaria and thyroid autoimmunity seems to be shown. It concerns asymptomatic Hashimoto's thyroïditis and more rarely Basedow's disease. The analysis of the literature doesn't allow establishing the role of thyroid hormone on the urticaria course. Recent observations showed a high rate of prevalence of Helicobacter pylori infection among patients suffering of chronic urticaria but some publications not found a statistically significant relation between these two pathologies. The differences observed in the urticaria course after eradication of Helicobacter pylori can result from a great variability in the methods used and the geographical origin of these series. In childhood, the causes being able to lead to a specific treatment are represented by various infections. Literature review does not reveal any controlled study and does not make it possible to establish the responsibility for these infections in the development of chronic urticaria and in the effectiveness of adapted treatment.
Recent studies suggest that autoimmune mechanisms may be involved in the etiology of chronic idiopathic urticaria (CIU). There is a higher prevalence of B12 deficiency in autoimmune diseases and possibly in gastric Helicobacter pylori (H. pylori) infection. The frequency of B12 deficiency in CIU is unknown. Our objective in this study was to determine the prevalence of B12 deficiency in patients with CIU and also its relationship to gastric H. pylori infection and serologic markers of autoimmunity in these groups. Thirty-three patients with CIU and 27 healthy controls were included in the study. Serum vitamin B12 levels, H. pylori infection and serological markers of autoimmunity (anti-thyroglobulin, thyroid microsomal, gastric parietal cell and antinuclear autoantibodies) were investigated. H. pylori infection was determined according to serology and gastric biopsy in 19 patients, serology and urea breath test in 4 patients and serology alone in the remaining 10 patients. Serum B12 levels were below the normal reference range in 11/33 (33.3%) patients with CIU. The mean serum B12 levels among patients with CIU and the controls were 281+/-127.5 pg/ml and 465.1+/-140.3 pg/ml (p=0.0001), respectively. Anti-thyroid antibodies were positive in 6 of 11 patients (54.5%) with low B12 levels, but only in 4 of 27 (14.8%) healthy controls (p=0.019). Anti-GPC antibodies were positive in 4 of 11 (36.4%) patients with CIU and low B12 levels, but only in 2 of 27 (7.4%) healthy controls (p=0.047). In CIU patients, there was no difference in the frequency of IgG H. pylori antibodies between those with low B12 levels and normal B12 levels. Among the 19 patients who had been performed gastric endoscopy, 15 patients (78.9%) had chronic antral gastritis, 2 patients (10.5%) had atrophic gastritis and there were normal findings in 2 patients (10.5%). In conclusion, serum B12 levels were found to be below the normal reference range in 33% of the patients with CIU. An association between low B12 levels and H. pylori could not be shown. The higher frequency of antithyroid and anti-GPC antibodies in patients with low B12 levels suggest that low B12 levels in CIU may be autoimmune in nature.
To investigate the association of chronic urticaria and autoimmune thyroid disease, a population of patients with thyroid autoimmunity as measured by thyroid autoantibody positivity was compared with a population of patients with thyroid disease without antibodies and an in-patient control group for the incidence and prevalence of skin disorders in particular chronic urticaria and angioedema.
Urticarial vasculitis is a subset of vasculitis characterized clinically by urticarial skin lesions and histologically by necrotizing vasculitis.
A review of patients with urticarial vasculitis was undertaken to further characterize the clinical and histologic findings and to differentiate this disorder from urticaria and other types of cutaneous vasculitis.
Seventy-two cases of biopsy-proven urticarial vasculitis were selected for a review of medical records, laboratory data, and histologic findings. Fifty cases of simple urticaria were also reviewed for purposes of comparison.
Systemic symptoms in patients with urticarial vasculitis included angioedema in 30 patients (42%), arthralgias in 35 (49%), pulmonary disease in 15 (21%), and abdominal pain in 12 (17%). Twenty-three patients (32%) had hypocomplementemia. Forty-six of 72 patients (64%) had lesions that lasted more than 24 hours, 23 of 72 (32%) had painful or burning lesions, and 25 of 72 (35%) had lesions that resolved with purpura. Sixteen biopsy specimens from the 23 patients with hypocomplementemia showed dermal neutrophilia in addition to the perivascular infiltrate. Of the 23 patients with hypocomplementemia, 20 (87%) had fluorescence of the blood vessels and 16 (70%) had fluorescence of the basement membrane zone as determined by routine direct immunofluorescence.
Patients with hypocomplementemia were more likely to have systemic symptoms such as urticaria that resolved with purpura, arthralgias, abdominal pain, and chronic obstructive pulmonary disease. The histologic pattern associated with hypocomplementemia is interstitial neutrophilic infiltrate of the dermis and an immunofluorescent pattern of immunoglobulins or C3 in the blood vessels and along the basement membrane zone.
From a pool of 624 patients with idiopathic chronic urticaria and angioedema, 90 patients had evidence of associated thyroid autoimmunity (TA). Since the number expected by chance alone is 37, given that less than 6% of normal subjects have TA, the association is significant (p less than 0.01; chi-square test). Age and sex distribution was typical of patients with TA. Clinically, most patients suffered relentless and severe urticaria and/or angioedema. With the exception of thyroid function and thyroid antibody tests, other laboratory tests were not rewarding. In most cases, treatment with 1 thyroxine did not improve urticaria or angioedema, but a few patients demonstrated a dramatic response. Awareness of the association resulted in the identification of previously undiagnosed thyroid disease. The authors hypothesize that a subset of idiopathic chronic urticaria and angioedema may be an autoimmune disease.
• Seventeen patients, constituting 12.1% of 140 consecutively seen cases of chronic urticaria, demonstrated thyroid autoimmunity with thyroid microsomal antibodies (TMAs) in serum titers greater than or equal to 1:1,600. Eight of these 17 patients had goiter or thyroid dysfunction. In a control group of 477 consecutively seen patients, only 27 (5.6%) had similar TMA titers. Routine and special immunologic test results in this group of 17 patients did not differ from those found in other patients with chronic urticaria and angioedema (CUA), and the only notable clinical feature was that all 17 had angioedema. The age and sex distribution and thyroid features of these 17 patients were similar to those described in autoimmune thyroiditis. Patients (especially women) with CUA should be tested for the presence of TMAs. In this subgroup, CUA may have an autoimmune basis.
(Arch Dermatol 1983;119:636-640)