Antineutrophil Cytoplasmic Antibody-Positive Crescentic Glomerulonephritis Associated With Anti-Thyroid Drug Treatment

D’Cruz, David; Chesser, Alistair; Lightowler, C.; Comer, M.; Hurst, Miriam; Baker, L. R. I.; Raine, A. E. G.

doi:10.1093/rheumatology/34.11.1090

Cited by 90 publications

(57 citation statements)

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“…Clinical signs were present in 2 of 6 ANCA-positive 110 Slot et al patients who had used PTU, in 2 patients using other antithyroid drugs, and in none of the patients who were not treated with antithyroid drugs. The presence of ANCA, and of ANCA-associated vasculitis, in patients using antithyroid drugs for treatment of hyperthyroidism have been recurrently reported (15)(16)(17)(18)(19)(20)(21)(22)(23)27). Reported prevalence of ANCA in patients treated with antithyroid drugs varies from 4% to 46%; prevalence of AAV is lower (0 -1.4%) (22,(27)(28)(29).…”

Section: Discussionmentioning

confidence: 99%

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Occurrence of antineutrophil cytoplasmic antibodies and associated vasculitis in patients with hyperthyroidism treated with antithyroid drugs: A long‐term followup study

Slot¹,

Links²,

Stegeman³

et al. 2005

Arthritis & Rheumatism

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Section: Discussionmentioning

confidence: 99%

“…There are several case reports implicating hydralazine (11)(12)(13)(14) and propylthiouracil (PTU) (15)(16)(17)(18)(19) in the induction of AAV. Occasionally, other drugs are mentioned, including other antithyroid drugs, such as carbimazole (17) and methimazole (20,21).…”

Section: Introductionmentioning

confidence: 99%

Occurrence of antineutrophil cytoplasmic antibodies and associated vasculitis in patients with hyperthyroidism treated with antithyroid drugs: A long‐term followup study

Slot¹,

Links²,

Stegeman³

et al. 2005

Arthritis & Rheumatism

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“…Numerous articles have appeared on ANCA positivity arising from administration of propylthiouracil (PTU) for anti-thyroid treatment in patients with Graves disease, hyperthyroidism, and thyrotoxicosis (13, [207][208][209]. The majority of these patients had ANCA directed against MPO, although ANCA that were simultaneously directed against other antigens such as human leukocyte elastase, lactoferrin, and even PR3 were also described (210,211).…”

Section: Pharmacologic Inductionmentioning

confidence: 99%

Hypotheses on the Etiology of Antineutrophil Cytoplasmic Autoantibody–Associated Vasculitis

Wijngaarden¹,

Rijn²,

Hagen³

et al. 2008

Clinical Journal of the American Society of Nephrology

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The first description of what is now known as antineutrophil cytoplasmic autoantibody-associated necrotizing vasculitis appeared more than 140 yr ago. Since then, many aspects of the pathogenic pathway have been elucidated, indicating the involvement of antineutrophil cytoplasmic autoantibodies, but why antineutrophil cytoplasmic autoantibodies are produced in the first place remains unknown. Over the years, many hypotheses have emerged addressing the etiology of antineutrophil cytoplasmic antibody production, but no exclusive factor or set of factors can so far be held responsible. Herein is reviewed the most influential hypotheses regarding the causes of antineutrophil cytoplasmic antibody-associated vasculitis with the aim of placing in an epidemiologic background the different hypotheses that are centered on environmental and genetic influences.Clin J Am Soc Nephrol 3: 237-252, 2008237-252, . doi: 10.2215 A ntineutrophil cytoplasmic autoantibody (ANCA)-associated necrotizing vasculitis was probably first described in 1866 by Kussmaul and Maier (1) as "polyarteritis nodosa." It was not until the early 1930s when the first case of what was later named Wegener's granulomatosis (WG) was described (2). The disease was named after Friedrich Wegener, who described it as an entity in 1939 (3). In 1985, antibodies associated with the disease were detected and later became known as ANCA (4). WG is a systemic autoimmune disease that can cause damage in various organs. Later, microscopic polyangiitis (MPA) was distinguished as a separate ANCA-associated vasculitis. The disease-or its immunosuppressive treatment-can cause high levels of morbidity and death, especially in patients with renal involvement. Animal experiments have shown that ANCA directed against myeloperoxidase (MPO) can cause vasculitis that resembles human vasculitic disease (5,6); however, the cause of ANCA production remains unresolved.Theories have been developed to explain how ANCA could interact with neutrophils, along with monocytes and most probably T lymphocytes, to form the lesions that are characteristic of ANCA-associated vasculitis, such as fibrinoid necrosis and granulomas (7). A recent theory of interest has been postulated by Pendergraft et al. (8), stating that an antibody against the complementary peptide of proteinase-3 (PR3) in an idiotypic/anti-idiotypic network is essential to the development of ANCA and to the development of clinical vasculitis, but why and how these ANCA are produced in the first place remains unanswered. Nonetheless, many hypotheses have been developed about the initiating factor for ANCA production. Many factors, either directly or indirectly, have been considered important in the development of ANCA: Silica exposure (9); genetic predisposition (10); bacterial infection by Staphylococcus aureus (11); viral infection by, for instance, parvovirus B19 (12); and thyroid drugs (13) all have been correlated with and held to contribute to the incidence of ANCA-associated vasculitis. Some of these hypotheses are still th...

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“…Thus, it has been reported that PTU can selectively accumulate into neutrophils where it can bind to myeloperoxidase, changing or inactivating the heme structure of the enzyme (Lee et al, 1988). It has been suggested that, in susceptible individuals, the enzyme altered by PTU could then stimulate the production of anti-myeloperoxidase antibodies, inducing neutrophils degranulation and vascular damage (D'Cruz et al, 1995). In particular, MPO-ANCA seems to play an important role in the development of tissue damage in vasculitis or glomerulonephritis (Ashizawa et al, 2003;Arimura et al, 1993).…”

Section: Autoimmune Markers Of Thionamides-related Vasculitismentioning

confidence: 99%

“…In 1995, D'Cruz et al published the first report of renal biopsy-proven vasculitis in two patients treated with antithyroid drugs. Both patients developed a crescentic glomerulonephritis and responded to immunosuppressive therapy and dismission of anti-thyroid drugs (D'Cruz et al, 1995). Recently, Chen YX et al published a retrospective study of 19 patients with ANCA-positive vasculitis associated with PTU treatment.…”

Section: Clinical Manifestations Of Thionamides-related Vasculitismentioning

confidence: 99%

Thionamides-Related Vasculitis in Autoimmune Thyroid Disorders: Review of Current Literature and Case Reports

Romeo¹,

Russo²,

Giandalia³

et al. 2011

Autoimmune Disorders - Current Concepts and Advances From Bedside to Mechanistic Insights

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Antineutrophil Cytoplasmic Antibody-Positive Crescentic Glomerulonephritis Associated With Anti-Thyroid Drug Treatment

Cited by 90 publications

References 0 publications

Occurrence of antineutrophil cytoplasmic antibodies and associated vasculitis in patients with hyperthyroidism treated with antithyroid drugs: A long‐term followup study

Occurrence of antineutrophil cytoplasmic antibodies and associated vasculitis in patients with hyperthyroidism treated with antithyroid drugs: A long‐term followup study

Hypotheses on the Etiology of Antineutrophil Cytoplasmic Autoantibody–Associated Vasculitis

Thionamides-Related Vasculitis in Autoimmune Thyroid Disorders: Review of Current Literature and Case Reports

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