Editorial
IgG4 (IgG4-RD) Related Diseases, With a Horizon Not Limited to Mikulicz's Disease
Enfermedades relacionadas con IgG4 (IgG4-RD), con horizonte no limitado a la enfermedad de Mikulicz
Carlos Abud-Mendoza
Unidad Regional de Reumatología y Osteoporosis, Hospital Central «Dr. Ignacio Morones Prieto», Facultad de Medicina de la Universidad Autónoma de San Luis Potosí, San Luis Potosí, Mexico
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For decades, Mikulicz's disease and Sjögren's syndrome were considered identical conditions.<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1–5</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">IgG1 immunoglobulin is most prevalent (>50%) and the IgG4 variety constitutes less than 5%. IgG4 has disulfide bonds linking the heavy chains unsteadily, allowing their separation and forming 2 antigen-binding sites, so that the bispecific antibody is asymmetric with an unclear in vivo role. IgG4 interacts with the Fc portion of IgG1–3 and not through the Fab-Fc, as occurs with other immunoglobulins, and has rheumatoid factor activity. Therefore, IgG4 has little or no cross-reactivity between antigens and rarely forms immune complexes having no complement activation capacity.<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">IgG4 is characteristically protagonic in:<ul class="elsevierStyleList" id="lis0005"><li class="elsevierStyleListItem" id="lsti0005"><span class="elsevierStyleLabel">1.</span><p id="par0020" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Antiinflammation</span>: through binding with soluble antigens blocks interaction with IgE and mast cells, with subsequent inhibition of the allergic response.</p></li><li class="elsevierStyleListItem" id="lsti0010"><span class="elsevierStyleLabel">2.</span><p id="par0025" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Physiopathogeny</span>: as in pemphigus foliaceus, where IgG4 is directed against desmoglein (junctional protein) and a third of patients with membranous glomerulonephritis, in whom IgG4 interacts with phospholipase A2 receptor type M of podocytes. There are antimetelloproteinase ADMATS13 IgG4 autoantibodies role in thrombotic thrombocytopenic purpura.<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1,6</span></a></p></li><li class="elsevierStyleListItem" id="lsti0015"><span class="elsevierStyleLabel">3.</span><p id="par0030" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Autoantibody reaction</span>: IgG4 interactions with other antibodies.</p></li></ul></p><p id="par0035" class="elsevierStylePara elsevierViewall">The clinical expression of IgG4-RD is almost universal<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1–5</span></a>; the 2 presentations classically described are salivary and lacrimal gland disease (Mikulicz's disease) and pancreatic disease, which may occur alone or accompanying other organic problems, such as biliary disease and salivary gland problems associated with a fibrosing inflammatory process of the pancreas.<a class="elsevierStyleCrossRefs" href="#bib0035"><span class="elsevierStyleSup">7–9</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">Most presentations of IgG4-RD occur between 55 and 60 years of age, predominantly in women. Characteristically, it causes growth or thickening of the affected organ and pseudotumor formation, which can lead to organ dysfunction (e.g., xerostomia and xerophthalmia due to salivary and lacrimal gland disease, chronic diarrhea, pancreatitis, dyspnea, interstitial pneumonitis, etc.).</p><p id="par0045" class="elsevierStylePara elsevierViewall">The differential diagnosis between Mikulicz's disease and Sjögren's syndrome is of great interest,<a class="elsevierStyleCrossRefs" href="#bib0050"><span class="elsevierStyleSup">10–12</span></a> with some overlap of clinical and serological manifestations. The first occurs typically in the sixth decade of life in females and glandular growth is persistent, with high levels of IgG4 and IgG4/IgG index, with lower prevalence of antinuclear antibodies (ANA) (≤30%), seronegative for anti-Ro and anti-La (SSA, SSB), glandular preservation, storiform fibrosis (from the center to the periphery) in advanced stages, venular obliteration (obliterative phlebitis) and excellent response to steroids, whereas Sjögren's is more common in the fifth decade of life in women, with more xerostomia and xerophthalmia, ANA (90%) and anti-SSA (50%), being able to evolve to glandular destruction and be unresponsive to steroids.</p><p id="par0050" class="elsevierStylePara elsevierViewall">Immunohistochemistry allows for an accurate diagnosis and helps exclude other entities such as lymphomas. In case of liver affection there is portal inflammation; in renal disease, tubulointerstitial infiltration may be found and, less frequently, glomerular disease (membranous nephropathy)<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">13</span></a> and when lymph nodes are affected there are 5 subtypes that might pose a histological diagnosis challenge when differentiating with Castleman's disease or hyperplasia.<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">14</span></a></p><p id="par0055" class="elsevierStylePara elsevierViewall">IgG4-RD has ethnic predilections; the Japanese are associated with DRB1 *04015 and 0405, and Koreans with DQB1 and relapses; other, different genes have been described for Chinese patients and for selected clinical expressions. Recognized initiator mechanisms are autoantigens in autoimmune pancreatitis, such as lactoferrin and carbonic anhydrase autoantibodies II of another IgG subclass.<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">15</span></a> Yamamoto et al. identified a 13.1<span class="elsevierStyleHsp" style=""></span>Kd antigen bound to an IgG4 molecule in patients with autoimmune pancreatitis and Mikulicz disease, not present in Sjögren patients or in healthy controls.<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">16</span></a></p><p id="par0060" class="elsevierStylePara elsevierViewall">Additionally, we have documented changes in the activation and regulation of Toll-like and NOD type receptors. Activation of Toll-like receptor 4 in patients with IgG4-RD leads to increased IL-10, an increased Th2 response and increased production of IgG4, but in healthy patients leads to an increased production of interferon and tumor necrosis factor.<a class="elsevierStyleCrossRefs" href="#bib0085"><span class="elsevierStyleSup">17–29</span></a></p><p id="par0065" class="elsevierStylePara elsevierViewall">The primary response modulator in IgG4-RD are Th2 lymphocytes (leading to an overproduction of IgG4 and eosinophils); it elevates the production of various cytokines 18- to 45-fold in patients with autoimmune pancreatitis, with lesser titers in autoimmune cholangitis and primary biliary cirrhosis.<a class="elsevierStyleCrossRefs" href="#bib0090"><span class="elsevierStyleSup">18–20</span></a> T regulatory cells (Tregs, CD25+ FoxP3+) are elevated in number or functionally, unlike what is characteristically observed in other rheumatic diseases, where they are diminished and increase after treatment. In IgG4-RD, increased conventional and memory Tregs are responsible for the production of IL-10, which in turn is responsible for the change to the IgG4 subclass. All this leads to the activation and infiltration of plasma cells, eosinophils and fibroblasts, with subsequent tissue damage in conjunction with the release of cytokines and, on occasion, immune complexes and complement activation, which typically depends on the coparticipation of IgG1; transforming growth factor beta participates in the formation of fibrosis.<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1,20–22</span></a></p><p id="par0070" class="elsevierStylePara elsevierViewall">The diagnosis is usually one of exclusion against common diseases, such as infections (viral, bacterial, mycobacterial and fungal) and neoplasia (lymphoma). Its recognition has increased due to its distinctive characteristics and classification criteria: (a) dysfunction of one or more organs, (b) radiographical evidence of involvement by IgG4-RD (e.g., pseudotumor, peripancreatic inflammation, interstitial pneumonitis), (c) serological: IgG4≥135<span class="elsevierStyleHsp" style=""></span>mg/dl, and (d) pathological: lymphoplasmacytic infiltration, storiform fibrosis, obliterative phlebitis, eosinophilia, immunohistochemistry showing IgG4+ (≥10 cells IgG4 in a high power field and/or IgG4+/IgG+ of 40%), with sensitivity of 92% and 88%–95% specificity. Eosinophilia occurs in 15%–20% of cases.<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1,2,4</span></a></p><p id="par0075" class="elsevierStylePara elsevierViewall">Despite its low prevalence, which puts them in the condition of an exclusion diagnosis, and sometimes constitute part of associated comorbid conditions, the clinician should consider IgG4-RD in the differential diagnosis of any disease with glandular, pulmonary, retroperitoneal, thyroid, biliopancreatic, eye, aortic, mediastinal, renal, urogenital and neurological manifestations. Thus, a third of vasculitis associated with antineutrophil cytoplasmic antibodies, such as granulomatous polyangiitis (PG) and GP with eosinophilia (Churg Strauss), occurs with increased IgG4 and almost 10% of the IgG4-RD meet criteria or are associated with Sjögren's syndrome, vasculitis, cancer, etc.<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1,11,13,21–31</span></a></p><p id="par0080" class="elsevierStylePara elsevierViewall">Although not <span class="elsevierStyleItalic">a prerequisite</span> for diagnosis, we must consider elevated levels of IgG4 (normal up to 30%). Of 3300 IgG4 determinations made by clinically suggestive signs, 158 (4.8%) had high titers (>140<span class="elsevierStyleHsp" style=""></span>mg/dl) and only 29 (18.4%) had IgG4-RD in possible or definitive titers,<a class="elsevierStyleCrossRef" href="#bib0110"><span class="elsevierStyleSup">22</span></a> a fact that evidences that most patients with clinical manifestations indicative of IgG4-RD, even with high levels of IgG4, have other diseases responsible for manifestations, such as vasculitis.<a class="elsevierStyleCrossRefs" href="#bib0110"><span class="elsevierStyleSup">22–31</span></a> According to the above criteria, we analyzed 23<span class="elsevierStyleHsp" style=""></span>712 biopsies performed from January 2011 to June 2012 and selected 34 cases potentially compatible with IgG4-RD according to conventional histopathology (granulomatous mastitis 17, sialadenitis 8, thyroiditis [2 and one of each: dacryoadenitis, pleomorphic parotid tumor, pericarditis, inflammatory lung tumor, or sclerosing myofibroblastic tumor, aortitis lymphoplasmacytic ileum tumor and SLE with inflammatory autoimmune pancreatitis and chronic sialadenitis]), and only in 10% did we confirm an IgG4-RD.</p><p id="par0085" class="elsevierStylePara elsevierViewall">The response to low-dose steroids is distinctive of the IgG4-RD, although it is of interest that up to 30% of patients with IgG4-RD have spontaneous resolution and a similar percentage is refractory or have relapsed; Rituximab is generally suitable for B cell depleting therapy,<a class="elsevierStyleCrossRef" href="#bib0160"><span class="elsevierStyleSup">32</span></a> although one can also use methotrexate, mycophenolic acid and azathioprine. There is evidence that treatment modifies the natural course of the disease, both in normalizing the organic functions and preventing fibrosis.<a class="elsevierStyleCrossRef" href="#bib0165"><span class="elsevierStyleSup">33</span></a></p></span>" "pdfFichero" => "main.pdf" "tienePdf" => true "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: Abud-Mendoza C. Enfermedades relacionadas con IgG4 (IgG4-RD), con horizonte no limitado a la enfermedad de Mikulicz. Reumatol Clin. 2013;9:133–5.</p>" ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0005" "bibliografiaReferencia" => array:33 [ 0 => array:3 [ "identificador" => "bib0005" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "IgG4-related disease" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:3 [ 0 => "J.H. Stone" 1 => "Y. Zen" 2 => "V. 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| Year/Month | Html | Total | |
|---|---|---|---|
| 2024 November | 7 | 13 | 20 |
| 2024 October | 47 | 26 | 73 |
| 2024 September | 71 | 24 | 95 |
| 2024 August | 67 | 34 | 101 |
| 2024 July | 64 | 33 | 97 |
| 2024 June | 73 | 23 | 96 |
| 2024 May | 69 | 31 | 100 |
| 2024 April | 72 | 19 | 91 |
| 2024 March | 55 | 28 | 83 |
| 2024 February | 43 | 25 | 68 |
| 2024 January | 51 | 29 | 80 |
| 2023 December | 45 | 30 | 75 |
| 2023 November | 45 | 22 | 67 |
| 2023 October | 50 | 28 | 78 |
| 2023 September | 69 | 30 | 99 |
| 2023 August | 70 | 22 | 92 |
| 2023 July | 71 | 36 | 107 |
| 2023 June | 54 | 29 | 83 |
| 2023 May | 72 | 26 | 98 |
| 2023 April | 51 | 11 | 62 |
| 2023 March | 73 | 31 | 104 |
| 2023 February | 80 | 37 | 117 |
| 2023 January | 64 | 37 | 101 |
| 2022 December | 68 | 46 | 114 |
| 2022 November | 70 | 37 | 107 |
| 2022 October | 63 | 42 | 105 |
| 2022 September | 57 | 37 | 94 |
| 2022 August | 47 | 43 | 90 |
| 2022 July | 42 | 49 | 91 |
| 2022 June | 55 | 45 | 100 |
| 2022 May | 43 | 48 | 91 |
| 2022 April | 54 | 46 | 100 |
| 2022 March | 55 | 54 | 109 |
| 2022 February | 36 | 29 | 65 |
| 2022 January | 58 | 45 | 103 |
| 2021 December | 30 | 46 | 76 |
| 2021 November | 36 | 41 | 77 |
| 2021 October | 49 | 45 | 94 |
| 2021 September | 32 | 42 | 74 |
| 2021 August | 47 | 35 | 82 |
| 2021 July | 34 | 24 | 58 |
| 2021 June | 37 | 54 | 91 |
| 2021 May | 55 | 35 | 90 |
| 2021 April | 77 | 93 | 170 |
| 2021 March | 61 | 24 | 85 |
| 2021 February | 55 | 31 | 86 |
| 2021 January | 37 | 23 | 60 |
| 2020 December | 37 | 19 | 56 |
| 2020 November | 46 | 16 | 62 |
| 2020 October | 31 | 9 | 40 |
| 2020 September | 39 | 26 | 65 |
| 2020 August | 34 | 20 | 54 |
| 2020 July | 24 | 15 | 39 |
| 2020 June | 37 | 17 | 54 |
| 2020 May | 28 | 38 | 66 |
| 2020 April | 26 | 34 | 60 |
| 2020 March | 16 | 6 | 22 |
| 2020 February | 2 | 0 | 2 |
| 2020 January | 4 | 0 | 4 |
| 2019 September | 4 | 0 | 4 |
| 2019 June | 1 | 0 | 1 |
| 2019 March | 1 | 0 | 1 |
| 2019 January | 1 | 0 | 1 |
| 2018 May | 7 | 0 | 7 |
| 2018 April | 61 | 7 | 68 |
| 2018 March | 66 | 8 | 74 |
| 2018 February | 69 | 3 | 72 |
| 2018 January | 26 | 5 | 31 |
| 2017 December | 68 | 14 | 82 |
| 2017 November | 36 | 8 | 44 |
| 2017 October | 30 | 8 | 38 |
| 2017 September | 47 | 8 | 55 |
| 2017 August | 59 | 17 | 76 |
| 2017 July | 44 | 17 | 61 |
| 2017 June | 76 | 7 | 83 |
| 2017 May | 81 | 15 | 96 |
| 2017 April | 61 | 9 | 70 |
| 2017 March | 62 | 25 | 87 |
| 2017 February | 40 | 3 | 43 |
| 2017 January | 43 | 8 | 51 |
| 2016 December | 75 | 16 | 91 |
| 2016 November | 59 | 8 | 67 |
| 2016 October | 77 | 14 | 91 |
| 2016 September | 61 | 19 | 80 |
| 2016 August | 52 | 10 | 62 |
| 2016 July | 34 | 10 | 44 |
| 2016 May | 0 | 8 | 8 |
| 2016 March | 0 | 9 | 9 |
| 2016 February | 1 | 18 | 19 |
| 2015 December | 2 | 0 | 2 |
| 2015 October | 0 | 9 | 9 |
| 2015 September | 1 | 0 | 1 |
| 2015 August | 1 | 0 | 1 |
| 2015 July | 35 | 6 | 41 |
| 2015 June | 65 | 14 | 79 |
| 2015 May | 94 | 16 | 110 |
| 2015 April | 63 | 20 | 83 |
| 2015 March | 55 | 11 | 66 |
| 2015 February | 81 | 16 | 97 |
| 2015 January | 60 | 12 | 72 |
| 2014 December | 63 | 14 | 77 |
| 2014 November | 56 | 13 | 69 |
| 2014 October | 76 | 14 | 90 |
| 2014 September | 57 | 18 | 75 |
| 2014 August | 61 | 16 | 77 |
| 2014 July | 76 | 18 | 94 |
| 2014 June | 94 | 21 | 115 |
| 2014 May | 82 | 19 | 101 |
| 2014 April | 81 | 17 | 98 |
| 2014 March | 91 | 29 | 120 |
| 2014 February | 80 | 17 | 97 |
| 2014 January | 64 | 21 | 85 |
| 2013 December | 58 | 20 | 78 |
| 2013 November | 53 | 21 | 74 |
| 2013 October | 73 | 12 | 85 |
| 2013 September | 53 | 10 | 63 |
| 2013 August | 70 | 32 | 102 |
| 2013 July | 46 | 29 | 75 |
| 2013 June | 69 | 38 | 107 |
| 2013 May | 19 | 13 | 32 |
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