IgG4-related disease: Difference between revisions

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| style="font-weight: bold;" | [[Scrotum]]
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| IgG4-related paratesticular pseudotumor,<ref name="pmid25026959" /><br />IgG4-related epididymo-orchitis<ref name="pmid25026959" />
| IgG4-related paratesticular pseudotumor,<ref name="pmid25026959" /><ref name="pmid25337295" /><br />IgG4-related epididymo-orchitis<ref name="pmid25026959" />
| Paratesticular fibrous pseudotumor, inflammatory pseudotumor of the [[spermatic cord]], pseudosarcomatous myofibroblastic proliferations of the spermatic cord, proliferative funiculitis, chronic proliferative periorchitis, fibromatous periorchitis, nodular periorchitis, reactive periorchitis, fibrous mesothelioma<ref name="pmid20957491" />
| Paratesticular fibrous pseudotumor, inflammatory pseudotumor of the [[spermatic cord]], pseudosarcomatous myofibroblastic proliferations of the spermatic cord, proliferative funiculitis, chronic proliferative periorchitis, fibromatous periorchitis, nodular periorchitis, reactive periorchitis, fibrous mesothelioma<ref name="pmid20957491" />


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<ref name="pmid25260440">
{{cite journal |author1=Bobby B Najari |author2=Brian D Robinson |author3=Stephen A Paget |author4=Darius A Paduch |date=October 2014 |title=Clinical, radiographic, and pathologic description of IgG4-related perivasal fibrosis: a previously undescribed etiology of chronic orchialgia |url=http://www.goldjournal.net/article/S0090-4295%2814%2900681-5/abstract |journal=[[Urology (journal)|Urology]] |publisher=Société Internationale d'Urologie |volume=84 |issue=4 |pages=748–750 |doi=10.1016/j.urology.2014.06.035 |pmid=25260440}}
{{cite journal |author1=Bobby B Najari |author2=Brian D Robinson |author3=Stephen A Paget |author4=Darius A Paduch |date=October 2014 |title=Clinical, radiographic, and pathologic description of IgG4-related perivasal fibrosis: a previously undescribed etiology of chronic orchialgia |url=http://www.goldjournal.net/article/S0090-4295%2814%2900681-5/abstract |journal=[[Urology (journal)|Urology]] |publisher=Société Internationale d'Urologie |volume=84 |issue=4 |pages=748–750 |doi=10.1016/j.urology.2014.06.035 |pmid=25260440}}
</ref>

<ref name="pmid25337295">
{{cite journal |author1=Takashi Karashima |author2=Yoshinori Taniguchi |author3=Tsutomu Shimamoto |author4=Tomoya Nao |author5=Hiroshi Nishikawa |author6=Satoshi Fukata |author7=Masayuki Kamada |author8=Keiji Inoue |author9=Kentaro Oko |author10=Hideki Nakajima |author11=Shigetoshi Sano |author12=Manabu Matsumoto |author13=Naoto Kuroda |author14=Yoshihiro Kamei |author15=Taro Shuin |date=9 December 2014 |title=IgG4-related disease of the paratestis in a patient with Wells syndrome: a case report |url=http://www.diagnosticpathology.org/content/9/1/225 |journal=Diagnostic Pathology |volume=9 |id=225 |doi=10.1186/s13000-014-0225-5 |pmc=4265405 |pmid=25337295}}
</ref>
</ref>


Revision as of 19:36, 28 August 2015

IgG4-related disease
SpecialtyRheumatology, immunology Edit this on Wikidata

IgG4-related disease (IgG4-RD) is a relapsing–remitting immune-mediated fibroinflammatory disease characterised by: a tendency to mass forming, tissue-destructive lesions in multiple sites; a prompt response usually to steroids; a characteristic histopathological appearance; and elevated serum IgG4 concentrations in approximately 60–70% of people during an acute phase.[1][2]

The disease, which was formerly also known as IgG4-related systemic disease, is so named because plasma cells producing the antibody subtype IgG4 are present in large amounts on tissue samples from involved organs, and because IgG4 antibody levels in the bloodstream are often elevated.

Inflammation results in fibrosis, the deposition of connective tissue, in affected anatomical sites which can lead to organ dysfunction, or even organ failure, if not treated.[3]

Early detection is important to avoid organ damage and potentially serious complications.[4]

Nomenclature

Names previously used for IgG4-RD:

IgG4-related systemic disease (IgG4-RSD)
IgG4-related sclerosing disease
IgG4-related systemic sclerosing disease
IgG4-related autoimmune disease
IgG4-associated multifocal systemic fibrosis
IgG4-associated disease
IgG4 syndrome
Hyper-IgG4 disease
Systemic IgG4-related plasmacytic syndrome
IgG4-positive multiorgan lymphoproliferative syndrome

Prior to 2011, IgG4-RD used to get mentioned in the medical literature under various different names.[1][5]

At the 2011 International Symposium on IgG4-Related Diseases, the consensus name of IgG4-related disease was endorsed for the condition.[1] This name had already been agreed upon as a consensus name among Japanese investigators,[1][2] notably choosing not to use the term 'systemic' as that might lead to malignant tumours in other organs getting incorrectly diagnosed as being just another manifestation of the IgG4-related condition.[5]

However, some experts at the international symposium did express reservations about naming the disease after IgG4, as its role in pathogenesis is questionable and the use of serum IgG4 concentrations as a biomarker is unreliable.[1]

Individual organ manifestations

IgG4-RD can involve one or multiple sites in the body. With multiorgan involvement, the sites involved can be affected at the same time (synchronously) or at different unrelated periods (metachronously).

Several different diseases that have been known for many years are now considered to be manifestations of IgG4-RD. These include type 1 autoimmune pancreatitis, retroperitoneal fibrosis, mediastinal fibrosis, Riedel's thyroiditis, Mikulicz's disease, Küttner's tumor and inflammatory pseudotumor are now regarded as forms of IgG4-RD.[6][7]

Nomenclature for individual organ involvement[1][8]
Organ or site Preferred names Previously used names
Head and neck
Salivary gland IgG4-related sialadenitis Chronic sclerosing sialadenitis,
Küttner's tumour (submandibular glands),
Mikulicz's disease (salivary and lacrimal glands)[9]
Lacrimal gland IgG4-related dacryoadenitis Mikulicz's disease (salivary and lacrimal glands)[9]
Orbit IgG4-related ophthalmic disease (IgG4-ROD) Idiopathic orbital inflammatory disease, orbital pseudotumor
Paranasal sinuses[10]   Chronic sinusitis, Eosinophilic angiocentric fibrosis (orbits and upper respiratory tract)
Pharynx IgG4-related pharyngitis[11]  
Thyroid gland IgG4-related thyroid disease Riedel's thyroiditis or Riedel's struma
Soft tissues of the head and neck   Idiopathic cervical fibrosis,[12] sclerosing cervicitis, cervical fibrosclerosis
Central Nervous System
Pituitary gland IgG4-related hypophysitis:
IgG4-related panhypophysitis (all of pituitary gland),
IgG4-related adenohypophysitis (anterior pituitary),
IgG4-related infundibuloneurohypophysitis (posterior pituitary and pituitary stalk)
 Autoimmune hypophysitis
Meninges IgG4-related pachymeningitis (dura mater),
IgG4-related leptomeningitis[13] (arachnoid and pia mater) 		Idiopathic hypertrophic pachymeningitis
Chest and abdomen
Pancreas IgG4-related pancreatitis Type 1 autoimmune pancreatitis, lymphoplasmacytic sclerosing pancreatitis, 'chronic pancreatitis with diffuse irregular narrowing of the main pancreatic duct'[14]
Lung IgG4-related lung disease Pulmonary inflammatory pseudotumour
Pleura IgG4-related pleuritis  
Liver IgG4-related hepatopathy  
Bile duct IgG4-related sclerosing cholangitis  
Gallbladder IgG4-related cholecystitis  
Aorta
(especially the infrarenal portion) 		IgG4-related aortitis,
IgG4-related periaortitis[15] 		Inflammatory aortic aneurysm,
Chronic periaortitis.
Branches of the aorta
(including coronary,[10] renal or iliac arteries) 		IgG4-related periarteritis[15]  
Pericardium IgG4-related pericarditis  
Mediastinum IgG4-related mediastinitis Fibrosing mediastinitis
Retroperitoneum IgG4-related retroperitoneal fibrosis Retroperitoneal fibrosis, Albarran-Ormond syndrome, Ormond's disease, perirenal fasciitis, Gerota's fasciitis/syndrome, periureteritis fibrosa, sclerosing lipogranuloma, sclerosing retroperitoneal granuloma, non-specific retroperitoneal inflammation, sclerosing retroperitonitis, retroperitoneal vasculitis with perivascular fibrosis.[16]
Mesentery IgG4-related mesenteritis (subtypes are: mesenteric panniculitis, mesenteric lipodystrophy and retractile mesenteritis)[16] Sclerosing mesenteritis, systemic nodular panniculitis, liposclerosis mesenteritis, mesenteric Weber-Christian disease, mesenteric lipogranuloma, xanthogranulomatous mesenteritis.[16]
Breast IgG4-related mastitis Sclerosing mastitis
Genitourinary
Kidney IgG4-related kidney disease (IgG4-RKD):
IgG4-related tubulointerstitial nephritis (IgG4-TIN),
IgG4-related membranous glomerulonephritis
 Idiopathic tubulointerstitial nephritis
Prostate IgG4-related prostatitis  
Vas deferens IgG4-related perivasal fibrosis[17][18] Chronic orchalgia
Scrotum IgG4-related paratesticular pseudotumor,[8][19]
IgG4-related epididymo-orchitis[8] 		Paratesticular fibrous pseudotumor, inflammatory pseudotumor of the spermatic cord, pseudosarcomatous myofibroblastic proliferations of the spermatic cord, proliferative funiculitis, chronic proliferative periorchitis, fibromatous periorchitis, nodular periorchitis, reactive periorchitis, fibrous mesothelioma[20]
Other
Lymph nodes IgG4-related lymphadenopathy  
Skin IgG4-related skin disease Angiolymphoid hyperplasia with eosinophilia,[21] cutaneous pseudolymphoma[22]
Nerve IgG4-related perineural disease[8][23]  

This is not a complete list, as IgG4-RD can involve any site in the body.

Other affected sites, confirmed on histology to be manifestations of IgG4-RD, include: heart;[24] hard palate,[25] esophagus,[26][27] stomach,[28] small intestine;[29] adrenal gland,[30] uterus,[31] ureter,[32] bladder,[33] urachus,[34] and synovium.[35]

Radiologic evidence in confirmed cases of IgG4-RD has also demonstrated involvement in the superior vena cava[24] and seminal vesicle.[36]

Symptoms

IgG4-related disease has been described as an indolent condition as usually symptoms, if any, tend to be mild. This can be in spite of considerable organ destruction. People are often described as being generally well at the time of diagnosis, although some may give a history of weight loss.

Pain is generally not a feature of the inflammation. However it may occur as a secondary effect, for example due to either obstruction or compression.

Often diagnosis is made due to the presence of painless swellings or mass lesions, or due to complications of masses, e.g. jaundice due to involvement of the pancreas, biliary tree or liver. Symptoms are commonly attributed to other conditions and other diagnoses may have been made years before diagnosis, e.g. urinary symptoms in men attributed to common prostate conditions. Lesions may also be detected incidentally on radiological images, but can be easily misdiagnosed as malignancies.

Reported cases do include some significant symptoms or findings however:

System Uncommon symptoms and complications
Neurological Seizures,[37][38] paralysis or hemiparesis,[37] cranial nerve palsies,[37] sensorineural hearing loss,[39] pituitary hormone deficiencies[40]
Eye Loss of vision,[37] proptosis[41]
Cardiac Constrictive pericarditis,[42] heart block,[24] ruptured aortic aneurysm,[43][44] aortic dissection,[45] sudden cardiac death[46][47]
Respiratory Airway obstruction,[48] pleural effusion[31][49]
Gastrointestinal Esophageal obstruction,[26][27] bowel obstruction[50]
Urological Renal failure,[51] hydronephrosis,[51][52] testicular pain[17]

Histology

Whatever area of the body is involved, the hallmark histopathological features of IgG4-RD are:[2][6][7]

  1. A dense lymphoplasmacytic (lymphocytes and plasma cells) infiltrate rich in IgG4-positive plasma cells.
    • IgG4 immunostaining needs to be specifically requested and performed in order to detect IgG4-positive plasma cells.
  2. Fibrosis, arranged at least focally[2] in a storiform pattern.
    • 'Storiform' is commonly referred to as meaning 'having a cartwheel pattern', but its literal meaning is the appearance of 'a woven mat [Latin: storea] (of rush or straw)'.
  3. Obliterative phlebitis.
    • The venous channels are obliterated by a dense lymphoplasmacytic infiltrate, within both the venous walls and the lumen.[2]

Other histopathological features associated with IgG4-RD are:

Submandibular gland research

In an article from 1977, histological research into 349 cases of Küttner's tumor (now known as IgG4-related sialadenitis) identified four distinct stages of the fibroinflammatory process:[53]

  • Stage 1: Focal periductal (around the salivary ducts) lymphocytic infiltration
  • Stage 2: Diffuse lymphocytic infiltration and severe periductal fibrosis (scarring)
  • Stage 3: Prominent lymphocytic infiltration, atrophy of parenchyma (functional area), and periductal sclerosis (hardening due to scarring)
  • Stage 4: Marked loss and sclerosis (hardening) of the parenchyma - similar to the process involved in cirrhosis where there is shrinkage and loss of functional areas of the liver

This may reflect the fibroinflammatory process in other organs involved in IgG4-RD.

Treatment

The goal of treatment is the induction and maintenance of remission so as to prevent progression of fibrosis and organ destruction in affected organ(s).

An international panel of experts have developed recommendations for the management of IgG4-RD.[3][54] They concluded that in all cases of symptomatic, active IgG4-RD that treatment is required. Some cases with asymptomatic IgG4-RD also require treatment, as some organs tend to not cause symptoms until the late stages of disease. Urgent treatment is advised with certain organ manifestations, such as aortitis, retroperitoneal fibrosis, proximal biliary strictures, tubulointerstitial nephritis, pachymeningitis, pancreatic enlargement and pericarditis.

Induction of remission

In untreated patients with active disease, the recommended first-line agent for induction of remission is glucocorticoids unless contraindications exist. Glucocorticoids characteristically result in a rapid and often dramatic improvement in clinical features and often a resolution of radiographic features. However, where advanced fibrotic lesions have resulted in irreversible damage, the response to glucocorticoids and other current treatment options may be poor or even absent.

Although not validated yet in clinical trials, the common induction regime is prednisolone 30–40 mg per day for 2–4 weeks, then gradually tapered over 3 to 6 months. Recurrences during or after tapering of glucocorticoids are frequent however. Steroid-sparing immunosuppressive agents might be considered, depending on local availability of these drugs, for use in combination with glucocorticoids from the start of treatment. Steroid-sparing agents that have been used include rituximab, azathioprine, methotrexate, and cyclophosphamide, although trials are needed to ascertain the effectiveness of each drug in IgG4-RD.

Maintenance

Following a successful induction of remission, maintenance therapy might be given in some cases, for example when there is a high risk of relapse or in patients with organ-threatening manifestations. Common maintenancy therapy is prednisolone 2.5–5 mg per day, or use of a steroid-sparing agent instead.

Relapse

Relapses are common, and a previous history of relapse appears to be a strong predictor of future relapse. When relapse occurs while off therapy and there has been a prolonged disease remission following initial glucocorticoid induction, then the relapse can usually be managed successfully with a re-induction strategy using glucocorticoids. Introducing a steroid-sparing agent might also need to be considered for relapses.

Other interventions

When organ involvement causes local mechanical problems, further organ-specific interventions may be necessary. For example, when a tumefactive lesion cause obstruction of the bile duct, it may be necessary to insert a biliary stent to allow the bile to drain freely.

Similarly, ureteral or vascular stents, surgical resection or radiotherapy may be considered for various different presenting problems.

References

  1. ^ a b c d e f John H. Stone; Arezou Khosroshahi; Vikram Deshpande; John K. C. Chan; J. Godfrey Heathcote; Rob Aalberse; Atsushi Azumi; Donald B. Bloch; William R. Brugge; Mollie N. Carruthers; Wah Cheuk; Lynn Cornell; Carlos Fernandez-Del Castillo; Judith A. Ferry; David Forcione; Günter Klöppe; Daniel L. Hamilos; Terumi Kamisawa; Satomi Kasashima; Shigeyuki Kawa; Mitsuhiro Kawano; Yasufumi Masaki; Kenji Notohara; Kazuichi Okazaki; Ji Kon Ryu; Takako Saeki; Dushyant Sahani; Yasuharu Sato; Thomas Smyrk; James R. Stone; Masayuki Takahira; Hisanori Umehara; George Webster; Motohisa Yamamoto; Eunhee Yi; Tadashi Yoshino; Giuseppe Zamboni; Yoh Zen; Suresh Chari (October 2012). "Recommendations for the nomenclature of IgG4-related disease and its individual organ system manifestations". Arthritis & Rheumatism. 64 (10): 3061–3067. doi:10.1002/art.34593. PMID 22736240.
  2. ^ a b c d e f g Vikram Deshpande; Yoh Zen; John KC Chan; Eunhee E Yi; Yasuharu Sato; Tadashi Yoshino; Günter Klöppe; J Godfrey Heathcote; Arezou Khosroshahi; Judith A Ferry; Rob C Aalberse; Donald B Bloch; William R Brugge; Adrian C Bateman; Mollie N Carruthers; Suresh T Chari; Wah Cheuk; Lynn D Cornell; Carlos Fernandez-Del Castillo; David G Forcione; Daniel L Hamilos; Terumi Kamisawa; Satomi Kasashima; Shigeyuki Kawa; Mitsuhiro Kawano; Gregory Y Lauwers; Yasufumi Masaki; Yasuni Nakanuma; Kenji Notohara; Kazuichi Okazaki; Ji Kon Ryu; Takako Saeki; Dushyant V Sahani; Thomas C Smyrk; James R Stone; Masayuki Takahira; George J Webster; Motohisa Yamamoto; Giuseppe Zamboni; Hisanori Umehara; John H Stone (18 May 2012). "Consensus statement on the pathology of IgG4-related disease". Modern Pathology. 25: 1181–1192. doi:10.1038/modpathol.2012.72. PMID 22596100.
  3. ^ a b Arezou Khosroshahi; Zachary S. Wallace; Jayne Littlejohn Crowe; Takashi Akamizu; Atsushi Azumi; Mollie N. Carruthers; Suresh T. Chari; Emanuel Della-Torre; Luca Frulloni; Hiroshi Goto; Phillip A. Hart; Terumi Kamisawa; Shigeyuki Kawa; Mitsuhiro Kawano; Myung-Hwan Kim; Yuzo Kodama; Kensuke Kubota; Markus M Lerch; Matthias Löhr; Yasufumi Masaki; Shoko Matsui; Tsuneyo Mimori; Seiji Nakamura; Takahiro Nakazawa; Hirotaka Ohara; Kazuichi Okazaki; Jay H. Ryu; Takako Saeki; Nicolas Schleinitz; Akira Shimatsu; Tooru Shimosegawa; Hiroki Takahashi; Masayuki Takahira; Atsushi Tanaka; Mark Topazian; Hisanori Umehara; George J. Webster; Thomas E. Witzig; Motohisa Yamamoto; Wen Zhang; Tsutomu Chiba; John H. Stone (July 2015). "International Consensus Guidance Statement on the Management and Treatment of IgG4-Related Disease". Arthritis & Rheumatology. 67 (7): 1688–1699. doi:10.1002/art.39132. PMID 25809420.
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  5. ^ a b Hisanori Umehara; Kazuichi Okazaki; Yasufumi Masaki; Mitsuhiro Kawano; Motohisa Yamamoto; Takako Saeki; Shoko Matsui; Takayuki Sumida; Tsuneyo Mimori; Yoshiya Tanaka; Kazuo Tsubota; Tadashi Yoshino; Shigeyuki Kawa; Ritsuro Suzuki; Tsutomu Takegami; Naohisa Tomosugi; Nozomu Kurose; Yasuhito Ishigaki; Atsushi Azumi; Masaru Kojima; Shigeo Nakamura; Dai Inoue; The Research Program for Intractable Disease by Ministry of Health, Labor and Welfare Japan G4 team (February 2012). "A novel clinical entity, IgG4-related disease (IgG4RD): general concept and details". Modern Rheumatology. 22 (1): 1–14. doi:10.1007/s10165-011-0508-6. PMC 3278618. PMID 21881964.{{cite journal}}: CS1 maint: numeric names: authors list (link)
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  9. ^ a b Tetsuo Himi; Kenichi Takano; Motohisa Yamamoto; Yasuyoshi Naishiro; Hiroki Takahashi (February 2012). "A novel concept of Mikulicz's disease as IgG4-related disease". Auris Nasus Larynx. 39 (1): 9–17. doi:10.1016/j.anl.2011.01.023. PMID 21571468.
  10. ^ a b Yueyang Guo; David Ansdell; Sharon Brouha; Andrew Yen (January 2015). "Coronary periarteritis in a patient with multi-organ IgG4-related disease". Journal of Radiology Case Reports. 9 (1): 1–17. doi:10.3941/jrcr.v9i1.1967. PMC 4391803. PMID 25926916.
  11. ^ Mollie N. Carruthers; Eli M. Miloslavsk; John H. Stone (August 2013). "Reply to "IgG4-related pharyngitis-an addition to the nomenclature of IgG4-related disease: comment on the article by Stone et al."". Arthritis & Rheumatism. 65 (8): 2217–2218. doi:10.1002/art.37998. PMID 23666890.
  12. ^ Wah Cheuk; Fiona K Y Tam; Alice N H Chan; Ivy S C Luk; Anthony P W Yuen; Wai-Kong Chan; Terry C W Hung; John K C Chan (November 2010). "Idiopathic cervical fibrosis--a new member of IgG4-related sclerosing diseases: report of 4 cases, 1 complicated by composite lymphoma". The American Journal of Surgical Pathology. 34 (11): 1678–1685. doi:10.1097/PAS.0b013e3181f12c85. PMID 20871392.
  13. ^ Shyamal H. Mehta; Jeffrey A. Switzer; Paul Biddinger; Amyn M. Rojiani (11 February 2014). "IgG4-related leptomeningitis: a reversible cause of rapidly progressive cognitive decline". Neurology. 82 (6): 540–542. doi:10.1212/WNL.0000000000000100. PMID 24384648.
  14. ^ Terumi Kamisawa; Yuyang Tu; Naoto Egawa; Nobuhiro Sakaki; Jun-ichi Ishiwata; Kouji Tsuruta; Atsutake Okamoto; Toshio Takahashi; Morio Koike (January 2001). "Clinicopathologic study on chronic pancreatitis with diffuse irregular narrowing of the main pancreatic duct". Nippon Shokakibyo Gakkai Zasshi (in Japanese). 98 (1): 15–24. doi:10.11405/nisshoshi1964.98.15. PMID 11201120.
  15. ^ a b Dai Inoue; Yoh Zen; Hitoshi Abo; Toshifumi Gabata; Hiroshi Demachi; Jyun Yoshikawa; Shiro Miyayama; Yasuni Nakanuma; Osamu Matsui (November 2011). "Immunoglobulin G4–related Periaortitis and Periarteritis: CT Findings in 17 Patients". Radiology. 261 (2). Radiological Society of North America: 625–633. doi:10.1148/radiol.11102250. PMID 21803920.
  16. ^ a b c Verghese George; Varaha Sairam Tammisetti; Venkateswar Rao Surabhi; Alampady K. Shanbhogue (July 2013). "Chronic Fibrosing Conditions in Abdominal Imaging". RadioGraphics. 33 (4). Radiological Society of North America: 1053–1080. doi:10.1148/rg.334125081. PMID 23842972.
  17. ^ a b Bobby B Najari; Brian D Robinson; Stephen A Paget; Darius A Paduch (October 2014). "Clinical, radiographic, and pathologic description of IgG4-related perivasal fibrosis: a previously undescribed etiology of chronic orchialgia". Urology. 84 (4). Société Internationale d'Urologie: 748–750. doi:10.1016/j.urology.2014.06.035. PMID 25260440.
  18. ^ Jin Hee Kim; Jae Ho Byun; Seung Soo Lee; Hyoung Jung Kim; Moon-Gyu Lee (January 2013). "Atypical Manifestations of IgG4-Related Sclerosing Disease in the Abdomen: Imaging Findings and Pathologic Correlations". American Journal of Roentgenology. 200 (1). American Roentgen Ray Society: 102–111. doi:10.2214/AJR.12.8783. PMID 23255748.
  19. ^ Takashi Karashima; Yoshinori Taniguchi; Tsutomu Shimamoto; Tomoya Nao; Hiroshi Nishikawa; Satoshi Fukata; Masayuki Kamada; Keiji Inoue; Kentaro Oko; Hideki Nakajima; Shigetoshi Sano; Manabu Matsumoto; Naoto Kuroda; Yoshihiro Kamei; Taro Shuin (9 December 2014). "IgG4-related disease of the paratestis in a patient with Wells syndrome: a case report". Diagnostic Pathology. 9. doi:10.1186/s13000-014-0225-5. PMC 4265405. PMID 25337295. 225.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  20. ^ Hans Bösmüller; Claus Hann von Weyhern; Patrick Adam; Vedat Alibegovic; Gregor Mikuz; Falko Fend (January 2011). "Paratesticular fibrous pseudotumor--an IgG4-related disorder?". Virchows Archiv: The European Journal of Pathology. 458 (1). European Society of Pathology: 109–113. doi:10.1007/s00428-010-0995-4. PMID 20957491.
  21. ^ Yasuhito Hamaguchi; Manabu Fujimoto; Yukiyo Matsushita; Seiko Kitamura-Sawada; Mitsuhiro Kawano; Kazuhiko Takehara (2011). "IgG4-related skin disease, a mimic of angiolymphoid hyperplasia with eosinophilia". Dermatology. 223 (4). Basel: Karger Publishers: 301–305. doi:10.1159/000335372. PMID 22269779.
  22. ^ Yoshiki Tokura; Hiroaki Yagi; H. Yanaguchi; Yuta Majima; Akira Kasuya; Taisuke Ito; M Maekawa; Hideo Hashizume (November 2014). "IgG4-related skin disease". British Journal of Dermatology. 171 (5). British Association of Dermatologists: 959–967. doi:10.1111/bjd.13296. PMID 25065694.
  23. ^ Dai Inoue; Yoh Zen; Yasuharu Sato; Hitoshi Abo; Hiroshi Demachi; Akio Uchiyama; Toshifumi Gabata; Osamu Matsui (2012). "IgG4-Related Perineural Disease". International Journal of Rheumatology. 2012. doi:10.1155/2012/401890. PMC 3317227. PMID 22523496. 401890.{{cite journal}}: CS1 maint: unflagged free DOI (link)
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External links

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