Rituximab Maintenance Therapy Reduces Rate of Relapse of Pancreaticobiliary Immunoglobulin G4-related Disease

Majumder, Shounak; Mohapatra, Sonmoon; Lennon, Ryan J.; Ramos, Guilherme Piovezani; Postier, Neil; Gleeson, Ferga C.; Levy, Michael J.; Pearson, Randall K.; Petersen, Bret T.; Vege, Santhi Swaroop; Chari, Suresh T.; Topazian, Mark D.; Witzig, Thomas E.

doi:10.1016/j.cgh.2018.02.049

Cited by 56 publications

(48 citation statements)

References 14 publications

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“…Rituximab is indicated for patients with recurrent or refractory disease, levels of IgG4 decline rapidly while levels of other IgG subclasses remain stable [17,18]. Unlike IgG4related Sclerosing Cholangitis in which elevated alkaline phosphatase levels are a predictor of relapse after RTX induction therapy in the IgG4-RD, predictive marker isn't known [19,20]; on the other hand the elevation of pretreatment levels of IgG4, immunoglobulin E (IgE) and blood eosinophil concentrations independently predicted future relapses [20]. The objective of the treatment of IgG4-RD is to alleviate symptoms and prevent disease-related complications and irreversible fibrosis [21].…”

Section: Discussionmentioning

confidence: 99%

Relapsing IgG4-related orbital inflammatory pseudotumor after achieving success with rituximab

Vega-Hinojosa¹,

M²,

M³

et al. 2019

Int. J. Clin. Rheumatol

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IgG4-related disease (IgG4-RD) is a disease of fibroinflammatory with infiltration of IgG4-positive plasma cells. The lesions show focal or diffuse nodular formations in one or multiple organs; due to the infiltration of lymphocytes and plasma cells with fibrosis. The IgG4-DR is recognized as an important cause of idiopathic inflammatory disease that must be differentiated with other pathologies. The measurement of normal IgG4 levels is not enough to exclude IgG4-RD. The treatment covers the symptomatic aspect and use of systemic corticosteroids (CS), and immunomodulatory and biological therapy. The relapsing is might be misdiagnosis. We propose to consider the imaging follow-up for the therapeutic management

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Section: Discussionmentioning

confidence: 99%

Relapsing IgG4-related orbital inflammatory pseudotumor after achieving success with rituximab

Vega-Hinojosa¹,

M²,

M³

et al. 2019

Int. J. Clin. Rheumatol

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“…Klinisk erfaring tilsier at rituksimab bør tilbys pasienter som ikke tolererer eller ikke oppnår ønsket effekt av prednisolon. Dokumentasjonen for vedlikeholdsbehandling med rituksimab er sparsom (14,15). Patogenesen ved IgG4-relatert sykdom er bare delvis kartlagt, men den gode responsen på rituksimab indikerer at Blymfocytter spiller en sentral rolle.…”

Section: Diskusjonunclassified

En mann i 50-årene med magesmerter, kløe og vekttap

Bjørlykke¹,

Eftang²,

Grzyb³

et al. 2020

Tidsskriftet

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“…Among the maintenance regimens, relapses occur in the lowest proportion of patients (w10%) receiving rituximab maintenance (every 6 months). 89 Relapse occurs in 25%-35% of patients who receive lowdose steroid and immunomodulator regimens for maintenance. 90,91 High-dose steroid treatment (40 mg/d for 4 weeks, followed by taper by 5 mg/wk, until patients are off the drugs) is an acceptable regimen for prednisolone 5,92,93 ; rates of response to steroid therapy are 79%-97%, 5,92 whereas rates of relapse to the maintenance therapy are 31%-60%.…”

Section: Diagnosis and Treatmentmentioning

confidence: 99%

“…95 A retrospective study showed lower relapse with maintenance rituximab vs observation following induction with rituximab. 96 In this study, 43 patients with pancreaticobiliary IgG4-RD received rituximab, 14 received induction doses only without maintenance therapy, and 29 received induction therapy plus maintenance rituximab. Both groups were followed for similar times after treatment (34 vs 27 months).…”

Section: Diagnosis and Treatmentmentioning

confidence: 99%

Gastrointestinal and Extra-Intestinal Manifestations of IgG4–Related Disease

et al. 2018

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IgG4-related disease (IgG4-RD) is a chronic relapsing multi-organ fibro-inflammatory syndrome of presumed autoimmune etiology. It is characterized by increased serum levels of IgG4 and tissue infiltration by IgG4 cells. Increased titers of autoantibodies against a spectrum of self-antigens and response to steroids have led to its characterization as an autoimmune disease. However, the pathognomonic antigens probably differ among manifestations, and different antigens or autoantibodies produce similar immune reactions in different organs. Little is known about the pathogenic effects, if any, of serum IgG4 or IgG4 plasma cells in tissues. Despite several animal models of the disease, none truly recapitulates human IgG4-RD. Histologic analyses of tissues from patients with IgG4-RD reveal a dense lymphoplasmacytic infiltrate rich in IgG4 plasma cells, storiform fibrosis, and obliterative phlebitis, although these features vary among organs. Typical presentation and imaging findings include mass-forming synchronous or metachronous lesions in almost any organ, but most commonly in the pancreas, bile duct, retroperitoneum, kidneys, lungs, salivary and lacrimal glands, orbit, and lymph nodes. In all organs, inflammation can be reduced by corticosteroids and drugs that deplete B cells, such as rituximab. Patients with IgG4-RD have relapses that respond to primary therapy. Intense fibrosis accompanies the inflammatory response, leading to permanent organ damage and insufficiency. Death from IgG4-RD is rare. IgG4-RD is a multi-organ disease with predominant pancreatico-biliary involvement. Despite its relapsing-remitting course, patients have an excellent prognosis.

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Rituximab Maintenance Therapy Reduces Rate of Relapse of Pancreaticobiliary Immunoglobulin G4-related Disease

Cited by 56 publications

References 14 publications

Relapsing IgG4-related orbital inflammatory pseudotumor after achieving success with rituximab

Relapsing IgG4-related orbital inflammatory pseudotumor after achieving success with rituximab

En mann i 50-årene med magesmerter, kløe og vekttap

Gastrointestinal and Extra-Intestinal Manifestations of IgG4–Related Disease

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