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Copyright ©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Feb 28, 2024; 30(8): 817-832
Published online Feb 28, 2024. doi: 10.3748/wjg.v30.i8.817
Autoimmune pancreatitis: Cornerstones and future perspectives
Camilla Gallo, Giulia Dispinzieri, Pietro Invernizzi, Sara Massironi, Division of Gastroenterology and Center for Autoimmune Liver Diseases, Department of Medicine and Surgery, Fondazione IRCCS San Gerardo dei Tintori; University of Milano-Bicocca, Monza 20900, Italy
Nicola Zucchini, Department of Pathology, Fondazione IRCCS San Gerardo dei Tintori, Monza 20900, Italy
ORCID number: Camilla Gallo (0000-0002-7598-7220); Pietro Invernizzi (0000-0003-3262-1998); Sara Massironi (0000-0003-3214-8192).
Author contributions: Gallo C writing and supervising; Dispinzieri G writing; Zucchini N writing and figures editing; Massironi S coordinationg and supervising; Invernizzi P supervising.
Conflict-of-interest statement: Authors declare no conflict of interests for this article.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Sara Massironi, MD, PhD, Chief Physician, Doctor, Medical Assistant, Research Scientist, Division of Gastroenterology and Center for Autoimmune Liver Diseases, Department of Medicine and Surgery, Fondazione IRCCS San Gerardo dei Tintori; University of Milano-Bicocca, 33 Via Pergolesi, Monza 20900, Italy. sara.massironi@libero.it
Received: November 15, 2023
Peer-review started: November 15, 2023
First decision: December 15, 2023
Revised: December 18, 2023
Accepted: January 25, 2024
Article in press: January 25, 2024
Published online: February 28, 2024

Abstract

Autoimmune pancreatitis (AIP) is an autoimmune subtype of chronic pancreatitis resulting from the aberrant immune response against the pancreas, leading to inflammation and fibrosis. Although AIP is rare, its incidence is increasing and is often misdiagnosed as other pancreatic diseases. AIP is commonly classified into two types. Type 1 AIP (AIP-1) is typically associated with elevated serum immunoglobulin G4 (IgG4) levels and systemic manifestations, while type 2 AIP is typically a more localized form of the disease, and may coexist with other autoimmune disorders, especially inflammatory bowel diseases. Additionally, there is emerging recognition of a third type (type 3 AIP), which refers to immunotherapy-triggered AIP, although this classification is still gaining acceptance in medical literature. The clinical manifestations of AIP mainly include painless jaundice and weight loss. Elevated serum IgG4 levels are particularly characteristic of AIP-1. Diagnosis relies on a combination of clinical, laboratory, radiological, and histological findings, given the similarity of AIP symptoms to other pancreatic disorders. The mainstay of treatment for AIP is steroid therapy, which is effective in most cases. Severe cases might require additional imm-unosuppressive agents. This review aims to summarize the current knowledge of AIP, encompassing its epidemiology, etiology, clinical presentation, diagnosis, and treatment options. We also address the challenges and controversies in diagnosing and treating AIP, such as distinguishing it from pancreatic cancer and managing long-term treatment, highlighting the need for increased awareness and knowledge of this complex disease.

Key Words: Autoimmunity, Pancreatitis, Autoimmune pancreatitis, Immunoglobulin G4, Steroids, Relapse

Core Tip: Autoimmune pancreatitis (AIP) is rare and often misdiagnosed. The lymphoplasmacytic sclerosing form, type 1 AIP (AIP-1), represents the pancreatic manifestation of immunoglobulin G4-related disease, while the idiopathic ductal centric form, type 2 AIP (AIP-2), is often associated with inflammatory bowel disease. AIP-1 presents with obstructive jaundice or abnormalities in exocrine and endocrine pancreatic function; AIP-2 usually shows abdominal pain and acute pancreatitis. The atypical mass-forming abnormality of the pancreas implies the need to histologically distinguish AIP form pancreatic ductal adenocarcinoma. Steroids are the first-line therapy for both AIP-1 and AIP-2, rituximab is a good alternative for AIP-1. Given the high relapse rate, long-term maintenance therapy is recommended. Scientific efforts are focusing on target therapies.



INTRODUCTION
Definition

Autoimmune pancreatitis (AIP) is a relatively rare, specific form of chronic benign pancreatic disease characterized by obstructive jaundice, with or without pancreatic masses, histologic evidence of a specific lymphoplasmacytic infiltrate and fibrosis, and a dramatic response to steroid therapy[1].

Two main forms of AIP have been described: Type 1 AIP (AIP-1), known as lymphoplasmacytic sclerosing pancreatitis, and type 2 AIP (AIP-2), known as idiopathic ductal centric pancreatitis[2], which differ mainly in epidemiology, patho-genesis, clinical presentation, histologic pattern, and natural history.

AIP-1 predominantly affects men in their sixth to seventh decade of life, and is usually painless, although mild epigastric pain may occur in about one third of patients[3]. It represents the pancreatic manifestation of immunoglobulin G4 (IgG4)-related disease (IgG4-RD), a rare, immune-mediated, systemic fibro-inflammatory multi-organ disease that often determines the growth of inflammatory pseudotumors in the affected organs. IgG4-RD usually affects two or more organs, with AIP-1 and IgG4-related cholangitis (IRC) being the most common manifestations (45% of cases overall). However, other possible typical localizations of the disease include retroperitoneal fibrosis, sialadenitis and dacryoadenitis (Mikulicz disease), Riedel’s thyroiditis, mediastinal lymphadenopathy, aortic and/or renal involvement, and interstitial lung disease[4]. Based on the distribution of organ involvement, four characteristic IgG4-RD phenotypes can be distinguished: Pancreatic-hepatobiliary disease, which is the most common; retroperitoneal fibrosis and/or aortitis; disease confined to the head and neck; Mikulicz syndrome with systemic involvement[5]. IgG4-RD is characterized by the following histologic features: lymphoplasmacytic infiltrates rich in IgG4+ plasma cells [> 10 per high-power field (HPF)], storiform fibrosis, and obliterative phlebitis. Circulating IgG4 levels may vary, but the ratio of circulating IgG4 to IgG levels is typically > 10%[6].

AIP-2 usually affects younger subjects without sex differences. It manifests as acute symptomatic pancreatitis, with specific involvement of a single organ. AIP-2 is caused by dysimmune fibro-inflammatory infiltration of the middle and small pancreatic ducts (PDs) and pancreatic acini, leading to the formation of pathognomonic granulocytic epithelial lesions (GELs)[7]. In 15%-30% of cases, AIP-2 is associated with inflammatory bowel disease (IBD), typically ulcerative colitis (UC). For this reason, anti-neutrophil cytoplasmic antibodies (p-ANCA and c-ANCA) can often be detected in patients with AIP-2[8], although no specific serological markers are currently available: Serum IgG4 Levels are usually normal or only slightly elevated.

A third type of AIP has recently been described: Type 3 AIP (AIP-3) is a mostly asymptomatic or rarely pauci-symptomatic form of pancreatic injury that exclusively affects patients with advanced malignancies. It is an iatrogenic entity caused by a non-specific, inflammatory T-cell mediated immune response against PDs and acini, triggered by immune checkpoint inhibitors (often anti-PD-1 and anti-CTLA4). The disease typically occurs 4-6 months, rarely more than 12 months, after the start of therapy. It is not characterized by pathognomonic histopathologic lesions, and it is usually seronegative, although elevated IgG4 levels have been occasionally described[9].

Epidemiology

Few data are available on the overall prevalence and incidence of AIPs. Among the possible immune-mediated pancreatic disorders, AIP-1 is the most common and accounts for the vast majority of cases[10]; it is more common in Asia than in the United States and European Union[11]. Regarding AIP-1, thanks to the increasing awareness of IgG4-RD and the dissemination of diagnostic guidelines, large-scale epidemiological data have recently been published, mainly from Japan. According to a nationwide epidemiological survey conducted in 2016, AIP-1 showed an incidence of 1-3 cases per 100,000 adults and a prevalence of approximately 10 cases per 100000 adults; compared with previously published data, these results have more than doubled in less than 5 years. The reported male-to-female sex ratio was 2.94:1, and the mean age at diagnosis was 64.8 years[12]. The first raw data published in Italy showed that AIP-1 affects approximately 6% of the general population, and accounts for 61% of AIP cases[3].

On the other hand, AIP-2 is more prevalent in Western countries than in Asia[13], with an estimated prevalence rate of 4.6–6% in acute and chronic pancreatitis and about 1-4 cases per 100000 adults in the general population[2-14]. Only two Asian studies investigated the epidemiology of AIP-2 in IBD patients and reported a prevalence of 0.3%-0.5%[15,16], which is approximately 100-fold higher than in the general population, and may even be underestimated due to the difficulty of diagnosing AIP-2, which often requires histological confirmation. On the other hand, 49%-67% of AIP-2 patients have concomitant IBD, which means that AIP-2 patients have a 12-15-fold higher risk of having a concurrent IBD compared to the general population[17]. According to an Italian multicenter study, AIP-2 accounts for 28% of all AIP cases. Compared to AIP-1, younger people are more likely to be affected, with no significant gender difference between men and women[3].

According to a recent American review on AIP-3, the incidence of AIP-3 among all immune-mediated adverse events with immune checkpoint inhibitors is between 0.6% and 4%[9].

Etiopathogenesis

Despite numerous attempts, the pathogenesis of AIP-1 is still unclear. As it is the pancreatic manifestation of IgG4-RD, it is a multifactorial disease in which both genetic and environmental factors play a pivotal role. Genome-wide association studies in IgG4-RD-affected patients revealed a significant association between mutations in human leukocyte antigen DRB1 genes encoding macrophage-type toll-like receptors (TLRs) II major histocompatibility complex (MHC)[4]. The overexpression of certain types of TLRs in the pancreas highlights the central role of the innate immune system in the development of AIP-1. Plasmacytoid dendritic cells (pDCs) may also play a key role in the pathogenesis of AIP: They are involved in host defense against microbial infections and are the major source of type 1 interferons (IFN-I)[18]. The unregulated production of IFN-I and, consequently, of interleukine (IL)-33 by pDCs could underlie AIP-1. IL-33, which is also produced by overexpression of certain types of TLRs, may promote activation of mainly Th2 cells and regulatory T cells that produce IL-4 and IL-10, respectively, which in turn are responsible for switching immunoglobulins to the IgG4 subclass[19]. The role of IgG4 in the development of AIP-1 and IgG4- RD is still unclear, but it is hypothesized that IgG4 may play a role in the activation of the complement system after the presence of immune complexes has been demonstrated in IgG4-RD-affected tissues[20].

In addition to the activation of T helper and T reg CD4+ lymphocytes that follows the interaction between TLRs and MHC-II, also the interaction between T follicular helper (Tfh) cells, especially circulating type 1 Tfh cells, and SLAMF7, a member of the Signaling Lymphocyte Activation Molecule family receptors, promotes IgG4 release[21]. SLAMF7 is implicated in homotypic interactions with activated B cells and, thus, it is involved in disease immunopathogenesis. SLAMF7+ CD4+ cytotoxic T cells (CTLs) are unusual CD4+ cells, which have been shown to express cytotoxic mediators that are typically expressed by CD8+ cells, and have been shown to have the potential to both stimulate fibroblast activation and interact with antigen-presenting B cells[22]. Recent studies have shown that SLAMF7+ CD4+ CTLs are increased in the peripheral blood of subjects with active IgG4-RD, and thus represent a key pathological factor in the disease[23].

Furthermore, cellular components that form the fibro-inflammatory pancreatic aggregate include eosinophils, which are attracted to the pancreatic site primarily by the chemotactic action of eotaxin. It is noteworthy that elevated levels of circulating eotaxin-1 and 3 have been detected in AIP-1 patients[24]. The presence of elevated levels of circulating IgE and IgG4 in IgG4-RD and AIP-1 and the presence of eosinophilic infiltrates in the pancreas suggest that, in addition to genetic predisposition, environmental factors play an important role in the development of AIP-1. Prolonged exposure to certain exogenous antigens and molecular mimicry between these antigens and some autoantigens may lead to overactivity of specific types of TLRs that trigger a dysimmune response directed against the endogenous autoantigens[4].

Regarding the pathogenesis of AIP-2, the Th-17 subset of CD4+ effector T cells plays a crucial role in infiltrating the periductal pancreatic tissue, where they release inflammatory cytokines, mainly IL-17, IL-21, IL-22, and IL-23[25]. The reasons leading to this hyperactivation of Th-17 cells and their migration into pancreatic tissue are not yet clear. However, there may be a link with genetic mutations in the genes for multiple endocrine neoplasia 1 and polycystic kidney and liver disease 1, which are frequently found in AIP-2 patients[26]. Moreover, the pathognomonic AIP-2 GELs consist not only of lymphocytes but mainly of neutrophils that migrate and aggregate in the periductal pancreatic tissue, attracted by the chemotactic function of IL-8, which in turn is stimulated by IL-17[27]. IL-8 was overexpressed not only in AIP-2 cases but also in UC patients, suggesting that it is an immunological biomarker for the coincidence of AIP-2 and UC[28].

The increasing awareness of the relationship between specific alterations in the composition of the gut microbiota and the innate immunological response, and thus the development of autoimmune diseases, led to the hypothesis of a possible role of the microbiota in the etiopathogenesis of AIP, particularly K. Pneumoniae[29]. This possible gut-pancreas axis could apply not only to AIP-2, for which the correlation data between IBD and changes in the gut microbiota are strong but also to AIP-1[30].

Finally, the etiopathogenesis of AIP-3 is closely related to the administration of checkpoint inhibitors, which trigger a non-specific inflammatory immune response mediated by T cells, mainly CD8+ T cells, resulting in an increased ratio of CD8+/CD4+ T lymphocytes[31,32]. In Figure 1, a concise overview of the etiopathogenetic mechanisms underlying AIP-1, AIP-2, and AIP-3 is provided.

Figure 1
Figure 1 Ethiopathology of different types of autoimmune pancreatitis. Ethiopathological mechanisms of type 1 autoimmune pancreatitis, type 2 autoimmune pancreatitis, and type 3 autoimmune pancreatitis. AIP: Autoimmune pancreatitis; IFN: Interferon; IL: Interleukine; TLRs: Toll-like receptors; pDCs: Plasmacytoid dendritic cells; IgG4: Immunoglobulin G4; AIP-1: Type 1 autoimmune pancreatitis; AIP-2: Type 2 autoimmune pancreatitis; AIP-4: Type 3 autoimmune pancreatitis.
CLINICAL AND SEROLOGICAL FEATURES

The two main forms of AIP described, AIP-1 and AIP-2, have two distinct clinical phenotypes. AIP-1 occurs mainly in older men and is usually painless. According to an international multicenter study, the most common symptom is obstructive jaundice, which occurs in 75% of cases[10] and is thought to be due to compression of the common bile duct by the mass/swelling of the pancreatic head or by direct infiltration of biliary wall with lymphocytes and plasma cells[33]. Less commonly, AIP-1 manifests with abdominal symptoms (in nearly 40% of patients), such as abdominal pain or malaise, and more rarely with acute pancreatitis. Other clinical manifestations include weight loss and abnormalities of exocrine and endocrine pancreatic function, with diabetes mellitus that may occur before (33%), concurrently (52%), or after steroid treatment[6]. It may also manifest as diffuse, focal, or segmental enlargement of the pancreas, mimicking PD adenocarcinoma (PDAC), from which it must be differentiated. As it is the pancreatic manifestation of IgG4-RD, AIP-1 usually occurs with the involvement of other organs, such as biliary stricture, renal involvement, orbital pseudotumor, extensive lymphadenopathy, and retroperitoneal fibrosis. The most common clinical presentation of IgG4-RD sees the involvement of the bilio-pancreatic district, such that AIP-1 and IRC occur together in 80% of cases. It should be noted that although the involvement of other organs supports the diagnosis of AIP, the absence of involvement of other organs does not exclude AIP-1, and isolated pancreatic involvement is seen in approximately 50% of patients[34]. IgG4-RD is a multisystemic fibroinflammatory disease characterized by elevated serum concentration of IgG4 and accumulation of IgG4-expressing plasma cells in the affected organs[35]. However, serum IgG4 plays an increasingly minor role in the diagnosis of AIP-1 and IgG4-RD. Recent studies have shown that up to half of patients with biopsy-proven and clinically active IgG4-RD may have normal serum IgG4 concentrations[36]. Furthermore, only 10% of patients with elevated serum IgG4 levels were diagnosed with IgG4-RD, underscoring the lack of specificity of this test[37].

While AIP-1 has a mostly asymptomatic clinical course, AIP-2 manifests more frequently with abdominal pain and acute pancreatitis. Acute pancreatitis occurs in nearly 50% of patients[28]. Other manifestations include painless ob-structive jaundice, focal pancreatic masses, and symptomatic PD strictures[38], similar to AIP-1 patients. Compared with AIP-1, AIP-2 typically affects younger patients, with an average age of 40 years, and has no gender predilection. Although AIP-2 can also occur with exclusive pancreatic involvement, a strong association between AIP-2 and concurrent IBD, especially UC, has been reported, as mentioned previously[17]. In most cases, the diagnosis of IBD precedes the diagnosis of AIP-2, but it is unclear whether active IBD plays a role in the development of AIP-2. According to an Italian retrospective study at IBD-AIP, 68% of patients had a prior or concomitant diagnosis of UC, but only 44% had active disease[39]. However, a French study with a similar group of patients shows that 80% of patients had a previous or concomitant diagnosis of IBD, and about 70% had active disease at the onset of AIP[40]. Table 1 resembles the differential characteristics between AIP-1 and AIP-2.

Table 1 Differential characteristics between type 1 and type 2 autoimmune pancreatitis.

AIP-1
AIP-2
Gender (M:F)3:11:1
Mean age at disease onset60-70 yr40-60 yr
EpidemiologyAsia > Western CountriesWestern Countries > Asia
Main clinical manifestationsPainless jaundice (75%); Abdominal symptoms (40%)Abdominal pain and acute pancreatitis (50%)
Weight loss
Diabetes and exocrine pancreatic insufficiency
Extrapancreatic manifestationsIgG4-related disease extrapancreatic manifestations (50%)IBD (49%-67%)
Hepatobiliary disease
Retroperitoneal fibrosis and/or aortitis
Head and neck involvement
Mikulicz syndrome
Serum IgG4 levelsElevated (circulating IgG4 to IgG levels typically > 10%) (50%)Normal (p-ANCA and c-ANCA autoantibodies often positive)
Histologic featuresLymphoplasmacytic infiltrates rich in IgG4+ plasma cellsGranulocytic epithelial lesions
Storiform fibrosis
Obliterative phlebitis
Steroid therapyResponsiveResponsive
RelapseHigh rate (39%)Rare
RADIOLOGICAL PRESENTATION

Contrast-enhanced (CE)-computed tomography (CT) and magnetic resonance imaging (MR) (MRI) have proven useful in the imaging diagnosis of AIP. Imaging abnormalities of the pancreas are virtually indistinguishable between AIP-1, AIP-2, and AIP-3[9,41]. The differential diagnosis between these three different nosographic entities is mainly based on the combination of history, clinical presentation, histopathologic findings, and, in the case of IgG4-RD-involvement of the pancreas, the possible presence of combined characteristic radiologic findings reflecting coexisting pathologies in other affected organs[42]. Furthermore, CE-CT and MRI scans do not always allow a correct differential diagnosis between mass-forming AIP and PDAC, which is challenging because of their common epidemiologic and clinical manifestations[43].

Typical CT features of AIP include focal or diffuse sausage-like swellings of the parenchyma with straight margins, rectangular shape of the tail (cut-tail sign), and consequent loss of the typical lobular structure[44] (Figure 2). An exception is elderly patients, in whom the age-related reduction in pancreatic volume may mask the presence of inflammatory swelling of the organ[45].

Figure 2
Figure 2 Radiological appearance of autoimmune pancreatitis-part 1. A: Unenhanced computed tomography scan appearance of a diffuse autoimmune pancreatitis (AIP): Sausage-like swelling of the parenchyma, with straight margins, and consequent loss of the typical lobular structure. A hypodense fibrotic capsule-like rim demarcates the swollen pancreas (blue arrow); B: Unenhanced T1 weighted magnetic resonance imaging (MRI) appearance of a diffuse AIP: Sausage-like swelling of the parenchyma, with straight margins, and rectangular shape of the tail (cut-tail sign) (orange arrow); C: Arterial phase of the contrast-enhanced T1 weighted MRI: Homogeneous reduced enhancement of the pancreatic parenchyma, with a more hypointense fibrotic capsule-like rim that demarcates the swollen pancreas (orange arrow).

Due to the presence of fibrosis, the arterial or pancreatic phase of the CE-CT scan typically shows a homogeneous reduced enhancement of the affected areas compared with the normal pancreatic parenchyma, whereas a gradually increasing enhancement is detectable in the delayed phases of the dynamic scan[46,47]. Small areas of normal pancreatic parenchyma may remain focal in association with the affected lesions: such areas maintain normal arterial blood flow and may therefore be visualized as punctate, speckled, or dotted contrast enhancement in the arterial phase[45]. These findings help to distinguish AIP from PDAC[48].

As a result of the physio-pathological accumulation of the fibrotic component at the periphery of the inflammatory areas (be it the pancreas as a whole or the intrapancreatic pseudotumor lesions), a capsular rim demarcates the swollen pancreas and/or the pseudotumoral affected areas, with a typical reduced enhancement in the arterial phase and a progressively increasing enhancement in the delayed phases[49]. PDAC may sometimes have a peripheral rim, but unlike the rim detectable in AIP, it is usually early enhanced in the arterial phase[50]; therefore, the CE behavior of the perilesional rim of AIP with mass-forming AIP may help distinguish AIP from PDAC.

As a consequence of inflammatory involvement of the main PD (MPD), the arterial phase of the CE-CT scan may show a marked hyperdense demarcation of the MPD walls, which are often also thickened (enhanced duct sign)[51].

In particular, the capsular rim and thickened and hyper-enhanced MPD are usually less common in AIP-2, but these differences are not sufficient to make a differential diagnosis with AIP-1 based on radiologic presentation alone[41].

The typical appearance of AIP at CE-MRI is characterized by a diffuse or focal signal of lower intensity on unenhanced T1-weighted MRI images, with an even more hypointense signal in line with the border delineating the entire pancreas or the affected pseudotumoral areas, which are heavily composed of fibrosis. On T2-weighted images, the areas affected by AIP show moderately higher signal intensity, still demarcated by a low-intensity fibrotic rim (Figure 3). The contrastographic behavior of AIP on MRI is the same as that described for CE-CT (Figure 2)[46,47].

Figure 3
Figure 3 Radiological appearance of autoimmune pancreatitis-part 2. A: Unenhanced T1 weighted magnetic resonance imaging (MRI) images of autoimmune pancreatitis (AIP): Diffuse hypointense pancreas, with an even more hypointense fibrotic capsule-rim; B: Unenhanced T2 weighted MRI images of diffuse AIP: The affected parenchyma shows a moderately higher intensity signal, with a persistently low-intensity fibrotic rim.

On diffusion-weighted images, the presence of highly cellular plasmocyte proliferation is reflected in a homogeneously hyperintense signal of the affected areas, with the mean apparent diffusion coefficient of the lesions being significantly lower in mass-forming AIP than in PDAC[52-54].

Magnetic resonance cholangiopancreatography images show typical multiple and long MPD skip narrowings without upstream dilatation but with prominent side branches of the PD[55], producing a characteristic radiological sign (icicle sign). In the case of mass-forming AIP, the MPD may penetrate the lesion without complete occlusion (the sign of ductal penetration)[56].

MR elastography results vary considerably depending on the pathological phases of AIP: Recent edematous inflammation is associated with lower stiffness values, whereas chronic fibrotic inflammation is associated with higher stiffness values. However, AIP is generally associated with lower median pancreatic stiffness values than PDAC[57,58].

Concerning the MRI differential diagnosis between mass-forming AIP and PDAC, a multicenter nationwide study highlighted the following features of AIP as the most reliable among all those mentioned above: The presence of long and multiple MPD strictures, the absence of upstream dilatation of the stricture, and the detection of PD side branches originating from a strictured segment (sensitivity 44%-71%, specificity 92%-P < 0.05)[50]. According to a recent Korean meta-analysis, the absence of MPD dilation has the highest pooled sensitivity (87%, 95%CI = 68%-96%), whereas the presence of a peripancreatic rim has the highest pooled specificity (100%, 95%CI = 88%-100%) in distinguishing the two diseases[43].

According to the results of a recent comparative meta-analysis between CT and MRI in terms of diagnostic accuracy in AIP, MRI had significantly higher summary sensitivity than CT (84% vs 59%, P = 0.02) but similar specificity (97% vs 99%, P = 0.18). In the subgroup analysis for mass-forming AIP, sensitivity for discriminating between mass-forming AIP and PDAC was higher for MRI than CT (76% vs 50%, P = 0.28), but specificity was similar for both methods (97% vs 98%, P = 0.07)[59].

On 18F-fluorodeoxyglucose (FDG) positron emission tomography (PET)-CT, AIP usually shows markedly increased diffuse uptake, which is different from the typical focal PDAC uptake[60]. Some other 18F-FDG parameters, including the SUVmax ratio between the pancreatic lesion and liver and uptake outside the pancreas in other organs, might help to distinguish the two diseases. Indeed, the SUVmax ratio between the pancreas and liver in delayed scans is usually higher in PDAC. On the contrary, the presence of increased uptake in the salivary glands, prostate (with a typical "V" shape), and mediastinal, hilar, and para-pancreatic lymph nodes are likely concomitant signs of IgG4- RD with pancreatic involvement[61,62].

Furthermore, since fibrosis is an important feature of IgG4-RD, 68Ga-fibroblast activation protein inhibitor-PET, which uses a recently introduced agent targeting fibroblast activation protein, proved to have high sensitivity in detecting IgG4-related pancreatic, biliary and lacrimal gland involvement, with significantly higher uptake than 18F-FDG-PET[63].

According to a very recent study focusing on the radiological appearance of AIP-3[32], it is consistently associated with acinar injury and pancreatic volume loss. The parenchymal loss is directly proportional to pancreatic enzyme elevation: higher pancreatic enzymes correspond to major parenchymal loss, while near-normal pancreatic enzymes are associated with near-normal radiological pancreatic aspect. These distinct radiological features suggest AIP-3 to be sustained by a novel mechanism of chronic pancreatic injury.

ENDOSCOPIC ULTRASOUND PRESENTATION AND ENDOSCOPIC ULTRASOUND-GUIDED TISSUE SAMPLING

In the complex scenario of AIP diagnosis, the role of endoscopic ultrasound (EUS) so far can be seen mainly in its ability to biopsy the affected pancreatic parenchyma and thus make a definite AIP diagnosis, which is also different from PDAC. The endoscopic approach of first choice for obtaining pancreatic specimens for histopathological evaluation should be EUS fine-needle biopsy (FNB): According to a recent meta-analysis, FNB needles seem to be more accurate than fine-needle aspiration (FNA) needles in diagnosing AIP, as they guarantee a core biopsy[64,65]. However, the diagnosis of AIP is challenging, even by using EUS and FNA/FNB. The sonographic and cross-sectional findings of AIP closely mimic PDAC, and tissue sampling techniques for diagnosis of AIP still remain suboptimal[66]. Although the diagnostic consistency of histologic diagnosis of type 1 AIP based on the findings obtained by an EUS-guided FNA/FNB is feasible, it remains a challenge and not conclusive[67].

The main EUS findings may be divided into diffuse and focal pictures of AIP. EUS characteristics suggestive of diffuse AIP included diffuse pancreatic enlargement with echo-poor echo texture, hyperechoic foci/stands or lobularity (parenchymal heterogeneity), loss of connection to the splenic vein, hyperechoic MPD walls thickening and peripancreatic hypoechoic margin; stones and cysts similar to those described in chronic alcoholic pancreatitis may occur in the late stages of AIP. In mass-forming AIP, EUS features included focal hypoechoic mass, absence of parenchymal heterogeneity, eventually PD dilation, and vessel involvement. In a recent retrospective study, these pictures were used to construct a prediction diagnostic model, that showed an area under the receiver operating characteristic curve of more than 0.95, with a good capability to distinguish focal AIP from PDAC. By using the optimal cutoff value, the efficacy of the model for diagnosing PDAC showed 83.7%-91.8% sensitivity and 93.3%-95.6% specificity[68]. It is likely that the use of EUS-based convolutional neural networks can help, showing in a recent study, a sensitivity of 99% and a specificity of 98% for distinguishing AIP from normal pancreas, a sensitivity of 94% and a specificity of 71% for distinguishing AIP from chronic pancreatitis, and a sensitivity of 90% and a specificity of 93% for distinguishing AIP from PDAC[66].

EUS elastography may show increased stiffness of the parenchyma. EUS is extremely useful in detecting other typical findings of IgG4- RD AIP, such as changes in the common bile duct and lymphoadenomegaly (Figure 4)[69].

Figure 4
Figure 4 Endoscopic ultrasound appearance of autoimmune pancreatitis. Endoscopic ultrasound aspect of a mass-forming autoimmune pancreatitis: Solitary, irregular hypoechoic mass, located in the head of the pancreas, without upstream dilatation of the main pancreatic duct.

Finally, regarding the natural history of the disease, the typical picture of AIP described above usually improves after steroid treatment: the swelling of the pancreas decreases, the capsular rim disappears, the multiple MPD stenoses improve, and the enhanced duct sign also disappears. Nevertheless, the global CE of the previously affected parenchyma may not completely normalize[54,70]. Table 2 resembles the main radiological features of AIP.

Table 2 Main radiological features of autoimmune pancreatitis.
CT scanDiffuse or focal sausage-like swelling
Cut-tail sign
Homogeneous reduced enhancement with dotted contrast enhancements of normal parenchyma
Hypo-enhanced capsule-like rim with delayed enhancement
Thickened hyperdense MPD walls
MRIDiffuse or focal lower intensity signal on T1-weighted MRI images, with an even more hypointense capsule-rim
Moderately higher intensity signal on T2-weighted images, still with a low-intensity fibrotic rim
DWI homogeneously hyperintensity
MRCPMultiple and long MPD skip narrowings
No upstream dilatation
Side PD branches (icicle sign)
Duct-penetrating sign, in case of mass-forming AIP
18F-FDG PET-CTDiffused or focal increased uptake
EUSDiffuse pancreatic enlargement, with echopoor echotexture, loss of interface with the splenic vein, concomitant intraparenchymal hyperechoic foci and strands
Hyperechoic MPD walls
Solitary, irregular, hypoechoic mass, in case of mass-forming AIP, generally in the head of the pancreas, without upstream dilatation of the MPD
ElastographyMagnified parenchymal stiffness
HISTOPATHOLOGICAL CHARACTERISTICS

The main morpho-histological features of AIP-1 are dense lymphoplasmacytic infiltrate of the affected areas, distributed mainly lobule-centered but sometimes involving the periductal areas with a resulting slit-like obstruction of the PD; storiform fibrosis composed of spindle-shaped cells and inflammatory cells on a background of delicate collagen; luminal obliteration of the interlobular vein by the lymphoplasmacytic infiltrate, forming obliterative phlebitis. Interobserver variability in the interpretation of storiform fibrosis and obliterative phlebitis is not negligible; additional elastic staining, such as Elastica van Gieson staining, should be considered because it may help reduce interobserver variability[71]. In contrast to the findings typical of AIP-2, organs affected by AIP-1 do not usually show neutrophilic infiltration or abscess formation.

In addition to these typical morphologic features, which have historically been the primary histologic diagnostic criteria for AIP-1, biopsy or resection specimens of AIP-1 exhibit a highly pathognomonic immunohistochemical pattern: Diffuse and massive IgG4+ plasma cell infiltration with > 10 per HPF in biopsy specimens and > 50 per HPF in surgical specimens. For diagnostic purposes, to date, minimally invasive small biopsies have largely replaced surgical resections, and although this development is an achievement for the field, it represents a major challenge for the surgical pathologist. In fact, according to recent studies, around one-half of all small biopsies do not usually meet the pathological criteria for IgG4-RD, being the lack of both storiform-type fibrosis and obliterative phlebitis the most common reason for diagnostic failure. However, despite the lower pathological quality of biopsy samples, which is mainly due to their smaller size, the IgG4/total IgG ratio on biopsy samples proved the same high diagnostic accuracy when compared to the one on resection specimens. Immunohistochemistry (IHC) for IgG4 and total IgG, and the evaluation of IgG4/total IgG ratio is thus mandatory for IgG4-RD diagnosis, being it the most sensitive tissue-based feature of IgG4-RD[72]. According to a recent meta-analysis, in fact, the use of IHC for IgG4 in the diagnosis of AIP-1 has a sensitivity and specificity of approximately 70% and 92%, respectively[73].

Although the IgG4/total IgG ratio is emphasized in most diagnostic algorithms, the optimal cutoff has not yet been shared univocally; to date, most studies have utilized a cutoff ranging from 30% to 40% with a higher cutoff corresponding to higher specificity, but proportionally lower sensitivity[74,75].

Of note, treatment can interfere with histological findings and cell counts; on the other hand, also prolonged disease can lead to possible false negative immunohistochemical patterns.

Currently, there are no specific serological markers for AIP-2, so the diagnosis is made based on histology[7]. AIP-2 is characterized by a large inflammatory infiltrate in the pancreas composed mainly of neutrophils but also containing lymphocytes and plasma cells. This inflammation occurs primarily in the PD area, where it forms structures known as GELs[7,76]. AIP-2 can also cause clusters of neutrophils to form inside the ducts. Unlike AIP-1, which is characterized by obliterative phlebitis and storiform fibrosis, these features are less common in AIP-2. In addition, the number of IgG4+ plasma cells is usually not significantly increased in AIP-2, although small pockets of these cells may be present[74].

The absence of established histologic patterns for AIP-3 raises questions about its categorization, even if it is important to consider that the field of AIP is still evolving, and our understanding of the disease continues to expand. Therefore, at this stage, referring to this subtype as AIP-3 allows for the recognition of a distinct subgroup within the spectrum of AIP, even in the absence of well-defined histologic patterns. However, it is crucial to continue research efforts to establish clearer diagnostic criteria and classification systems for AIP-3 and other potential subtypes to improve the accuracy of diagnosis and guide appropriate treatment strategies. Figure 5 Histological samples of AIP-1.

Figure 5
Figure 5 Histology of autoimmune pancreatitis. A: Histological samples of type 1 autoimmune pancreatitis. Hematoxylin eosin (HE) 4, Duct centric lymphoplasmacytic infiltrate; B: HE 10, storiform fibrosis with intense lymphoplasmacytic infiltrate and obliterative phlebitis (arrow); C: HE 4, lobule complete effacement by inflammatory cells and fibrosis; D: Immunoglobulin G4 (IgG4) IIC 20, moderate increase of IgG4+ plasma cells.
DIAGNOSIS

According to the International Consensus Diagnostic Criteria for AIP, a definitive diagnosis of AIP-1 can be made in diffuse pancreatitis based on clinical, radiological, and serological features. In the presence of atypical mass-forming imaging and concomitant absence of other diagnostic criteria (mainly IgG4-RD extrapancreatic involvement or elevated IgG4+ plasma cells count), histologic evaluation by surgical or EUS-FNB tissue sampling is mandatory to make the definitive diagnosis and differentiate AIP from PDAC. In the latter scenario, the AIP-1 diagnosis can be definitively established if three or more of the following four histologic features are present: lymphoplasmacytic cell infiltration, > 10 per HPF IgG4+ plasma cells (in case of biopsy sampling, otherwise > 50 per HPF in case of surgical specimen), storiform fibrosis, or obliterative phlebitis. In the presence of fewer than three of these histologic features, increased plasma IgG4 cell counts, along with typical imaging features, may help determine the diagnosis: (1) Serum IgG4 level has proven to be a valuable tool in the diagnosis of AIP and it is one of the five cardinal features of Mayo's HISORt criteria for the diagnosis of AIP-1[77], which are based on 5 main diagnostic criteria: Histologic findings, imaging, serology, involvement of other organs, and response to steroid therapy. Indeed, in most cases, AIP patients exhibit significantly elevated levels of serum IgG4, typically exceeding a defined threshold of 135 mg/dL. However, it is important to note that elevated IgG4 levels alone are not sufficient for an AIP diagnosis, as they may also be observed in other conditions, such as IgG4-RD involving multiple organ systems. Therefore, a comprehensive diagnostic approach combining clinical presentation, radiologic imaging, serologic markers (including IgG4 levels), and histopathologic evaluation is critical for accurate diagnosis and differentiation of AIP from mimicking diseases.

With the exact purpose of excluding disease mimics, in 2019 the ACR/EULAR diagnostic criteria were developed. They consist of a three-step classification process: first, at least one of 11 possible organs must be involved in a manner consistent with IgG4-RD; second, 32 clinical, serological, radiological, and pathological exclusion criteria must be verified; third, eight weighted inclusion criteria domains, addressing clinical findings, serological results, radiological assessments, and pathological interpretations, have to be applied. A case meets the classification criteria for IgG4-RD if the entry criteria are met, no exclusion criteria are present, and the total points is ≥ 20[5].

In the case of an uncertain histologic diagnosis, systems for grading the likelihood of AIP (highly suggestive, probable, inconclusive) based on various combinations of features have been proposed, but they remain to be clinically validated[78-81]. A biopsy showing little or no evidence of AIP cannot exclude AIP with certainty unless a positive alternative diagnosis can be made[75].

Ongoing research in the field of AIP is investigating potential future markers for diagnosis. These markers include subclass analysis of IgG4, serum cytokines [such as IL-6 and tumor necrosis factor (TNF)-alpha], serum microRNAs (e.g., miR-21 and miR-375), autoantibodies targeting pancreatic antigens and advanced imaging techniques (e.g., EUS and MRI). However, further research is needed to validate their clinical utility in routine AIP diagnosis. Integration of these markers with existing diagnostic criteria may improve accuracy in diagnosing AIP.

Definitive AIP-2 diagnosis is histologic and requires the presence of GELs; lobular neutrophil infiltration strengthens the diagnosis[41].

AIP-3 can be diagnosed in the presence of a compatible drug history and by excluding other causes of pancreatitis.

INDUCTION THERAPY FOR AIP

According to recent literature data, approximately 25% of cases of AIP show spontaneous resolution of symptoms without medical treatment, with some case series reporting resolution rates up to 55%[82]. Nevertheless, experts from different countries have proposed detailed treatment criteria for acute AIP. A consensus statement published in 2016 stated that therapy is recommended for symptomatic disease (abdominal pain, back pain, fever, obstructive jaundice) or in the case of AIP-1, for asymptomatic patients with persistent pancreatic mass on imaging or persistent liver test abnormalities in case of concomitant IRC[82]. In addition to the above criteria, following the latest United European Gastroenterology (UEG) recommendations, treatment is indicated for subclinical conditions that may lead to severe or irreversible organ failure[75].

Steroids are the first-line therapy for patients with active AIP-1 and 2[75,82]. They inhibit dendritic cell maturation and downstream signal transduction of TLRs; they also inhibit the expression of many proinflammatory cytokines involved in AIP pathogenesis. Based on UEG and Swedish Society of Gastroenterology recommendations, the initial dose of prednisone should be 0.6-0.8 mg/kg per day (typically 30-40 mg/d). The treatment duration at the full dose is one month, with an initial assessment of response to treatment approximately 2 wk after initiation (especially in cases of a diagnostic steroid study). Thereafter, treatment should be gradually tapered by 5 mg/wk to a maintenance dose of 2.5-5 mg/d over 2-3 months[83].

Up to 97%-100% of AIP, patients respond to steroid treatment[84,85]. Clinical complete remission is defined as the disappearance of symptoms, normalization of IgG or IgG4 serum levels, and disappearance of typical AIP features on imaging, i.e., mainly shrinkage of the enlarged pancreatic parenchyma and regression of the narrowing of the multistrictured MPD. Incomplete remission is achieved only when one or 2 of these 3 categories are met. Imaging response to steroids is an optional diagnostic criterion, as mentioned earlier. In a small proportion of cases, AIP patients do not show any steroid response[84,85]. Furthermore, some comorbidities may contraindicate long-term steroid treatment[86]. In such cases, rituximab, a monoclonal antibody directed against CD20 B-cell-specific antigen, is the second-line good alternative therapeutic choice for acute AIP-1[75,87], whether monotherapy with immunomodulators (such as azathioprine, 6-mercaptopurine, mycophenolate mofetil, cyclosporine A, tacrolimus, methotrexate, and cyclophosphamide) did not prove sufficient efficacy, but reliable data specifically on AIP-2 are lacking[88].

If rituximab therapy is required for induction remission, the most common regimen includes 1 g of intravenous rituximab on days 0 and 14[75], and it has been shown to guarantee complete remission in up to 83% of patients[89,90]. On the other hand, given their low efficacy as monotherapy, immunomodulators steroid-sparing agents are used mainly in combination with low-dose steroids in steroid-refractory conditions[91].

Minipulse steroid therapy (two administrations of methylprednisolone 500 mg/day for three days with an interval of four days) was described in several Japanese protocols[92].

Specifically concerning AIP-2, colchicine has recently been reported to be a successful treatment option: it inhibits neutrophils and thus reduces the formation of the pathognomonic GELs[93]. There is also emerging evidence suggesting the potential use of biologic medications in the treatment of AIP-2. While corticosteroids remain the first-line therapy for AIP-2, there have been reports of cases where biologic agents, such as anti-TNF-alpha and ustekinumab, have shown promise in managing steroid-refractory or steroid-dependent AIP-2. These patients have often been effectively treated with anti-TNF-alpha agents, which are also indicated for frequent concomitant IBD[7]. In a recent letter by Lauri, two cases of AIP-2 were reported to have been safety and successfully treated with ustekinumab, a monoclonal antibody that targets interleukin-12 and interleukin-23, used for concomitant IBD. This treatment option highlights the potential efficacy of ustekinumab in managing AIP-2, although further research and clinical trials are needed to validate its effectiveness in a larger patient population[94].

AIP-3 therapy is essentially based on the discontinuation of immune checkpoint inhibitors and supportive therapy. Indeed, the role of corticosteroids and immunosuppressants is not well understood. A retrospective study of 82 patients with AIP-3 found no statistically significant differences in the duration of symptoms or hospitalization between patients treated with corticosteroids and patients not treated with them[95]. Furthermore, steroid use in these immunocompromised patients with advanced malignancies carries a significantly increased risk of infectious events[96].

DISEASE RELAPSES

Relapses are significantly more common with AIP-1 (nearly 60% of cases) than with AIP-2 (9%-25%); the relapse rate in AIP-IBD patients appears to be similar to that of isolated AIP-2[97].

The main factors predicting relapse are young age, high serum IgG4 levels at disease onset, persistently high serum levels after treatment, diffuse enlargement of the pancreas, concurrent evidence of IRC, especially if proximal, or extensive multiorgan involvement[98]. Also, elevated levels of circulating IgE and/or eosinophils, and the presence of rich-in-eosinophils pancreatic infiltrate at histology represent other risk factors for disease relapse that need to be considered. Lastly, prolonged exposure to certain exogenous antigens may lead to overactivity of specific types of TLRs that may perpetuate a dysimmune response[4].

Given the high relapse rate in AIP-1, long-term maintenance therapy is recommended, especially for patients with a known high risk of relapse. Current guidelines recommend low-dose (5 mg/d) maintenance treatment with steroids for 2-3 years[99]. To reduce the risk of adverse events and lifetime cumulative steroid dose, the use of steroid-sparing agents is an alternative treatment strategy. According to a recent meta-analysis, nearly 40% of the cases relapse on immunosuppressive agents (azathioprine, mycophenolate mofetil, methotrexate, tacrolimus, and cyclophosphamide). To date, no study that compares the efficacy of different immunosuppressive has been published and the interpretation of the efficacy of conventional immunosuppressive medications is hampered by concomitant glucocorticoid use[100]. Also in the case of maintenance therapy, rituximab with the same induction scheme proved to be superior to immunomodulatory drugs in terms of efficacy[101]: 100% rituximab vs 81% azathioprine vs 72% other immunosuppressant[100].

In AIP-2, maintenance therapy is unnecessary in most patients unless certified risk factors are present; in the latter case, anti-TNF-alpha agents have been shown to be effective[7].

In cases of proven recurrent AIP, re-administration of a high dose of glucocorticoids with a slow steroid taper is effective[99].

Concerning AIP-3, it is not appropriate to refer to the risk of disease recurrence but rather to emphasize that after the acute event has resolved, the disease evolves in up to 36% of cases to a treatment-emergent stage of glandular atrophy with endocrine and exocrine insufficiency, associated with markedly reduced overall survival[102].

CONCLUSION

Given the multitude of mechanisms that explain the etiopathogenesis of AIP, great scientific efforts are being made to find new effective target therapies. As mentioned earlier, given the chemotactic role of eotaxin on inflammatory cells, attention is being paid to the development of targeted anti-eotaxin therapy[24]. Because increased production of IFN-I and IL-33 by pDCs promotes the chronic inflammation and fibrosis characteristic of AIP and IgG4- RD, neutralization of IFN-I and IL-33 may represent a new therapeutic option for these diseases. The anti-IFN-I therapeutics anifrolumab and sifalimumab and the anti-IL-33 therapeutic etokimab have been successfully used in systemic lupus erythematosus, but reliable data are not yet available for AIP in humans[35].

In addition, targeted therapies against B-cell lineage plasmablasts and CD4+ T cells (such as anti-CD19 inebilizumab, an inhibitor of B-cell activating factor ianalumab, anti-CD80/86 abatacept, anti-LOX2 simtuzumab, anti-SLAMF7 elotuzumab, or anti-CD38 daratumumab) have recently been proposed[103].

Finally, regarding the possible role of the microbiota in the etiopathogenesis of AIP, manipulation of the gut microbiota through prebiotics, probiotics, symbiotics, and fecal microbiota transplantation may represent a future prophylactic perspective, possibly targeting IgG4-RD and/or IBD patients. Indeed, early studies in mice have shown that sterilization of the gut leads to a significant reduction in the accumulation of pDCs in the pancreas that produce IFN-I and IL-33[104].

Footnotes

Provenance and peer review: Invited article; Externally peer reviewed.

Peer-review model: Single blind

Specialty type: Gastroenterology and hepatology

Country/Territory of origin: Italy

Peer-review report’s scientific quality classification

Grade A (Excellent): A

Grade B (Very good): 0

Grade C (Good): 0

Grade D (Fair): 0

Grade E (Poor): 0

P-Reviewer: Liu C, China S-Editor: Qu XL L-Editor: A P-Editor: Chen YX

References
1.  Shimosegawa T, Chari ST, Frulloni L, Kamisawa T, Kawa S, Mino-Kenudson M, Kim MH, Klöppel G, Lerch MM, Löhr M, Notohara K, Okazaki K, Schneider A, Zhang L; International Association of Pancreatology. International consensus diagnostic criteria for autoimmune pancreatitis: guidelines of the International Association of Pancreatology. Pancreas. 2011;40:352-358.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 1050]  [Cited by in F6Publishing: 962]  [Article Influence: 74.0]  [Reference Citation Analysis (0)]
2.  Sah RP, Chari ST, Pannala R, Sugumar A, Clain JE, Levy MJ, Pearson RK, Smyrk TC, Petersen BT, Topazian MD, Takahashi N, Farnell MB, Vege SS. Differences in clinical profile and relapse rate of type 1 versus type 2 autoimmune pancreatitis. Gastroenterology. 2010;139:140-8; quiz e12.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 336]  [Cited by in F6Publishing: 286]  [Article Influence: 20.4]  [Reference Citation Analysis (0)]
3.  Barresi L, Tacelli M, Crinò SF, Attili F, Petrone MC, De Nucci G, Carrara S, Manfredi G, Capurso G, De Angelis CG, Crocellà L, Fantin A, Dore MF, Garribba AT, Tarantino I, De Pretis N, Pagliari D, Rossi G, Manes G, Preatoni P, Barbuscio I, Tuzzolino F, Traina M, Frulloni L, Costamagna G, Arcidiacono PG, Buscarini E, Pezzilli R; Italian Association of Hospital Gastroenterologists and Endoscopists (AIGO), Italian Association for the Study of the Pancreas (AISP). Multicentric Italian survey on daily practice for autoimmune pancreatitis: Clinical data, diagnosis, treatment, and evolution toward pancreatic insufficiency. United European Gastroenterol J. 2020;8:705-715.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 12]  [Cited by in F6Publishing: 14]  [Article Influence: 3.5]  [Reference Citation Analysis (0)]
4.  Löhr JM, Vujasinovic M, Rosendahl J, Stone JH, Beuers U. IgG4-related diseases of the digestive tract. Nat Rev Gastroenterol Hepatol. 2022;19:185-197.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 7]  [Cited by in F6Publishing: 34]  [Article Influence: 17.0]  [Reference Citation Analysis (0)]
5.  Wallace ZS, Naden RP, Chari S, Choi HK, Della-Torre E, Dicaire JF, Hart PA, Inoue D, Kawano M, Khosroshahi A, Lanzillotta M, Okazaki K, Perugino CA, Sharma A, Saeki T, Schleinitz N, Takahashi N, Umehara H, Zen Y, Stone JH; Members of the ACR/EULAR IgG4-RD Classification Criteria Working Group. The 2019 American College of Rheumatology/European League Against Rheumatism classification criteria for IgG4-related disease. Ann Rheum Dis. 2020;79:77-87.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 336]  [Cited by in F6Publishing: 317]  [Article Influence: 79.3]  [Reference Citation Analysis (1)]
6.  Khandelwal A, Inoue D, Takahashi N. Autoimmune pancreatitis: an update. Abdom Radiol (NY). 2020;45:1359-1370.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 35]  [Cited by in F6Publishing: 37]  [Article Influence: 9.3]  [Reference Citation Analysis (0)]
7.  de Pretis N, Frulloni L. Autoimmune pancreatitis type 2. Curr Opin Gastroenterol. 2020;36:417-420.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 8]  [Cited by in F6Publishing: 17]  [Article Influence: 4.3]  [Reference Citation Analysis (0)]
8.  Zen Y, Grammatikopoulos T, Hadzic N. Autoimmune pancreatitis in children: insights into the diagnostic challenge. J Pediatr Gastroenterol Nutr. 2014;59:e42-e45.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 15]  [Cited by in F6Publishing: 22]  [Article Influence: 2.2]  [Reference Citation Analysis (0)]
9.  Sayed Ahmed A, Abreo M, Thomas A, Chari ST. Type 3 autoimmune pancreatitis (immune checkpoint inhibitor-induced pancreatitis). Curr Opin Gastroenterol. 2022;38:516-520.  [PubMed]  [DOI]  [Cited in This Article: ]  [Reference Citation Analysis (0)]
10.  Kamisawa T, Chari ST, Giday SA, Kim MH, Chung JB, Lee KT, Werner J, Bergmann F, Lerch MM, Mayerle J, Pickartz T, Lohr M, Schneider A, Frulloni L, Webster GJ, Reddy DN, Liao WC, Wang HP, Okazaki K, Shimosegawa T, Kloeppel G, Go VL. Clinical profile of autoimmune pancreatitis and its histological subtypes: an international multicenter survey. Pancreas. 2011;40:809-814.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 207]  [Cited by in F6Publishing: 168]  [Article Influence: 12.9]  [Reference Citation Analysis (0)]
11.  Hardacre JM, Iacobuzio-Donahue CA, Sohn TA, Abraham SC, Yeo CJ, Lillemoe KD, Choti MA, Campbell KA, Schulick RD, Hruban RH, Cameron JL, Leach SD. Results of pancreaticoduodenectomy for lymphoplasmacytic sclerosing pancreatitis. Ann Surg. 2003;237:853-8; discussion 858.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 107]  [Cited by in F6Publishing: 138]  [Article Influence: 6.6]  [Reference Citation Analysis (0)]
12.  Masamune A, Kikuta K, Hamada S, Tsuji I, Takeyama Y, Shimosegawa T, Okazaki K; Collaborators. Nationwide epidemiological survey of autoimmune pancreatitis in Japan in 2016. J Gastroenterol. 2020;55:462-470.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 68]  [Cited by in F6Publishing: 68]  [Article Influence: 17.0]  [Reference Citation Analysis (0)]
13.  Hart PA, Kamisawa T, Brugge WR, Chung JB, Culver EL, Czakó L, Frulloni L, Go VL, Gress TM, Kim MH, Kawa S, Lee KT, Lerch MM, Liao WC, Löhr M, Okazaki K, Ryu JK, Schleinitz N, Shimizu K, Shimosegawa T, Soetikno R, Webster G, Yadav D, Zen Y, Chari ST. Long-term outcomes of autoimmune pancreatitis: a multicentre, international analysis. Gut. 2013;62:1771-1776.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 382]  [Cited by in F6Publishing: 337]  [Article Influence: 30.6]  [Reference Citation Analysis (0)]
14.  Kanno A, Masamune A, Okazaki K, Kamisawa T, Kawa S, Nishimori I, Tsuji I, Shimosegawa T; Research Committee of Intractable Diseases of the Pancreas. Nationwide epidemiological survey of autoimmune pancreatitis in Japan in 2011. Pancreas. 2015;44:535-539.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 115]  [Cited by in F6Publishing: 98]  [Article Influence: 10.9]  [Reference Citation Analysis (0)]
15.  Ueki T, Kawamoto K, Otsuka Y, Minoda R, Maruo T, Matsumura K, Noma E, Mitsuyasu T, Otani K, Aomi Y, Yano Y, Hisabe T, Matsui T, Ota A, Iwashita A. Prevalence and clinicopathological features of autoimmune pancreatitis in Japanese patients with inflammatory bowel disease. Pancreas. 2015;44:434-440.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 31]  [Cited by in F6Publishing: 31]  [Article Influence: 3.4]  [Reference Citation Analysis (0)]
16.  Park SH, Kim D, Ye BD, Yang SK, Kim JH, Yang DH, Jung KW, Kim KJ, Byeon JS, Myung SJ, Kim MH. The characteristics of ulcerative colitis associated with autoimmune pancreatitis. J Clin Gastroenterol. 2013;47:520-525.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 34]  [Cited by in F6Publishing: 36]  [Article Influence: 3.3]  [Reference Citation Analysis (0)]
17.  Massironi S, Fanetti I, Viganò C, Pirola L, Fichera M, Cristoferi L, Capurso G, Invernizzi P, Danese S. Systematic review-pancreatic involvement in inflammatory bowel disease. Aliment Pharmacol Ther. 2022;55:1478-1491.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 10]  [Cited by in F6Publishing: 4]  [Article Influence: 2.0]  [Reference Citation Analysis (0)]
18.  Swiecki M, Colonna M. The multifaceted biology of plasmacytoid dendritic cells. Nat Rev Immunol. 2015;15:471-485.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 800]  [Cited by in F6Publishing: 741]  [Article Influence: 82.3]  [Reference Citation Analysis (0)]
19.  Kurimoto M, Watanabe T, Kamata K, Minaga K, Kudo M. IL-33 as a Critical Cytokine for Inflammation and Fibrosis in Inflammatory Bowel Diseases and Pancreatitis. Front Physiol. 2021;12:781012.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in F6Publishing: 10]  [Reference Citation Analysis (0)]
20.  Kawa S. The Immunobiology of Immunoglobulin G4 and Complement Activation Pathways in IgG4-Related Disease. Curr Top Microbiol Immunol. 2017;401:61-73.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 9]  [Cited by in F6Publishing: 15]  [Article Influence: 1.9]  [Reference Citation Analysis (0)]
21.  Higashioka K, Ota Y, Maehara T, Moriyama M, Ayano M, Mitoma H, Akahoshi M, Arinobu Y, Horiuchi T, Nakamura S, Akashi K, Niiro H. Association of circulating SLAMF7(+)Tfh1 cells with IgG4 levels in patients with IgG4-related disease. BMC Immunol. 2020;21:31.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 7]  [Cited by in F6Publishing: 5]  [Article Influence: 1.3]  [Reference Citation Analysis (0)]
22.  Mattoo H, Mahajan VS, Maehara T, Deshpande V, Della-Torre E, Wallace ZS, Kulikova M, Drijvers JM, Daccache J, Carruthers MN, Castelino FV, Stone JR, Stone JH, Pillai S. Clonal expansion of CD4(+) cytotoxic T lymphocytes in patients with IgG4-related disease. J Allergy Clin Immunol. 2016;138:825-838.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 215]  [Cited by in F6Publishing: 240]  [Article Influence: 30.0]  [Reference Citation Analysis (0)]
23.  Della-Torre E, Bozzalla-Cassione E, Sciorati C, Ruggiero E, Lanzillotta M, Bonfiglio S, Mattoo H, Perugino CA, Bozzolo E, Rovati L, Arcidiacono PG, Balzano G, Lazarevic D, Bonini C, Falconi M, Stone JH, Dagna L, Pillai S, Manfredi AA. A CD8α- Subset of CD4+SLAMF7+ Cytotoxic T Cells Is Expanded in Patients With IgG4-Related Disease and Decreases Following Glucocorticoid Treatment. Arthritis Rheumatol. 2018;70:1133-1143.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 73]  [Cited by in F6Publishing: 74]  [Article Influence: 12.3]  [Reference Citation Analysis (0)]
24.  Mari A, Kadah A, Mahamid M, Sbeit W, Khoury T. IgG4 Related Autoimmune Pancreatitis: An Overview and the Emerging Role of Serum Eotaxin as a Potential Treatment Target. Isr Med Assoc J. 2019;21:620-623.  [PubMed]  [DOI]  [Cited in This Article: ]
25.  Loos M, Lauffer F, Schlitter AM, Kleeff J, Friess H, Klöppel G, Esposito I. Potential role of Th17 cells in the pathogenesis of type 2 autoimmune pancreatitis. Virchows Arch. 2015;467:641-648.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 9]  [Cited by in F6Publishing: 11]  [Article Influence: 1.2]  [Reference Citation Analysis (0)]
26.  Dong F, Chen QQ, Zhuang ZH, He QL, Wang FQ, Liu QC, Liu HK, Wang Y. Multiple gene mutations in patients with type 2 autoimmune pancreatitis and its clinical features. Cent Eur J Immunol. 2014;39:77-82.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 2]  [Cited by in F6Publishing: 7]  [Article Influence: 0.7]  [Reference Citation Analysis (0)]
27.  Ku Y, Hong SM, Fujikura K, Kim SJ, Akita M, Abe-Suzuki S, Shiomi H, Masuda A, Itoh T, Azuma T, Kim MH, Zen Y. IL-8 Expression in Granulocytic Epithelial Lesions of Idiopathic Duct-centric Pancreatitis (Type 2 Autoimmune Pancreatitis). Am J Surg Pathol. 2017;41:1129-1138.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 19]  [Cited by in F6Publishing: 20]  [Article Influence: 2.9]  [Reference Citation Analysis (0)]
28.  Hart PA, Levy MJ, Smyrk TC, Takahashi N, Abu Dayyeh BK, Clain JE, Gleeson FC, Pearson RK, Petersen BT, Topazian MD, Vege SS, Zhang L, Chari ST. Clinical profiles and outcomes in idiopathic duct-centric chronic pancreatitis (type 2 autoimmune pancreatitis): the Mayo Clinic experience. Gut. 2016;65:1702-1709.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 57]  [Cited by in F6Publishing: 51]  [Article Influence: 6.4]  [Reference Citation Analysis (0)]
29.  Kamata K, Watanabe T, Minaga K, Hara A, Sekai I, Otsuka Y, Yoshikawa T, Park AM, Kudo M. Gut microbiome alterations in type 1 autoimmune pancreatitis after induction of remission by prednisolone. Clin Exp Immunol. 2020;202:308-320.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 4]  [Cited by in F6Publishing: 4]  [Article Influence: 1.0]  [Reference Citation Analysis (0)]
30.  Schepis T, De Lucia SS, Nista EC, Manilla V, Pignataro G, Ojetti V, Piccioni A, Gasbarrini A, Franceschi F, Candelli M. Microbiota in Pancreatic Diseases: A Review of the Literature. J Clin Med. 2021;10.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 17]  [Cited by in F6Publishing: 18]  [Article Influence: 6.0]  [Reference Citation Analysis (0)]
31.  Liu Y, Zhang H, Zhou L, Li W, Yang L, Li K, Liu X. Immunotherapy-Associated Pancreatic Adverse Events: Current Understanding of Their Mechanism, Diagnosis, and Management. Front Oncol. 2021;11:627612.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 11]  [Cited by in F6Publishing: 22]  [Article Influence: 7.3]  [Reference Citation Analysis (0)]
32.  Thomas AS, Abreo M, Sayed SA, Sireesha Yedururi YW, Chari ST. Autoimmune Pancreatitis Secondary to Immune Checkpoint Inhibitor Therapy (Type 3 AIP): Insights Into a New Disease From Serial Pancreatic Imaging. Gastroenterology. 2023;164:154-155.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in F6Publishing: 3]  [Reference Citation Analysis (0)]
33.  Adsay NV, Basturk O, Thirabanjasak D. Diagnostic features and differential diagnosis of autoimmune pancreatitis. Semin Diagn Pathol. 2005;22:309-317.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 21]  [Cited by in F6Publishing: 24]  [Article Influence: 1.3]  [Reference Citation Analysis (0)]
34.  Nagpal SJS, Sharma A, Chari ST. Autoimmune Pancreatitis. Am J Gastroenterol. 2018;113:1301.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 49]  [Cited by in F6Publishing: 47]  [Article Influence: 7.8]  [Reference Citation Analysis (0)]
35.  Minaga K, Watanabe T, Hara A, Yoshikawa T, Kamata K, Kudo M. Plasmacytoid Dendritic Cells as a New Therapeutic Target for Autoimmune Pancreatitis and IgG4-Related Disease. Front Immunol. 2021;12:713779.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 3]  [Cited by in F6Publishing: 4]  [Article Influence: 1.3]  [Reference Citation Analysis (0)]
36.  Wallace ZS, Deshpande V, Mattoo H, Mahajan VS, Kulikova M, Pillai S, Stone JH. IgG4-Related Disease: Clinical and Laboratory Features in One Hundred Twenty-Five Patients. Arthritis Rheumatol. 2015;67:2466-2475.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 355]  [Cited by in F6Publishing: 408]  [Article Influence: 45.3]  [Reference Citation Analysis (0)]
37.  Bledsoe JR, Della-Torre E, Rovati L, Deshpande V. IgG4-related disease: review of the histopathologic features, differential diagnosis, and therapeutic approach. APMIS. 2018;126:459-476.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 67]  [Cited by in F6Publishing: 72]  [Article Influence: 12.0]  [Reference Citation Analysis (0)]
38.  Majumder S, Takahashi N, Chari ST. Autoimmune Pancreatitis. Dig Dis Sci. 2017;62:1762-1769.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 40]  [Cited by in F6Publishing: 34]  [Article Influence: 4.9]  [Reference Citation Analysis (0)]
39.  Conti Bellocchi MC, Marconato E, Lamonaca L, Cattani Mottes M, Ciccocioppo R, Carrara S, de Pretis N, Gabbrielli A, Crinò SF, Frulloni L. The features and clinical outcomes of inflammatory bowel disease associated with autoimmune pancreatitis: A greater awareness is needed. Medicine (Baltimore). 2022;101:e28602.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 1]  [Cited by in F6Publishing: 1]  [Article Influence: 0.5]  [Reference Citation Analysis (0)]
40.  Lorenzo D, Maire F, Stefanescu C, Gornet JM, Seksik P, Serrero M, Bournet B, Marteau P, Amiot A, Laharie D, Trang C, Coffin B, Bellaiche G, Cadiot G, Reenaers C, Racine A, Viennot S, Pauwels A, Bouguen G, Savoye G, Pelletier AL, Pineton de Chambrun G, Lahmek P, Nahon S, Abitbol V; GETAID-AIP study group. Features of Autoimmune Pancreatitis Associated With Inflammatory Bowel Diseases. Clin Gastroenterol Hepatol. 2018;16:59-67.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 38]  [Cited by in F6Publishing: 47]  [Article Influence: 7.8]  [Reference Citation Analysis (0)]
41.  Zen Y. Type 2 Autoimmune Pancreatitis: Consensus and Controversies. Gut Liver. 2022;16:357-365.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 3]  [Cited by in F6Publishing: 11]  [Article Influence: 3.7]  [Reference Citation Analysis (1)]
42.  Negrelli R, Boninsegna E, Avesani G, Zamboni GA, Brozzi L, Frulloni L, Manfredi R, Pozzi Mucelli R. Type 1 and Type 2 Autoimmune Pancreatitis: Distinctive Clinical and Pathological Features, But Are There Any Differences at Magnetic Resonance? Experience From a Referral Center. Pancreas. 2018;47:1115-1122.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 8]  [Cited by in F6Publishing: 11]  [Article Influence: 1.8]  [Reference Citation Analysis (0)]
43.  Ha J, Choi SH, Kim KW, Kim JH, Kim HJ. MRI features for differentiation of autoimmune pancreatitis from pancreatic ductal adenocarcinoma: A systematic review and meta-analysis. Dig Liver Dis. 2022;54:849-856.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 7]  [Cited by in F6Publishing: 2]  [Article Influence: 1.0]  [Reference Citation Analysis (0)]
44.  Haaga JR, Alfidi RJ, Zelch MG, Meany TF, Boller M, Gonzalez L, Jelden GL. Computed tomography of the pancreas. Radiology. 1976;120:589-595.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 104]  [Cited by in F6Publishing: 101]  [Article Influence: 2.1]  [Reference Citation Analysis (0)]
45.  Ogawa H, Takehara Y, Naganawa S. Imaging diagnosis of autoimmune pancreatitis: computed tomography and magnetic resonance imaging. J Med Ultrason (2001). 2021;48:565-571.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 3]  [Cited by in F6Publishing: 3]  [Article Influence: 1.0]  [Reference Citation Analysis (0)]
46.  Rehnitz C, Klauss M, Singer R, Ehehalt R, Werner J, Büchler MW, Kauczor HU, Grenacher L. Morphologic patterns of autoimmune pancreatitis in CT and MRI. Pancreatology. 2011;11:240-251.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 31]  [Cited by in F6Publishing: 34]  [Article Influence: 2.6]  [Reference Citation Analysis (0)]
47.  Takahashi N, Fletcher JG, Hough DM, Fidler JL, Kawashima A, Mandrekar JN, Chari ST. Autoimmune pancreatitis: differentiation from pancreatic carcinoma and normal pancreas on the basis of enhancement characteristics at dual-phase CT. AJR Am J Roentgenol. 2009;193:479-484.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 69]  [Cited by in F6Publishing: 71]  [Article Influence: 4.7]  [Reference Citation Analysis (0)]
48.  Wakabayashi T, Kawaura Y, Satomura Y, Watanabe H, Motoo Y, Okai T, Sawabu N. Clinical and imaging features of autoimmune pancreatitis with focal pancreatic swelling or mass formation: comparison with so-called tumor-forming pancreatitis and pancreatic carcinoma. Am J Gastroenterol. 2003;98:2679-2687.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 119]  [Cited by in F6Publishing: 124]  [Article Influence: 5.9]  [Reference Citation Analysis (0)]
49.  Suzuki K, Itoh S, Nagasaka T, Ogawa H, Ota T, Naganawa S. CT findings in autoimmune pancreatitis: assessment using multiphase contrast-enhanced multisection CT. Clin Radiol. 2010;65:735-743.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 50]  [Cited by in F6Publishing: 50]  [Article Influence: 3.6]  [Reference Citation Analysis (0)]
50.  Sugumar A, Levy MJ, Kamisawa T, Webster GJ, Kim MH, Enders F, Amin Z, Baron TH, Chapman MH, Church NI, Clain JE, Egawa N, Johnson GJ, Okazaki K, Pearson RK, Pereira SP, Petersen BT, Read S, Sah RP, Sandanayake NS, Takahashi N, Topazian MD, Uchida K, Vege SS, Chari ST. Endoscopic retrograde pancreatography criteria to diagnose autoimmune pancreatitis: an international multicentre study. Gut. 2011;60:666-670.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 113]  [Cited by in F6Publishing: 118]  [Article Influence: 9.1]  [Reference Citation Analysis (0)]
51.  Kawai Y, Suzuki K, Itoh S, Takada A, Mori Y, Naganawa S. Autoimmune pancreatitis: assessment of the enhanced duct sign on multiphase contrast-enhanced computed tomography. Eur J Radiol. 2012;81:3055-3060.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 11]  [Cited by in F6Publishing: 12]  [Article Influence: 1.0]  [Reference Citation Analysis (0)]
52.  Muhi A, Ichikawa T, Motosugi U, Sou H, Sano K, Tsukamoto T, Fatima Z, Araki T. Mass-forming autoimmune pancreatitis and pancreatic carcinoma: differential diagnosis on the basis of computed tomography and magnetic resonance cholangiopancreatography, and diffusion-weighted imaging findings. J Magn Reson Imaging. 2012;35:827-836.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 89]  [Cited by in F6Publishing: 92]  [Article Influence: 7.1]  [Reference Citation Analysis (0)]
53.  Choi SY, Kim SH, Kang TW, Song KD, Park HJ, Choi YH. Differentiating Mass-Forming Autoimmune Pancreatitis From Pancreatic Ductal Adenocarcinoma on the Basis of Contrast-Enhanced MRI and DWI Findings. AJR Am J Roentgenol. 2016;206:291-300.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 60]  [Cited by in F6Publishing: 62]  [Article Influence: 7.8]  [Reference Citation Analysis (0)]
54.  Sekito T, Ishii Y, Serikawa M, Tsuboi T, Kawamura R, Tsushima K, Nakamura S, Hirano T, Fukiage A, Mori T, Ikemoto J, Kiyoshita Y, Saeki S, Tamura Y, Miyamoto S, Chayama K. The role of apparent diffusion coefficient value in the diagnosis of localized type 1 autoimmune pancreatitis: differentiation from pancreatic ductal adenocarcinoma and evaluation of response to steroids. Abdom Radiol (NY). 2021;46:2014-2024.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 3]  [Cited by in F6Publishing: 3]  [Article Influence: 1.0]  [Reference Citation Analysis (0)]
55.  Hur BY, Lee JM, Lee JE, Park JY, Kim SJ, Joo I, Shin CI, Baek JH, Kim JH, Han JK, Choi BI. Magnetic resonance imaging findings of the mass-forming type of autoimmune pancreatitis: comparison with pancreatic adenocarcinoma. J Magn Reson Imaging. 2012;36:188-197.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 84]  [Cited by in F6Publishing: 85]  [Article Influence: 7.1]  [Reference Citation Analysis (0)]
56.  Kim HJ, Kim YK, Jeong WK, Lee WJ, Choi D. Pancreatic duct "Icicle sign" on MRI for distinguishing autoimmune pancreatitis from pancreatic ductal adenocarcinoma in the proximal pancreas. Eur Radiol. 2015;25:1551-1560.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 43]  [Cited by in F6Publishing: 36]  [Article Influence: 3.6]  [Reference Citation Analysis (0)]
57.  Shi Y, Cang L, Zhang X, Cai X, Wang X, Ji R, Wang M, Hong Y. The use of magnetic resonance elastography in differentiating autoimmune pancreatitis from pancreatic ductal adenocarcinoma: A preliminary study. Eur J Radiol. 2018;108:13-20.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 16]  [Cited by in F6Publishing: 19]  [Article Influence: 3.2]  [Reference Citation Analysis (0)]
58.  Ohno E, Hirooka Y, Kawashima H, Ishikawa T, Tanaka H, Sakai D, Ishizu Y, Kuzuya T, Nakamura M, Honda T. Feasibility and usefulness of endoscopic ultrasonography-guided shear-wave measurement for assessment of autoimmune pancreatitis activity: a prospective exploratory study. J Med Ultrason (2001). 2019;46:425-433.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 17]  [Cited by in F6Publishing: 18]  [Article Influence: 3.6]  [Reference Citation Analysis (0)]
59.  Ha J, Choi SH, Byun JH, Kim KW, Kim SY, Kim JH, Kim HJ. Meta-analysis of CT and MRI for differentiation of autoimmune pancreatitis from pancreatic adenocarcinoma. Eur Radiol. 2021;31:3427-3438.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 6]  [Cited by in F6Publishing: 7]  [Article Influence: 1.8]  [Reference Citation Analysis (0)]
60.  Lee TY, Kim MH, Park DH, Seo DW, Lee SK, Kim JS, Lee KT. Utility of 18F-FDG PET/CT for differentiation of autoimmune pancreatitis with atypical pancreatic imaging findings from pancreatic cancer. AJR Am J Roentgenol. 2009;193:343-348.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 112]  [Cited by in F6Publishing: 117]  [Article Influence: 7.8]  [Reference Citation Analysis (0)]
61.  Zhang J, Jia G, Zuo C, Jia N, Wang H. (18)F- FDG PET/CT helps differentiate autoimmune pancreatitis from pancreatic cancer. BMC Cancer. 2017;17:695.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 27]  [Cited by in F6Publishing: 34]  [Article Influence: 4.9]  [Reference Citation Analysis (0)]
62.  Cheng MF, Guo YL, Yen RF, Chen YC, Ko CL, Tien YW, Liao WC, Liu CJ, Wu YW, Wang HP. Clinical Utility of FDG PET/CT in Patients with Autoimmune Pancreatitis: a Case-Control Study. Sci Rep. 2018;8:3651.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 26]  [Cited by in F6Publishing: 30]  [Article Influence: 5.0]  [Reference Citation Analysis (0)]
63.  Luo Y, Pan Q, Yang H, Peng L, Zhang W, Li F. Fibroblast Activation Protein-Targeted PET/CT with (68)Ga-FAPI for Imaging IgG4-Related Disease: Comparison to (18)F-FDG PET/CT. J Nucl Med. 2021;62:266-271.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 56]  [Cited by in F6Publishing: 96]  [Article Influence: 24.0]  [Reference Citation Analysis (0)]
64.  de Pretis N, Crinò SF, Frulloni L. The Role of EUS-Guided FNA and FNB in Autoimmune Pancreatitis. Diagnostics (Basel). 2021;11.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 5]  [Cited by in F6Publishing: 15]  [Article Influence: 5.0]  [Reference Citation Analysis (0)]
65.  Kanno A, Tamada K, Fukushima N, Lefor AK, Yamamoto H. Endoscopic ultrasound-guided tissue acquisition for the histopathological diagnosis of autoimmune pancreatitis. J Med Ultrason (2001). 2021;48:555-563.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 1]  [Cited by in F6Publishing: 5]  [Article Influence: 1.7]  [Reference Citation Analysis (0)]
66.  Marya NB, Powers PD, Chari ST, Gleeson FC, Leggett CL, Abu Dayyeh BK, Chandrasekhara V, Iyer PG, Majumder S, Pearson RK, Petersen BT, Rajan E, Sawas T, Storm AC, Vege SS, Chen S, Long Z, Hough DM, Mara K, Levy MJ. Utilisation of artificial intelligence for the development of an EUS-convolutional neural network model trained to enhance the diagnosis of autoimmune pancreatitis. Gut. 2021;70:1335-1344.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 44]  [Cited by in F6Publishing: 59]  [Article Influence: 19.7]  [Reference Citation Analysis (1)]
67.  Notohara K, Kamisawa T, Furukawa T, Fukushima N, Uehara T, Kasashima S, Iwasaki E, Kanno A, Kawashima A, Kubota K, Kuraishi Y, Motoya M, Naitoh I, Nishino T, Sakagami J, Shimizu K, Tomono T, Aishima S, Fukumura Y, Hirabayashi K, Kojima M, Mitsuhashi T, Naito Y, Ohike N, Tajiri T, Yamaguchi H, Fujiwara H, Ibuki E, Kobayashi S, Miyaoka M, Nagase M, Nakashima J, Nakayama M, Oda S, Taniyama D, Tsuyama S, Watanabe S, Ikeura T, Kawa S, Okazaki K. Concordance of the histological diagnosis of type 1 autoimmune pancreatitis and its distinction from pancreatic ductal adenocarcinoma with endoscopic ultrasound-guided fine needle biopsy specimens: an interobserver agreement study. Virchows Arch. 2022;480:565-575.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 4]  [Cited by in F6Publishing: 6]  [Article Influence: 3.0]  [Reference Citation Analysis (0)]
68.  Guo T, Xu T, Zhang S, Lai Y, Wu X, Wu D, Feng Y, Jiang Q, Wang Q, Qian J, Yang A. The role of EUS in diagnosing focal autoimmune pancreatitis and differentiating it from pancreatic cancer. Endosc Ultrasound. 2021;10:280-287.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 2]  [Cited by in F6Publishing: 9]  [Article Influence: 3.0]  [Reference Citation Analysis (0)]
69.  Buscarini E, De Lisi S, Arcidiacono PG, Petrone MC, Fuini A, Conigliaro R, Manfredi G, Manta R, Reggio D, De Angelis C. Endoscopic ultrasonography findings in autoimmune pancreatitis. World J Gastroenterol. 2011;17:2080-2085.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in CrossRef: 26]  [Cited by in F6Publishing: 17]  [Article Influence: 1.3]  [Reference Citation Analysis (0)]
70.  Manfredi R, Frulloni L, Mantovani W, Bonatti M, Graziani R, Pozzi Mucelli R. Autoimmune pancreatitis: pancreatic and extrapancreatic MR imaging-MR cholangiopancreatography findings at diagnosis, after steroid therapy, and at recurrence. Radiology. 2011;260:428-436.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 80]  [Cited by in F6Publishing: 70]  [Article Influence: 5.4]  [Reference Citation Analysis (0)]
71.  Yoon SB, Moon SH, Song TJ, Kim JH, Kim MH. Endoscopic ultrasound-guided fine needle aspiration versus biopsy for diagnosis of autoimmune pancreatitis: Systematic review and comparative meta-analysis. Dig Endosc. 2021;33:1024-1033.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 27]  [Cited by in F6Publishing: 26]  [Article Influence: 8.7]  [Reference Citation Analysis (0)]
72.  Arora K, Rivera M, Ting DT, Deshpande V. The histological diagnosis of IgG4-related disease on small biopsies: challenges and pitfalls. Histopathology. 2019;74:688-698.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 24]  [Cited by in F6Publishing: 34]  [Article Influence: 6.8]  [Reference Citation Analysis (0)]
73.  Yoon SB, Moon SH, Kim JH, Song TJ, Kim MH. The use of immunohistochemistry for IgG4 in the diagnosis of autoimmune pancreatitis: A systematic review and meta-analysis. Pancreatology. 2020;20:1611-1619.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 11]  [Cited by in F6Publishing: 7]  [Article Influence: 1.8]  [Reference Citation Analysis (0)]
74.  Deshpande V, Zen Y, Chan JK, Yi EE, Sato Y, Yoshino T, Klöppel G, Heathcote JG, Khosroshahi A, Ferry JA, Aalberse RC, Bloch DB, Brugge WR, Bateman AC, Carruthers MN, Chari ST, Cheuk W, Cornell LD, Fernandez-Del Castillo C, Forcione DG, Hamilos DL, Kamisawa T, Kasashima S, Kawa S, Kawano M, Lauwers GY, Masaki Y, Nakanuma Y, Notohara K, Okazaki K, Ryu JK, Saeki T, Sahani DV, Smyrk TC, Stone JR, Takahira M, Webster GJ, Yamamoto M, Zamboni G, Umehara H, Stone JH. Consensus statement on the pathology of IgG4-related disease. Mod Pathol. 2012;25:1181-1192.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 1714]  [Cited by in F6Publishing: 1637]  [Article Influence: 136.4]  [Reference Citation Analysis (0)]
75.  Löhr JM, Beuers U, Vujasinovic M, Alvaro D, Frøkjær JB, Buttgereit F, Capurso G, Culver EL, de-Madaria E, Della-Torre E, Detlefsen S, Dominguez-Muñoz E, Czubkowski P, Ewald N, Frulloni L, Gubergrits N, Duman DG, Hackert T, Iglesias-Garcia J, Kartalis N, Laghi A, Lammert F, Lindgren F, Okhlobystin A, Oracz G, Parniczky A, Mucelli RMP, Rebours V, Rosendahl J, Schleinitz N, Schneider A, van Bommel EF, Verbeke CS, Vullierme MP, Witt H; UEG guideline working group. European Guideline on IgG4-related digestive disease - UEG and SGF evidence-based recommendations. United European Gastroenterol J. 2020;8:637-666.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 60]  [Cited by in F6Publishing: 97]  [Article Influence: 24.3]  [Reference Citation Analysis (0)]
76.  Zhang L, Chari S, Smyrk TC, Deshpande V, Klöppel G, Kojima M, Liu X, Longnecker DS, Mino-Kenudson M, Notohara K, Rodriguez-Justo M, Srivastava A, Zamboni G, Zen Y. Autoimmune pancreatitis (AIP) type 1 and type 2: an international consensus study on histopathologic diagnostic criteria. Pancreas. 2011;40:1172-1179.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 112]  [Cited by in F6Publishing: 91]  [Article Influence: 7.0]  [Reference Citation Analysis (0)]
77.  Chari ST, Smyrk TC, Levy MJ, Topazian MD, Takahashi N, Zhang L, Clain JE, Pearson RK, Petersen BT, Vege SS, Farnell MB. Diagnosis of autoimmune pancreatitis: the Mayo Clinic experience. Clin Gastroenterol Hepatol. 2006;4:1010-6; quiz 934.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 722]  [Cited by in F6Publishing: 756]  [Article Influence: 42.0]  [Reference Citation Analysis (0)]
78.  Culver EL, Sadler R, Bateman AC, Makuch M, Cargill T, Ferry B, Aalberse R, Barnes E, Rispens T. Increases in IgE, Eosinophils, and Mast Cells Can be Used in Diagnosis and to Predict Relapse of IgG4-Related Disease. Clin Gastroenterol Hepatol. 2017;15:1444-1452.e6.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 97]  [Cited by in F6Publishing: 91]  [Article Influence: 13.0]  [Reference Citation Analysis (0)]
79.  Yan T, Ke Y, Chen Y, Xu C, Yu C, Li Y. Serological characteristics of autoimmune pancreatitis and its differential diagnosis from pancreatic cancer by using a combination of carbohydrate antigen 19-9, globulin, eosinophils and hemoglobin. PLoS One. 2017;12:e0174735.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 14]  [Cited by in F6Publishing: 11]  [Article Influence: 1.6]  [Reference Citation Analysis (0)]
80.  van Heerde MJ, Buijs J, Hansen BE, de Waart M, van Eijck CH, Kazemier G, Pek CJ, Poley JW, Bruno MJ, Kuipers EJ, van Buuren HR. Serum level of Ca 19-9 increases ability of IgG4 test to distinguish patients with autoimmune pancreatitis from those with pancreatic carcinoma. Dig Dis Sci. 2014;59:1322-1329.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 7]  [Cited by in F6Publishing: 13]  [Article Influence: 1.3]  [Reference Citation Analysis (0)]
81.  Chang MC, Liang PC, Jan S, Yang CY, Tien YW, Wei SC, Wong JM, Chang YT. Increase diagnostic accuracy in differentiating focal type autoimmune pancreatitis from pancreatic cancer with combined serum IgG4 and CA19-9 levels. Pancreatology. 2014;14:366-372.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 31]  [Cited by in F6Publishing: 32]  [Article Influence: 3.2]  [Reference Citation Analysis (0)]
82.  Okazaki K, Chari ST, Frulloni L, Lerch MM, Kamisawa T, Kawa S, Kim MH, Lévy P, Masamune A, Webster G, Shimosegawa T. International consensus for the treatment of autoimmune pancreatitis. Pancreatology. 2017;17:1-6.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 129]  [Cited by in F6Publishing: 135]  [Article Influence: 16.9]  [Reference Citation Analysis (0)]
83.  Kamisawa T, Okazaki K, Kawa S, Shimosegawa T, Tanaka M; Research Committee for Intractable Pancreatic Disease and Japan Pancreas Society. Japanese consensus guidelines for management of autoimmune pancreatitis: III. Treatment and prognosis of AIP. J Gastroenterol. 2010;45:471-477.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 192]  [Cited by in F6Publishing: 204]  [Article Influence: 14.6]  [Reference Citation Analysis (0)]
84.  Kamisawa T, Shimosegawa T, Okazaki K, Nishino T, Watanabe H, Kanno A, Okumura F, Nishikawa T, Kobayashi K, Ichiya T, Takatori H, Yamakita K, Kubota K, Hamano H, Okamura K, Hirano K, Ito T, Ko SB, Omata M. Standard steroid treatment for autoimmune pancreatitis. Gut. 2009;58:1504-1507.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 500]  [Cited by in F6Publishing: 460]  [Article Influence: 30.7]  [Reference Citation Analysis (0)]
85.  Matsubayashi H, Yoneyama M, Nanri K, Sugimoto S, Shinjo K, Kakushima N, Tanaka M, Ito S, Takao M, Ono H. Determination of steroid response by abdominal ultrasound in cases with autoimmune pancreatitis. Dig Liver Dis. 2013;45:1034-1040.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 8]  [Cited by in F6Publishing: 11]  [Article Influence: 1.0]  [Reference Citation Analysis (0)]
86.  Kamisawa T, Okazaki K, Kawa S, Ito T, Inui K, Irie H, Nishino T, Notohara K, Nishimori I, Tanaka S, Nishiyama T, Suda K, Shiratori K, Tanaka M, Shimosegawa T; Working Committee of the Japan Pancreas Society and the Research Committee for Intractable Pancreatic Disease supported by the Ministry of Health, Labour and Welfare of Japan. Amendment of the Japanese Consensus Guidelines for Autoimmune Pancreatitis, 2013 III. Treatment and prognosis of autoimmune pancreatitis. J Gastroenterol. 2014;49:961-970.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 147]  [Cited by in F6Publishing: 140]  [Article Influence: 14.0]  [Reference Citation Analysis (0)]
87.  Akiyama M, Takeuchi T. IgG4-Related Disease: Beyond Glucocorticoids. Drugs Aging. 2018;35:275-287.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 35]  [Cited by in F6Publishing: 26]  [Article Influence: 4.3]  [Reference Citation Analysis (0)]
88.  Hart PA, Topazian MD, Witzig TE, Clain JE, Gleeson FC, Klebig RR, Levy MJ, Pearson RK, Petersen BT, Smyrk TC, Sugumar A, Takahashi N, Vege SS, Chari ST. Treatment of relapsing autoimmune pancreatitis with immunomodulators and rituximab: the Mayo Clinic experience. Gut. 2013;62:1607-1615.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 282]  [Cited by in F6Publishing: 242]  [Article Influence: 22.0]  [Reference Citation Analysis (0)]
89.  Blaho M, Dítě P, Kunovský L, Kianička B. Autoimmune pancreatitis - An ongoing challenge. Adv Med Sci. 2020;65:403-408.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 10]  [Cited by in F6Publishing: 13]  [Article Influence: 3.3]  [Reference Citation Analysis (0)]
90.  Lanzillotta M, Della-Torre E, Wallace ZS, Stone JH, Karadag O, Fernández-Codina A, Arcidiacono PG, Falconi M, Dagna L, Capurso G. Efficacy and safety of rituximab for IgG4-related pancreato-biliary disease: A systematic review and meta-analysis. Pancreatology. 2021;21:1395-1401.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 5]  [Cited by in F6Publishing: 15]  [Article Influence: 5.0]  [Reference Citation Analysis (0)]
91.  Buechter M, Klein CG, Kloeters C, Schlaak JF, Canbay A, Gerken G, Kahraman A. Tacrolimus as a reasonable alternative in a patient with steroid-dependent and thiopurine-refractory autoimmune pancreatitis with IgG4-associated cholangitis. Z Gastroenterol. 2014;52:564-568.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 12]  [Cited by in F6Publishing: 11]  [Article Influence: 1.1]  [Reference Citation Analysis (0)]
92.  Sugimoto M, Takagi T, Suzuki R, Konno N, Watanabe K, Nakamura J, Kikuchi H, Waragai Y, Asama H, Takasumi M, Hikichi T, Watanabe H, Obara K, Ohira H. Efficacy of Steroid Pulse Therapy for Autoimmune Pancreatitis Type 1: A Retrospective Study. PLoS One. 2015;10:e0138604.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 13]  [Cited by in F6Publishing: 13]  [Article Influence: 1.4]  [Reference Citation Analysis (0)]
93.  Chiabrando F, Lanzillotta M, Palumbo D, Pedica F, Caruso M, Capurso G, Della-Torre E. Treating Type 2 Autoimmune Pancreatitis With Colchicine: A Case Series. Ann Intern Med. 2021;174:1775-1776.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 2]  [Cited by in F6Publishing: 3]  [Article Influence: 1.0]  [Reference Citation Analysis (0)]
94.  Lauri G, D'Amico F, Allocca M, Palumbo D, Della-Torre E, De Cobelli F, Doglioni C, Giorgio Arcidiacon P, Capurso G, Danese S. Ustekinumab as Induction and Maintenance Therapy in Patients with Inflammatory Bowel Disease and Type II Autoimmune Pancreatitis: Report of Two Cases. J Crohns Colitis. 2023;17:1552-1554.  [PubMed]  [DOI]  [Cited in This Article: ]  [Reference Citation Analysis (0)]
95.  Abu-Sbeih H, Tang T, Lu Y, Thirumurthi S, Altan M, Jazaeri AA, Dadu R, Coronel E, Wang Y. Clinical characteristics and outcomes of immune checkpoint inhibitor-induced pancreatic injury. J Immunother Cancer. 2019;7:31.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 58]  [Cited by in F6Publishing: 78]  [Article Influence: 15.6]  [Reference Citation Analysis (0)]
96.  Abu-Sbeih H, Tang T, Ali FS, Johnson DH, Qiao W, Diab A, Wang Y. The Impact of Immune Checkpoint Inhibitor-Related Adverse Events and Their Immunosuppressive Treatment on Patients’ Outcomes. J Immunother Precis Oncol. 2018;1:7-18.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 26]  [Cited by in F6Publishing: 26]  [Article Influence: 6.5]  [Reference Citation Analysis (0)]
97.  Sandanayake NS, Church NI, Chapman MH, Johnson GJ, Dhar DK, Amin Z, Deheragoda MG, Novelli M, Winstanley A, Rodriguez-Justo M, Hatfield AR, Pereira SP, Webster GJ. Presentation and management of post-treatment relapse in autoimmune pancreatitis/immunoglobulin G4-associated cholangitis. Clin Gastroenterol Hepatol. 2009;7:1089-1096.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 164]  [Cited by in F6Publishing: 134]  [Article Influence: 8.9]  [Reference Citation Analysis (0)]
98.  Tacelli M, Celsa C, Magro B, Barresi L, Guastella S, Capurso G, Frulloni L, Cabibbo G, Cammà C. Risk Factors for Rate of Relapse and Effects of Steroid Maintenance Therapy in Patients With Autoimmune Pancreatitis: Systematic Review and Meta-analysis. Clin Gastroenterol Hepatol. 2019;17:1061-1072.e8.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 24]  [Cited by in F6Publishing: 29]  [Article Influence: 5.8]  [Reference Citation Analysis (0)]
99.  Kubota K, Kamisawa T, Okazaki K, Kawa S, Hirano K, Hirooka Y, Uchida K, Shiomi H, Ohara H, Shimizu K, Arakura N, Kanno A, Sakagami J, Itoi T, Ito T, Ueki T, Nishino T, Inui K, Mizuno N, Yoshida H, Sugiyama M, Iwasaki E, Irisawa A, Shimosegawa T, Takeyama Y, Chiba T. Low-dose maintenance steroid treatment could reduce the relapse rate in patients with type 1 autoimmune pancreatitis: a long-term Japanese multicenter analysis of 510 patients. J Gastroenterol. 2017;52:955-964.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 55]  [Cited by in F6Publishing: 63]  [Article Influence: 9.0]  [Reference Citation Analysis (0)]
100.  Brito-Zerón P, Kostov B, Bosch X, Acar-Denizli N, Ramos-Casals M, Stone JH. Therapeutic approach to IgG4-related disease: A systematic review. Medicine (Baltimore). 2016;95:e4002.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 86]  [Cited by in F6Publishing: 81]  [Article Influence: 10.1]  [Reference Citation Analysis (0)]
101.  Soliman H, Vullierme MP, Maire F, Hentic O, Ruszniewski P, Lévy P, Rebours V. Risk factors and treatment of relapses in autoimmune pancreatitis: Rituximab is safe and effective. United European Gastroenterol J. 2019;7:1073-1083.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 31]  [Cited by in F6Publishing: 33]  [Article Influence: 6.6]  [Reference Citation Analysis (0)]
102.  Das JP, Postow MA, Friedman CF, Do RK, Halpenny DF. Imaging findings of immune checkpoint inhibitor associated pancreatitis. Eur J Radiol. 2020;131:109250.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 14]  [Cited by in F6Publishing: 18]  [Article Influence: 4.5]  [Reference Citation Analysis (0)]
103.  Okazaki K, Ikeura T, Uchida K. Recent progress on the treatment of type 1 autoimmune pancreatitis and IgG4-related disease. Mod Rheumatol. 2023;33:237-241.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 1]  [Cited by in F6Publishing: 1]  [Article Influence: 1.0]  [Reference Citation Analysis (0)]
104.  Kamata K, Watanabe T, Minaga K, Hara A, Yoshikawa T, Okamoto A, Yamao K, Takenaka M, Park AM, Kudo M. Intestinal dysbiosis mediates experimental autoimmune pancreatitis via activation of plasmacytoid dendritic cells. Int Immunol. 2019;31:795-809.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 16]  [Cited by in F6Publishing: 24]  [Article Influence: 6.0]  [Reference Citation Analysis (0)]