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At least 19 recordsLinked to original sources
PubMed1988

Clinicopathological study of myoepithelial sialadenitis and chronic sialadenitis (sialolithiasis).

To determine any overlap in pathological features between myoepithelial sialadenitis and chronic sialadenitis/sialolithiasis histological sections from 69 cases of myoepithelial sialadenitis (MESA) (n = 7) and chronic sialadenitis/sialolithiasis (n = 62) were reviewed over a 10 year period. Three of the cases with MESA contained calculi and four of those originally diagnosed as chronic sialadenitis/sialolithiasis showed epimyoepithelial island formation. The presence of calculi should not rule out a diagnosis of MESA, particularly in the parotid gland where calculi are uncommon; as the incidence of MESA may very well be underestimated and diagnosed as chronic sialadenitis, these patients, who are at increased risk of developing lymphoma, could be lost to follow up.

Adult↗
PubMed2001

Focal sialadenitis in patients with ankylosing spondylitis and spondyloarthropathy: a comparison with patients with rheumatoid arthritis or mixed connective tissue disease.

OBJECTIVES: To investigate the occurrence of and risk factors for focal sialadenitis in patients with rheumatoid arthritis (RA), mixed connective tissue disease (MCTD), ankylosing spondylitis (AS), and spondyloarthropathy (SpA). METHODS: A total of 85 patients (25 with RA, 19 with MCTD, 19 with AS, 22 with SpA) participated in the study. Each patient filled out a questionnaire for eye and oral symptoms and for the use of medication, and was interviewed; other tests included Schirmer's test, laboratory tests, collection of unstimulated and stimulated whole saliva, and minor salivary gland biopsy. A focus score of > or =1 was regarded as an indicator of focal sialadenitis. RESULTS: Focal sialadenitis was observed in 68% (57/84) of all patients. It affected 80% (20/25) of the patients with RA, 94% (17/18) of those with MCTD, 58% (11/19) of those with AS, and 41% (9/22) of those with SpA (chi(2) test, p=0.0013). Salivary secretion correlated negatively with the focus scores-that is, severity of focal sialadenitis. Patients with focal sialadenitis had both decreased salivary secretion and decreased tear secretion significantly more often than did patients without (chi(2) test, p=0.0074 and p=0.048 respectively). Patients with positive rheumatoid factor (RF), antinuclear antibodies (ANA), or SSA or SSB antibodies had sialadenitis significantly more often than did patients with negative antibodies. In the subgroup of patients with AS or SpA, no associations were found between focal sialadenitis and the presence of these antibodies. CONCLUSION: In addition to patients with RA or MCTD, focal sialadenitis also affects a very high proportion of patients with AS or SpA. Focus scores are significantly higher in patients with RA or MCTD than in those with AS or SpA. A significant association exists between focal sialadenitis and RF, ANA, SSA and SSB. However, in the subgroup of patients with AS or SpA, no associations were found between focal sialadenitis and serological markers or clinical symptoms.

Adult↗
PubMed1998

Parotid and submandibular sialadenitis treated by salivary gland excision.

BACKGROUND: The purpose of the present study was to compare and contrast the clinicopathological features and treatment outcome of chronic sialadenitis involving the parotid and submandibular glands, among patients who were treated by excision of the affected gland. METHODS: In a series of 88 patients treated over an 8-year period, 47 had parotid sialadenitis and 41 had submandibular sialadenitis. In the parotid group, 63% of patients were symptomatic for longer than 6 months compared with 27% in the submandibular group. Calculi were implicated in the disease process in 24% of patients with parotid sialadenitis, compared with 73% of patients with submandibular disease. RESULTS: Patients with parotid sialadenitis had superficial (n = 14) or near-total parotidectomy (n = 35), while those with submandibular sialadenitis underwent total gland excision. Complications occurred twice as frequently in the parotidectomy group. The rate of temporary facial nerve weakness was 29% after parotidectomy while marginal mandibular nerve dysfunction occurred after 12% of submandibular excisions. Both procedures were highly effective in permanently relieving the symptoms of sialadenitis. CONCLUSIONS: Parotid sialadenitis is infrequently associated with stones and tends to run a longer course before surgical intervention is necessary. Submandibular sialadenitis usually presents earlier, is secondary to calculi and requires early intervention.

Chronic Disease↗
PubMed2007

Sialoendoscopic treatment for radioiodine induced sialadenitis.

BACKGROUND AND OBJECTIVE: The use of radioiodine (RI) for the ablation of residual thyroid tissue and metastatic thyroid cancer lesions after thyroidectomy has become established as standard treatment in the management of differentiated thyroid cancer and subsequent sialadenitis is the most common complication of RI therapy. The purpose of this study was to establish a new treatment modality for RI-induced sialadenitis. METHOD: The study group consisted of 115 patients with a mean age of 47.7 (range, 24-78) years. All patients received RI therapy after total thyroidectomy. The incidence of RI-induced sialadenitis, salivary gland involvement, administered RI dose, treatment modality, and result of treatment by interventional sialoendoscopy were evaluated. RESULTS: The incidence of RI-induced sialadenitis was 18% (21/115), with involvement of the parotid more frequent than the submandibular gland. The average development period of RI-induced sialadenitis was 4.8 months. The average RI dosage for the sialadenitis group was higher than for the nonsialadenitis group, suggesting that RI-induced sialadenitis may be dose related, although the data were not statistically significant because of the small numbers in the high-dose group. Conservative management was effective in 71% (15/21) of the cases, and interventional sialoendoscopy was successful in 50% of those cases that did not respond to conservative treatment. The causes of treatment failure in the remaining cases were a totally obstructed parotid duct and stenosis at the bifurcation site. CONCLUSION: Sialadenitis is the most common complication after RI therapy. Sialadenitis was successfully managed by conservative treatment in most cases, and interventional sialoendoscopy is an alternative method of treatment in selected cases such as in partial ductal stenosis.

Adult↗
PubMed2002

The genetic control of sialadenitis versus arthritis in a NOD.QxB10.Q F2 cross.

The non-obese diabetic (NOD) mouse spontaneously develops diabetes and sialadenitis. The sialadenitis is characterized by histopathological changes in salivary glands and functional deficit similar to Sjögren's syndrome. In humans, Sjögren's syndrome could be associated with other connective tissue disorders, such as rheumatoid arthritis. In the present study the genetic control of sialadenitis in mice was compared to that of arthritis. We have previously reported a NOD locus, identified in an F2 cross with the H2(q) congenic NOD (NOD.Q) and C57BL/10.Q (B10.Q) strains, that promoted susceptibility to collagen-induced arthritis. The sialadenitis in NOD.Q showed a similar histological phenotype as in NOD, whereas no submandibular gland infiltration was found in B10.Q. The development of sialadenitis was independent of immunization with type II collagen and established arthritis. To identify the genetic control of sialadenitis, a gene segregation experiment was performed on an (NOD.QxB10.Q)F2 cross and genetic mapping of 353 F2 mice revealed one significant locus associated with sialadenitis on chromosome 4, LOD score 4.7. The NOD.Q allele-mediated susceptibility under a recessive inheritance pattern. The genetic control of sialadenitis seemed to be unique in comparison to diabetes and arthritis, as no loci associated with these diseases have been identified at the same location.

Animals↗
PubMed1999

Genetic basis of autoimmune sialadenitis in MRL/lpr lupus-prone mice: additive and hierarchical properties of polygenic inheritance.

OBJECTIVE: To clarify the mode of inheritance of autoimmune sialadenitis in MRL/MpJ-lpr/lpr (MRL/lpr) lupus-prone mice and identify the susceptibility loci. METHODS: MRL/lpr, C3H/HeJ-lpr/lpr (C3H/lpr), (MRL/lpr x C3H/lpr)F1 intercross, and MRL/lpr x (MRL/lpr x C3H/lpr)F1 backcross mice were prepared, and sialadenitis in individual mice was analyzed by histopathologic grading. The genomic DNA of the backcross mice was examined by simple sequence-length polymorphism analysis, and the highly associated polymorphic microsatellite markers with sialadenitis were determined as sialadenitis susceptibility loci. RESULTS: Four susceptible gene loci recessively associated with sialadenitis were mapped on chromosomes 10, 18, 4, and 1, respectively. These loci manifested additive and hierarchical properties in the development of sialadenitis. CONCLUSION: The results indicate that sialadenitis in MRL/lpr mice is under the control of polygenic inheritance, possibly involving allelic polymorphism.

Animals↗
PubMed2001

Treatment of chronic sialadenitis in a murine model of Sjögren's syndrome by local fasL gene transfer.

OBJECTIVE: Infection of Fas (Fas/CD95)-mutant C57BL/6 (B6)-lpr/lpr mice with murine cytomegalovirus (MCMV) leads to a chronic sialadenitis similar to that of Sjögren's syndrome (SS). The aim of this study was to evaluate whether chronic sialadenitis would also occur in Fas ligand (FasL/CD95L)-mutant B6-gld/gld mice upon infection with MCMV and whether the expression of FasL by local gene transfer using recombinant adenoviral vectors would be an effective therapeutic strategy. METHODS: B6-gld/gld mice were infected intraperitoneally with MCMV, and salivary glands were analyzed histologically at different time points. For treatment of sialadenitis, recombinant adenoviral vectors expressing the fasL gene (AdLoxpFasL + AxCANCre) or the lacZ gene (AdCMVLacZ) were locally injected into the salivary glands of MCMV-infected B6-gld/gld mice and uninfected B6-+/+ and B6-gld/gld mice. RESULTS: Following MCMV infection, B6-gld/gld mice developed an acute and chronic sialadenitis characterized by multiple foci of infiltrating T cells. After local injection of adenoviral vectors, high levels of lacZ or fasL gene expression could be detected in acinar and ductal cells. Treatment of acute and chronic sialadenitis in B6-gld/gld mice with local fasL gene transfer resulted in a significant reduction in the number of inflammatory foci and tissue destruction in salivary glands compared with mice treated with AdCMVLacZ. Despite high levels of FasL expression after injection of recombinant vectors, <5% of ductal and acinar cells were TUNEL positive, demonstrating that, in this model of SS, acinar and ductal cells were not highly sensitive to FasL-mediated apoptosis. CONCLUSION: Chronic sialadenitis similar to that of SS developed in B6-gld/gld mice after MCMV infection. FasL expression was reconstituted by local gene transfer, resulting in significant reduction of infiltrating mononuclear cells, which indicates that local gene transfer of fasL might be a novel treatment for chronic sialadenitis.

Animals↗
PubMed1988

Effects of immunomodulating treatment on autoimmune sialadenitis in MRL/Mp-lpr/lpr mice.

The autoimmune MRL/Mp-lpr/lpr (MRL/l) mouse spontaneously develops sialadenitis with a morphological and phenotypical pattern similar to that seen in human Sjögren's syndrome (SS). This makes the MRL/l mouse a suitable model for therapeutical studies of autoimmune sialadenitis. We have, by histological and immunohistochemical techniques, analyzed the therapeutical effect of treatment with LS2616, a recently synthesized oxokinolinamide derivative, on sialadenitis in submandibular glands of MRL/l mice. The results were compared with effects obtained after treatment with cyclophosphamide (CY) and physiologic saline. Administration of both LS2616 and CY to MRL/l mice has previously been found to result in prolongation of survival and amelioration of organ pathology. However, only CY treatment reduced sialadenitis, while LS2616 increased the semiquantitatively assessed focal inflammation of salivary glands in 6 months old mice. No differences in T-cell phenotypes of infiltrating lymphoid cells in salivary glands between different treatment regims could be noted. However, the frequency of B-cells in the sialadenitis was decreased in the CY treated group. In contrast, CY but not LS2616 treatment normalized expression of T-helper and cytotoxic T-cell phenotypes as well as reduced the B-cell portion in lymph nodes. It is concluded that CY treatment can suppress sialadenitis although both LS2616 and CY are effective in prolongation lifespan of MRL/l mice. This may implicate different immunopathogenic mechanisms for development of sialadenitis versus other organ lesions in the autoimmune disease of MRL/l mice.

Adjuvants, Immunologic↗
PubMed1977

[On the pathogenesis of the Küttner tumor of the submandibular gland -- Analysis of 349 cases with chronic sialadenitis of the submandibular (author's transl)].

In view of the etiology and pathogenesis of the so-called Kütter tumor (chronic sialadenitis of the submandibular gland) gland resections of 349 patients (salivary gland register at the Institute of Pathology, University of Hamburg; period 165--1974) were analyzed pathohistologically. In 143 cases (41%) a sialolithiasis of the submandibular gland occurred simultaneously. Regarding the degree of the inflammation 4 stages were distinguished (stage 1 = focal sialadenitis; stage 2= diffuse lymphocytic sialadenitis with salivary gland fibrosis; stage 3 = chronic sclerosing sialadenitis with salivary gland sclerosis; stage 4= chronic progressive sialadenitis with salivary gland cirrhosis). Twenty-five per cent of the cases were classified in stage 1, 19% in stage 2, 38% in stage 3, and 18% in stage 4. A predominance of the male sex (70%) was observed especially in stage 4. The initial stage is characterized by a periductally lymphocytic infiltration, ectasias of the ducts, and alteration of the secret in the duct lumens (spheroliths, microliths). In stages 2--3 an increase of the inflammatory infiltration with lymph follicles, considerable alterations of the ducts (metaplasias, dysplasias, regenerates of the ducts), and a parenchymal reduction were found. This process is combined with an increase of the interstitial connective tissue and a cicatrication of the salivary gland parenchyma. In the final stage, 4, a cirrhotic gland transformation with progressive loss of the parenchyma and considerable duct destruction appeared. From the pathogenetic course of the inflammation and the comparison with other forms of sialadenitis, the conclusion is drawn that two etiologic factors are important in the Küttner tumor: an initial disturbance of secretion with an obstructive electrolyte sialadenitis and an immune reaction of the salivary duct system with the final phase of an obstructive, progressive immunosialadenitis.

Adolescent↗
PubMed2005

Up-regulation of surfactant protein A in chronic sialadenitis.

OBJECTIVES: Salivary secretions play a critical role in maintaining the health of the oral cavity, which is the first gate of entry to the airways and thus is exposed to a variety of environmental insults. Surfactant protein A (SP-A) is a member of the collectin family and plays an important role in first-line airway defense. The objectives of this study were to examine the expression of SP-A messenger RNA and protein in human salivary glands and to investigate its up-regulation during inflammatory conditions. DESIGN: Reverse transcription-polymerase chain reaction was performed on salivary gland tissues from patients and a control group. The expression levels of SP-A to GAPDH (glyceraldehyde-3-phosphate dehydrogenase) transcripts were semiquantified by densitometry. We also characterized the cellular localizations of SP-A protein immunohistochemically. SETTING: Tertiary academic institution. PATIENTS: Ten patients with chronic sialadenitis and 10 patients with healthy salivary glands. RESULTS: Surfactant protein A messenger RNA and protein were detected in glands of patients who were healthy and in those with chronic sialadenitis. The expression levels of SP-A messenger RNA in the salivary glands of patients with chronic sialadenitis was significantly increased compared with those in healthy salivary glands. Immunohistochemical staining revealed SP-A immunoreactivity in the ductal epithelia of healthy salivary glands and in the salivary glands of those with chronic sialadenitis, and stronger immunoreactivity was observed in those with chronic sialadenitis tissues. CONCLUSIONS: Surfactant protein A is present in the salivary gland epithelium and is up-regulated in individuals with chronic sialadenitis. These results suggest that salivary gland SP-A may play an important role in the innate host defense of human salivary glands.

Chronic Disease↗
PubMed2006

Antagonist of interferon-inducible protein 10/CXCL10 ameliorates the progression of autoimmune sialadenitis in MRL/lpr mice.

OBJECTIVE: Mononuclear cell infiltration of the salivary glands is a major feature of Sjögren's syndrome (SS) and its animal model. Local generation of chemokines and the presence of chemokine receptors on the infiltrating cells may be involved in this process. We undertook the present study to investigate the expression of chemokines during the development of autoimmune sialadenitis in MRL/lpr mice and the therapeutic effect of chemokine antagonists on sialadenitis. METHODS: NH2-terminal-truncated interferon-inducible protein 10 (IP-10)/CXCL10 analogs were transfected into a nonmetastatic fibroblastoid cell line, MRL/N-1, and injected subcutaneously into MRL/lpr mice, and the effects on sialadenitis were monitored. RESULTS: IP-10 analogs truncated by 5 or more amino acid residues from the N-terminal failed to induce chemotaxis and calcium influx by CXCR3-expressing cells. Of these, the most potent antagonist (AT) (IP-10-AT) was a molecule with methionine added after removal of the 5 N-terminal amino acid residues. Significantly increased expression of the Th1-associated chemokines IP-10, monokine induced by interferon-gamma/CXCL9, and interferon-inducible T cell chemoattractant/CXCL11 was induced in the ductal epithelium by interferon-gamma produced in the salivary glands, whereas expression of the Th2-associated chemokines thymus and activation-regulated chemokine (TARC)/CCL17 and monocyte-derived chemokine/CCL22 was almost undetectable during sialadenitis. Inoculation of IP-10-AT into MRL/lpr mice during the early stage of sialadenitis significantly reduced periductal mononuclear cell infiltration and parenchymal destruction compared with these features in control and TARC-AT-bearing mice. This was due to a significant reduction in infiltration of CXCR3+ T cells, predominantly Th1 cells, resulting in decreased interferon-gamma production. CONCLUSION: We prepared a novel potent IP-10 antagonist and demonstrated its ability to ameliorate the progression of autoimmune sialadenitis. This agent may provide a new therapeutic approach to SS.

Animals↗
PubMed1997

Effects of sialadenitis after cellular transfer in autoimmune MRL/lpr mice.

The MRL/Mp mice bearing a lymphoproliferative gene, lpr (MRL/Mp-lpr/lpr), provide an appropriate model for the study of autoimmune mechanisms leading to the destruction of salivary and lacrimal gland tissue in Sjögren's syndrome. By 7-8 weeks of age, progressive focal inflammatory cell infiltrates are observed in salivary glands. We examined the possibility of transferring this disorder into syngeneic, young animals. Spleen cells and infiltrating mononuclear cells (MNC) enzymatically eluted from salivary glands were used. The results showed that sialadenitis could be transferred in vivo to young MRL/lpr mice by splenic and salivary gland MNC. The most striking finding was observed in male recipients where the highest incidence of sialadenitis (5/5) was seen in the group injected intravenously with a small dose (1 x 10(6) of salivary gland MNC, CD8+ splenic cells alone were not able to transfer disease. On the other hand, CD4+ splenic cells induced a more severe sialadenitis compared to the control animals. The transfer of pooled cells from salivary glands resulted in the most severe and accelerating sialadenitis (P < 0.05) in female recipients compared with the control animals. Overall, the highest sialadenitis scores (> 0.10) were obtained only after transfer of CD4+ spleen cells and infiltrating salivary gland MNC. These findings indicate that sialadenitis in MRL/lpr mice is mediated by cellular mechanisms and suggest that the infiltrating MNC have the ability to accelerate autoimmune disease in the salivary glands.

Adoptive Transfer↗
PubMed1995

Short-term administration of selected anti-T-cell receptor V beta chain specific MoAb reduces sialadenitis in MRL/lpr mice.

Sialadenitis develops spontaneously in MRL/Mp mice bearing a lymphoproliferative gene, lpr (MRL/Mp-lpr/lpr). Based on recent observations of an oligoclonal expansion of T-cell receptor (TCR) expressing V beta chain families (V beta 4, V beta 8.1,2, V beta 10b) in salivary glands of these mice we have initiated selective antibody therapy. Treatment with monoclonal antibodies (MoAb) specific for T cells expressing a mixture of TCR V beta 4, V beta 8.1,2 and V beta 10b was applied to MRL/lpr mice before and after the spontaneous development of sialadenitis. The in vivo treatment with V beta 4, V beta 8.1,2 and V beta 10b MoAb did not prevent the development of sialadenitis. However, in animals with established sialadenitis, treatment with the MoAb significantly decreased the inflammation compared with the control groups. Immunohistochemical staining of cell phenotypes demonstrated a change in the ratio of CD4/CD8 in the animals with established sialadenitis. Altogether, these findings illustrate that it is possible to modulate sialadenitis and infiltrate cell phenotypes in vivo in MRL/lpr mice with specific anti-TCR V beta MoAb treatment.

Animals↗
PubMed2002

Iodide-induced sialadenitis complicating coronary angiography.

Sialadenitis is an uncommon complication of intravenous administration of iodinated contrast medium. We present two cases of iodide-induced sialadenitis following coronary angiography. Clinical features and clues to differentiation from suppurative sialadenitis are discussed. The mechanism for aseptic iodide-induced sialadenitis remains unclear, but prognosis with conservative treatment is apparently good. Sialadenitis may recur with subsequent administration of contrast medium.

Aged↗
PubMed2006

Surgical treatment of chronic parotid sialadenitis.

OBJECTIVE: To review the results of surgical management of chronic parotid sialadenitis refractory to medical therapy, with particular respect to long-term symptom resolution and development of post-operative complications. METHODS: A retrospective review of parotidectomies performed for chronic intractable parotid sialadenitis. Information was collected about presentation, pre-operative investigations, surgical treatment, post-operative complications and outcome. RESULTS: 36 parotidectomies were performed for chronic sialadenitis between 1991 and 2002. Age at presentation was 56+/-9.6 years, with median symptom duration of 2.3 years. For patients with non-specific presentations, magnetic resonance imaging (MRI) was the most useful pre-operative investigation. Superficial parotidectomy with duct preservation was the main treatment with a 94 per cent success rate, and near-total parotidectomy was reserved for patients with extensive deep-lobe involvement. Duct ligation significantly increased the risk of transient facial palsy. There was a 56 per cent and 22 per cent incidence of temporary facial paresis and Frey's syndrome, respectively. CONCLUSIONS: Controversies exist regarding the optimal pre-operative investigation and surgical treatment of chronic parotid sialadenitis. We advocate magnetic resonance image (MRI) scanning for patients with non-specific symptoms of sialadenitis, and sialography in the presence of reasonable clinical suspicion. We propose superficial parotidectomy without parotid duct ligation as the standard of care, with near-total parotidectomy reserved for extensive deep-lobe disease.

Adolescent↗
PubMed1989

Epithelial HLA-DR expression in labial salivary glands in Sjögren's syndrome and non-specific sialadenitis.

The expression of the Class II major histocompatibility antigen HLA-DR was quantified in the epithelial cells of labial salivary glands from patients with Sjögrens Syndrome (SS) and compared with similar expression in glands showing non-specific sialadenitis and normal controls. In all glands more duct cells were positive than acinar cells but only in sialadenitis and SS was strong epithelial staining seen. The proportions of duct and acinar cells expressing HLA-DR were increased between normals and sialadenitis (P less than 0.01) and between sialadenitis and SS (P less than 0.001). However, for all cases increased expression of HLA-DR correlated to the increased proportion of inflammatory cells in the gland (P less than 0.01). The results indicate that although HLA-DR is expressed on the epithelial cells in the glandular lesions of SS, this is not specific as it is also seen in sialadenitis. This supports the view that such expression is secondary to an inflammatory infiltrate and may not be of importance in initiating autoimmune tissue damage.

Adolescent↗
PubMed2005

IgG4-related sclerosing disease incorporating sclerosing pancreatitis, cholangitis, sialadenitis and retroperitoneal fibrosis with lymphadenopathy.

BACKGROUND AND AIMS: Autoimmune pancreatitis is usually associated with elevated serum IgG4 concentrations, and sometimes with sclerosing cholangitis and Sjögren's syndrome. This study aimed to elucidate the proposed entity of IgG4-related sclerosing disease. METHODS: Subjects were patients with autoimmune pancreatitis (n = 26), sclerosing sialadenitis (n = 5), chronic alcoholic pancreatitis (n = 20), sialolithiasis (n = 34), Sjögren's syndrome (n = 50), and primary sclerosing cholangitis (n = 3). Sections of various organs and tissues of these patients were examined immunohistochemically using antibodies to CD4-T, CD8-T, and CD20-B cell subsets and IgG4, and serum IgG4 concentrations were measured. RESULTS: Patients with autoimmune pancreatitis were associated with sclerosing cholangitis (n = 23), sclerosing sialadenitis (n = 2), retroperitoneal fibrosis (n = 2), and abdominal (n = 5) and cervical (n = 4) lymphadenopathy. They demonstrated infiltrations of more abundant IgG4-positive plasma cells in the pancreas, peripancreatic retroperitoneal tissues, extrahepatic bile duct, gallbladder, stomach, minor salivary gland, and abdominal lymph nodes compared with those of other diseases (p < 0.01). Such infiltrations were also observed in the minor salivary gland and submandibular gland of patients with sclerosing sialadenitis (p < 0.01). Serum IgG4 concentrations were significantly elevated in patients with autoimmune pancreatitis and sclerosing sialadenitis (p < 0.01). CONCLUSION: We propose a new clinicopathological entity of IgG4-related sclerosing disease incorporating sclerosing pancreatitis, cholangitis, sialadenitis and retroperitoneal fibrosis with lymphadenopathy.

Aged↗