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ID PMID Title PublicationDate abstract
8738962 Anti-Fc gamma receptor autoantibodies from patients with Sjögren's syndrome do not react 1996 Apr Sera from patients with primary Sjögren's syndrome (pSS) have been examined for the presence of cell-free Fc-gamma receptor (Fc gamma R) IIIb, which is expressed in polymorphonuclear leukocytes (PMN), and the production of related autoantibody. Sera from 66 patients with pSS were evaluated by an ELISA using recombinant human Fc gamma RIIIb as the substrate and by flow cytometry. Cell-free Fc gamma RIIIb was also detected by an ELISA. The fine specificity of autoantibodies was established by inhibition with a preparation of Fc gamma RI plus Fc gamma RII, and two ELISAs using Fc gamma RI and Fc gamma RII as the substrates respectively. Anti-Fc gamma RIIIb activity was found in 30 patients (45%), but 25 of them did not react with autologous PMN, whereas they bound to Fc gamma RIIIb eluted from the same PMN in ELISA and Western blotting. Autoantibodies from one serum recognized the three receptors, six with Fc gamma RII in addition to Fc gamma RIII, and three sera were specific for the latter receptor. None of these reacted with Fc gamma RI- and Fc gamma RII-carrying cells. Cell-free Fc gamma RIIIb, but negligible amounts of Fc gamma RIIIa, were detectable in the patient sera. The membrane expression of CD15, an early activation marker, was diminished, while that of three PMN late activation markers was markedly enhanced. Taken together, these results suggest that autoantibodies are produced following the shedding of Fc gamma RIIIb upon PMN activation. A credible candidate for this activation is IgG-containing immune complexes.
8070162 Distribution of vasoactive intestinal peptide (VIP) and its binding sites in labial saliva 1994 May OBJECTIVE: Tissue distribution of vasoactive intestinal peptide (VIP)-containing nerves and their target cells were studied in labial salivary glands in patients with Sjögren's syndrome and in healthy controls. METHODS: Immunoperoxidase staining was used to demonstrate VIP-containing nerve fibers, and receptor autoradiography with 125I-Bolton Hunter (BH)-VIP was used to demonstrate VIP positive binding sites. RESULTS: VIP-containing nerves were seen around salivary acini, salivary ducts, blood vessels and deep parenchyma, but were absent from large inflammatory cell foci in patients with Sjögren's syndrome. Receptor autoradiography with 125I-BH-VIP disclosed VIP binding sites on mucous acinar cells and blood vessels, whereas salivary ducts contained no VIP receptors. VIP binding sites were also absent from the centers of large inflammatory cell foci/acinar atrophy. CONCLUSION: The topology of VIP and its receptor suggests that VIP may act on the vascular and secretory components of the salivary gland. However, VIP causes only a slight increase in non-adrenergic, non-cholinergic salivary secretion. It is therefore more likely that this extensive tissue distribution of VIP and its receptors reflects its recently suggested trophic effects on salivary gland tissue. This is further supported by the observation that VIP-IR nerves/VIP binding sites were absent in areas of focal lymphocytoid infiltrates/acinar atrophy in patients with Sjögren's syndrome.
8385303 Oral manifestations of cytomegalovirus infection. 1993 Apr Disease caused by cytomegalovirus is reported with increasing frequency. Cytomegalovirus is an important pathogen in immunocompromised and immunosuppressed patients. The most common manifestation of cytomegalovirus infection of the gastrointestinal tract including the oral mucosa is ulceration. The role of cytomegalovirus in xerostomia, Sjögren's syndrome, and Kaposi's sarcoma is continuing to be investigated. This article reviews the oral manifestations of cytomegalovirus, including recently reported oral manifestations.
8432914 HLA antigens in anti-Ro(SS-A)-positive patients with recurrent annular erythema. 1993 Feb BACKGROUND: Recurrent annular erythema associated with the anti-Ro(SS-A) antibody response has recently been reported in Orientals. The association is assumed to represent a distinct clinical entity. OBJECTIVE: Our purpose was to extend knowledge on the immunogenetic spectrum of the disease. METHODS: Sixteen anti-Ro(SS-A)-positive Japanese patients with recurrent annular erythema and Sjögren's syndrome were studied. The standard complement-dependent microcytotoxicity assay was used to type the HLA-A, -B, -C, -DR, and -DQ, as well as the HLA-DRw52 and -DRw53 antigens. RESULTS: All 16 patients were positive for HLA-DRw52 antigens as compared with 52% of control subjects (p < 0.01 relative risk 14.8). No significant deviations were noted in the phenotype frequencies for HLA-A, -B, -C, and -DQ antigens. CONCLUSION: HLA-DRw52 is closely related to annular erythema in anti-Ro(SS-A)-positive Japanese patients with Sjögren's syndrome.
1468597 [A case of Hashimoto's thyroiditis associated with renal tubular acidosis, Sjögren syndro 1992 Nov 20 This report describes a 48-year old female patient with Hashimoto's thyroiditis, distal-type renal tubular acidosis (d-RTA), Sjögren syndrome (SjS), and empty sella syndrome (ESS). She has been receiving replacement of thyroxine for Hashimoto's thyroiditis since 1967. She felt muscle weakness and numbness in the extremities and was found to have low serum potassium (2.9 mEq/l) in 1987. Since then she has been administrated potassium chloride orally. She was admitted to our hospital because of recurrence of muscle weakness and numbness of the extremities in November 1990. Laboratory examination revealed that her serum levels of antimicrosomal antibody and anti-thyroglobulin antibody were highly positive (MCHA: x 2(10) x 100, and TGHA: x 100). Furthermore, she was revealed to have 1) d-RTA by oral tolerance tests with the administration of NH4Cl and NaHCO3, 2) SjS by Schirmer test and sialography, and 3) ESS by computed tomography and magnetic resonance imaging examinations of the pituitary. Association of Hashimoto's thyroiditis, d-RTA, SjS and ESS in this case may possibly be caused by common autoimmune mechanism.
1335373 [Preparation of a monoclonal antibody against EA p138 of Epstein-Barr virus: its applicati 1992 Aug A monoclonal antibody against Epstein-Barr virus (EBV) encoded early antigen (EA) p138 was prepared with the use of a lysoprotein from the recombinant plasmid pUCARG1140. By using this specific monoclonal antibody and immunofluorescence as well as immunoenzyme methods, 4 of 13 lacrimal, 15 of 37 labial and all 7 renal biopsy tissues from patients with Sjogren's syndrome (SS) were found to have positive staining of epithelial cells, whereas those of control persons were all negative. These results suggest that EBV has been in the stage of active replication in the aforementioned tissues of SS and this virus may have a close association with SS in terms of pathogenesis.
7562780 C5 deficiency in a patient with primary Sjögren's syndrome. 1995 Jul We report a case of C5 deficiency in combination with Sjögren's syndrome (SS). Our patient presented with polyarthritis and complaints of oral and ocular dryness. In the serum there was a very low titer of total hemolytic complement (CH50) due to a deficiency of the fifth complement component. C5 deficiency is often associated with recurrent life threatening infections, membranous glomerulonephritis, and discoid lupus erythematosus, but it has not been described in association with primary SS.
9063835 [HIV-associated cysts of the parotid glands. An histomorphologic and magnetic resonance to 1996 Nov BACKGROUND: Multiple and bilateral parotid Lymphoepithelial cysts (LEC) are encountered in 3-6% of HIV-infected patients. The formal pathogenesis of LEC is controversial. They are thought to develop from embryological salivary gland inclusions in intraparotid lymphnodes. METHODS: Seventeen operative parotid specimens from HIV-infected patients were examined histologically and immunohistologically. Findings of magnetic resonance imaging (MRI) were correlated with the histological results. RESULTS: A continuous spectrum of a lymphoepithelial salivary gland lesion is found, developing initially from a lymphoid infiltration of salivary lobules to lymphoepithelial duct lesions with cystic dilatation up to large ductal cysts (diameter up to 3.5 cm) with highgrade parenchymal atrophy. The ductal and cystic lesions demonstrate an intense basal cell hyperplasia without participation of myoepithelial cells. The MRI findings indicate involvement of the entire tissue of both parotid glands. CONCLUSIONS: The preferred hypothesis of a development of HIV-associated Lymphoepithelial cysts from preexisting salivary lymphnode inclusions cannot be verified. Our results demonstrate a continuous development of the cysts from a Sjögren-like cystic lymphoepithelial lesion of parotid glands. The enormous cystic dilatation of the duct lesions presumably is a consequence of ductal obstruction through basal cell hyperplasia of striated ducts and intense intraglandular lymphofollicular hyperplasia.
8613065 Serum antibodies to carbonic anhydrase I and II in patients with idiopathic chronic pancre 1996 May BACKGROUND & AIMS: Patients with idiopathic chronic pancreatitis and Sjögren's syndrome show immune responses against a 60-kilodalton protein isolated from human pancreas extracts. Monoclonal antibody SP3-1, raised against the 60-kilodalton protein, reacts with ductal cells in several exocrine organs and cross-reacts with human carbonic anhydrase II. The present study evaluated serum from patients with these diseases for antibodies to human carbonic anhydrase I and II. METHODS: An enzyme-linked immunosorbent assay was used to quantify serum antibody against carbonic anhydrase I and II. RESULTS: Serum antibodies against carbonic anhydrase I and II were detected in 7 and 11 of 33 patients with idiopathic chronic pancreatitis, respectively, and in 8 and 13 of 21 patients with Sjögren's syndrome, respectively. The positive prevalence rates of patients with antibodies of carbonic anhydrase II were significantly different among patients with idiopathic chronic pancreatitis and Sjögren's syndrome compared with normal patients (1 of 21). There were no significant differences in the prevalence rates of patients with alcoholic chronic pancreatitis (3 of 20), gallstone-related chronic pancreatitis (0 of 7), and primary biliary cirrhosis (1 of 11). CONCLUSIONS: The results suggest that carbonic anhydrase II is one candidate target antigen recognized during the autoimmune pathophysiology observed in idiopathic chronic pancreatitis and Sjögren's syndrome.
7548243 [Pulmonary infiltrations in Sjögren syndrome--a radiodiagnostic study]. 1995 Jul We report on the radiological findings of 8 female patients with primary Sjögren's syndrome and pulmonary infiltrations. In the chest x-ray, all patients featured an interstitial diffuse bilateral reticular pattern which was most prominent in the bases. The apices of the upper lobes were not involved. There were no pleural effusions. The radiologic appearances changed only slowly. In three cases the lesions progressed to form a patchy confluent pattern. 4 of 8 patients developed within 24 months a nodal or extranodal lymphoma of low-grade malignancy.
7741662 Increased beta 2-microglobulin in both parotid and submandibular/sublingual saliva from pa 1994 Oct Samples of unstimulated saliva from patients with sialoadenopathy were collected by microcapillary tube (1 microliter), and their beta 2-microglobulin (B2-MG) content determined by a sandwich enzyme immunoassay. A higher than normal (control) concentration of the globulin was present in both parotid and submandibular/sublingual saliva from the patients with Sjögren's syndrome but not in the samples from the patients with sialoadenitis or diabetes mellitus. The increase in B2-MG in saliva from patients with Sjögren's syndrome may reflect that immunolopathological events are important in the degeneration of both glands in this disease. Therefore, the determination of B2-MG in saliva may be a simple, non-invasive technique for confirming the diagnosis of Sjögren's syndrome as an autoimmune disease.
7908513 [Sulfasalazine therapy for hypergammaglobulinemia in patients with Sjögren's syndrome]. 1994 Jan Steroid therapy has been used in patients with Sjögren's syndrome and hyperviscosity syndrome due to hypergammaglobulinemia. We report here the use of sulfasalazine therapy on patients with Sjögren's syndrome and serum immunoglobulin G levels of more than 3000 mg/dl. Sulfasalazine was used because of its inhibitory effect on B cells. Serum levels of immunoglobulin G and A were decreased after 8 weeks' administration of 1000 mg/day sulfasalazine. However four of the eleven patients experienced a side effect (skin rash). Sulfasalazine therapy could be used continuously and appeared to be an effective therapy.
1352097 Primary Sjögren's syndrome with antibodies to HTLV-I: clinical and laboratory features. 1992 Jun The prevalence of antibodies to human T lymphotropic virus type I (HTLV-I) was studied in patients with primary Sjögren's syndrome. Thirteen of 36 serum samples were positive by enzyme linked immunosorbent assay (ELISA) and particle agglutination assay for antibodies to HTLV-I and were confirmed by western blotting. The presence of antibodies to HTLV-I may signify an HTLV-I carrier state. These patients had a high occurrence of extraglandular manifestations such as uveitis, myopathy, and recurrent high fever compared with patients who did not have antibodies to HTLV-I. Patients with antibodies to HTLV-I had an increased spontaneous proliferation of peripheral blood mononuclear cells compared with those without the antibodies. The proportions of activated and memory T cells (HLA-DR+ CD3+, CD25+ CD3+, and CD29+ CD4+ cells) were higher in HTLV-I carriers than in non-carriers. The presence of antibodies to HTLV-I in some patients with primary Sjögren's syndrome suggests that HTLV-I may cause primary Sjögren's syndrome or its extraglandular manifestations, or both.
1376444 CD5+ B lymphocytes and other lymphocyte subsets in primary Sjögren's syndrome. 1992 Apr CD5+ B cells and other lymphocyte subsets were analyzed by flow cytometry in patients with primary Sjögren's syndrome (pSS), in healthy subjects (HS) and in patients with various control diseases. When compared with HS, patients with pSS were found to have similar levels of CD5+ B cells and decreased levels of CD8+ T cells (P = 0.0003). When compared with patients with various other diseases, however, the number of CD5+ B cells in pSS was more than twice as high (P = 0.0002), whereas no difference was found between numbers of CD8+ T cells. When the number of CD5+ B cells was expressed as a percentage of total B cells, the results obtained were similar to those with absolute numbers. Determination of lymphocyte subsets may be used as a diagnostic aid for Sjögren's syndrome in selected patients with suspected immunological diseases of unknown type.
8698925 Acquired generalized hypohidrosis/anhidrosis with subclinical Sjögren's syndrome: report 1996 Aug The pathogenesis and the underlying pathologic changes of acquired generalized hypohidrosis/anhidrosis (AGHA) are largely unknown. We studied a case of AGHA in a young woman suffering from heat intolerance and progressive loss of sweating. Pathologic study of affected skin revealed unique syringolymphoid hyperplasia with T cell infiltration, suggesting a T cell-mediated autoimmune disease. The patient also had subclinical Sjögren's syndrome and diffuse hair loss. The pathogenesis of the latter two conditions is believed to be related to the patient's AGHA.
8738057 Glomerular filtration rate in primary Sjögren's syndrome with renal disease. 1996 Apr Renal disease in Primary Sjögren's syndrome (SS) is often overlooked, because of a paucity of symptoms. Distal renal tubular acidosis (dRTA) and tubulointerstitial nephritis (TIN) might be present. Only a few cases of SS with decreased glomerular filtration rate (GFR) have been reported. We have studied GFR in 27 female SS-patients, mean age 62 years (37-78). GFR was measured as the single injection 51Cr-EDTA plasma clearance. Eighteen women had normal GFR (group 1), and nine (33%) had values below the lower normal limit (group 2). In group 2, dRTA was present in 8/9 urolithiasis in 6/9, previous upper urinary tract infection (UTI) in 2/9 and TIN in 5/6 patients who were kidney biopsied. Among patients with dRTA 8/18 (44%) had decreased GFR. We conclude that decreased GFR is not unusual in SS-patients with dRTA, and decreased GFR is mostly associated with TIN. Urolithiasis and UTI may contribute to decreased GFR in some individuals.
8875029 Current concepts of autoimmune exocrinopathy: immunologic mechanisms in the salivary patho 1996 Sjögren's syndrome is a systemic autoimmune disorder characterized by symptoms of oral and ocular dryness and a chronic, progressive loss of salivary and lacrimal function. The exocrine involvement is the result of a focal, peri-ductal mononuclear cell infiltrate and the subsequent loss of secretory epithelial cells. The mechanisms of this autoimmune exocrinopathy are not understood fully. Many recent investigations have described alterations in a number of immune mediators within the salivary glands. These studies provide new insights into the immune regulation of normal salivary gland functions and the mechanisms of gland damage in Sjögren's syndrome.
8391219 Epstein-Barr virus and the lacrimal gland pathology of Sjögren's syndrome. 1993 Jul The lacrimal gland (LG) immunopathology of Sjögren's syndrome (SS) consists of a proliferation of B and CD4 lymphocytes surrounding epithelial structures (Pepose JS, et al: Ophthalmology 1990, 97:1599-1605). Based on the detection of EBV genomes in a greater percentage of SS than normal LG biopsies, we previously postulated that Epstein-Barr virus (EBV) is a risk factor for LG lymphoproliferation in SS (Pflugfelder SC, et al: Ophthalmology 1990, 97:976-984). The purpose of this study was to determine the cellular site(s) of infection, virus type, and antigen expression of EBV infecting normal and SS LGs. EBV DNA was detected by in situ hybridization in intraductal epithelia in 13-33% of lobules in 21% of normal LGs and in cells in areas of B lymphoproliferation as well as the majority of epithelia in 86% of SS LGs. EBV genomic sequences were amplified from 36% of normal and 88% of SS LG biopsies by polymerase chain reaction. Only type 1 EBV sequences were amplified in SS LGs; in contrast EBV nuclear antigen 2-deleted but not type 1 sequences were amplified in normal LGs. Immunohistochemistry with EBV-specific monoclonal antibodies was performed on normal and SS LGs. No EBV antigens were detected in normal LGs. In contrast, latent antigens (latent membrane protein, EBV nuclear antigen 2) were detected in lymphocytes in areas of B lymphoproliferation, and early and late lytic cycle antigens were observed in epithelia in SS LGs. These studies suggest that EBV may play a role in the LG B lymphoproliferation and epithelial pathologic changes observed in SS.
8480145 Pulmonary pseudolymphoma presented with a mass lesion in a patient with primary Sjögren's 1993 A 61-year-old woman with primary Sjögren's syndrome (SS) presented with fever, dry cough, dyspnea on exertion, and a mass lesion with reticular shadowing at both bases on her chest X-ray. Pulmonary pseudolymphoma was diagnosed by transbronchial lung biopsy which revealed infiltration of T cell-like slightly atypical lymphoid cells. After three infusions of cyclophosphamide (750 mg every 4 weeks) combined with prednisolone, the pulmonary mass lesion was diminished and her symptoms improved. Evaluation of the 12 reported cases of pulmonary pseudolymphoma with SS that presented with mass lesions showed an increase in IgM level, frequent pulmonary fibrosis, precedence of SS, and better prognosis with immunosuppressants in those patients.
8882053 Thrombotic thrombocytopenic purpura in adult Still's disease. 1996 Feb We describe 2 patients with adult Still's disease who developed thrombotic thrombocytopenic purpura (TTP) and were successfully treated. Although TTP has been associated with autoimmune diseases, usually with systemic lupus erythematosus or various forms of vasculitis, it has rarely been observed in patients with adult Still's disease. This uncommon coexistence of 2 clinical entities may indicate similar pathogenetic mechanisms.