Guest guest Posted February 6, 2001 Report Share Posted February 6, 2001 American College of Rheumatology 1999 Annual Scientific Meeting [Medscape, 1999. © 1999 Medscape, Inc.] Epidemiology, Diagnostics, and Management Borenstein, MD Sjogren syndrome was addressed in a State of the Art Lecture by Roland Jonsson, DMD,PhD, professor of immunology at the University of Bergen in Norway. He reviewed the clinical manifestations and research advances associated with Sjogren syndrome and the presentation of more than 40 abstracts. Sjogren syndrome was named for the Swedish ophthalmologist Henrik Sjogren, who first described the clinical and pathological findings of xerostomia (dry mouth) and keratoconjunctivitis sicca (dry eye).[1] Primary Sjogren syndrome is the disorder that occurs independent of any additional connective tissue disease, whereas secondary Sjogren syndrome occurs in the setting of other connective tissue diseases, such as rheumatoid arthritis, systemic lupus erythematosus, or polymyositis. Epidemiology Sjogren syndrome is a disease that affects all populations throughout the world and occurs in all age groups. The peak incidence is in the fourth and fifth decades of life, with a female-male ratio of 9:1. The prevalence of primary Sjogren syndrome varies from 0.08% in a population study in California to 2.7% in Sweden,[2,3] with an average prevalence of 0.2%. The variation in frequency of the illness in these population studies may be explained in part by different classification criteria. The variation in other associated illnesses, such as lymphoma, demyelinating disorders, or vasculitis, may also result from a lack of agreement on diagnostic criteria. Classification Criteria The most recent European criteria from 1993[4] include an emphasis on patients' subjective complaints. The criteria include the presence of four of six symptoms, including (1) ocular symptoms, (2) oral symptoms, (3) evidence of keratoconjunctivitis sicca, (4) focal sialadenitis by minor salivary gland involvement, (5) instrumental evidence of salivary gland involvement, and (6) presence of autoantibodies. Ocular symptoms include dry eyes for more than 3 months, recurrent sensation of sand or gravel in the eyes, or use of tear substitutes more than three times a day. Oral symptoms include the daily feeling of dry mouth for more than 3 months, recurrent or persistent swollen salivary glands, or use of liquid to aid in swallowing dry food. Ocular signs are characterized by a positive result on the Shirmer test (<5 mm in 5 minutes) or a Rose Bengal staining score of more than 4 according to the van Bijsterveld scoring system. Focal sialadenitis is distinguished by lymphoid infiltration in exocrine glands. The grading system of 1 to 4 corresponds to increasing lymphocytic infiltration with increasing destruction of salivary gland structures. Objective salivary gland testing includes salivary scintigraphy, parotid sialography, or unstimulated salivary flow (<1.5 mL in 15 minutes). Antibodies to Ro(SS-A) or La(SS-, antinuclear antibodies, and rheumatoid factors are associated with Sjogren syndrome. For primary Sjogren syndrome, the presence of four of six criteria has a sensitivity of 93.5% and specificity of 94.0%. The San Diego criteria for Sjogren syndrome include manifestations of both primary and secondary Sjogren syndrome. Primary Sjogren syndrome is characterized by the following: 1. Symptoms and objective signs of ocular dryness (Schirmer test result of <8-mm wetting per 5 minutes and positive Rose Bengal staining of cornea or conjunctiva to demonstrate keratoconjunctivitis sicca). 2. Symptoms and objective signs of dry mouth (decreased parotid flow rate using Lashley cups and abnormal findings on biopsy specimen of minor salivary gland, with a focus score of >2 based on an average of four evaluable lobules). 3. Serologic evidence of systemic autoimmunity (elevated rheumatoid factor >1:320 or elevated antinuclear antibody >1:320 or presence of anti-SS-A[Ro] or anti-SS-B[La]antibodies). Secondary Sjogren syndrome is defined by characteristic signs and symptoms of Sjogren syndrome plus clinical features of rheumatoid arthritis, systemic lupus erythematosus, polymyositis, scleroderma, or biliary cirrhosis. The European and San Diego classification systems are the two most currently referenced criteria. Clinical Features Sjogren syndrome encompasses a wide clinical spectrum from specific autoimmune exocrinopathy to a systemic disorder characterized by multiple organ failure, including the kidney, nervous, and musculoskeletal systems. The illness is caused by a CD4 T lymphocyte infiltration of lacrimal and salivary glands. Namekawa et al further characterized the areas of salivary gland destruction to contain CD4+CD28- cytotoxic T lymphocytes.[5] The disease starts insidiously, with increasing dryness of the eyes and mouth. Individuals describe the feeling of having sand in their eyes, whereas others notice increasing difficulty with eating dry foods, such as bread or crackers. Extraglandular manifestations of Sjogren syndrome include fatigue and musculoskeletal pain. Strombeck et al[6] presented a visual analog pain scale and Short Form 36 data obtained from patients with primary Sjogren syndrome, rheumatoid arthritis, and fibromyalgia. The patients with Sjogren syndrome had a significant decrease in quality of life similar to those of the rheumatoid arthritis and fibromyalgia groups, which was related to the degree of pain felt by these individuals. In regard to Sjogren syndrome and arthritis, Brennan et al presented data on the frequency of sialadenitis and early synovitis in a cohort of 10 patients.[7] Six individuals had positive lip biopsy specimens, whereas only four had symptoms of xerostomia. The histologic biopsy specimen characteristics were similar for a control group of patients with Sjogren syndrome and the subjects with early synovitis, suggesting that the arthritis associated with Sjogren syndrome may be mediated by similar cells to those found in salivary glands. Autoantibodies and Pathogenesis The immune disorder associated with Sjogren syndrome is characterized by B-cell activation, the production of multiple autoantibodies, and the loss of immune tolerance. The antibodies correlate with the extent and severity of disease in Sjogren syndrome and are potentially involved in the pathogenic development of autoimmune exocrinopathy. Anti-Ro/SS-A and anti-La/SS-B are the clinically important autoantibodies in primary Sjogren syndrome. Anti-Ro precipitins occur in approximately 60% to 75% of primary Sjogren syndrome cases and are also observed in cases of secondary Sjogren syndrome.[8] The two Ro proteins (Ro52 and Ro60) localize to surface membrane outcroppings on apoptotic cells, and these blebs may become targets of the autoimmune response.[9] Anti-La occurs in 40% of patients with primary Sjogren syndrome. The La antigen is a RNA polymerase I.[10] Dr. Jonsson suggested that the pathogenic role of anti-Ro and anti-La in Sjogren syndrome included the association among leukopenia, lymphopenia, and hypogammaglobulinemia with more severe salivary disease. An association between surface expression of La on conjunctival cells and aberrant expression pattern of La on labial salivary glands exists in patients with Sjogren syndrome, as does local salivary production of anti-Ro and anti-La and the presence of Ro52 and 60. Additional proof of nonspecific B-cell activation may be found in the number of autoantibodies produced by patients with Sjogren syndrome. These antibodies include those directed against carbonic anhydrase, proteasomal subunits, and alpha-fodrin. Antiphospholipid antibodies of the immunoglobulin A isotype were reported in 20% of patients with Sjogren syndrome without signs of antiphospholipid syndrome, but the clinical importance of these antibodies remains to be determined. In contrast, the presence of muscarinic M3 receptor antibodies that decrease salivary flow may explain impaired glandular function in individuals with less extensive lymphocytic infiltration of salivary glands.[11] Immunopathogenesis and Apoptosis The immunohistology of exocrine glands in Sjogren syndrome shows a predominant T-cell infiltration with fewer B cells and macrophages. The T cells are thought to play a prominent role in the destruction of salivary glands, but the exact mechanism of damage remains unknown. On recognition of a proper major histocompatibility complex antigen complex on a target cell, cytotoxic T cells should induce cell death by one of two independent pathways: the perforin-mediated or Fas-mediated pathway. However, apoptosis is deficient in the lymphocytes of patients with Sjogren syndrome. Although the expression of fas, fasL,bcl-2, and other apoptosis-associated proteins has been detected in minor salivary glands from patients with Sjogren syndrome,[12] studies have shown a low degree or absence of cell death among infiltrating mononuclear cells.[13] In addition to the damage caused by the absence of apoptosis, injury to epithelial cells may also dampen the response of these cells to muscarinic stimulation.[14] These damaged cells would explain the severe dryness that was out of proportion to the actual number of apoptotic cells seen in salivary gland biopsy specimens. Glandular hypofunction is not solely a result of the destruction of salivary glands, because normal acinar cells may be observed in patients with Sjogren syndrome, and lymphocytic glandular infiltration is not always accompanied by decreased salivation. Therapy Treatment of Sjogren syndrome is directed at decreasing the symptoms; no therapy is currently available to decrease lymphocytic infiltration of salivary glands or reverse the imbalance of apoptosis of lymphocytes. Oral therapies are prescribed to increase the production of saliva and tears. A study by LeVeque et al reported on the long-term effect of pilocarpine hydrochloride on increases in salivary flow in patients with Sjogren syndrome.[15] There were 212 patients with Sjogren syndrome who received 2.5 to 30 mg per day of pilocarpine during a 15-month period. Increased salivary flow was sustained during the study without evidence of tachyphylaxis. Adverse events were limited to sweating in 49%, urinary frequency in 16.5%, flushing in 11.3%, and chills in 8%. Pilocarpine is safe and effective therapy for xerostomia associated with Sjogren syndrome. For dry eye symptoms, Tsubota et al[16] reported on Cevimeline, a drug studied in Japan. This drug is an analog of acetylcholine chloride and binds preferentially to muscarinic M3 receptors. In a double-blind study of 60 patients, 53% of the 19 patients taking 20 mg three times daily and 53% of 15 patients taking 30 mg three times daily significantly improved compared with the placebo group. Eye symptoms decreased with less eye pain, and Rose Bengal staining decreased at 2 weeks into therapy. This preliminary study needs to be extended to document the continued efficacy and safety of this agent for longer periods. References 1. Sjogren H. Zur kenntnis der keratoconjunctivitis sicca. Acta Opthalmol. 1933;11(suppl 2):1-151. 2.Fox RI, C, Curd J, et al. Suggested criteria for classification. Scand J Rheumatol. 1986;61:28-30. 3.Manthorpe R, Oxholm P, Prause JU, et al. The Copenhagen criteria for Sjogren's syndrome. Scand J Rheumatol. 1986;61:19-21. 4.Vitali C, Bombardieri S, Moutsopoulos H, et al. Preliminary criteria for the classification of Sjogren's syndrome: results of a prospective concerted action supported by the European community. Arthritis Rheum. 1993;36:340-347. 5.Strombeck B, Ekdahl C, sson L, Manthorpe R, Wikstrom I. Health-related quality of life in primary Sjogren's syndrome, rheumatoid arthritis and fibromyalgia compared to normal population data using SF-36. Arthritis Rheum. 1999;42(suppl):S222. 6.Namekawa T, Matsumura R, Sumida T, et al. Involvement of cytotoxic CD4+ CD28-T cells in the tissue destruction of salivary glands from patients with Sjogren's syndrome. Arthritis Rheum. 1999;42(suppl):S140. 7.Reichlin M, Scofield RH. SS-A(Ro) autoantibodies. In: JB, Schoenfeld Y, eds. Autoantibodies. Amsterdam, Netherlands: Elsevier; 1996:789-797. 8.Brennan MT, Pilemer SR, Goldbach-Mansky R, et al. Focal sialadenitis in patients with early synovitis. Arthritis Rheum. 1999;42(suppl):S137. 9.Casciola-Rosen LA, Anhalt G, Rosen A. Autoantigens targeted in systemic lupus erythematosus are clustered in two populations of surface structures on apoptotic keratinocytes. J Exp Med. 1994;179:1317-1330. 10.Chan EKL, Andrade LEC. Antinuclear antibodies in Sjogren's syndrome. Rheum Clin North Am. 1992;18:551-570. 11.Bacman S, LC, Sterin-Borda L, et al. Autoantibodies against lascrimal gland M3 muscarinic acetylcholine receptors in patients with primary Sjogren's syndrome. Invest Opthalmol Vis Sci. 1998;39:151-156. 12.Kong L, Ogawa N, Nakabayashi T, et al. Fas and Fas ligand expression in the salivary glands of patients with primary Sjogren's syndrome. Arthritis Rheum. 1997;40:87-97. 13.Nakamura H, Koji T, Tominaga M, et al. Apoptosis in labial salivary glands from Sjogren's syndrome (SS) patients: companion with human T lymphotropic virus-I (HTLV-I)-seronegative and -seropositive SS patients. Clin Exp Immunol. 1998:114:106-112. 14.Masago R, Kong L, Aiba-Masago S, et al. Fas-mediated signaling abnormalities in salivary epithelial cells created by aborted apoptosis: a model for SS. Arthritis Rheum. 1999;42(suppl):S402. 15.LeVeque F, Khan Z, Salisbury PL, et al. Sustained increases in salivary flow and safety findings following extended use of pilocarpine tablets for the treatment of dry mouth symptoms in patients with Sjogren's syndrome (SS). Arthritis Rheum. 1999;42(suppl):S139. 16.Tsubota K, Ono M, Takamura E, et al. Efficacy of civimeline, a muscarinic agonist in treating dry eye symptoms in patients with Sjogren's Syndrome. Arthritis Rheum. __________________________________________________ Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 6, 2001 Report Share Posted February 6, 2001 American College of Rheumatology 1999 Annual Scientific Meeting [Medscape, 1999. © 1999 Medscape, Inc.] Epidemiology, Diagnostics, and Management Borenstein, MD Sjogren syndrome was addressed in a State of the Art Lecture by Roland Jonsson, DMD,PhD, professor of immunology at the University of Bergen in Norway. He reviewed the clinical manifestations and research advances associated with Sjogren syndrome and the presentation of more than 40 abstracts. Sjogren syndrome was named for the Swedish ophthalmologist Henrik Sjogren, who first described the clinical and pathological findings of xerostomia (dry mouth) and keratoconjunctivitis sicca (dry eye).[1] Primary Sjogren syndrome is the disorder that occurs independent of any additional connective tissue disease, whereas secondary Sjogren syndrome occurs in the setting of other connective tissue diseases, such as rheumatoid arthritis, systemic lupus erythematosus, or polymyositis. Epidemiology Sjogren syndrome is a disease that affects all populations throughout the world and occurs in all age groups. The peak incidence is in the fourth and fifth decades of life, with a female-male ratio of 9:1. The prevalence of primary Sjogren syndrome varies from 0.08% in a population study in California to 2.7% in Sweden,[2,3] with an average prevalence of 0.2%. The variation in frequency of the illness in these population studies may be explained in part by different classification criteria. The variation in other associated illnesses, such as lymphoma, demyelinating disorders, or vasculitis, may also result from a lack of agreement on diagnostic criteria. Classification Criteria The most recent European criteria from 1993[4] include an emphasis on patients' subjective complaints. The criteria include the presence of four of six symptoms, including (1) ocular symptoms, (2) oral symptoms, (3) evidence of keratoconjunctivitis sicca, (4) focal sialadenitis by minor salivary gland involvement, (5) instrumental evidence of salivary gland involvement, and (6) presence of autoantibodies. Ocular symptoms include dry eyes for more than 3 months, recurrent sensation of sand or gravel in the eyes, or use of tear substitutes more than three times a day. Oral symptoms include the daily feeling of dry mouth for more than 3 months, recurrent or persistent swollen salivary glands, or use of liquid to aid in swallowing dry food. Ocular signs are characterized by a positive result on the Shirmer test (<5 mm in 5 minutes) or a Rose Bengal staining score of more than 4 according to the van Bijsterveld scoring system. Focal sialadenitis is distinguished by lymphoid infiltration in exocrine glands. The grading system of 1 to 4 corresponds to increasing lymphocytic infiltration with increasing destruction of salivary gland structures. Objective salivary gland testing includes salivary scintigraphy, parotid sialography, or unstimulated salivary flow (<1.5 mL in 15 minutes). Antibodies to Ro(SS-A) or La(SS-, antinuclear antibodies, and rheumatoid factors are associated with Sjogren syndrome. For primary Sjogren syndrome, the presence of four of six criteria has a sensitivity of 93.5% and specificity of 94.0%. The San Diego criteria for Sjogren syndrome include manifestations of both primary and secondary Sjogren syndrome. Primary Sjogren syndrome is characterized by the following: 1. Symptoms and objective signs of ocular dryness (Schirmer test result of <8-mm wetting per 5 minutes and positive Rose Bengal staining of cornea or conjunctiva to demonstrate keratoconjunctivitis sicca). 2. Symptoms and objective signs of dry mouth (decreased parotid flow rate using Lashley cups and abnormal findings on biopsy specimen of minor salivary gland, with a focus score of >2 based on an average of four evaluable lobules). 3. Serologic evidence of systemic autoimmunity (elevated rheumatoid factor >1:320 or elevated antinuclear antibody >1:320 or presence of anti-SS-A[Ro] or anti-SS-B[La]antibodies). Secondary Sjogren syndrome is defined by characteristic signs and symptoms of Sjogren syndrome plus clinical features of rheumatoid arthritis, systemic lupus erythematosus, polymyositis, scleroderma, or biliary cirrhosis. The European and San Diego classification systems are the two most currently referenced criteria. Clinical Features Sjogren syndrome encompasses a wide clinical spectrum from specific autoimmune exocrinopathy to a systemic disorder characterized by multiple organ failure, including the kidney, nervous, and musculoskeletal systems. The illness is caused by a CD4 T lymphocyte infiltration of lacrimal and salivary glands. Namekawa et al further characterized the areas of salivary gland destruction to contain CD4+CD28- cytotoxic T lymphocytes.[5] The disease starts insidiously, with increasing dryness of the eyes and mouth. Individuals describe the feeling of having sand in their eyes, whereas others notice increasing difficulty with eating dry foods, such as bread or crackers. Extraglandular manifestations of Sjogren syndrome include fatigue and musculoskeletal pain. Strombeck et al[6] presented a visual analog pain scale and Short Form 36 data obtained from patients with primary Sjogren syndrome, rheumatoid arthritis, and fibromyalgia. The patients with Sjogren syndrome had a significant decrease in quality of life similar to those of the rheumatoid arthritis and fibromyalgia groups, which was related to the degree of pain felt by these individuals. In regard to Sjogren syndrome and arthritis, Brennan et al presented data on the frequency of sialadenitis and early synovitis in a cohort of 10 patients.[7] Six individuals had positive lip biopsy specimens, whereas only four had symptoms of xerostomia. The histologic biopsy specimen characteristics were similar for a control group of patients with Sjogren syndrome and the subjects with early synovitis, suggesting that the arthritis associated with Sjogren syndrome may be mediated by similar cells to those found in salivary glands. Autoantibodies and Pathogenesis The immune disorder associated with Sjogren syndrome is characterized by B-cell activation, the production of multiple autoantibodies, and the loss of immune tolerance. The antibodies correlate with the extent and severity of disease in Sjogren syndrome and are potentially involved in the pathogenic development of autoimmune exocrinopathy. Anti-Ro/SS-A and anti-La/SS-B are the clinically important autoantibodies in primary Sjogren syndrome. Anti-Ro precipitins occur in approximately 60% to 75% of primary Sjogren syndrome cases and are also observed in cases of secondary Sjogren syndrome.[8] The two Ro proteins (Ro52 and Ro60) localize to surface membrane outcroppings on apoptotic cells, and these blebs may become targets of the autoimmune response.[9] Anti-La occurs in 40% of patients with primary Sjogren syndrome. The La antigen is a RNA polymerase I.[10] Dr. Jonsson suggested that the pathogenic role of anti-Ro and anti-La in Sjogren syndrome included the association among leukopenia, lymphopenia, and hypogammaglobulinemia with more severe salivary disease. An association between surface expression of La on conjunctival cells and aberrant expression pattern of La on labial salivary glands exists in patients with Sjogren syndrome, as does local salivary production of anti-Ro and anti-La and the presence of Ro52 and 60. Additional proof of nonspecific B-cell activation may be found in the number of autoantibodies produced by patients with Sjogren syndrome. These antibodies include those directed against carbonic anhydrase, proteasomal subunits, and alpha-fodrin. Antiphospholipid antibodies of the immunoglobulin A isotype were reported in 20% of patients with Sjogren syndrome without signs of antiphospholipid syndrome, but the clinical importance of these antibodies remains to be determined. In contrast, the presence of muscarinic M3 receptor antibodies that decrease salivary flow may explain impaired glandular function in individuals with less extensive lymphocytic infiltration of salivary glands.[11] Immunopathogenesis and Apoptosis The immunohistology of exocrine glands in Sjogren syndrome shows a predominant T-cell infiltration with fewer B cells and macrophages. The T cells are thought to play a prominent role in the destruction of salivary glands, but the exact mechanism of damage remains unknown. On recognition of a proper major histocompatibility complex antigen complex on a target cell, cytotoxic T cells should induce cell death by one of two independent pathways: the perforin-mediated or Fas-mediated pathway. However, apoptosis is deficient in the lymphocytes of patients with Sjogren syndrome. Although the expression of fas, fasL,bcl-2, and other apoptosis-associated proteins has been detected in minor salivary glands from patients with Sjogren syndrome,[12] studies have shown a low degree or absence of cell death among infiltrating mononuclear cells.[13] In addition to the damage caused by the absence of apoptosis, injury to epithelial cells may also dampen the response of these cells to muscarinic stimulation.[14] These damaged cells would explain the severe dryness that was out of proportion to the actual number of apoptotic cells seen in salivary gland biopsy specimens. Glandular hypofunction is not solely a result of the destruction of salivary glands, because normal acinar cells may be observed in patients with Sjogren syndrome, and lymphocytic glandular infiltration is not always accompanied by decreased salivation. Therapy Treatment of Sjogren syndrome is directed at decreasing the symptoms; no therapy is currently available to decrease lymphocytic infiltration of salivary glands or reverse the imbalance of apoptosis of lymphocytes. Oral therapies are prescribed to increase the production of saliva and tears. A study by LeVeque et al reported on the long-term effect of pilocarpine hydrochloride on increases in salivary flow in patients with Sjogren syndrome.[15] There were 212 patients with Sjogren syndrome who received 2.5 to 30 mg per day of pilocarpine during a 15-month period. Increased salivary flow was sustained during the study without evidence of tachyphylaxis. Adverse events were limited to sweating in 49%, urinary frequency in 16.5%, flushing in 11.3%, and chills in 8%. Pilocarpine is safe and effective therapy for xerostomia associated with Sjogren syndrome. For dry eye symptoms, Tsubota et al[16] reported on Cevimeline, a drug studied in Japan. This drug is an analog of acetylcholine chloride and binds preferentially to muscarinic M3 receptors. In a double-blind study of 60 patients, 53% of the 19 patients taking 20 mg three times daily and 53% of 15 patients taking 30 mg three times daily significantly improved compared with the placebo group. Eye symptoms decreased with less eye pain, and Rose Bengal staining decreased at 2 weeks into therapy. This preliminary study needs to be extended to document the continued efficacy and safety of this agent for longer periods. References 1. Sjogren H. Zur kenntnis der keratoconjunctivitis sicca. Acta Opthalmol. 1933;11(suppl 2):1-151. 2.Fox RI, C, Curd J, et al. Suggested criteria for classification. Scand J Rheumatol. 1986;61:28-30. 3.Manthorpe R, Oxholm P, Prause JU, et al. The Copenhagen criteria for Sjogren's syndrome. Scand J Rheumatol. 1986;61:19-21. 4.Vitali C, Bombardieri S, Moutsopoulos H, et al. Preliminary criteria for the classification of Sjogren's syndrome: results of a prospective concerted action supported by the European community. Arthritis Rheum. 1993;36:340-347. 5.Strombeck B, Ekdahl C, sson L, Manthorpe R, Wikstrom I. Health-related quality of life in primary Sjogren's syndrome, rheumatoid arthritis and fibromyalgia compared to normal population data using SF-36. Arthritis Rheum. 1999;42(suppl):S222. 6.Namekawa T, Matsumura R, Sumida T, et al. Involvement of cytotoxic CD4+ CD28-T cells in the tissue destruction of salivary glands from patients with Sjogren's syndrome. Arthritis Rheum. 1999;42(suppl):S140. 7.Reichlin M, Scofield RH. SS-A(Ro) autoantibodies. In: JB, Schoenfeld Y, eds. Autoantibodies. Amsterdam, Netherlands: Elsevier; 1996:789-797. 8.Brennan MT, Pilemer SR, Goldbach-Mansky R, et al. Focal sialadenitis in patients with early synovitis. Arthritis Rheum. 1999;42(suppl):S137. 9.Casciola-Rosen LA, Anhalt G, Rosen A. Autoantigens targeted in systemic lupus erythematosus are clustered in two populations of surface structures on apoptotic keratinocytes. J Exp Med. 1994;179:1317-1330. 10.Chan EKL, Andrade LEC. Antinuclear antibodies in Sjogren's syndrome. Rheum Clin North Am. 1992;18:551-570. 11.Bacman S, LC, Sterin-Borda L, et al. Autoantibodies against lascrimal gland M3 muscarinic acetylcholine receptors in patients with primary Sjogren's syndrome. Invest Opthalmol Vis Sci. 1998;39:151-156. 12.Kong L, Ogawa N, Nakabayashi T, et al. Fas and Fas ligand expression in the salivary glands of patients with primary Sjogren's syndrome. Arthritis Rheum. 1997;40:87-97. 13.Nakamura H, Koji T, Tominaga M, et al. Apoptosis in labial salivary glands from Sjogren's syndrome (SS) patients: companion with human T lymphotropic virus-I (HTLV-I)-seronegative and -seropositive SS patients. Clin Exp Immunol. 1998:114:106-112. 14.Masago R, Kong L, Aiba-Masago S, et al. Fas-mediated signaling abnormalities in salivary epithelial cells created by aborted apoptosis: a model for SS. Arthritis Rheum. 1999;42(suppl):S402. 15.LeVeque F, Khan Z, Salisbury PL, et al. Sustained increases in salivary flow and safety findings following extended use of pilocarpine tablets for the treatment of dry mouth symptoms in patients with Sjogren's syndrome (SS). Arthritis Rheum. 1999;42(suppl):S139. 16.Tsubota K, Ono M, Takamura E, et al. Efficacy of civimeline, a muscarinic agonist in treating dry eye symptoms in patients with Sjogren's Syndrome. Arthritis Rheum. __________________________________________________ Quote Link to comment Share on other sites More sharing options...
Guest guest Posted July 15, 2003 Report Share Posted July 15, 2003 It is Sjoegren's syndrome - a comprehensive and unpleasant auto-immune condition. Let's see what the various suggestions are for this! Savage MA RSHom FSHom 26 Winstanley Road Saffron Walden Essex CB11 3EQ 01799 524442 Mobile: 07889 989398 Email: roger.jo@... Sjpgren syndrome Hi-Have anyone ever heard of the above syndrome. I have never been diagnosed with it but I have all the symtoms and an auto immune disease too. If you have had any experience in treating it with QXCI I would like to hear from you. Thanks. ............................................. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted April 1, 2012 Report Share Posted April 1, 2012 Thanks Ebtessam and RasheedaYes from that point of view you are right But I read in scully that in sjogren ,lymphocytes and plasma cell infiltrate salivary glands making acinar destruction.Doesn't that make it type 4 then? What do you think? Other opinions please?BalsamSent from my iPadOn 1 Apr 2012, at 12:59, ebtessam elhamalawy <ebtessamhamalawy@...> wrote: hi basmala I believe its type 3 CHCH BY IMMUNOCOMPLEX FORMAITON THAT AFFECTS MULTIPLE ORGANSBEST REGARDSEBTISAM From: Balsam_Majid <balsam_majid@...> " " < > Sent: Sunday, 1 April 2012, 12:08 Subject: Sjogren syndrome What type of hypersensitivity is sjogren syndrome plz? Sent from my iPad = Quote Link to comment Share on other sites More sharing options...
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