HIGLIGHTS OF THE 11TH INTERNATIONAL CONGRESS ON BEHCET’S DISEASE
October 27 – 31, 2004; Antalya
Izzet Fresko MD
Division of Rheumatology
Department of Internal Medicine
Cerrahpasa Medical Faculty
University of Istanbul
Istanbul,
Turkey
The 11th International Congress of Behçet’s Disease (BD) was held in Antalya, Turkey during 27-31 October 2004 under the auspices of the International Society for Behçet’s Disease and the Turkish Society for Education and Research in Rheumatology. Two hundred and sixty four medical doctors participated in the meeting and 250 abstracts were presented.
Dr. Maurizio Cutolo from Italy opened the congress with a lecture on gender and disease. He stressed the roles of testosterone and 17-beta estradiol on the generation of the immune response with special emphasison the apoptotic effects of the former on lymphocytes. He then gave an overview on the gender differences observed during the course of BD. He hypothesized that inflammatory diseases with a male predominance might be caused by a chronic infection related to the immunosuppressive properties of androgens although there is no data at the moment to support this (1).
EPIDEMIOLOGY
Two groups reported that there was a decrease in the total number of patients with BD in Japan with a trend towards milder forms such as less severe eye involvement (2,3,4). There was a very low prevalence of BD in Thailand with 23 cases diagnosed in a university hospital in 24 years (5), a neurological involvement frequency of 23% in Lebanon (6) and a group of patients with severe disease who had a high prevalence of gastrointestinal and neurological involvement (22% and 38%) from Italy; a country where severe cases are not expected (7). However, there were biases of referral and ascertainment in these studies and the definitions of neurological and gastroenterological involvement were not clear. A study among hospital workers in Cerrahpasa Medical Faculty, Istanbul found prevalences of BD and rheumatoid arthritis that were similar to those reported in field surveys. The authors suggested that this may form the basis of low cost epidemiological studies among hospital employees in different locations (8). A Tunisian group claimed that BD patients with a late disease onset (>40 years) were mostly males (M/F=2.6/1) who had frequent articular involvement (9) whereas an Iranian group showed that they were frequently women who had more frequent eye disease (10). Females tended to have more severe oral ulcerations (11) and more frequent episodes of erythema nodosum and arthritis compared to males (12) in spite of the consensus that males usually have a more severe disease course.
Quality of life was a major issue. Several studies from Turkey showed that increased disease activity resulted in a worse quality of life irrespective of the index used (Oral health impact profile-14, Short Form-36). Females tended to have lower scores although they were as responsive to changes in disease activity as males (13,14). It was not known however whether the lower performance in females was due to a methodological problem, to an issue related to the female sex or to a specific feature of BD. A British group developed a quality of life measure specific to Behçet’s disease and claimed that it had excellent scaling and psychometric properties (15). However it lacked questions that addressed vision loss. Another study showed that patients with BD had more psychiatric symptoms and a poorer quality of life than controls but did not explore the relationship between the two (16). A survey of socioeceonomic status among patients with BD in Istanbul showed that they tended to be poorer from patients with ankylosing spondylitis and inflammatory bowel disease and the disease burden was higher among the less well to do (17).
The Iranians presented an arithmetical extrapolation of the original version of the classification tree where each symptom is numerically graded (18). They claimed that it was more sensitive and specific than the International Study Group criteria in classifying BD.
GENETICS:
The genetics panel had 4 invited speakers. Silman from the UK discussed the methodological problems of genetic studies. He adressed the issues of sample selection, genotyping and analysis and discussed the sources of error in interpreting data, emphasizing the large numbers of subjects required (over 2000) to obtain sufficient power (19). Gül from Turkey discussed the limitations of linkage studies and whole genome analyses and emphasized the possible role of modest risk alleles that may have important roles in diseases with high frequencies in the population (common disease/common variant hypothesis). He also stressed the possible role of the epistatic interactions between non-HLA loci with the HLA-B locus such as HLA-B51 and killer immunoglobulin-like receptors (KIR) and the novel methods such as SEREX used to identify candidate genes (20). Wallace from the UK commented on genes in linkage disequilibrium with HLA-B51. He emphasized the role of TNF, MIC and TAP polymorphisms (TNFB*2, TNFb*1, MICA009/A6 allele, TAP2*0101) in disease pathogenesis and their roles as severity or susceptibility alleles. He concluded that the strongest association was still between HLA-B51 and BD (21). Weinberger from Israel explored the animal models that examined the mechanisms of activation of T-cells by HLA-B51, HLA-B51 related peptides or peptides that may cross react with those mentioned above. He showed that the sera of some patients with BD had antibodies to α-tropomyosin (TPM) and rats vaccinated with this 35-45 kD protein developed arthritis, uveitis and skin inflammation. He proposed that TPM caused inflammation in rats either due to “molecular mimicry” with HLA-B51 or due to its presention by B51 to T-cell receptors. He concluded that it remains to be explained how these phenomena are associated with particular genes (22).
A Japanese group showed that the nucleotide sequences of HLA-B510101 were completeley identical among Italian, Jordanian, Turkish and Japanese BD patients and that HLA-B510101 had a common ancestral origin. However there were 7 single nucleotide polymorphisms in all ethnic groups that permitted the generation of 5 different haplotypes (23).
There were numerous abstracts on the association of various genetic polymorphisms with BD. Two studies explored mannose binding lectin gene polymorphisms. The first found a modest association of the disease with the HYPA haplotype (24) and the second with the mutant type codon 54 (25). A Turkish study claimed that patients with BD had a higher frequency of the GSTM1 null phenotype of the glutathione S-transferase gene; an enzyme involved in the detoxification and activation of various chemicals (26). The allelic frequencies and the untranslated and/or promoter regions of IL-12 p40, interferon regulatory factor 1, IL-8 and mannose binding lectin genes were determined in 87 patients with BD and 65 controls. There were no differences between the two groups (27). One study on 22 single nucleotide polymorphisms in cytokine genes revealed that there were differences in IL-1RA mspal 11100, TGF-β, IL-2 and IL-6 genotypes among BD patients and controls (28). Another study failed to show any relationship in the genetic ability to produce tumour necrosis factor-α, IL-6, TGF-β1, Interferon-γ and IL-10 and the severity of BD (29). HLA-G polymorphisms; a gene that protects target tissues from NK or T cell induced cytolysis, were examined in a group of patients with BD in a Korean study. The 3741*+14bp and 1597*delC containing haplotype was increased more than two fold in BD patients compared to controls but the functional significance of this finding was unknown (30). There were two studies on killer immunoglobulin-like receptor gene polymorphisms. The first found a selective decrease of KIR3DS1 alleles in BD patients especially among those who were B-51 negative and an increase in 3DL1 alleles. The authors suggested that the epistatic interaction between the Bw4 epitopes of HLA-B51 with the KIR3DL1 molecules was important in the pathogenesis (31). The second study found a negative association between BD and KIR3DL1 and KIR2DS alleles (32). There was an equal frequency of C5a receptor polymorphism (C/T transition at position 450) among 54 BD patients and 126 controls. However the polymorphism was protective for uveitis (33). Another study from Turkey explored the -318*C/T and +49*A/G single nucleotide polymorphisms of CTLA-4 and CD28 among patients with BD. There was no statistically significance difference among the patients and controls but +49*A/G was associated with arthritis (34). CTLA-4 +49*A/G allele was more frequent in ocular involvement and erythema nodosum (35). The last three studies explored FcγRIIa, IIIa and IIIb receptor, endothelial nitric oxide synthase and heat shock protein (HSP) 60/65 gene polymorphisms in BD. The first study found relationships between FcγRIIIa polymorphisms and arthritis and FcγRIIIb polymorphisms and vascular involvement (36). The second study claimed that the Glu298Asp polymorphism in exon 7 of the eNOS gene was a susceptibility gene for BD in Turkish patients (37) and the third study showed a very weak association between the GAT/GAA heterozygote single nucleotide polymorphism of the HSP 60/65 gene and vascular BD (38).
BASIC SCIENCE
There were several studies on the various aspects of innate immunity. The expression of toll like receptors were investigated in two abstracts. The first study found an increased expression of toll like receptors of 2,4,6,9 and 10 in the oral biopsy samples of patients with BD compared to controls (39). The second study showed lower baseline expression of toll like receptor 6 in patients with BD compared to normal controls and increased expression of receptors 1 and 2 on granulocytes after stimulation with lipopolysaccharide (LPS), heat schock protein 60 (HSP) and streptococcus sanguis extract (ST). Receptor 6 was increased only after LPS and HSP stimulation. In contrary, monocyte receptor 2 and 6 expressions decreased significantly after LPS and HSP stimulation. The authors concluded that monocytes and granulocytes had different roles in disease pathogenesis (40). A Japanese group found an increased expression of anti mannan antibodies against Saccharomyces Cerevisiae (ASCA) or Rhodotorula glutinis (ARGA) in a limited number of patients with BD although the titers were lower than those found in Crohn’s disease. They thought that their presence was a useful serological marker for BD (41). Another study explored the relationship between serum mannose binding lectin levels and streptococcus mutans colonization of the mouth. They found that patients with lower serum mannose binding lectin levels tended to have higher levels of streptococcus mutans colonization in saliva (42). The expression of human neutrophil anti microbial peptides (HNP 1-3) were examined in skin biopsies of patients with BD. Their expressions were increased in positive pathergy specimens and in spontaneous skin lesions compared to normal controls. The authors claimed that alpha defensins were major effector molecules in BD (43). A multiplex bead analysis of cytokines from sera of patients with BD showed that IL-8 was the dominant cytokine. The cytokine profile was consistent with that seen in an innate rather than an adaptive immune response (44).
Three studies evaluated neutrophil functions. One study found an increased expression of Fc γ receptor 1 (CD64) in neutrophils among patients with active BD. However the levels were normal in patients in remission and it was not possible to differentiate patients with active BD patients from patients with infections (45). Another study found an increased oxidative burst reaction in the nutrophils and monocytes of patients with BD in response to monosodium urate crystals. However the reaction was not specific to BD and the response was not correlated to the MSU skin test results (46). A group investigated the effects of testosterone on neutrophil activity in BD by measuring oxidative burst responses. Oxidative burst index was significantly higher in male patients without testosterone treatment. Treatment with testosterone induced an oxidative burst in female patients. It also increased the apoptosis ratio in BD patients in general (47). Another study from the UK showed that serum levels of IL-15; a cytokine involved in the stimulation of neutrophils and in the delay of their apoptosis, were elevated in patients with BD compared to controls (48).
Several reports on oral immunology explored the relationships between saliva and oral epithelial cells, T cells, cytokeratins, differentiation markers and adhesion molecules. The first study showed that IL-1a expression was significantly higher in the saliva of BD patients compared to healthy controls. A peculiar finding was the dramatically stimulated epithelial cell proliferation in response to the saliva of healthy controls compared to patients with BD (49). The second study showed that mitogen stimulated T cells from BD patients secreted several cytokines that were capable of inducing proliferation and differentiation of buccal epithelial cells (50). The third study demonstrated that cytokeratins 6 and 16, ICAM-1, VCAM and alpha-6 integrin were upregulated in oral ulcer punch biopsies of patients with BD providing evidence for T-cell mediated activation of epithelial cells and abnormalities of the keratinocyte differentiation pathway in BD mucosa (51).
A few studies explored the Th1/Th2 polarization in BD and the cell types and cytokines involved in this polarization. One study found an upregulated expression of IL-12 receptor in circulating T-cells of patients with active BD (52), and another found a correlation between interferon-γ, IL-12 and IL-18 levels with disease activity in BD although the levels of these cytokines were lower than those found in normal controls (53). A group from Tunisia reported increased levels of interferon-γ producing CD8+ T cells in patients with active and inactive BD (54). An abstract from Japan revealed that BD patients receiving conventional therapies had high levels of interferon-γ, IL-12 and TNF-α. A single infusion of infliximab reduced circulating TNF-α secreting cells while the levels re-increased after infliximab was stopped (55).
Alpha enolase is the target of serum anti endothelial cell antibodies and it is a protein that may have an important role in fibrinolysis. It was suggested that α enolase antibodies could be used as a diagnostic test in BD (56). There was cross reactivity between the antibody response to human α enolase with the response to Streptococcus cell wall antigen (57). The antibodies were positive in systemic lupus erythematosus, rheumatoid arthritis, dermatomyositis, scleroderma, Takayasu’s arteritis and mixed connective tissue disease.as well as in BD (58). Patients with gastrointestinal BD had higher degrees of α enolase antibodies compared to patients with inflammatory bowel diseases (59).
The possible role of chemokines in the pathogenesis of BD were investigated. One study found increased synovial fluid levels of IL-8 in patients with BD and rheumatoid arthritis and lower expression of ELR(+)CXC angiogenic chemokines in BD compared to rheumatoid arthritis. The results were compatible with the superficial and non destructive synovitis of BD compared to rheumatoid arthritis (60). Another study showed that the CXCR4 gene was upregulated in patients with active BD and I-309 was strongly expressed in dermal microvascular endothelial cells (61). CXCR3 was the principal chemokine receptor involved in BD, particularly during central nervous system manifetations (62).
There were a few abstracts on the microbiological aspects of the disease. An abstract from Japan showed that peripheral blood mononuclear cells from patients with BD produced lower levels of IL-12, TNF-α and IL-8 compared to normal controls when they were stimulated by human homologous oligopeptides of Streptococcal heat shock protein 60. They claimed that the tolerance produced could be used as a therapeutic tool (63). The streptococci isolated from patients with BD were heterogenous. At least two species within the mitis group were involved (64). Pustular pathergy lesions in BD were not sterile and Staphylococcus aureus, coagulase negative Staphylococci and Propionibacterium acnes were grown from the specimens obtained (65).
Two studies explored the levels of vascular endothelial growth factor (VEGF) in BD; an angiogenic factor induced by hypoxia. The first evaluated its role in the uveitis of BD with the hypothesis that ischemic neovascularization plays an important role in the eye involvement of this condition. They found increased levels in patients with active and inactive uveitis and in patients with proliferative diabetic retinopathy. They concluded that VEGF was a non specific marker of BD uveitis without any relation to disease activity (66). An Austrian group showed that VEGF levels were high in a small cohort of patients with BD compared to controls (67).
A Japanese study showed the presence of anti-cofilin autoantibodies in the sera of patients with BD. However the results were not specific to BD. They could not comment on the pathological role of these antibodies (68). The decrease in oral aphthae during smoking in BD was due to a specific anti inflammatory effect of nicotine and biochanin A, a phytoestrogen (69). Another German study investigated the role of human recombinant interferon α on intracellular cytokines in T cells. Human recombinant interferon α acted by up-regulating reduced IL-2 levels in CD3+/CD4+ T cells in patients with BD (70)
Studies on experimental uveitis models showed that human cationic antimicrobial protein 18 peptide was beneficial in ameliorating streptococcal cell wall induced uveitis in mice (71), and α melanocyte stimulating hormone was useful in treating endotoxin induced uveitis in rats (72).
CLINICAL AND LABORATORY FINDINGS
An study from the UK compared the nature, location and the frequency of oral ulcers in recurrent aphthous stomatitis (ROU) and BD. They found that in contrary to ROU, BD patients tended to have more severe oral ulcers with healing times of more than a week (73). It was not possible to differentiate the papulopustular lesions of BD from non specific follicular lesions on clinical grounds although histopathologically, a perivascular infiltrate or leukocytoclastic vasculitis was more prominent in patients with BD (74). Erythema nodosum like lesions were usually seen in patients with phlebitis reinforcing the notion that it is not easy to differentiate them from superficial thrombophlebitis (75). An Iraqi group reported an exceptionally high frequency of epididymo-orchitis during the course of the disease (39%) although referral bias was a probability (76). There was a decrease in the positivity of pathergy in an Iranian series from 72% to 33% during the last two decades (77). A Turkish group reported that optic disc neovascularization was an important but often neglected complication of ocular involvement of BD and suggested that interferon α2 was the agent of choice for its management (78). Two studies evaluated left ventricular end diastolic function of the heart in patients with BD. The first, which utilized tissue Doppler imaging did not find any abnormalities in diastolic filling (79) whereas the second found a significant degree of impairment with the same technique (80). Four studies evaluated hearing loss in BD. Three of them reported sensorineural hearing loss and one claimed that there was no impairment in hearing and that cochlear functions were spared (81, 82, 83, 84). Atopy, a condition that is believed to protect the patient against Th1 cell mediated diseases, was investigated in two studies. None of them found a significant difference in its frequency between the patients with BD and the controls (85,86). A Korean group found 11 female cases of BD who had coexistent autoimmune diseases including 5 with Sjogren’s syndrome, challenging the notion that they are not prevalent in this condition (87). Two retrospective studies investigated the relationship between BD and pregnancy. The first claimed that disease activity increased in a group of patients with BD in the post-partum period (88) whereas the second showed that pregnancy does not have a deleterious effect on the course of BD and that it may even ameliorate it. However pregnancy complications, cesarean section and miscarriages were more frequent in patients with BD (89). Two studies suggested that serum IL-8 levels were not reliable markers of disease activity in BD (90,91). Anti saccharomyces cerevisiae (ASCA) antibodies were negative in 98% of patients with BD (92) and were not positive in first degree relatives of another group of patients (93).
VASCULAR INVOLVEMENT AND THROMBOPHILIA
Dorian Haskard from the UK gave a lecture on endothelial dysfunction in BD. He empasized the importance of the impairment of endothelial dependent vascular relaxation in response to increased blood flow as a measure of global endothelial dysfunction and suggested that it was due to the quenching of nitric oxide by superoxide radicals. He also presented data that showed the relationship between anti endothelial cell antibodies, local leucocyte recruitment at sites of vascular endothelial cell activation and tissue injury. Finally he commented on the upregulated expression of decay accelerating factor (DAF), a cytoprotective protein in the vasculitides, the role of statins in inducing this upregulation and the their potential roles in the treatment of vascular inflammation (94).
A study showed that chronic venous insufficiency had serious socioeconomical and physical impacts on the patients (95). A Turkish group claimed that the medical treatment of the Budd-Chiari syndrome was beneficial although the nature of the treatment was not specified (96). A French case series showed that arterial involvement was present in 9.5% of the patients with an association with venous thrombosis in 68% of the cases. The lesions were multiple in 22 patients and 65% had relapses (97). A Greek study demonstrated that corticosteroids reduced systemic arterial stiffness in BD (98). Two abtracts proposed that erythrocyte deformability had an important role in the thrombotic tendency of BD (99, 100) and several others suggested that hyperhomocysteinemia (101), increased platelet reactivity (102), decreased NO production (103) and increased lipoprotein A levels (104) were operative.
NEUROLOGICAL INVOLVEMENT
There were three plenary lectures on neurological involvement in BD. The first was on the histopathology of the central nervous system lesions. Prof Hirohata from Japan showed that active neurological involvement was associated with the perivascular infiltration of CD45+RO T lymphocytes, CD68+ monocytes with few CD20+ B lymphocytes. Most of the neurons were undergoing apoptosis. Clinically inactive lesions demonstrated atrophy, and isomorphic gliosis (105). The second was on headache in BD. Prof Siva from Istanbul demonstrated that headache was very common in BD both in patients with and without neurological involvement. Most of the episodes were not associated with any organic lesions but a non-structural migraine type headache linked to disease exacerbations were noteworthy (106). The third was on the etiopathogenesis of neurological involvement. Saruhan Direskeneli’s group showed that antibodies to heat shock protein 65 and αβ-crystallin and high levels of CXCL10, CXCL8 were prominent in the cerebrospinal fluids of neuro-Behcet patients. Limited numbers of oligoclonal IgG bands with different banding patterns were also observed, compared to those seen in multiple sclerosis (107). A French study evaluated the neuro-ophthalmic manifestations of BD and reported that they could be observed before BD was diagnosed. Diplopia, 6th and 3rd cranial nerve palsies and optic neuritis were the most common manifestations (108). A study explored the relationship between cyclosporine use and neurological involvement. It demonstrated that the incidence of new onset neurological disease was significantly higher in patients with cyclosporine A compared to those on other medications (109). Patients with BD tended to have more “frontal” cognitive dysfunction compared to patients with multiple sclerosis (110).
PROGNOSIS
A survey of “silent” neurological involvement (non specific headache at initial presentation with abnormal neurological findings at clinical examination) showed that they had a tendency to develop overt neurological attacks during follow up although their mortality and disability rates were lower than classical neuro Behçet patients. Some of them had pathological MR findings before the attacks (111). A study on the long term course of deep vein thrombosis in BD revealed that the risk of recurrence was high especially in males with procoagulant polymorphisms. The frequency of post-thrombotic syndrome (PTS) was 22% and it was mainly seen among patients who had a recurrence. Immunosuppressive drugs had a favorable effect on the prevention of recurrence and on the development of PTS (112). The frequency of pediatric cases was was 0.2% among all cases with BD in Cerrahpasa Medical Faculty, Istanbul and males had more severe disease as in adults. There was an 8% mortality among the boys and the main causes of death were pulmonary artery aneurysms, Budd-Chiari syndrome, suicide and pneumonia. Genital ulcers, papulopustular lesions, erythema nodosum and arthritis were less common than that observed in the adult population (113). When the mortality and morbidity of the 1990-91 cohort of adult patients with BD was compared to that of the 1977-1983 cohort in the same center, it was seen that the prognosis of eye and vascular disease was more favorable in the new cohort although there was no change in the overall mortality rate (114). The prognosis of pulmonary artery aneuryms were also better compared to twenty years ago probably due to earlier diagnosis and prolonged immunosuppression with cyclophosphamide and steroids (115).
MANAGEMENT
A Turkish group showed in a controlled study that depot corticosteroids were only beneficial for erythema nodosum in the females (116). A double blind controlled trial of methotrexate (MTX) in patients with eye disease demonstrated that the combination of MTX with corticosteroids were not superior to prednisolone alone in the suppression of uevitis at least in the short term (117). Interferon alpha was effective among a group of patients with “isolated” uveitis (118) and lead to a good visual prognosis among patients with BD with severe ocular disease (119). It was suggested that patients should be carefully selected with particular attention to compliance. Concomitant corticosteroid use should also be limited to 10 mg/day (120). Sfikakis from Greece demonstrated that a single infusion of 5mg/kg of infliximab was effective for a whole month in suppressing severe ocular inflammation (121) but both a French and a Turkish series revealed that relapses occured in some patients when infliximab was infused at 8 week intervals, necessitating more frequent administration (122,123). Anti nuclear antibodies developed at six months in 76% of the patients and anti-ds DNA and anti β2 glycoprotein antibodies were also common (124). Granulocyte apheresis was beneficial in a group of patients with eye disease refractory to conventional therapy (125). Lactobacilli lozenges were effective in the treatment of oral ulcers (126) and topical granulocyte colony stimulating factor worked in oral and genital ulcers (127). Topical pimecrolimus was efficient in the management of genital ulcers (128,129).
REFERENCES:
1. Cutolo M. Gender and disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: L1.
2. Kurosawa M, Inaba Y, Nishibu A, Kaneko F, Kawakami Y, Tamakoshi A, Kawamura T. Nationwide epidemiologic survey of Behçet’s Disease in 2003 in Japan. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: A1.
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12. Elezoglou AV, Sfikakis PP, Frangiadaki K, Vassilopoulos D, Markomihelakis N, Vaiopoulos G, Kaklamanis Ph. Effects of gender on the clinical features and severity of Adamantiades-Behçet’s Disease in Greece. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: A17.
13. Mumcu G, Inanc M, Ergun T, Islek U, Yavuz S, Fresko I, Sur H, Atalay T, Direskeneli H. Gender effects quality of life in Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: A18.
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29. Hershkowitz C, Klein T. Krause I, Weinberger A. Cytokine gene polymorphism in HLA-B5 positive Israeli patients with Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: B10.
30. Choi JS, Nam JH, Bang D, Lee ES, Lee S, Park KS. HLA-G 3741 14p insertion in the 3-UTR in Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: B11.
31. Duymaz-Tozkir J, Duyar FA, Saruhan Direskeneli G, Gul A. Killer immunoglobulin-like receptor gene 3DL1/3DS1 polymorphism in Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: B12.
32. Lingdi XU, Lian Fan, Yu Lun. Association of killer cell immunoglobulin like receptor (KIR) gene polymorphism with Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: B13.
33. Erken E, Gunesacar R, Ozer HTE. C5a receptor polymorphism in Behçet’s Disease. Negative association with uveitis. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: B14.
34. Gunesacar R, Erken E, Ozer HTE. Analysis of CTLA-4 and CD28 gene polymorphisms in patients with Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: B15.
35. Sallakcy N, Bacanli A, Coskun M, Yavuzer U, Yegin O, Alpsoy E. CTLA-4 gene polymorphism in Turkish patients with Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: B16.
36. Aksu K, Berdeli A, Keser G, Inal V, Kabasakal Y, Oksel F, Kobak S, Kocanogullari H, Doganavsargil E. Fcgamma RIIa, IIIa and IIIb receptor gene polymorphisms in Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: B17.
37. Oksel F, Ozmen M, Aksu K, Keser G, Berdeli A. Endothelial nitric oxide synthase gene polymorphisms in Turkish patients with Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: B18.
38. Ozbalkan S, Ertenli I, Kiraz S, Ozturk MA, Apras S, Akdogan A, Misirlioglu M, Tuncer S, Calguneri M. Heat shock protein (HSP) 60/65 gene polymorphism in Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: B19.
39. Durrani O, Wallace GR, Hamburger J, Williams H, Fortune F, Stewart J, Murray PL. Toll like receptor expression in oral ulcer biopsies frok Behçet’s Disease patients. A role for innate immune system in BD. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: C1.
40. Elbir Y, Tulunay A, Ozilhan G, Akdeniz T, Eksioglu-Demiralp E, Direskeneli H, Yavuz S. Toll like receptors in etiopathogenesis of Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: C2.
41. Isogai E, Isogai H, Matuo K, Kaneko F, Sugiyama T, Ohno S. Anti-mannan antibodies and mannose-binding protein in patients with Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: C3.
42. Mumcu G. Inanc N, Elbir Y, Ergun T, Yavuz S, Direskeneli H. Low serum mannose binding lectin levels predispose to S.Mutans colonization in Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: C4.
43. Mertens D, Koetter I, Gunaydin I, Fresko I, Yazici H. Mueller C. Expression of alpha defensins HNP 1-3 in Behçet’s Disease: Effector molecules of spontaneous and pathergy induced papulopustular lesions? Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: C6.
44. Wallace GR, Pryce K, Curnow SJ, Fortune F, Stewart JE, Stanford MR, Murray PI. Multiplex bead analysis of cytokines in serum from patients with Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: C20.
45. Ureten K, Ertenli I, Akif Ozturk M, Kiraz S, Mesut Onat A, Tuncer M, Okur H, Akdogan A, Apras S, Calgüneri M. Neutrophil CD64 expression in Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: C7.
46. Gogus F, Fresko I, Elbir Y, Demiralp E, Direskeneli H. Oxidative burst response to monosodium urate crystals in patients with Behçet’s Syndrome. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: C8.
47. Ozilhan G, Tulunay A, Elbir Y, Akdeniz T, Direskeneli H, Eksioglu-Demiralp E, Yavuz S. Effects of testosterone on neutrophil activity in Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: C9.
48. Stanford MR, Modi NC, Knight BC, Stewart JE, Fortune F, Wallace GR. Serum levels of IL-15 in Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: C24.
49. Stewart JE, Mumcu G, Wallace G, Stanford MR, Fortune F. Effects of serum and saliva from patients with Behçet’s Disease on epithelial and inflammatory cell responses. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: C10.
50. Freysdottir J, Dalghous AM, Stewart JE, Fortune F. Cross-talk between oral epithelium and T cells in Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: C12.
51. Kose O, Stewart JE, Waseem A, Stanford M, Fortune F. Immunohistochemical expression analyses of cytokeratins, differentiation markers and adhesion molecules in oral ulcers of Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: C39.
52. Takeno M, Nagafuchi H, Shimoyama Y, Ishigatsubo Y, Suzuki N. Upregulated expression of IL-12 receptor is associated with active disease in Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: C23.
53. Durusoy C, Seckin D, Arykan S, Akalyn N, Alpsoy E. The levels of interferon-gamma, interleukin-12 and interleukin-18 in patients with Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: C28.
54. Houman MH, Hamzaoui A, Smiti-Khanfir M, Ben Ghorbel I, Fki M, Hamzaoui K. Characterization of a cytotoxic CD8+ T cell population in patients with Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: C11.
55. Takeno M, Nakamura S, Ohno S, Ishigatsubo Y. Treatment with anti-TNF alpha monoclonal antibody modulates cytokine profile in patients with Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: C21.
56. Lee KH, Chung HS, Kim HS, Oh SH, Ha MK, Lee S, Bang D. Antiendothelial cell antibodies and alpha enolase. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: L7.
57. Chang YJ, Wu WH, Lee JH, Bang D, Lee KH. The cross-reactivity of anti human alpha enolase in the sera of Behçet’s Disease patients to streptococcus sanguis antigen. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: C14.
58. Chang JY, Lee JH, Bang D, Ha KW, Park YB, Lee SK, Lee KH. Anti alpha enolase antibody in sera from patients with Behçet’s Disease and rheumatological disorders. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: C16.
59. Chang JY, Lee JH, Bang D, Ha KW, Choi CH, Kim WH, Lee KH. Anti alpha enolase antibody in sera from patients with gastrointestinal Behçet’s Disease and chronic inflammatory bowel disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: C17.
60. Erdem H, Pay S, Serdar M, Simsek I, Dinc A, Pekel A, Musabak U, Turan M. Synovial ELR (+) (angiogenic) CXC chemokine expression in patients with inflammatory arthritides: Do lower levels prevent the development of pannus and sequential erosive changes in patients with Behçet’s Disease? Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: C32.
61. Heo JH, Sohn S, Lee S, Lee E-S. Expression of chemokines in patients with Behçet’s Disease in relation to clinical activity. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: C34.
62. Houman MH, Hamzaoui A, Smiti-Khanfir M, Ben Ghorbel I, Ennaifer R, Fki M, Hamzaoui K. Chemokine receptors expression in Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: C35.
63. Yanagihori H, Oyama N, Inoue T, Nakamura K, Oguma K, Kaneko F. Human homologue of streptococcal heat shock protein (HSP) 60 induces “biological tolerance” in patients with Behçet’s Disease: the possible implication in advanced treatment strategy. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: C13.
64. Kawamura Y, Mishima N, Itoh Y, Ohkusu K, Isogai E, Ezaki T. Taxonomic study of strains isolated from the Behçet’s Disease patients. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: C19.
65. Hatemi G, Bahar H, Melikoglu M, Arzuhal N, Mat C, Yazici H. Microbiology of pustular pathergy lesions and skin flora of Behçet’s Syndrome patients. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: C18.
66. Yilmaz OS, Dinc A, Erdem H, Simsek I, Pay S, Pekel A. Vascular endothelial growth factor (VEGF) and tumour necrosis factor-alpha (TNF-alpha) serum levels in patients with Behçet’s uveitis. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: C30.
67. Baltaci M, Eller GN, Vielandner M, Dejaco C, Veidinger F, Zouboulis CC, Patsch JR, Fritsch P, Schirmer M. Vasculitis, other organ involvements and vascular endothelial growth factor in Behçet’s Disease: first results from the Austrian Behçet’s Register. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: C31.
68. Nakano H, Ooka S, Matsuda T, Sekine T, Nishioka K, Ozaki S, Kato T. Identification of cofilin-1 as an autoantigen in patients with Behçet’s Disease by a proteomic approach. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: C36.
69. Kalayciyan A, Orawa H, Fimmel S, Perschel FH, Gonzalez JB, Fitzmer RG, Orfanos CE, Zouboulis CC. Nicotine and biochanin A, but not cigarette smoke induce anti-inflammatory effects on keratinocytes and endothelial cells in patients with Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: C44.
70. Groll S, Amberger M, Gunaydin I, Vontheim R, Koetter I. Intracellular cytokines in Behçet’s Disease and ankylosing spondylitis and effects of Interferon-a-2a treatment on their expression. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: C29.
71. Isogai E, Okumura K, Isogai H, Kaneko F, Oguma K, Ohno S. Effect of human cationic antimicrobial protein 18 peptide on streptococcal cell wall induced uveitis in mice and on apoptosis in human active cells. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: C47.
72. Nishida T, Ohgami K, Shiratori K, Ilieva IB, Miyata S, Itoh Y, Mizuki N, Ohno S, Taylor AW. Suppression of alpha melanocyte stimulating hormone against rat endotoxin-induced uveitis and the time course of inflammatory agents in aqueous humour. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: C48.
73. Ifeacho SN, Malhi G, Hamburger J, Murray PI. Recurrent aphthous stomatitis and Behçet’s Disease: is there a link? Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: D1.
74. Boyvat A, Heper AO, Kocyigit P, Erekul S, Gurgey E. Can specific vessel based papulopustular lesions of Behçet’s Disease be differentiated from non-specific follicular lesions clinically? Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: D5.
75. Chams-Davatchi C, Davatchi F, Shahram F, Nadji A, Chams H, Jamshidi AR. Relationship of skin lesions with other manifestations of Behçet’s Disease. Analysis of 5369 patients. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: D6.
76. Abdulla TAS. Epididymo-orchitis in patients with Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: D9.
77. Davatchi F, Chams-Davatchi C, Jamshidi AR, Nadji A, Shahram F, Shams H, Akbarian M, Gharibdoost F, Ziaie N, Sedigh M. Is pathergy test still worthwile? Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: D10.
78. Tugal-Tutkun I, Onal S, Altan-Yaycioglu R, Urgancioglu M. Optic disk neovascularization in Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: D15.
79. Gurler O, Okan T, Baris N, Ilknur T, Onen F, Goldeli O, Akkoc N. Assessment of left ventricular diastolic functions by conventional and new methods in Behçet’s patients. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: D21.
80. Arslan S, Bozkurt E, Sari RA, Erol MK, Senocak H. Left ventricular diastolic function abnormalities in Behçet’s Disease: Standard Doppler and tissue Doppler study. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: D22.
81. Atef MR, Ghasemi MM, Bakhshaei M. Hearing in Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: D23.
82. Kalyoncu U, Calguneri M, Sarac S, Akdogan A, Turkyilmaz D, Ureten K, Oguz KK, Apras S, Karadag O, Onat AM, Kiraz S, Ertenli I. Hearing loss in Behçet’s Disease: a controlled study. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: D24.
83. Choung Y-H, Lee E-S, Park K, Lee J. Audio-vestibular involvement in patients with Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: D25.
84. Yilmaz M, Bayazit Y, Gunduz B, Yilmaz O, Kemaloglu Y, Onder M, Gurer MA. Oto acoustic emission findings in Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: D26.
85. Temel M, Atagunduz P, Tasan D, Bicakcigil M, Ergun T, Yavuz S, Direskeneli H. Atopy in Behçet’s Disease is associated with disease severity. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: D28.
86. Gul U, Gonul M, Kulcu Cakmak S, Kilic A, Olcay I. Atopy in Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: D29.
87. Bin Cho S, Bang D, Lee KH, Lee ES, Lee S. Coexistence of Behçet’s Disease and autoimmune disease: Clinical features of 11 patients. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: D31.
88. Monselise A, Krause I, Molad Y, Hershkowitz C, Weinberger A. Behçet’s Disease and pregnancy outcome: a retrospective study. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: D34.
89. Jadaon J, Shushan A, Sela H, Oscan C, Rojansky N. Behçet’s Disease and pregnancy. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: D33.
90. Zouboulis CC, Kalayciyan A, Kaklamanis Ph, Katsantonis J, Adler Y. Serum IL-8 is not a reliable marker for the activity of Adamantiades-Behcet’s disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: D35.
91. Kalayciyan A, Kaklamanis Ph, Orawa H, Perschel FH, Fitzner RG, Zouboulis CC. C-reactive protein but not serum IL-8 is a relaible marker of activity in Adamantiades-Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: D36.
92. Charuel JL, Sbai A, Diemert MC, Musset L, Wechsler B, Piette JC. Anti saccharomyces cerevisiae antibodies and Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: D38.
93. Monselise A, Krause I, Molad Y, Monselise Y, Weinberger A. Anti saccharomyces cerevisiae antibodies (ASCA) among family members of Behçet’s Disease patients. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: D39.
94. Haskard DO. Endothelial dysfunction in vasculitis and in Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: L6.
95. Ergun T, Akpinar I, Mumcu G, Erdem F, Yavuz S, Adademir T, Bakar O, Direskeneli H. Chronic venous insufficiency in patients with Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: E4.
96. Korkmaz C. Budd-Chiari Syndrome caused by Behçet’s Syndrome: 4 cases. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: E5.
97. Asli B, Wechsler B, Duhaut P, Du-Boutin LTH, Cacoub P, Amoura Z, Bletry O, Papo T, Kieffer E, Cluzel P, Piette JC. Arterial involvement in Behçet’s Disease: a report of 63 cases. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: E8.
98. Protogerou A, Lekakis J, Ikonomidis I, Stamatelopoulos K, Aznaouridis K, Karatzis E, Papamichael Ch, Marcomihelakis N, Kaklamanis Ph, Mavrikakis M. Effect of different drugs on systemic arterial stiffness in patients with Adamantiades-Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: E13.
99. Uskudar O, Erdem A, Demiroglu H, Dikmenoglu N. Decreased erythrocyte deformability in Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: E16.
100. Yapislar H, Aydogan S, Borlu M, Yerer B, Simsek N, Kutlugun C, Ozyurt K, Ascioglu O. Lipid peroxidation, erythrocyte anti-oxidant enzymes and erythrocyte deformability in patients with Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: E17.
101. Aslan H, Aldemir D, Pay S, Ogus E, Gok F, Turkoglu S. Serum homocysteine and cysteine levels and their relations with the thrombosis in patients with Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: E18.
102. Akar S, Ozcan MA, Ates A, Gurler O, Ozsan H, Piskin O, Akkoc N, Ozkan S, Demirkan F, Onen F. Circulated activated platelets and increased platelet reactivity in patients with Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: E20.
103. Yapislar A, Aydogan S, Borlu M, Kutlugun C, Simsek N, Ozyurt K, Atasavun C, Ascioglu O. Decreased NO production and increased platelet aggregability in patients with Behçet’s disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: E24.
104. Akdemir S, Sari RA, Kiziltunc A, Gundogdu M, Kiki I. The role of lipoprotein (a) and anticardiolipin antibodies in the formation of venous thrombosis in Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: E25.
105. Hirohata S. Histopathology of central nervous system lesions of Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: L10.
106. Saip S, Siva A, Altintas A, Kiyat A, Seyahi E, Hamuryudan V. Headache in Behçet’s Syndrome. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: L9.
107. Saruhan Direskeneli G. Neuro-Behçet’s: Etiopathogenesis. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: L8.
108. Sbai A, Wechsler B, Cassoux N, Du-Boutin LTH, Bodaghi B, Duhaut P, Dormont D, Lafitte C, Amoura Z, Cacoub P, Le Hoang P, Piette JC. Neuro-ophthalmic manifestations in Behçet’s Disease: evaluation of 112 patients. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: F1.
109. Kotter I, Gunaydin I, Battra M, Vonthein R, Stuebiger N, Fierlbeck G, Melms A. Central-nervous system manifestations in patients with Behçet’s Disease during otherwise effective treatment with Cyclosporin A. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: F8.
110. Akman-Demir G, Emir O, Oktem-Tanor O, Akca S, Tumac Coban O, Serdaroglu P, Eraksoy M, Gurvit H. Cognitive impairment in MS and neuro-Behçet’s Disease: a comparative study of two diseases affecting executive functions. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: F9.
111. Yesilot N, Shehu M, Akman-Demir G, Serdaroglu P. Subclinical “silent” neurological involvement in Behçet’s Disease: 8 year follow-up. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: G4.
112. Karaman O, Celebi-Onder S, Kamali S, Inanc M, Ocal L, Aral O, Konice M, Gul A. Long Term course of deep vein thrombosis in Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: G6.
113. Seyahi E, Ozdogan H, Yurdakul S, Ugurlu S, Ozyazgan Y, Mat C, Melikoglu M, Fresko I, Hamuryudan V, Yazici H. The outcome of children with Behçet’s Syndrome. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: G7.
114. Seyahi E, Ugurlu S, Ozyazgan Y, Mat C, Melikoglu M, Fresko I, Hamuryudan V, Yurdakul S, Yazici H. The mortality and morbidity of Behçet’s Syndrome in a recent cohort. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: G8.
115. Hamuryudan V, Oz B, Tuzun H, Yazici H. The prognosis and management of pulmonary artery aneurysms of Behçet’s Syndrome. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: H31.
116. Mat C, Yurdakul S, Ozyazgan Y, Uysal S, Uysal O, Yazici H. A double blind trial of depot corticosteroids in Behçet’s Syndrome. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: H1.
117. Shahram F, Shams H, Akhyani M, Moradzadeh K, Nadji A, Tehrani A, Jamshidi A, Davatchi F. A double blind trial of methotrexate in ocular lesions of Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: H3.
118. Stuebiger N, Deuter CME, Gunaydin I, Zierhut M, Koetter I. Isolated ocular Behçet’s Disease: Therapy with interferon alpha2a. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: H9.
119. Deuter CME. Kotter I, Stubiger N, Gunaydin I, Zierhut M. Behçet’s Disease: Visual prognosis after treatment with interferon alpha2a. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: H10.
120. Zierhut M, Stubiger N, Gunaydin I, Deuter C, Kotter I. Behçet’s disease: what we have learned from the treatment with interferon alfa2a in ocular Behçet. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: H11.
121. Sfikakis PP, Kaklamanis Ph, Theodossiadis PG, Elezoglou A, Marchomichelakis N. Rapid effects of infliximab in patients with Adamantiades-Behçet’s Disease and sight threatening ocular inflammation: a 4 week study in 26 patients. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: H13.
122. Wechsler B, Bodaghi B, Fain O, Du-Boutin LTH, Cassoux N, Le Hoang P, Piette JC. Long term follow up of infliximab in refractory pan uveitis due to Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: H14.
123. Gul A, Tugal Tutkun I, Mudun B, Inanc M, Kamali S, Kasapoglu E, Urgancioglu M. Efficacy of infliximab in the treatment of uveitis resistant to the combination of azathioprine and cyclosporine in Behçet’s Disease: Results of an open label trial. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: H15.
124. Elezoglou A, Kafasi N, Vaiopoulos G, Choremi E, Kaklamanis Ph, Sfikakis PP. Induction of autoantibodies during prolonged infliximab therapy for Admantiades-Behcet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: H18.
125. Namba K, Sonoda KH, Kitamei H, Kitaichi N, Ishibashi T, Ohno S. Efficacy of granulocyte apheresis therapy for the patients with Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: H19.
126. Tasli ML, Mat C, De Simone C, Yazici H. Lactobacilli lozenges in the management of oral ulcers of Behçet’s syndrome. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: H21.
127. Yerebakan O, Bacanli A, Parmaksizoglu B, Yilmaz E, Alpsoy E. Topical granulocyte-colony stimulating factor for the treatment of oral and genital ulcers of patients with Behçet’s Disease. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: H20.
128. Onder M, Guler Ozden M, Gurer MA. Topical pimecrolimus 1% cream for genital ulcer treatment in Behçet’s cases-preliminary report. Book of Abstracts. 11th International Congress on Behçet’s Disease, Antalya, 2004: Abs no: H24.
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