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PubMed2006

Subclavian artery pseudoaneurysm in Behcet's disease.

Behcet's disease (BD) is an autoimmune, multisystemic, and chronic inflammatory disease. Although it affects all systems, involvement of the vascular system is of vital importance. Pseudoaneurysm ruptures in the arteries are the major causes of sudden deaths in BD. Although pseudoaneurysms in aorta and pulmonary arteries are rare, it is even more rare in the subclavian arteries. In our case, a pulsatile mass in the right clavicular area was determined to be associated with BD and this case is presented because subclavian artery pseudoaneurysm is seen rarely in BD.

Adult↗
PubMed2006

Skewed Th1 responses caused by excessive expression of Txk, a member of the Tec family of tyrosine kinases, in patients with Behcet's disease.

Behcet's disease (BD) is characterized by recurrent attacks of uveitis, oral aphtha, genital ulcers and skin lesions. The etiology and pathogenesis of BD are largely unknown. It has been reported that excessive Th1 cell function is involved in the pathogenesis of BD. Previously, we found that Txk, a member of the Tec family of tyrosine kinases, acts as a Th1 cell-specific transcription factor that is involved in the effector function of Th1 cells. Thus, we studied Th1 cytokine production and Txk expression of T-lymphocytes in patients with BD. Peripheral blood lymphocytes produced excessive Th1-associated cytokines including interferon-gamma (IFN-gamma) and interleukin (IL)-12 in patients with BD. Circulating CD3+ and purified CD4+ T cells expressed excessive Txk protein. The extent of IFN-gamma production by the lymphocytes correlated with the expression of Txk protein in the immunoblotting analysis. The majority of cells infiltrating into the skin lesions of patients with BD expressed IFN-gamma. IL-12 and IL-18 were found in the mononuclear cell aggregates in the skin and intestinal lesions of those with BD. Lymphocytes accumulating in the skin and intestinal lesions expressed higher levels of Txk as compared with other Th2-associated diseases. IFN-gamma, IL-18 and IL-12 detected in skin lesions may induce preferential development of Th1 cells in patients with BD. Collectively, Th1 cells expressing Txk and Th1-associated cytokines may play a critical role in the development of skin and intestinal lesions in patients with BD. This review may serve as a reminder of the importance of excessive Th1 cell function in the pathogenesis of BD and may contribute to the discovery of new molecular targets for the development of a specific therapeutic strategy for BD.

Behcet Syndrome↗
PubMed2002

Coagulation parameters and plasma total homocysteine levels in Behcet's disease.

Behcet's disease (BD) is a multisystemic inflammatory disorder of unknown etiology that is sometimes associated with thrombosis in addition to systemic manifestations. However, the mechanism of hypercoagulability is not known. We evaluated the coagulation and fibrinolytic activities and the plasma total homocysteine levels of Korean BD patients in two cross-sectional studies. In the first study regarding coagulation and fibrinolytic activities, the levels of fibrinogen and von Willebrand factor (vWF) antigen were significantly higher in the BD patients than in the healthy controls (387.7+/-24.3 versus 240.6+/-8.8 mg/dl, p<0.001, and 131.9+/-8.8 versus 105.2+/-0.3%, p<0.01, respectively). The level of antithrombin III (AT III) was significantly lower in the BD patients (92.8+/-3.2 versus 106.3+/-2.6%, p<0.005). No differences were observed in the levels of plasminogen, protein C, or protein S activities. Activated protein C (APC) resistance was not observed in any BD patients. In the second study, the plasma total homocysteine levels of patients with a history of thrombosis (11.9+/-3.0 micromol/l) or disease activity (12.5+/-3.8 micromol/l) were found to be significantly higher than those of the controls (9.2+/-2.6 micromol/l, p<0.05, both). The plasma homocysteine concentrations in the thrombosis patients were positively correlated with plasma vWF levels; a relationship which suggests injury of the vascular endothelium (Spearman coefficient=0.857, p<0.01). Therefore, coagulation abnormality did not contribute to thrombotic complications, and higher levels of homocysteine may play a role in the hypercoagulablity of BD patients.

Adult↗
PubMed2006

Asymmetric dimethylarginine and nitric oxide levels as signs of endothelial dysfunction in Behcet's disease.

Behcet's disease (BD) has been known for many years, yet the etiology of the systemic vasculitis remains unknown. Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide (NO) synthase. ADMA is involved in endothelial dysfunction in various vascular diseases and its level in BD is unclear. This study was performed to evaluate the relationship between ADMA and NO levels in plasma of patients with BD. There were 3 groups of 30 subjects: (a) controls, (b) BD patients with mucocutaneous involvement, and (c) BD patients with vascular involvement. Plasma NO levels were assayed by spectrophotometry and plasma ADMA levels were assayed by an ELISA test. Plasma ADMA levels were higher in both groups of BD patients than in the controls; the ADMA levels were higher in the BD patients with vascular involvement than in the mucocutaneous group. Plasma NO levels were lower in both groups of BD patients than in controls; plasma NO levels were lower in the BD patients with vascular involvement than in mucocutaneous group. In the combined groups of 60 BD patients, there was significant inverse correlation between the plasma concentrations of ADMA and NO (r = -0.570, p <0.001). Plasma lipid profiles did not differ significantly between the BD patients and the controls. These results are evidence for increased plasma ADMA levels and decreased plasma NO levels as risk factors for cardiovascular events in BD patients. Inhibition of NO synthesis by ADMA may contribute to vascular involvement in BD.

Adult↗
PubMed2006

Evaluation of left ventricular diastolic dysfunction with conventional and current Doppler techniques in Behcet's disease.

Behcet's disease (BD) is a systemic vasculitis characterized by genital and oral ulcers, uveitis, and other organs' involvement. Left ventricular (LV) diastolic dysfunction has been documented in BD. However, conventional echocardiographic techniques have serious limitations like its dependence on preload, afterload and heart rate. Recently, new techniques like colour M-mode and tissue Doppler imagining (TDI) have provided additional concept in the assessment of diastolic function. The aim of the present study was to investigate the LV diastolic dysfunction with conventional and new echocardiographic techniques in BD. Forty-eight patients with BD (25 women, 23 men) and 26 healthy volunteers (15 women, 11 men) were enrolled in the study. LV diastolic functions were examined with mitral inflow pulse wave Doppler, TDI and mitral flow propagation rate (MFPR). The following were accepted as diastolic dysfunction: in mitral inflow pulse wave Doppler, E/A<1, isovolumic relaxation time (IVRT)>110 ms and deceleration time of E wave (DT)>240 ms; in TDI of mitral ring with pulse wave, E'/A'<1; and in MFPR, velocity slope (Vp)<45 cm/s. The two groups were comparable in age, sex, heart rate, body mass index, smoking, hyperlipidemia and basic echocardiographic measurements. LV diastolic dysfunction was significantly higher in BD group according to E/A<1 (p<0.05). When echocardiographic measurements were compared one by one for two groups, As' (late diastolic TDI wave in septal wall) was found to be significantly higher in BD group (p<0,0001). IVRT was longer in BD group than in controls, but it did not reach statistical significance (p=0,06). Diastolic dysfunction of LV is more frequent in patients with BD than in control according to E/A and As'. Conventional and current techniques like TDI and colour M-mode Doppler echocardiography could be used to investigate diastolic functions in BD.

Adult↗
PubMed2005

Association of vascular endothelial growth factor gene polymorphisms with behcet disease in a Korean population.

Vascular endothelial growth factor (VEGF) is important for angiogenesis and inflammation, both of which are codependent and contribute to the pathophysiology of Behcet disease (BD). The increased expressions of VEGF have been observed in the active stage and in the ocular inflammation of BD. Polymorphisms of the VEGF gene have been associated with chronic inflammatory disease including rheumatoid arthritis. We sought to investigate whether polymorphisms on the regulatory region of the VEGF gene are associated with susceptibility of Korean patients with BD. One hundred one native Korean patients with BD and 138 healthy unrelated controls were recruited. Genotype and allele frequencies of the four selected polymorphisms (-2578, -1154, -634, and 936) were not different between the BD group and controls. Among the BD patients, the frequency of the -634 CC genotype decreased in patients with uveitis (2.6% vs. 20.6%, adjusted OR = 0.100, 95% CI 0.011-0.875, p = 0.037), although it became insignificant after correction for multiple comparisons. These results indicate that the VEGF gene polymorphisms are not associated with BD in the Korean population, but they may be involved in the development of the ocular inflammation of BD.

Adult↗
PubMed2005

Constitutional trisomy 8 mosaicism with myelodysplastic syndrome complicated by intestinal Behcet disease and antithrombin III deficiency.

Trisomy 8 is the most common acquired chromosomal abnormality associated with myeloid malignancy. As a constitutional trisomy 8 mosaicism (T8M), it exhibits an extremely variable phenotype. In addition, Behcet disease (BD) has been reported as an unusual complication of myelodysplastic syndrome (MDS). To our knowledge, 12 case reports of various hematologic malignancies in patients with T8M and 18 case reports of MDS with acquired trisomy 8 complicated by BD have been published to date. We report a case of constitutional T8M with MDS complicated by intestinal BD and antithrombin III deficiency.

Antithrombin III Deficiency↗
PubMed2002

Determination of Behcet disease with the application of FFT and AR methods.

In this study, Doppler signals recorded from ophthalmic artery of 86 patients were processed by personal computer using fast Fourier transform, Burg autoregressive (AR), and least-squares AR methods. By using these spectrum analysis techniques, the variations in the shape of the Doppler spectrums as a function of time were presented in the form of sonograms in order to obtain medical information. These sonograms were then used to compare the applied methods in terms of their frequency resolution and the effects in determination of Behcet disease.

Adult↗
PubMed1999

[Behcet disease].

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Behcet Syndrome↗
PubMed1954

[Behcet disease].

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Behcet Syndrome↗
PubMed2004

Elevated serum granulocyte colony-stimulating factor levels in patients with active phase of sweet syndrome and patients with active behcet disease: implication in neutrophil apoptosis dysfunction.

BACKGROUND: Sweet syndrome (SS), an acute inflammatory disease, has clinical and laboratory features similar to those of Behçet disease (BD). Serum levels of granulocyte colony-stimulating factor (G-CSF) are elevated in patients with SS, and exogenous administration of G-CSF has repeatedly been implicated in the causation of SS. Granulocyte colony-stimulating factor is a hematopoietic growth factor that regulates the production and differentiation of neutrophils. OBJECTIVES: To clarify the role of elevated serum G-CSF levels in patients with active SS and active BD compared with those with inactive SS or BD and healthy controls. To then analyze neutrophil apoptosis in the active state of SS and BD; and to also investigate the influence of autologous serum on neutrophil apoptosis. METHODS: Serum G-CSF was examined in 5 patients with active SS, 7 with inactive SS, 7 with active BD, 9 with inactive BD, and 5 healthy controls by means of an enzyme immunoassay kit. We measured apoptotic cells in the neutrophil fraction of peripheral blood collections in patients with active diseases and controls by means of flow cytometry. RESULTS: Serum G-CSF level was significantly higher in patients with active SS than in those with inactive SS. The difference in serum G-CSF levels among patients with active and inactive BD was also significant. Serum G-CSF level was significantly higher in patients with active SS than in those with active BD. Neutrophil apoptosis was significantly higher in patients with active SS than healthy controls. This increased apoptosis rate was also seen in patients with active BD. The increased rate of neutrophil apoptosis was significantly suppressed when the neutrophils were cultured for 18 hours in the presence of autologous active SS serum. Similarly, neutrophil apoptosis was suppressed in the presence of autologous serum in patients with active BD, but not significantly so. CONCLUSIONS: These findings indicate that increased production of G-CSF in patients with SS and BD may play an important role in the manifestation of these disorders. Given the suppression of neutrophil apoptosis in the active state in the presence of the influence of autologous serum, which includes elevated G-CSF level, we propose that serum G-CSF plays a significant role in the suppression of neutrophil apoptosis. Furthermore, G-CSF-induced suppression of neutrophil apoptosis appears to be deeply involved in the pathogenesis of SS and BD.

Acute Disease↗