Hyperhomocysteinaemia in Behçet's disease.

OBJECTIVE: Arterial and venous thrombosis are among the clinical features of Behçet's disease (BD), the pathogenesis of which is not completely understood. In this study, we investigated whether hyperhomocysteinaemia, being a well known risk factor for thrombosis, is also a contributive risk factor for the arterial and venous thrombosis of BD. METHODS: Eighty-four patients fulfilling the criteria of the International Study Group for Behçet's Disease (54 males, 30 females, mean age 36+/-9 yr) were enrolled. All the patients were carefully screened for a history of venous thrombosis and were separated into two groups with respect to thrombosis history. Thirty-six healthy individuals (23 males, 13 females), matched for age and sex with the BD group, were included as a negative control group. Patients were excluded if they had any condition that might affect plasma homocysteine concentration. As methotrexate (MTX) causes hyperhomocysteinaemia, we also included 29 rheumatoid arthritis patients (five males, 24 females) receiving MTX weekly. Fasting plasma homocysteine concentrations were measured by high-performance liquid chromatography. The data were analysed with the chi(2) test and Student's t-test. RESULTS: The highest homocysteine concentrations were found in the MTX group (17.5+/-5.3 micromol/l). Mean plasma homocysteine concentrations in BD patients were significantly higher than in the healthy controls (11.5+/-5.3 vs. 8.8+/-3.1 micromol/l, P<0.001). Among BD patients with a history of thrombosis, 20 of 31 (64%) had hyperhomocysteinaemia, and this was significantly higher than in those without thrombosis (9%). On the other hand, there was no significant difference between patients with non-thrombotic BD and healthy controls (P>0.05). In patients with thrombosis, we found no correlation between the duration of the post-thrombotic period and homocysteine concentration. Among all the variables investigated, only hyperhomocysteinaemia was found to be related to thrombosis. CONCLUSION: Hyperhomocysteinaemia may be assumed to be an independent risk factor for venous thrombosis in BD. Unlike the factor V Leiden mutation, hyperhomocysteinaemia is a correctable risk factor. This finding might lead to new avenues in the prophylaxis of thrombosis in BD.

Hypothalamus-hypophysis-thyroid axis, triiodothyronine and antithyroid antibodies in patients with primary and secondary Sjögren's syndrome.

It has been well established that, anti-thyroglobulin antibodies (ATG) and anti-microsomal antibodies (AMC) may be present in various thyroid disorders and other systemic autoimmune diseases, including Sjögren's syndrome (SS). However, presence of circulating autoantibodies to thyroid hormones, i.e. both to triiodothyronine (T3) and tetraiodothyronine (T4), has not been studied extensively in SS. Autoantibodies to T3 and T4 are very important, because serum T3 and T4 levels may be detected spuriously higher or lower, due to the presence of these autoantibodies. Their presence should be suspected when measured serum thyroid hormone levels are not consistent with clinical status of the patient. SS is a slowly progressive, inflammatory autoimmune disease, affecting primarily the exocrine glands. Thyroid gland, being a target in some autoimmune diseases, is well known to be affected in SS as well. Keeping this possibility in mind, we investigated T3 autoantibody levels and thyroid gland involvement in patients with SS. Twenty-six SS patients (F/M:22/4) with a mean age of 46.6 years, were recruited in this study. Twelve of them were accepted as primary SS (pSS), while others had secondary SS (sSS) (7 with rheumatoid arthritis (RA), 3 with systemic lupus erythematosus (SLE), 3 with progressive systemic sclerosis (PSS) and 1 with sarcoidosis). Thyroid function tests, including T3, T4, fT3, fT4, TSH, ATG, AMC, T3 antibody measurements, thyroid scintigraphy, thyroid ultrasonography and TRH stimulation tests were performed in all patients. We compared our results with those of the twenty healthy normal controls. Serum ATG and/or AMC were detected in three patients with pSS (25%) and no patients with sSS. No significant difference could be shown in the other parameters, including T3 autoantibodies and thyroid function tests. TRH stimulation test was also normal, showing that the hypothalamus-hypophysis-thyroid axis was not affected in patients both with pSS and sSS. In conclusion, we found that T3 autoantibody levels in pSS, were not significantly higher than sSS and normal controls.

Prevalences of hepatitis A, B, C and E viruses in Behçet's disease.

OBJECTIVE: To determine whether Behçet's disease (BD), being a systemic vasculitis of unknown aetiology, is associated with hepatitis viruses (HAV, HBV, HCV and HEV). METHODS: In addition to 124 patients [male:female (M/F): 73/51], all fulfilling the diagnostic criteria of the International Study Group for BD (1991), 14 patients with systemic necrotizing vasculitis (M/F: 7/7), 47 patients with ankylosing spondylitis (M/F: 36/11) and 51 healthy controls (M/F: 22/29) were also included in this study. Serological markers of four different types of hepatitis (anti-HAV IgM, total anti-HAV, HBsAg, anti-HBs, total anti-HBc, anti-HBc IgM, anti-HCV and anti-HEV) were studied in all cases. RESULTS: There was no difference between the groups with respect to HAV, HCV and HEV serologies. Anti-HBs positivity was observed less frequently in BD compared with healthy controls and systemic vasculitis (P<0.05). CONCLUSION: Serological evidence of previous HAV, HCV and HEV infections was not significantly different between Behçet's patients and other groups. However, previous HBV infection was found in a significantly lower number of BD patients as compared with healthy controls and systemic vasculitic patients.

Adhesive arachnoiditis causing cauda equina syndrome in ankylosing spondylitis: CT and MRI demonstration of dural calcification and a dorsal dural diverticulum.

We present the radiological features of a 42-year-old man with long-standing inactive ankylosing spondylitis (AS), demonstrating that arachnoiditis is a cause of a cauda equina syndrome (CES) in this disease. CT showed a dorsal arachnoid diverticulum causing scalloped erosion of the laminae, and punctate and curvilinear dural calcification. MRI revealed adhesion and convergence of the cauda equina dorsally into the arachnoid pouch, causing the dural sac to appear empty canal. To the best of our knowledge, dural calcification on CT is a new finding in AS, which may be related to the CES. Our findings support the hypothesis that chronic adhesive arachnoiditis with subsequent loss of meningeal elasticity may be the main cause of CES in AS.

Spinal abnormalities similar to ankylosing spondylitis in a 58-year-old woman with ochronosis.

Ochronotic arthropathy (spondylosis or peripheral arthropathy) is a late complication of alkaptonuria. There is a tendency for HLA-B27 positive patients with alkaptonuria to develop ochronotic spondylosis. A 58-year-old white woman, presented with ochronotic spondylosis. She was HLA-B27 positive. Her family history was positive for alkaptonuria. Ochronotic patients with HLA-B27 positivity develop spinal changes similar to ankylosing spondylitis (AS).

[Lupus anticoagulant and antiphospholipid antibody values in a family with systemic lupus erythematosus]. / Lupus-Antikoagulans- (LA-) und antiphospholipide Antikörper- (APA-) Werte bei einer Familie mit systemischem Lupus erythematodes (SLE).

The Lupus Anticoagulant (LA) is an immunoglobulin directed towards the phospholipid portion of the prothrombin activator complex. This immunoglobulin because first identified in the plasma of patients with Systemic Lupus Erythematodes, was named as Lupus Anticoagulant. Although initially described in patients with SLE, it was subsequently observed in other diseases and also in patients without any manifest disease. SLE or similar diseases are present in 35% of LA (+) patients. The LA prevalence in SLE patients has been found as 34% whereas ACA prevalence was found as 44%. While searching for the presence of LA and the levels of APA in cases having unexplained recurrent fetal losses, a family (a mother and 3 daughters) was discovered, whose each member has been diagnosed as SLE at different times and with different symptoms. Data suggesting the presence of LA and high APA levels were determined in all the members of the family and also it was realised that cause who had recurrent fetal losses had the highest APA levels. In addition to immunoassay methods to detect APA, examination of coagulation tests in patients with unexplained thrombosis and/or fetal losses, would be of great help.