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Orexin-A is a neuropeptide involved in the regulation of food intake and the sleep-wake cycle. This study investigated plasma orexin-A levels in a sleep clinic cohort, adjusting for smoking habits, in 76 participants comprising 41 with obstructive sleep apnoea (OSA) (apnoea-hypopnoea index [AHI] 44.1 ± 19.1 events/h) and 35 without OSA (AHI 6.3 ± 4.7 events/h). Plasma orexin-A levels were significantly lower in OSA patients (15.0 ± 4.6 ng/ml) compared with those without OSA (31.4 ± 6.5 ng/ml). In non-OSA subjects, there was no significant difference between never smokers and ex/current smokers in plasma orexin-A levels (32.9 ± 9.5 versus 29.7 ± 8.9 ng/ml, respectively) whereas, in the OSA sub-group, orexin-A levels were significantly lower in never smokers than in ex/current smokers (4.0 ± 1.2 versus 21.4 ± 7.0 ng/ml). A significant inverse relationship was found between plasma orexin-A levels and AHI amongst never smokers, but there was no significant relationship amongst ex/current smokers. These results confirm previous studies demonstrating lower levels of plasma orexin-A in OSA patients and indicate that smoking may affect orexin-A levels and AHI.

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 χ² test and Student's t-test.
Results. The highest homocysteine concentrations were found in the MTX group (17.5±5.3 μmol/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 μmol/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.

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.

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&lt;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.

Since prolactin (PRL) has been implicated as playing a role in the pathogenesis of certain autoimmune diseases and since Behçet's Syndrome (BS) is a unique systemic vasculitis, we investigated serum PRL levels in patients with BS. We found that mean PRL levels in patients with clinically active BS, were not significantly higher than patients with clinically inactive BS and healthy controls. This finding may be regarded as evidence that a contribution of hyperprolactinemia to the aetiopathogenesis of BS seems unlikely.