In multivariate regression analysis, duration of anemia was independently associated with the presence of PAH in SLE patients (P=0.006). When patients were divided into three groups according to tertiles of Hb well as PASP, serum IL-6 significantly increased across the tertiles of PASP (P for trend=0.038), but decreased across the tertiles of Hb (P for trend=0.001). Conclusions: Our study suggests that prolonged exposure to anemic hypoxia, which is associated with increased serum IL-6, might be a component of pathogenesis of PAH in SLE patients. Acknowledgedments: Nothing specified.

Systemic lupus erythematosus (SLE) is associated with increased cardiovascular risk. We aimed to evaluate arterial stiffness and the ankle brachial index (ABI), two markers of subclinical cardiovascular disease, in SLE. We studied 55 patients with SLE (12.7% males, age 53.3 ± 15.3 years) and 61 age- and gender-matched controls. Arterial stiffness was evaluated by measuring pulse wave velocity (PWV), augmentation index (AIx) and central systolic, diastolic, pulse and mean blood pressure (BP). Peripheral arterial disease was defined as ABI ≤ 0.90. Regarding markers of arterial stiffness, patients with SLE had lower PWV and AIx than controls (p < 0.01 and p < 0.05, respectively). However, after adjusting for differences in cardiovascular risk factors between patients with SLE and controls, PWV and AIx did not differ between the two groups. Central systolic, diastolic, pulse and mean BP also did not differ between the two groups. In patients with SLE, PWV correlated independently with systolic BP (B = 0.05, p < 0.001) and waist/hip ratio (B = 6.72, p < 0.05). Regarding ABI, the lowest ABI was lower in patients with SLE than in controls (p < 0.005). However, after adjusting for differences in cardiovascular risk factors between patients with SLE and controls, the lowest ABI did not differ between the two groups. The prevalence of PAD also did not differ between patients with SLE and controls (10.0 and 5.4%, respectively; p = NS). Markers of arterial stiffness and the ABI do not appear to differ between patients with SLE and age- and gender-matched controls. However, given the small sample size, larger studies are needed to clarify whether SLE promotes arterial stiffness and PAD.

Thiolat and colleagues reported a significant expansion in the number of Treg cells in 15 rheumatoid arthritis (RA) patients after 3 months of treatment with tocilizumab (TCZ) (1). We have observed that the increase in Treg cell frequency occurs even sooner after the initiation of TCZ treatment (shortly after the first infusion) and is sustained over at least 12 months of regular drug administration.We studied 22 patients with active RA who were administered TCZ monthly (5 patients received 12 infusions, 4 received 8, 3 received 6, 3 received 4, and 7 received 2) along with disease-modifying antirheumatic drugs (DMARDs) at stable doses. Corticosteroids were not used throughout the study. Levels of CD25 high FoxP3ϩCD4ϩ Treg cells were assessed before every TCZ infusion. After the first infusion, Treg cell frequencies were significantly increased and the 28-joint Disease Activity Score (2) was decreased (Table 1); this increment was sustained over the subsequent months.Related studies have assessed Treg cell levels after 2 months (3) or 3 months (1,4) of TCZ administration. Our results show that a significant increase in Treg cell frequency occurs after only 1 infusion; furthermore, the increase remains stable over time. Whether TCZ or another drug(s) is the direct cause of the Treg cell expansion or whether this is the result of disease remission remains a matter of controversy. In this context, corticosteroids (used in moderate doses in previous studies) (4) are known to increase Treg cell levels in other systemic autoimmune diseases, e.g., systemic lupus erythematosus (5). In our patients (who did not receive corticosteroids during the study), DMARDs were administered at stable doses; therefore, it is quite unlikely that the Treg cell expansion could be attributed to these drugs.In conclusion, TCZ is expected to skew the Th17/Treg cell balance toward the protective Treg cell arm (6,7) The exact mechanism(s) behind this action, the duration of the increase in Treg cell frequency, and its clinical significance remain to be determined.

Increase in Tregs during SLE remission is independent of the therapeutic regimen used and probably represents an epiphenomenon of disease remission. Time to Tregs restoration was significantly shorter in patients treated with iv MP and IVIGs compared to CYP pulse therapy.

Cyclophosphamide pulse therapy was associated with a significant increase of the CD4(+) CD25(high) FOXP3(+) Tregs in patients with active LN and NPSLE. This effect is probably indirect and may partially explain the beneficial role of cyclophosphamide in such cases.

No abstract

The disease affects, mainly, the large-and medium-sized extracranial branches of the carotid artery and, classical clinical features, such as headache, jaw claudication, scalp tenderness and visual impairment, are closely related to this marked cranial tropism of GCA. [3] On a histopathological basis, GCA involves all layers of the arterial wall, including the adventitia. Inflammatory lesions consist of activated T cells, dendritic cells (DCs) and macrophages. These lesions are believed to be the histopathologic hallmark of GCA and are characterized by a predominance of mononuclear infiltrates or granulomas, usually with multinucleated giant cells. [4] Besides the inflammation of the carotid branches, involvement of the great arteries, such as the aorta and its main tributaries, was initially recognized in the late 1930s and reported sporadically thereafter in necropsy or histopathologic studies of surgically resected tissues. [5,

Environmentally induced systemic sclerosis is a well-recognized condition, which is correlated with exposure to various chemical compounds or drugs. However, development of scleroderma-like disease after exposure to silicone has always been a controversial issue and, over time, it has triggered spirited debate whether there is a certain association or not. Herein, we report the case of a 35-year-old female who developed Raynaud's phenomenon and, finally, systemic sclerosis shortly after silicone breast implantation surgery.