Association of anticardiolipin antibodies, complement and leptin with the severity of coronary artery disease expressed as syntax score.

Chronic inflammation plays a role in all stages of atherosclerosis leading to coronary artery disease (CAD), with elevated inflammatory markers being associated with the worse clinical outcome. The goal of the current study was to examine possible association between pro-inflammatory/pro-coagulant factors; anticardiolipin (aCL) autoantibodies, complement C3, C4 and leptin, and the severity of CAD expressed as SYNTAX score. Patients with symptoms of cardiac ischemia undergoing coronary angiography were recruited, and their blood levels of aCL-IgG, aCL-IgM, complement C3, C4 and leptin were assessed. Their association with the SYNTAX score, calculated based on coronary angiography findings, was analyzed. All patients had aCL antibody titer within the normal range. A significant positive association was found for aCL-IgG and SYNTAX score. Male patients had higher average aCL-IgG concentration and SYNTAX score than female patients. No association was found between SYNTAX score and C3 and C4. On the other hand, leptin was negatively associated with SYNTAX score. Our study demonstrates an association between the extent of CAD and aCL-IgG even in the absence of systemic autoimmune disease and at the aCL-IgG levels that are within the normal range. Also, association of lower leptin levels with more severe CAD suggests that its pro-inflammatory effects might not contribute to the pathogenesis of CAD, and that leptin might even exert protective effects on coronary vasculature.

Relationship between vitamin D, IFN-γ, and E2 levels in systemic lupus erythematosus.

In this study, we investigated the relationship between vitamin D, interferon-gamma (IFN-γ), and estradiol (E2) in females of childbearing age with inactive systemic lupus erythematosus (SLE). The study included 22 SLE patients, and 21 age- and gender-matched healthy individuals. Serum concentrations of 25-hydroxyvitamin D3 (25(OH)D3), E2, and IFN-γ were measured by radioimmunoassay using the gamma-counter and ELISA. Patients and control subjects were divided into two groups based on their vitamin D levels (25(OH)D3 ≤ 20 ng/mL; 25(OH)D3 > 20 ng/mL). The median values of IFN-γ and E2 were higher in SLE patients compared to the controls, irrespective of vitamin D level (p = 0.001, p = 0.009, p = 0.003, and p = 0.003, respectively). In SLE patients, there was a negative correlation between IFN-γ and 25(OH)D3 (rs = -0.330; p = 0.03) and a positive correlation between IFN-γ and E2 (rs = 0.404; p = 0.007). This study demonstrates an interesting interplay between vitamin D, INF-γ, and E2 in SLE patients with inactive disease.

Possible implications of TGF-alpha in oesophageal dysmotility in systemic sclerosis.

OBJECTIVES: Hypoxia is a characteristic feature of systemic sclerosis (SSc).Transforming growth factor alpha (TGF-α) has an important role in excessive inflammation under hypoxic conditions. Since oesophageal dysmotility is one of the most common signs of SSc, the aim of this study was to explore the relation between TGF-α and oesophageal dysmotility in SSc. METHODS: The study included 35 patients with SSc and 32 healthy controls matched for sex and age. Serum concentrations of TGF-α were measured using ELISA. Oesophageal motility was assessed by oesophageal scintigraphy. A multiple-swallow test was performed in the study population with 99mTc-DTPA. A region of interest over the entire oesophagus was defined and the retention index (RI) was calculated. RESULTS: Statistically significant differences in serum concentration of TGF-α as well as of RI of 99mTc-DTPA were found between patients with SSc and healthy controls. A statistically significant correlation was found between serum concentrations of TGF-α and RIs of 99mTc-DTPA. This correlation was inverse, i.e. when serum concentrations of TGF-α increased, the RI of 99mTc-DTPA decreased (Spearman rho =-0361, p=0.033). CONCLUSIONS: These results point to a possible relation between TGF-α and oesophageal dysmotility in SSc. Although the results do not explain the exact role of this cytokine in the pathogenesis of esophageal changes, the finding of inverse correlation between TGF-α and oesophageal dysmotility is intriguing and requires further investigation.

Vascular manifestations of systemic lupus erythematosis.

Systemic lupus erythematosus (SLE) is an autoimmune connective disease, where vascular lesions are one of the typical symptoms. The differentiation of the type of vascular complications in SLE is very difficult, sometimes impossible, and requires an in-depth immune and histopathological approach, and extensive clinical experience. It may play a key role in the choice of treatment strategy and prediction of patient prognosis. SLE is a prototype of a multisystem autoimmune connective tissue disease, marked by immune complex-mediated lesions of blood vessels in diverse organs. Therefore, awareness of the aetiology, pathophysiology, the clinical and histopathogical setting, and SLE-associated vascular complications is of great clinical significance. In this review, the spectrum of vascular abnormalities and the options currently available to treat the vascular manifestations of SLE are discussed.

Drug-induced vasculitis: a clinical and pathological review.

Drug-induced vasculitis is an inflammation of blood vessels caused by the use of various pharmaceutical agents. Vasculitis causes changes in the walls of blood vessels, including thickening, weakening, narrowing and scarring. Inflammation can be short-term (acute) or long-term (chronic) and can be so severe that the tissues and organs supplied by the affected vessels do not get enough blood. The shortage of blood can result in organ and tissue damage, even death. Drug-induced vasculitis is the most common form of vasculitis. The differential diagnosis between drug-induced and idiopathic vasculitic conditions may be difficult in the individual patient. Withdrawal may be helpful to distinguish between these syndromes. Withdrawal of the offending agent alone is often sufficient to induce prompt resolution of clinical manifestations, obviating the need for immunosuppressive and anti-inflammatory drugs. Increasing understanding of the pathophysiological characteristics of all inflammatory vasculitides should lead to better diagnostic and therapeutic approaches to drug-induced vasculitis.

Infectious disease as aetiological factor in the pathogenesis of systemic sclerosis.

Systemic sclerosis is an autoimmune disease characterised by vascular obliteration, excessive extracellular matrix deposition and fibrosis of the connective tissues of the skin, lungs, gastrointestinal tract, heart, and kidneys. The pathogenesis of systemic sclerosis is extremely complex; at present, no single unifying hypothesis explains all aspects. Over the last 20 years increasing evidence has accumulated to implicate infectious agents in the aetiology of systemic sclerosis. Increased antibody titres, a preponderance of specific strains in patients with systemic sclerosis, and evidence of molecular mimicry inducing autoimmune responses suggest mechanisms by which infectious agents may contribute to the development and progression of systemic sclerosis. Here we review the current state of knowledge of infectious risk factors in systemic sclerosis and the possible mechanisms by which infectious exposures might induce pathologic processes.

The level of anti-topoisomerase I antibodies highly correlates with metacarpophalangeal and proximal interphalangeal joints flexion contractures in patients with systemic sclerosis.

BACKGROUND: It is found that an antibody directed against DNA topoisomerase I (anti-topo I abs) is detected almost exclusively in systemic sclerosis (SSc). These antibodies are predictors of pulmonary fibrosis and peripheral vascular disease. OBJECTIVE: Metacarpophalangeal (MCP) and proximal interphalangeal (PIP) joints flexion contractures are assessed as markers of active SSc. The aim of this study was to find out is there any relationship between anti-topo I abs and MCP and PIP joints flexion contractures. METHODS: Twenty-eight patients with active disease who fulfilled the American College of Rheumatology criteria for SSc were included in this study. Twenty eight healthy control subjects were also investigated. Clinical and radiological assessments of the hands were carried out. The flexion ranges in the 8 finger joints by goniometric measurement were obtained. Anti-topo I abs with an enzyme linked immunosorbent assay (ELISA) were measured. RESULTS: MCP and PIP joints flexion contractures and the levels of anti-topo I abs were significantly higher in patients with systemic sclerosis than in healthy control. The anti-topo I abs were found in 16 of 28 patients with systemic sclerosis. Sixteen of 28 patients with active disease had MPC and proximal PIP joints flexion contractures. In 16 SSc patients with anti-topo I abs, 13 had metacarpophalangeal and proximal interphalangeal joints flexion contractures. In only 3 patients of 16 with the flexion contractures the levels of anti-topo I abs were negative. The patients with MPC and PIP joints flexion contractures had higher mean value of anti-topo I abs titers (53.718 +/-50.977 vs 8.127 +/- 8.915, P < 0.0001) than did those with no contractures. Furthermore, the titers of anti-topoisomerase I antibody positively correlated with the flexion contractures (r = 0.4252, P = 0.0241). Radiologically, joint space narrowing and flexion contractures of the fingers were seen significantly more frequently in the SSc patients with anti-topo I abs (P < 0.05). CONCLUSION: Serum level of anti-topoisomerase I antibodies is in direct relationship with MPC and PIP joints flexion contractures.