10 research outputs found

    Vitamin D Status in Patients with Systemic Lupus Erythematosus in Serbia: Correlation with Disease Activity and Clinical Manifestations

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    BACKGROUND: Numerous studies indicate potential role of vitamin D as an important factor in the development of many autoimmune diseases including systemic lupus erythematosus (SLE). Patients with SLE are especially prone to the development of vitamin D deficiency due to the nature of their illness.AIM: The aims of our study were to determine the prevalence of vitamin D insufficiency and deficiency in patients with SLE in Serbia, to identify clinical variables associated with vitamin D status and to examine the impact of vitamin D status on disease activity and presence of specific lupus autoantibodies.MATERIAL AND METHODS: The study included 46 patients with SLE. Serum 25(OH)D concentration was measured by electrohemiluminiscent immunoassay.RESULTS: The mean serum concentration of 25(OH)D was 11.9 ± 7.3 ng/ml. The prevalence of insufficiency was 32.6%, while the prevalence of deficiency was 67.4%. There was no association between vitamin D status and photosensitivity, skin lesions, arthritis and lupus nephritis. Vitamin D status was not associated with the presence of specific autoantibodies. There was no correlation between disease activity assessed by SLEDAI scale with the concentration of 25(OH)D. Patients who used vitamin D supplements and calcium did not have a significantly higher concentration of 25(OH)D.CONCLUSION: In conclusion, vitamin D deficiency is common in patients with SLE

    Role of Vitamin D in Systemic Lupus Erythematosus

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    Vitamin D is a steroid hormone that in addition to its well known role in the metabolism of calcium and phosphorus exerts immunoregulatory properties. Data from animal studies and from prospective clinical trials on patients with rheumatoid arthritis, multiple sclerosis and type 1 diabetes point to the potential role of vitamin D as important environmental factor in the development of autoimmune diseases. Such role of vitamin D in systemic lupus erythematosus (SLE) has not yet been sufficiently studied. This review shows the sources, metabolism and mechanism of action of vitamin D, its effect on the cells of the immune system, prevalence and causes of vitamin D deficiency in patients with SLE, the link between vitamin D status and disease activity as well as recommendations for vitamin D supplementation

    Systemic Lupus Erythematosus and Antiphospholipid Syndrome

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    Antiphospholipid syndrome is an autoimmune disorder defined as association of vascular thrombosis and/or pregnancy complications with presence of antiphospholipid antibodies (lupus anticoagulant, anticardiolipin and anti-β2 glycoprotein I). It is the most common cause of acquired thrombophilia, and can occur as an independent entity or in relation with other diseases, especially systemic lupus erythematosus. Presence of antiphospholipid syndrome in systemic lupus erythematosus is additional vaso occlusive factor in already present inflammation, bringing further risk for thrombotic events. Clinical and serological manifestations of antiphospholipid syndrome and systemic lupus erythematosus are very similar, so possible connection for these two autoimmune disorders is assumed

    Systemic Lupus Erythematosus and Secondary Antiphospholipid Syndrome after Thymectomy for Myasthenia Gravis - A Case Report

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    INTRODUCTION: Systemic lupus erythematosus (SLE) and myasthenia gravis (MG) are autoimmune diseases that show some similarities: a higher incidence in young women, relapsing-remitting course and positive anti-nuclear antibodies (ANA). However, they are two different clinical syndromes, which can coexist or precede each other. Thymectomy is a therapeutic option for patients with severe MG or thymoma. There are many cases of SLE after thymectomy described in the literature, so the question arises whether thymectomy predisposes patients to SLE and what are imunopathogenetic mechanisms behind this process.CASE REPORT: We report a case of a patient who was diagnosed with SLE and secondary antiphospholipid syndrome (APS) 28 years after thymectomy for MG. Clinical picture of SLE was characterized by cutaneous and articular manifestations, polyserositis, lupus nephritis and immunological parameters showed positive ANA, anti-ds-DNA, excessive consumption of complement components, positive cryoglobulins. Clinical and laboratory immunological parameters for the diagnosis of secondary APS where also present. The patient was initially treated with glucocorticoids followed by mycophenolate mofetil. During one year follow-up patient was in a stable remission of SLE.CONCLUSION: Thymectomy for MG may predispose SLE development in some patients. Further studies are needed to better understand the connection between these two autoimmune diseases

    LC/DAD determination of biogenic amines in serum of patients with diabetes mellitus, chronic urticaria or Hashimoto's thyroiditis

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    Biogenic amines are integral part of nearly every cell. In the present study, the method of acidic extraction of histamine (His), of polyamines putrescine (Put), spermidine (Spd) and catecholamines epinephrine (Epi) and norepinephrine (NE) from human serum, precolumn derivatization with dansyl chloride, and LC/DAD analysis of the biogenic amines was used with the aim of monitoring differences of their levels in patients with diabetes mellitus, chronic urticaria, and Hashimoto's thyroiditis, compared to healthy subjects, and to observe them as possible markers for immune mediated diseases. The retention times were used for the determination of serum biogenic amines. Statistically significant differences were found in the levels of putrescine and histamine in diabetes mellitus patients, of the levels of putrescine, histamine, spermidine and epinephrine in chronic urticaria patients and of the levels of putrescine and spermidine levels in Hashimoto's thyroiditis patients, compared to those of healthy controls. Norepinephrine was found only in the serum of patients with chronic urticaria. The values of recovery, evaluated in controls, varied between 85.7 and 106.7 %. The statistically significant changes in putrescine, histamine, spermidine and epinephrine levels in patients compared with those in healthy people reflects the existence of biochemical disturbances in the mentioned immune-mediated diseases

    Enhanced Liver Fibrosis Score as a Biomarker for Vascular Damage Assessment in Patients with Takayasu Arteritis—A Pilot Study

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    Takayasu Arteritis (TA) is characterized by granulomatous panarteritis, vessel wall fibrosis, and irreversible vascular impairment. The aim of this study is to explore the usefulness of the Enhanced Liver Fibrosis score (ELF), procollagen-III aminoterminal propeptide (PIIINP), tissue inhibitor of matrix metalloproteinase-1 (TIMP-1), and hyaluronic acid (HA) in assessing vascular damage in TA patients. ELF, PIIINP, TIMP-1, and HA were measured in 24 TA patients, and the results were correlated with the clinical damage indexes (VDI and TADS), an imaging damage score (CARDS), and disease activity scores (NIH and ITAS2010). A mean ELF score 8.42 (±1.12) and values higher than 7.7 (cut-off for liver fibrosis) in 21/24 (87.5%) of patients were detected. The VDI and TADS correlated significantly to ELF (p < 0.01). Additionally, a strong association across ELF and CARDS (p < 0.0001), PIIINP and CARDS (p < 0.001), and HA and CARDS (p < 0.001) was observed. No correlations of the tested biomarkers with inflammatory parameters, NIH, and ITAS2010 scores were found. To our knowledge, this is the first study that suggests the association of the serum biomarkers PIIINP, HA, and ELF score with damage but not with disease activity in TA patients. The ELF score and PIIINP may be useful biomarkers reflecting an ongoing fibrotic process and quantifying vascular damage

    Large-Vessel Giant Cell Arteritis following COVID-19—What Can HLA Typing Reveal?

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    Giant cell arteritis (GCA) is an immune-mediated vasculitis that affects large arteries. It has been hypothesized that viruses may trigger inflammation within the vessel walls. Genetic studies on human leukocyte antigens (HLAs) have previously reported HLA-DRB1*04 as a susceptible allele for GCA and HLA-DRB1*15 as a protective allele for GCA. Here, we discuss the clinical presentation, laboratory findings, HLA class I and class II analysis results, and management of patients with extracranial large-vessel (LV) GCA, detected at least six weeks after recovery from COVID-19. This case series encompassed three patients with LV-GCA (two males and a female with an age range of 63–69 years) whose leading clinical presentation included the presence of constitutional symptoms and significantly elevated inflammatory markers. The diagnosis of LV-GCA was confirmed by CT angiography and FDG-PET/CT, revealing inflammation in the large vessels. All were treated with corticosteroids, while two received adjunctive therapy. By analyzing HLA profiles, we found no presence of the susceptible HLA-DRB1*04 allele, while the HLA-DRB1*15 allele was detected in two patients. In conclusion, LV-GCA may be triggered by COVID-19. We highlight the importance of the early identification of LV-GCA following SARS-CoV-2 infection, which may be delayed due to the overlapping clinical features of GCA and COVID-19. The prompt initiation of therapy is necessary in order to avoid severe vascular complications. Future studies will better define the role of specific HLA alleles in patients who developed GCA following COVID-19

    Large-Vessel Giant Cell Arteritis following COVID-19—What Can HLA Typing Reveal?

    No full text
    Giant cell arteritis (GCA) is an immune-mediated vasculitis that affects large arteries. It has been hypothesized that viruses may trigger inflammation within the vessel walls. Genetic studies on human leukocyte antigens (HLAs) have previously reported HLA-DRB1*04 as a susceptible allele for GCA and HLA-DRB1*15 as a protective allele for GCA. Here, we discuss the clinical presentation, laboratory findings, HLA class I and class II analysis results, and management of patients with extracranial large-vessel (LV) GCA, detected at least six weeks after recovery from COVID-19. This case series encompassed three patients with LV-GCA (two males and a female with an age range of 63–69 years) whose leading clinical presentation included the presence of constitutional symptoms and significantly elevated inflammatory markers. The diagnosis of LV-GCA was confirmed by CT angiography and FDG-PET/CT, revealing inflammation in the large vessels. All were treated with corticosteroids, while two received adjunctive therapy. By analyzing HLA profiles, we found no presence of the susceptible HLA-DRB1*04 allele, while the HLA-DRB1*15 allele was detected in two patients. In conclusion, LV-GCA may be triggered by COVID-19. We highlight the importance of the early identification of LV-GCA following SARS-CoV-2 infection, which may be delayed due to the overlapping clinical features of GCA and COVID-19. The prompt initiation of therapy is necessary in order to avoid severe vascular complications. Future studies will better define the role of specific HLA alleles in patients who developed GCA following COVID-19
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