Vitamin D and Demyelinating Diseases: Neuromyelitis Optica (NMO) and Multiple Sclerosis (MS)Read the full article
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Significance of Anti-TPO as an Early Predictive Marker in Thyroid Disease
Even though most thyroid subjects are undiagnosed due to nonspecific symptoms, universal screening for thyroid disease is not recommended for the general population. In this study, our motive is to showcase the early appearance of thyroid autoantibody, anti-TPO, prior to the onset of thyroid hormone disruption; hence the addition of anti-TPO in conjunction with traditional thyroid markers TSH and FT4 would aid to reduce the long-term morbidity and associated health concerns. Here, a total of 4581 subjects were tested multiple times for TSH, FT4, anti-TPO, and anti-Tg and followed up for 2 years. We streamlined our subjects into two groups, A1 (euthyroid at first visit, but converted to subclinical/overt hypothyroidism in follow-up visits) and A2 (euthyroid at first visit, but converted to hyperthyroidism in follow-up visits). According to our results, 73% of hypothyroid subjects (from group A1) and 68.6% of hyperthyroid subjects (from group A2) had anti-TPO 252 (±33) and 277 (±151) days prior to the onset of the thyroid dysfunction, respectively. Both subclinical/overt hypothyroidism and hyperthyroidism showed a significantly higher percentage of subjects who had anti-TPO prior to the onset of thyroid dysfunction compared to the combined control group. However, there was no significant difference in the subjects who had anti-Tg earlier than the control group. Further assessment showed that only anti-TPO could be used as a standalone marker but not anti-Tg. Our results showcase that anti-TPO appear prior to the onset of thyroid hormone dysfunction; hence testing anti-TPO in conjunction with TSH would greatly aid to identify potentially risk individuals and prevent long-term morbidity.
Galectin-1, -4, and -7 Were Associated with High Activity of Disease in Patients with Rheumatoid Arthritis
Background. Due to the variety of functions that galectins (Gal) possess, it is clear that they participate in the pathogenesis of rheumatoid arthritis (RA). Although some studies demonstrate their functions, there is still no correlation with the clinical data of the disease, having the physiological meaning still unknown. Objectives. To compare serum levels of Gal-1, -4, and -7 in patients with RA and healthy controls and to correlate them with clinical parameters. Methods. Serum samples were collected from patients with RA and healthy donors to determine the serum levels of Gal-1, -4, and -7. Results. Serum levels of Gal-1, -4, and -7 were significantly higher in RA patients compared to controls. We evaluated disease activity (CDAI) with serum levels of galectins and found that patients who were high in disease activity had high levels of galectin compared to the moderate activity group. Galectin-4 had higher levels in patients who were in high activity when compared to the group in remission or low activity. Evaluating the activity of the individual disease (DAS28), patients in high individual activity had high levels of Gal-4 when compared to the group in remission or low activity. We also found an association between positive rheumatoid factor and Gal-1 and Gal-4 levels. Conclusion. Our results show for the first time the relationship between serum levels of galectin and the clinical parameters of patients with RA. Demonstrating their role in pathogenesis, new studies with galectins are needed to assess how they function as a biomarker in RA.
Neuronal Antibodies and Associated Syndromes
Introduction. Multiple well-recognized conditions, such as Lambert–Eaton myasthenic syndrome (LEMS) and myasthenia gravis (MG), have been associated with neuronal antibodies. Materials and Methods. A search was performed using Embase, PubMed, and CINAHL. An initial search of each database was conducted using keywords and terms related to the aim of the current review. Additional articles were obtained by examining the reference lists and citations in the selected records. Results. The studies identified through the search process used different designs and methods to explore neuronal antibodies and associated syndromes. Previous studies have shown that neurological and psychiatric disorders can be mediated and influenced by various antibodies. The identification of autoantibodies can help with the accurate diagnosis of conditions and commencement of early treatment. Discussion. A review of selected studies identified in the literature implicated that classic anti-neuronal antibodies, such as anti-Ri and anti-Hu, play a role in the development of neurological diseases. More recent studies have indicated that other novel antibodies act on neuronal cell surface antigens to contribute to the development of neurological disorders. Conclusion. Existing research provides evidence revealing a spectrum of antibodies linked to the development and progression of neurological diseases. However, further antibody testing and studies should be performed to validate the relationship between conditions and antibodies.
Case Reports of DRESS Syndrome and Symptoms Consistent with DRESS Syndrome Following Treatment with Recently Marketed Monoclonal Antibodies
Background. Monoclonal antibodies constitute a potent and broadly tolerable drug class, representing for some conditions the first newly approved treatment in years. As such, many are afforded “fast-track” or “breakthrough therapy” designations by the U.S. Food and Drug Administration, leading to provisional approval before Phase III clinical trials are reported. Although these drugs are usually safe, some patients experience life-threatening complications—myositis and encephalitis have led to permanent or temporary recalls. Drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome is a hypersensitivity condition easily missed due to its long incubation period and nonspecific presentation. This minireview is primarily intended as an abbreviated guide for practitioners who may be using these powerful treatments. Methodology. We searched PubMed using a string of symptoms consistent with DRESS syndrome and monoclonal antibodies approved by the FDA since 2015. Then, we excluded studies reporting dermatological complications of reactivation of nonherpetic infection, immunodeficiency-related infection, or reactions to the injection site or infusion. We searched for and accessed prior reviews and background studies via PubMed, Mendeley, and Google Scholar. Results. Two cases of DRESS syndrome were identified in the literature, both the result of treatment with daclizumab. There was one additional case of encephalitis without cutaneous symptoms caused by daclizumab. Drug-induced hypersensitivity dermatitis was reported following treatment with nivolumab and two cases of combination treatment with ipilimumab and either nivolumab or durvalumab produced maculopapular rash and bullae in the first patient and lichenoid dermatitis and blisters in the second patient. Conclusions. Daclizumab was the only recently approved monoclonal antibody associated with DRESS syndrome as such. Limitations in the diagnostic reliability of DRESS syndrome as a clinical entity and the lack of negative clinical trial reporting suggest enhanced vigilance on the part of clinicians and regulators may be warranted.
Therapeutic Plasma Exchange as Management of Complicated Systemic Lupus Erythematosus and Other Autoimmune Diseases
Introduction. Autoimmune diseases include a diverse and complex group of pathologies with a broad clinical spectrum due to the production of autoantibodies, which generates multisystemic compromise. Therapeutic plasma exchange (TPE) is a good additive treatment for immunosuppression due to its action over the autoantibodies. Objectives. To describe the main clinical characteristics and outcomes of patients with systemic lupus erythematosus and other systemic autoimmune diseases managed with TPE. Methodology. This descriptive retrospective study enrolled patients with systemic autoimmune diseases who received TPE. Results. In total, 66 patients with a median age of 33.5 years (24-53 years) were included; the majority were females [n=51 (77.27%)]. Forty (60.61%) patients were diagnosed with systemic lupus erythematosus. In these cases, the main indication for TPE was diffuse alveolar hemorrhage (DAH; n=20, 30.3%) and neurolupus (n=9, 13.6%). No TPE-related deaths occurred, and the main complication was hemorrhage, without significant differences among the four types of TPE solutions used. The overall outcome was improvement in 41 (62.12%) patients. Conclusion. TPE is safe and effective in patients with severe manifestations of autoimmune diseases.
Identification of Levels of Serum Amyloid A and Apolipoprotein A1 in Serum Proteomic Analysis of Neuropsychiatric Systemic Lupus Erythematosus Patients
Neuropsychiatric Systemic Lupus Erythematosus (NPSLE) has multiple pathogenic mechanisms that cause diverse manifestations and whose diagnosis is challenging because of the absence of appropriate diagnostic tests. In the present study the application of proteomics using two-dimensional electrophoresis (2D) and mass spectrometry (MS) allowed the comparison of the protein profile of the serum low and high abundance protein fractions of NPSLE patients (NPSLE group) and SLE without neuropsychiatric syndromes (SLE group), Neuropsychiatric syndromes not associated with SLE (NPnoSLE groups), and healthy controls (CTRL group). The gels obtained were digitalized and analyzed with the PDQuest software. The statistical analysis of the spots was performed using the nonparametric Kruskal Wallis and Dunn's multiple comparison tests. Two spots showed significant differences and were identified by MS. Spot 4009 was significantly lower in NPSLE with regard to NPnoSLE (p= 0,004) and was identified as apolipoprotein A1 (APOA1) (score 809-1132). Spot 8001 was significantly higher in NPSLE regarding CTRL and NPnoSLE (p= 0,01 y 0,03, respectively) and was identified as serum amyloid A (SAA) (score 725-2488). The proinflammatory high density lipoproteins (HDL) have been described in SLE. In this HDL the decrease of APOA1 is followed by an increase in SAA. This altered level of both proteins may be related to the inflammatory state that is characteristic of an autoimmune disease like SLE, but this is not specific for NPSLE.