These altogether could contribute significantly to arsenic-induced immunosuppression observed in the arsenic-exposed individuals.
BackgroundArsenic is a natural drinking water contaminant affecting 26 million people in West Bengal, India. Chronic arsenic exposure causes cancer, cardiovascular disease, liver disease, neuropathies and ocular diseases. The aims of the present study were to assess bioindicators of hepatocellular injury as indicated by the levels of liver enzymes, to determine the auto immune status, as indicated by the amounts of anti-nuclear antibodies (ANA) and anti-dsDNA antibodies in their serum, and to predict cardiovascular risk in the arsenic exposed population.MethodsEffect of chronic arsenic exposure on liver was determined by liver function tests. Autoimmune status was measured by measuring ANA and anti-dsDNA in serum. Inflammatory cytokines associated with increased cardiovascular disease risk, IL6, IL8 and MCP-1 were determined.ResultsOur results indicated that serum levels of bilirubin, alanine transaminase, aspartate transaminase, alkaline phosphatase and ANA were increased in the arsenic exposed population. Serum levels of IL6 and IL8 also increased in the arsenic exposed group.ConclusionsChronic arsenic exposure causes liver injury, increases the serum levels of autoimmune markers and imparts increased cardiovascular risk.
BackgroundDiagnosis of Giant Cell Arteritis(GCA) is difficult since its manifestations are protean1. Under-diagnosis is associated with ischaemic complications whereas over diagnosis is associated with inappropriate glucocorticoids (GC)2.GCA is diagnosed by different specialties, including family physicians, who would benefit from a clinical prediction score.A fast track pathway also requires clinical triage in terms of probability of disease. We evaluated all referred patients (08/16–08/17) to develop a pre-test probability score(PTBS) to support a diagnostic pathway and decision-making.MethodsThe PTBS was generated from long standing clinical experience. Information collected at initial assessment was given varying positive weightage. This included baseline demographics (age-gender), symptomatology at presentation(onset, headache and scalp tenderness, ischaemic symptoms, constitutional symptoms, polymyalgia),C-Reactive protein(CRP) and examination findings(ischaemic ophthalmic complications, temporal artery abnormalities, extra-cranial abnormalities, cranial nerve palsies). Negative weightage was given for competing diagnoses (infection, cancer, head and neck pathology, systemic rheumatological diseases). The PTBS was compared with the final diagnosis as GCA or non-GCA 6 months after the initial assessment. Analysis was performed in Stata SE, version 13.1.Results122 PTBS were collected of which CRP was missing in 1 case which was excluded from the analysis.23 had a final diagnosis of GCA at 6 months follow up. The rest consist our control group(99 patients). The area under the ROC curve for the 121 cases was 0.953 (figure 1). Using the bootstrap method gave an estimated area under the ROC curve (95% confidence interval) of 0.953 (0.911, 0.994). At the point of inflection, corresponding to a cut point of 9.5, sensitivity was 95.7%, and specificity was 86.7%;the likelihood ratio for a positive test was 7.2 and the likelihood ratio for a negative test, 0.050. At this cut point, 88.4% cases were correctly classified.ConclusionsThis single centre retrospective study suggests that PTBS is a useful standardised assessment tool for rating pre-test probability for GCA with high levels of sensitivity and specificity. PTBS may reduce variation in clinical assessment and aid decision making.A patient with low probability score(<9.5) can be managed with colour doppler ultrasound examination(US) which if negative will exclude the disease and the clinician can reassure patient.A patient with high PTBS and positive US can safely have the diagnosis confirmed and treated with GC. With intermediate scores, conflicting PTBS and US findings, equivocal US, additional investigations including TA biopsy and/or other imaging scans may be needed. Our results need validation in a prospective study and in internal and external validation cohorts. PTBS has the potential for forming the basis for education programme for the correct and early diagnosis of GCA and limit inappropriate GC in non GCA mimics.References[1] Murchison AP, et al. Vali...
In West Bengal, India, at present, more than 26 million people are exposed to arsenic through drinking water. Among them, only 15-20% manifest arsenic-induced noncancerous, precancerous, and cancerous skin lesions, indicating that genetic variants play important role in arsenic susceptibility. Chronic arsenic exposure has been associated with impairment of immune systems in the exposed individuals. Because cytokines are important immune mediators, alteration in expression of these gene products may lead to arsenic-specific disease manifestations. The aim of the present work was to investigate the association between the TNF-α-308G>A (rs1800629) and IL10 -3575T>A (rs1800890) polymorphisms and arsenic-induced dermatological and nondermatological health outcomes. A case-control study was conducted in West Bengal, India, involving 207 cases with arsenic-induced skin lesions and 190 controls without skin lesions having similar arsenic exposure. The polymorphisms were determined using conventional PCR-sequencing method. ELISA was done to determine the serum levels of the two cytokines tumor necrosis factor α (TNF-α) and interleukin 10 (IL10). Associations between the polymorphisms studied and nondermatological health effects in the study subjects were determined from our epidemiological survey data. Individuals with GA/AA (-308 TNF-α) and TA/AA (-3575 IL10) genotypes were at higher risk of developing arsenic-induced skin lesions, ocular, and respiratory diseases. Also the -308 TNF A allele corresponded to a higher production of TNF-α, and -3575 IL10 A allele corresponded to a lower production of IL10. Thus, the polymorphisms studied impart significant risk toward development of arsenic-induced dermatological and nondermatological health effects in the chronically exposed population of West Bengal, India.
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