Patients with diagnosed inflammatory bowel disease (IBD) will commonly experience a clinical relapse in spite of a prolonged therapy-induced period of clinical remission. The current methods of assessing subclinical levels of low-grade inflammation which predispose patients to relapse are not optimal when considering both cost and patient comfort. Over the past few decades, much investigation has discovered that proteins such as calprotectin that are released from inflammatory cells are capable of indicating disease activity. Along with C-reactive protein and erythrocyte sedimentation rate, calprotectin has now become part of the current methodology for assessing IBD activity. More recently, research has identified that other fecal and serum biomarkers such as lactoferrin, S100A12, GM-CSF autoantibodies, α1-antitrypsin, eosinophil-derived proteins, and cytokine concentrations have variable degrees of utility in monitoring gastrointestinal tract inflammation. In order to provide direction toward novel methods of predicting relapse in IBD, we provide an up-to-date review of these biomarkers and their potential utility in the prediction of clinical relapse, given their observed activities during various stages of clinical remission.
The complex nature of inflammatory bowel disease (IBD) often results in treatment failure for many patients. With some patients cycling through multiple therapies before achieving a sustained period of remission, the ability to predict a patient's response to therapeutics could decrease the time from active disease to clinical remission and mucosal healing. The prospect of such individualized treatment of IBD would be aided by accurate biomarkers, both fecal and serological, which have to date shown value as indicators of IBD activity. Here we review the utility of generic biomarkers for inflammation or mucosal healing, such as calprotectin, C-reactive protein (CRP), and fecal hemoglobin (fHb) as predictors of response to treatment of IBD. We further provide a deeper insight into the utility of monitoring the thiopurine treatment by thiopurine metabolites or alternative hematologic parameters. In light of multiple recent publications of biomarkers and biological therapy, our focus in this review is predicting response to thiopurine treatment only, that is, Azathioprine and 6-Mercaptopurine.
There are increasing reports of immune‐mediated and para‐infectious syndromes beyond the well‐known respiratory manifestations of severe‐acute‐respiratory syndrome coronavirus 2 (SARS‐CoV‐2) infection. However, the spectrum of severe neurological sequelae of SARS‐CoV‐2 remains undefined. We present the case of a 66‐year‐old female with rapidly progressive lower limb neurology 3 days post SARS‐CoV‐2 infection. Clinical and radiological findings were in keeping with transverse myelitis and treatment success was achieved with methylprednisolone and remdesivir. This report will discuss the associations between SARS‐CoV‐2 and acute transverse myelitis. We believe this is one of few described cases of early SARS‐CoV‐2‐associated transverse myelitis secondary to neurotropism and the first successfully treated with the inclusion of remdesivir in the therapeutic regimen.
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