Treatment of inflammatory myopathy: emerging therapies and therapeutic targets

Despite the lack of placebo-controlled trials, glucocorticoids are considered the mainstay of initial treatment for idiopathic inflammatory myopathy and myositis-associated interstitial lung disease. Glucocorticoid-sparing agents are often given concomitantly with other immunosuppressive agents, particularly in patients with moderate or severe disease. First-line conventional immunosuppressive drugs include either methotrexate or azathioprine, and when they fail, more aggressive therapy includes mycophenolate mofetil, tacrolimus or cyclosporine, intravenous immunoglobulin, rituximab, or cyclophosphamide, used alone or in various combinations. Further investigations are required to assess the role of more novel therapies in the treatment of myositis and myositis-associated interstitial lung disease.     

Detection of Helicobacter pylori Gene by Means of Immunomagnetic Separation-Based Polymerase Chain Reaction in Feces

Background: Detection of Helicobacter pylori is usually performed by culture, polymerase chain reaction (PCR), histology, or urease test on gastric biopsy samples. Although methods based on feces are non-invasive, their sensitivity has been relatively low. In this study, to improve its sensitivity, immunomagnetic separation (IMS) was used as a pre-PCR step for direct detection of H. pylori in feces. Methods: Fresh fecal samples were taken from 72 patients attending for endoscopy. Of these, 57 patients had a positive H. pylori status according to the results of culture, histology, and PCR on gastric biopsy samples. Anti-H. pylori antibody-sensitized immunomagnetic beads were used to concentrate the bacteria. PCR was then performed to detect the H. pylori urease A-encoding gene. Results: Of the 57 H. pylori-positive patients, 35 (61.4%) had positive fecal samples by IMS-based PCR method. None of the 15 H. pylori-negative patients had positive fecal samples. The sensitivity of this method was 61.4%, and the specificity 100.0%. Conclusions: This study confirms that non-invasive diagnosis of H. pylori infection could be made from feces by using IMS-based PCR.     

Maternal country of birth and previous pregnancies are associated with breast milk characteristics

Populations in high infectious exposure countries are at low risk of some immune-mediated diseases such as Crohn's disease and allergy. This low risk is maintained upon immigration to an industrialized country, but the offspring of such immigrants have a higher immune-mediated disease risk than the indigenous population. We hypothesize that early life exposures in a developing country shape the maternal immune system, which could have implications for the offspring born in a developed country with a low infectious load. The aim of this study was to investigate if exposures in childhood (indicated by country of origin) and subsequent exposures influence immunologic characteristics relevant to stimulation of offspring. Breast milk components among 64 mothers resident in Sweden, 32 of whom immigrated from a developing country, were examined using the ELISA and Cytometric Bead Array methods. Immigrants from a developing country had statistically significantly higher levels of breast milk interleukin-6 (IL-6), IL-8 and transforming growth factor-β1. A larger number of previous pregnancies were associated with down-regulation of several substances, statistically significant for soluble CD14 and IL-8. The results suggest that maternal country of birth may influence adult immune characteristics, potentially relevant to disease risk in offspring. Such a mechanism may explain the higher immune-mediated disease risk among children of migrants from a developing to developed country. Older siblings may influence disease risk through the action of previous pregnancies on maternal immune characteristics.     

Mitogen activated protein kinases: a role in inflammatory bowel disease?

Since their discovery more than 15 years ago, the mitogen activated protein kinases (MAPK) have been implicated in an ever‐increasingly diverse array of pathways, including inflammatory signalling cascades. Inflammatory bowel diseases (IBD), such as ulcerative colitis and Crohn's disease, are characterized by the perpetual production of inflammatory mediators. Research into the transduction pathway behind this over‐production has highlighted the potential mediating role for the MAPKs and their related signalling components. This review highlights some of the research into the role for the MAPKs and their related signalling proteins in influencing the progression of IBD.     

短潜伏期体感诱发电位在慢性炎性脱髓鞘性多发性神经根神经病中的诊断作用

目的探讨短潜伏期体感诱发电位(SSEP)对慢性炎性脱髓鞘性多发性神经根神经病(CIDP)的诊断作用。方法 48例确诊或可能CIDP患儿及40例健康对照儿童进行肌电图神经传导和/或SSEP检查(健康对照仅行SSEP检查)。肌电图神经传导检查采用4道肌电图仪进行,包括至少4条运动神经和2条感觉神经;SSEP主要观察正中神经的N6(肘部电位),N13(颈髓电位),N20(皮质电位);胫神经的N8(腘窝电位),N22(腰髓电位),P39(皮质电位)。结果肌电图神经传导检测提示,48例患儿中35例运动、感觉神经均脱髓鞘,符合CIDP确诊标准;8例为感觉神经脱髓鞘,5例为轴突变性为主。40例患儿SSEP异常(未符合CIDP确诊标准的8例感觉受累患儿和5例继发轴突变性患儿的SSEP均异常),其中7例可见臂丛神经干和/或后根水平传导异常,33例同时有腰骶丛和/或后根损害。与健康对照相比,CIDP患儿N13、N22波幅潜伏期明显延长(P0.05)。结论 SSEP可用于CIDP辅助诊断,特别是对于感觉神经受累为主或继发轴突变性的CIDP患儿。     

CASE OF INFLAMMATORY FIBROID POLYP OF THE ESOPHAGOGASTRIC JUNCTION

Upper gastrointestinal endoscopy of a 25‐year‐old man with heartburn revealed an elevated lesion in the esophagogastric junction (EGJ). Piecemeal endoscopic mucosal resection (EMR) followed by histopathological examination led to a diagnosis of inflammatory fibroid polyp (IFP). After EMR, the heartburn persisted despite giving a proton pump inhibitor (PPI), and the residual lesion gradually enlarged and a transverse mucosal break developed on the esophageal side of it. However, the combined administration of the PPI and an H2 receptor antagonist reduced the heartburn, and led to endoscopic regression of the lesion and disappearance of the transverse mucosal break. IFP of the esophagogastric junction is extremely rare, and this case is interesting in that potent inhibition of gastric acid secretion resulted in the regression of the lesion.     

NT-proBNP与炎症因子在先兆子痫的诊疗价值及临床意义

目的 探讨NT-proBNP与炎症因子对先兆子痫的诊疗价值及临床意义.方法 选取该院2015年2月至2016年2月正常妊娠孕妇81例为A组,轻度先兆子痫患者81例为B组,重度先兆子痫患者81例为C组,行NT-proBNP与炎症因子检测.比较各组NT-proBNP与炎症因子差异,分析NT-proBNP、炎症因子与先兆子痫的相关性.结果 治疗前NT-proBNP、C反应蛋白(CRP)、白细胞介素(IL)-6、肿瘤坏死因子α(TNF-α)比较,从高到低为C、B、A组(P＜0.05).治疗后,B组与C组NT-proBNP、CRP、IL-6、TNF-α降低(P＜0.05).治疗后NT-proBNP、CRP、IL-6、TNF-α比较,从高到低为C、B、A组(P＜0.05).NT-proBNP、CRP、1L-6、TNF-α与先兆子痫呈正相关(r=0.569、0.602、0.418、0.427,P=0.000).并发症发生率比较,从高到低为C、B、A组(P＜0.05).结论 先兆子痫患者NT-proBNP与炎症因子有升高趋势,可将其作为先兆子痈评价的有效指标.     

Melatonin attenuates methamphetamine‐induced overexpression of pro‐inflammatory cytokines in microglial cell lines

Abstract: Methamphetamine (METH), the most commonly abused drug, has long been known to induce neurotoxicity. METH causes oxidative stress and inflammation, as well as the overproduction of both reactive oxygen species (ROS) and reactive nitrogen species (RNS). The role of METH‐induced brain inflammation remains unclear. Imbroglio activation contributes to the neuronal damage that accompanies injury, disease and inflammation. METH may activate microglia to produce neuroinflammatory molecules. In highly aggressively proliferating immortalized (HAPI) cells, a rat microglial cell line, METH reduced cell viability in a concentration‐ and time‐dependent manner and initiated the expression of interleukin 1β (IL‐1β), interleukin 6 (IL‐6) and tumor necrosis factor α. METH also induced the production of both ROS and RNS in microglial cells. Pretreatment with melatonin, a major secretory product of the pineal gland, abolished METH‐induced toxicity, suppressed ROS and RNS formation and also had an inhibitory effect on cytotoxic factor gene expression. The expression of cytotoxic factors produced by microglia may contribute to central nervous system degeneration in amphetamine abusers. Melatonin attenuates METH toxicity and inhibits the expression of cytotoxic factor genes associated with ROS and RNS neutralization in HAPI microglia. Thus, melatonin might be one of the neuroprotective agents induced by METH toxicity and/or other immunogens.