Overview of the microbiota in the gut-liver axis in viral B and C hepatitis

Viral B and C hepatitis are a major current health issue, both diseases having a chronic damaging effect on the liver and its functions. Chronic liver disease can lead to even more severe and life-threatening conditions, such as liver cirrhosis and hepatocellular carcinoma. Recent years have uncovered an important interplay between the liver and the gut microbiome: the gut-liver axis. Hepatitis B and C infections often cause alterations in the gut microbiota by lowering the levels of ‘protective’ gut microorganisms and, by doing so, hinder the microbiota ability to boost the immune response. Treatments aimed at restoring the gut microbiota balance may provide a valuable addition to current practice therapies and may help limit the chronic changes observed in the liver of hepatitis B and C patients. This review aims to summarize the current knowledge on the anato-functional axis between the gut and liver and to highlight the influence that hepatitis B and C viruses have on the microbiota balance, as well as the influence of treatments aimed at restoring the gut microbiota on infected livers and disease progression.     

基于“脑-肠轴”学说论治慢性乙型肝炎合并肠易激综合征

慢性乙型肝炎合并肠易激综合征的发病机制尚未完全清楚,西医疗效亦不容乐观,但"脑-肠轴异常"理论被认为是本病发病的关键,此恰与中医理论不谋而合,且中医理论认识更深、更广。基于"脑-肠轴"学说,以针刺头针胃区和头针肠区作为切入点,运用"调神针法"调节"脑神"进而调节"五脏神",以达到阴平阳秘,百病不生的状态,从而治愈本病。     

促性腺激素释放激素类似物激发试验尿检法对儿童促性腺激素释放激素类似物疗效的判断价值

目的 探讨促性腺激素释放激素类似物(GnRHa)激发试验时免疫化学发光分析法(ICMA)检测的无创性尿促性腺激素(UGn)可否用于儿童GnRHa的疗效判断.方法 患儿23例(男4例,女19例).中枢性性早熟17例(均为女童),予GnRHa治疗.青春期预测终身高矮小6例(男4例,女2例),予GnRHa联合生长激素治疗.在治疗前和治疗3个月均行GnRHa激发试验,留激发试验0～3.5 h尿,其中18例留取了激发试验前1d同一时段的日间自发性尿,应用ICMA检测促黄体生成素(LH)和卵泡刺激素(FSH).结果 1.治疗前后GnRHa激发试验时UGn显著性检验:治疗前后的尿促黄体生成素(ULH)水平分别为(1.27±1.63) IU和(0.07±0.06) IU,尿卵泡刺激素(UFSH)水平分别为(6.38±3.85)IU和(0.54±0.30) IU.2.GnRHa激发试验时血清Gn峰值和UGn对GnRHa疗效评估:当血清LH峰值(PLH)和FSH峰值(PFSH)分别≤2.30IU·L-1和2.39 IU·L-时,其判断疗效的灵敏度分别为95.45％和100％,特异度均为100％；当ULH水平和UFSH水平分别≤0.083 IU和1.089 IU时,其灵敏度分别为90.91％和100％,特异度均为100％.3.GnRHa激发试验时血清Gn和UGn分别与其激发试验前的比值对GnRHa疗效评估:当血清PLH/日间自发性血清LH、血清PFSH/日间自发性血清FSH分别≤5.40和2.16时,其灵敏度和特异度均为100％；当其激发试验时ULH水平/日间自发性ULH水平、激发试验时UFSH水平/日间自发性UFSH水平分别≤6.076和2.480时,其灵敏度和特异度也均达100％.结论 GnRHa激发试验时ICMA检测的无创性3.5 h UGn水平、激发试验时3.5 h UGn水平/日间自发性UGn水平指标可能对儿童GnRHa疗效具有判断价值,其中UFSH水平及其与日间自发性UFSH水平比值指标价值可能更大.     

Are Cushing's disease patients curable?

Treatment of Cushing's disease remains a challenge. Whereas pituitary surgery can “cure” the patient and restore a completely normal pituitary adrenal axis, there are immediate failures and late recurrences which ultimately require alternate therapeutic approaches. These are numerous, but so are their drawbacks, and all appear to be “default options”. For the future, pituitary adenoma has to remain the “reasonable obsession” of efficient and optimistic therapists…     

Bone formation in axial spondyloarthritis: Is disease modification possible?

Axial spondyloarthritis (SpA) is a chronic disease characterised by new bone formation (NBF) in the axial skeleton as well as at peripheral entheseal sites. NBF is thought to arise in areas of previous inflammation or osteitis visualised on MRI, with mechanical stress playing a role in disease pathogenesis. The interface between bone and immune cells is complex with the RANKL-OPG system being key to NBF. The IL-17/23 axis and other cytokines such as TNFα and MIF are thought to play a central role. The transition from inflammation to NBF is mediated via the Wnt, BMP and Hedgehog signalling pathways. An altered microbiome has been reported in SpA, which is a potential trigger of NBF in SpA. There is now data to show that treatment with TNF inhibitors prevents NBF and hence modifies disease progression. More research into identifying newer targets for disease modification is needed to alter the course of the disease.     

Role of negative affects in pathophysiology and clinical expression of irritable bowel syndrome

Irritable bowel syndrome(IBS)is regarded as a multifactorial disease in which alterations in the brain-gut axis signaling play a major role.The biopsychosocial model applied to the understanding of IBS pathophysiology assumes that psychosocial factors,interacting with peripheral/central neuroendocrine and immune changes,may induce symptoms of IBS,modulate symptom severity,influence illness experience and quality of life,and affect outcome.The present review focuses on the role of negative affects,including depression,anxiety,and anger,on pathogenesis and clinical expression of IBS.The potential role of the autonomic nervous system,stress-hormone system,and immune system in the pathophysiology of both negative affects and IBS are taken into account.Psychiatric comorbidity and subclinical variations in levels of depression,anxiety,and anger are further discussed in relation to the main pathophysiological and symptomatic correlates of IBS,such as sensorimotor functions,gut microbiota,inflammation/immunity,and symptom reporting.