《中西医结合防治小儿腹泻病专家共识》解读

小儿腹泻病是儿童消化系统最常见的疾病,2022年中国中西医结合学会儿科专业委员会制定了《中西医结合防治小儿腹泻病专家共识》。现结合临床实践及最新的研究结果,对《中西医结合防治小儿腹泻病专家共识》中小儿腹泻病的发病机制、诊断和治疗中的重点内容进行解读,以期加深医务工作者对《中西医结合防治小儿腹泻病专家共识》的认识,促进中西医结合规范化治疗小儿腹泻病。     

Pathogenesis of idiopathic IgA nephropathy

Despite a prodigious amount of work on the physiology of IgA production in man, and many studies on the immunopathology of IgA nephropathy, ranging from the immunogenetics to the immune response to chemical characteristics of the IgA, we are hardly any nearer to defining the pathogenesis of this disease. One of the main changes in our understanding has been to recognise that the bone marrow, now known to produce normally one-third of the body's IgA, overproduces this immunoglobulin in IgA nephropathy. This alters the previous notion that IgA nephropathy was due simply to IgA production in the mucosa, although a mucosal component is not excluded. Certain characteristics of the IgA in the diseased kidney and the circulation have been defined: it is of subclass IgA1 and has a higher proportion of light chains and negative charge than in normal subjects. The specificities of the IgA, either in the kidney or in complexes, have not helped to clarify the pathogenesis. They have been found for a wide range of endogenous and exogenous antigens, suggesting that the antibody activity represents polyclonal B cell activation. These findings have not helped to confirm the prevailing theory that IgA nephropathy is an immune complex disease. Other theories put forward are that IgA nephropathy is an autoimmune disease, glomerular components or IgA itself being among the candidate antigens, or that there is primary dysregulation of the IgA immune system. At this stage of development in our understanding of this common nephropathy, it is important to guard against the assumption that idiopathic IgA nephropathy is one disease and is the result of a single pathogenetic mechanism.     

The rheumatic poison: a survey of some published investigations of the immunopathogenesis of Henoch-Schönlein purpura

Laboratory studies of the pathophysiology of Henoch-Schönlein purpura (HSP) have become more numerous in recent years with the recognition of the disease's links with the mucosal immune system in general and IgA nephropathy in particular. There are weak genetic associations with C4 null phenotypes and with HLA B35 and DR4. Studies of plasma proteins in HSP patients show an increased IgA concentration, activation of the alternative pathway of complement and consumption of factor XIII. High molecular weight (polymeric) IgA has been detected in affected individuals, which some investigators have called immune complexes. Many patients synthesise an IgA rheumatoid factor in the acute phase, but other autoantibodies are largely absent. In vitro studies of lymphocytes from HSP patients have demonstrated an increased number of IgA-bearing and secreting B-cells, with altered T-cell regulation of antibody synthesis. While these observations point to immune dysregulation — primarily of IgA production — as a consistent feature of acute HSP, there is as yet insufficient information available to allow a consistent theory of pathogenesis to be formulated.     

慢性光化性皮炎的病因诊断及治疗

目的;探讨慢性光化性皮炎（ＣＡＤ）的病因,诊断及治疗,方法：查阅文献,对引起ＣＡＤ的光敏物、发病机理及治疗进行分析,结果：约１１％的ＣＡＤ患者有光敏物接触史;６２％光敏性隐匿;２７％有慢性皮炎病史;结论：ＣＡＤ发病与光变态反应有关,避光治疗有效。     

Hypozincaemia in febrile convulsion

To understand further the role of trace elements in the pathogenesis of febrile convulsions, serum zinc (Zn), copper (Cu), magnesium (Mg) and CSF Zn, Cu, Mg and protein levels were measured by spectrometry in patients with febrile convulsion (n=19), bacterial meningitis (n=9), viral CNS infection (n=16) and in the control groupn=10) which consisted of children with signs of meningeal irritation due to upper respiratory tract infection but normal CSF findings. Samples were obtained within 6 h after admission to hospital. Mean serum and CSF Zn levels in the febrile convulsion group were significantly lower than in the other groups (for serum Zn: 0.66±0.03 mg/l vs 0.98±0.07 mg/l, 1.06±0.08 mg/l, 1.05±0.09 mg/lP<0.05; for CSF Zn: 22.96±1.62 g/l vs 75.47 ±6.9 g/l, 50.32±5.235 g/l, 39.85 ±2.81 g/lP<0.05). A linear relationship was established between serum Zn and CSF Zn levels (P<0.001). Mean CSF Zn, Cu and protein levels in the bacterial meningitis group were significantly higher than in the other groups (for CSF Cu 63.94±6.33 g/l vs 38.77±2.70 g/l, 35.84±3.48 g/l, 33.86±2.88 g/lP<0.05; for CSF protein 0.80 ± 0.12 g/l vs 0.22±0.02 g/l, 0.53±0.08 g/l, 0.19±0.01 g/lP<0.05). In children with meningitis, the elevation of the mean CSF Zn and Cu levels may result from the breakdown of the blood-brain barrier and subsequent leakage of trace elements and protein from serum to CSF. There was no significant difference between the four groups in terms of mean serum Mg and mean CSF Mg levels.Conclusion Serum and CSF Zn levels are decreased in children with febrile seizures. Zinc deprivation may play a role in the pathogenesis of febrile seizures.     

中医药治疗恶性肿瘤的研究进展

阐述了中医对恶性肿瘤病因病机的认识及治则治法，对目前中医药治疗恶性肿瘤的几种新思路进行了探讨．在指出中医药治疗恶性肿瘤中存在的问题的同时，提出了笔者的几点建议。     

儿童颅骨生长性骨折

目的 探讨儿童颅骨生长性骨折(Growing skull fractwre，GSF)的发病机制、诊治方法。方法 对我院1992年1月2002年4月10年间收治的6例GSF患儿的临床资料进行回顾行分析。结果 6例均有明确颅脑损伤病史，平均发病年龄2．99岁，头部包块、颅骨缺损及神经功能障碍等症状常见，颅骨平片见以骨折线为长轴的梭形颅骨缺损，CT检查显示包块为蛛网膜囊肿或脑膨出，术中见硬脑膜缺损大于颅骨缺损；Goldstein分型：Ⅰ型2例，Ⅱ型2例，Ⅲ型2例；GOS5分者3例(2例Ⅰ型和1例Ⅱ型)，4分者2例(Ⅱ型和Ⅲ型各1例)，3分者1例(Ⅲ型)。结论 ①颅骨骨折致硬脑膜破损为GSF发病的病理基础，婴幼儿期颅脑发育、外伤后局部颅内压力增高、骨折缘缺血为发病的重要因素；②GSF患儿颅骨缺损范围与病程不呈正相关，颅脑CT在GSF的诊断方面优于颅骨平片；③GSF一经确诊即应手术治疗，扩大开颅术能显露硬脑膜残缘，严密修补硬脑膜是手术成功的关键，Medepor材料适用于GSF患儿。Goldstein分型对指导预后有一定意义。     

The pathogenesis of multiple sclerosis: a commentary

A series of recently published articles by a group of Austrian, German and American neuropathologists have proposed the existence of several different pathogenetic pathways in multiple sclerosis (MS). These studies were based on both biopsy and autopsy material. A review of the available published clinical, imaging and cerebrospinal fluid data suggest that some the cases used in those studies were more probably instances of disseminated encephalomyelitis rather than MS. This has serious implications regarding the specificity and significance of the findings in regard to MS pathogenesis. The specific myelinoclastic sequence and the variable clinical course of MS are determined by the individual's genetic endowment and immunologic history. Regardless of pathogenetic pathway and clinical course, the final pathologic picture of MS is always the same. The MS brain is genetically programmed to produce a unique, pathognomonic change, the plaque with sharply demarcated borders.     

浅析围绝经期睡眠障碍的中医发病机制

目的：探讨围绝经期睡眠障碍的中医发病机制。方法：分析肾、心、肝三脏与围绝经期睡眠障碍的关系。结论：心肾不交、肝阳上亢是围绝经期睡眠障碍的主要病理机制。     

禹余粮丸方考及验案举例

宋赵开美本《伤寒论》88条中提出禹余粮丸,但只见方名,未列药物。后世医家对于该方是否存在以及药味多少争论不一,笔者对此进行了简单的回顾与梳理,并举验案,以供同道参考。