地白液治疗传染性软疣的疗效观察

目的 观察地白液治疗传染性软疣的效果。方法 地白液涂搽疣体 ,2 0天为一疗程 :对照组用5 %新洁尔灭溶液外涂疣体 ,2 0天为一疗程。结果 治疗组 10 2例 ,治愈 84例 ,治愈率为 82 .35 %;对照组 73例 ,治愈 5 8例 ,治愈率为 79.4 5 %。结论 地白液和新洁尔灭溶液外用治疗传染性软疣均有很好疗效。

中药表面麻醉液外涂治疗传染性软疣60例

目的 减轻传染性软疣患者治疗中的痛苦。方法 利用多味中药配制成麻醉液在疣体上表面纱垫外敷 1 0分钟后 ,用血管钳夹挤皮损。结果 患者疼痛明显减轻 ,优于 2 %碘酊和利多卡因对照组。结论 利用中药表面麻醉液在挑疣中止痛 ,费用低 。

儿童传染性单核细胞增多症96例诊治体会

目的:探讨儿童传染性单核细胞增多症的临床特点。方法:对96例儿童传染性单核细胞增多症患儿的临床资料进行回顾性分析。结果:传染性单核细胞增多症96例患儿中3～6岁患儿65例,占67.7%;96例患儿均发热,其中高热患儿81例,占84.3%;伴淋巴结肿大72例,占75%;伴咽峡炎者86例,占89.6%,其中扁桃体表面附着白色渗出物75例,占78.1%;伴肝脏肿大46例,占47.9%;脾脏肿大42例,占43.8%;鼻塞59例,占61.5%;眼睑浮肿者41例,占42.7%;皮疹者28例,占29.2%;伴有其他症状者34例,占35.4%;所有病例异型淋巴细胞增高均大于10%,其中3例达到50%以上,占3.1%。结论:传染性单核细胞增多症好发于3～6岁儿童,其临床特点为发热,咽峡炎,淋巴结及肝脾肿大,外周血淋巴细胞显著增多并出现异型淋巴细胞,异型淋巴细胞增高大于10%,感染后体内出现EB病毒IgM抗体阳性率100%。早期诊断及早期治疗是关键。

EB病毒感染所致传染性单核细胞增多症55例分析

目的总结小儿传染性单核细胞增多症的临床特征,以得到早期诊断及治疗。方法收集符合EBV感染的传染性单核细胞增多症55例,进行回顾性分析。结果本病的临床表现主要为:发热98.2%(54/55);咽峡炎100%(55/55);淋巴结肿大87.2%(48/55);肝脏肿大32.7%(18/55);脾脏肿大49.1%(27/55);双眼睑水肿54.5%(30/55);鼻塞29.0%(16/55);皮疹23.6%(13/55)。实验室检查:外周血常规白细胞数>10×109/L者96%(53/55);EBV-DNA检测均阳性,可伴肝功能受损、心肌损害、肺炎等,更昔洛韦治疗有效。结论传染性单核细胞增多症临床表现复杂多样,可伴多器官多系统损害,大多预后良好。EBV-DNA检测具有特异性,可提高对本病的早期诊断。更昔洛韦治疗有效。

小儿急性传染性单核细胞增多症116例护理体会

目的探讨小儿急性传染性单核细胞增多症的治疗及护理措施。方法116例患儿在常规治疗的基础上,采用心理护理及对高热患儿的精心护理,认真观察病情,严格执行医嘱,按传染病常规护理,加强营养,指导患儿加强锻炼。结果116例患儿采用抗病毒药物及对症精心护理后,全部痊愈出院,平均住院日12 d。结论对症治疗加精心护理,可加速患儿痊愈,值得临床推广。

The role of Toll-like receptors in non-infectious lung injury

The role of Toll-like receptors （TLRs） in pathogen recognition has been expeditiously advanced in recent years. However, investigations into the function of TLRs in non-infectious tissue injury have just begun. Previously, we and others have demonstrated that fragmented hyaluronan （HA） accumulates during tissue injury. CD44 is required to clear HA during tissue injury, and impaired clearance of HA results in unremitting inflammation. Additionally, fragmented HA stimulates the expression of inflammatory genes by inflammatory cells at the injury site. Recently, we identified that HA fragments require both TLR2 and TLR4 to stimulate mouse macrophages to produce inflammatory chemokines and cytokines. In a non-infectious lung injury model, mice deficient in both TLR2 and TLR4 show an impaired transepithelial migration of inflammatory cells, increased tissue injury, elevated lung epithelial cell apoptosis, and decreased survival. Lung epithelial cell overexpression of high molecular mass HA protected mice against acute lung injury and apoptosis, in part through TLR-dependent basal activation of NF-κB. The exaggerated injury in TLR2 and TLR4 deficient mice appears to be due to impaired HA-TLR interactions on epithelial cells. These studies identify that host matrix component HA and TLR interactions provide signals that initiate inflammatory responses, maintain epithelial cell integrity, and promote recovery from acute lung injury.

Current treatment indications and strategies in chronic hepatitis B virus infection

The optimal approach to the management of several marginal cases with chronic hepatitis B virus (HBV) infection is controversial. Serum HBV DNA and ami-notransferase levels, and the degree of necroinflammation and fibrosis determine the therapeutic decisions. All patients with elevated aminotransferase (> twice the upper limit of normal) and serum HBV DNA above 20 000 IU/mL should be treated. Liver biopsy is important for therapeutic decisions in cases with mild aminotransferase elevations and serum HBV DNA below 20 000 IU/mL. Chronic HBV patients who do not receive treatment should be followed for life. There are seven agents licensed for chronic hepatitis B: standard and pegylated interferon-alpha, lamivudine, adefovir, entecavir, telbivudine and tenofovir. One-year courses with pegylated interferon-alpha induce sustained off-therapy remission in 30%-32% of patients with HBeAg-positive chronic hepatitis B and in a smaller proportion of patients with HBeAg-negative chronic hepatitis B. Oral antivirals achieve initial on-therapy responses in the majority of patients, but are intended as long-term therapies. Viral suppression has favourable effects on patients' outcome and modifies the natural course of the disease. Viral resistance, however, is the major drawback of long-term oral antiviral therapy. Lamivudine monotherapy is associated with the highest and ente-cavir monotherapy with the lowest resistance rate so far. There has been no resistance to tenofovir, but afteronly 18 mo of treatment to date. The optimal first-line anti-HBV therapy with the best long-term cost/benefit ratio remains unclear. If oral antiviral agents are used, compliance should always be ascertained and HBV DNA levels should be regularly tested.

Concept on the pathogenesis and treatment of primary biliarycirrhosis

Primary biliary cirrhosis (PBC) is an organ-specific autoimmune disease that predominantly affects women and is characterized by chronic, progressive destruction of small intrahepatic bile ducts with portal inflammation and ultimately fibrosis, leading to liver failure in the absence of treatment. Little is known about the etiology of PBC. PBC is characterized by anti-mitochondrial antibodies and destruction of intrahepatic bile ducts. The serologic hallmark of PBC is the presence of auto-antibodies to mitochondria, especially to the E2 component of the pyruvate dehydrogenase complex (PDC). Current theories on the pathogenesis of PBC favor the hypothesis that the disease develops as a result of an inappropriate immune response following stimulation by an environmental or infectious agent. Some reports suggest that xenobiotics and viral infections may induce PBC. The pathogenetic mechanism is believed to be caused by a defect in immunologic tolerance, resulting in the activation and expansion of self-antigen specific T and B lymphocyte clones and the production of circulating autoantibodies in addition to a myriad of cytokines and other inflammatory mediators. This leads to ductulopenia and persistent cholestasis, by developing end-stage hepatic-cell failure. In this review are given our own and literary data about mechanisms of development of intrahepatic cholestasis and possible ways of its correction.

Potential prospects of nanomedicine for targeted therapeutics in inflammatory bowel diseases

Inflammatory bowel diseases (IBDs) such as Crohn's disease are highly debilitating. There are inconsistencies in response to and side effects in the current conventional medications, failures in adequate drug delivery, and the lack of therapeutics to offer complete remission in the presently available treatments of IBD. This suggests the need to explore beyond the horizons of conventional approaches in IBD therapeutics. This review examines the arena of the evolving IBD nanomedicine, studied so far in animal and in vitro models, before comprehensive clinical testing in humans. The investigations carried out so far in IBD models have provided substantial evidence of the nanotherapeutic approach as having the potential to overcome some of the current drawbacks to conventional IBD therapy. We analyze the pros and cons of nanotechnology in IBD therapies studied in different models, aimed at different targets and mechanisms of IBD pathogenesis, in an attempt to predict its possible impact in humans.

Chinese Medicine in the Management of New and Emerging Infectious Diseases

Emerging infectious diseases are an important problem in medicine,and many continue to pose a global threat.However,the management of new and emerging infections is usually difficult due to a lack of knowledge and tools to address the problem.The use of Chinese medicine to manage new and emerging infectious diseases,however,has attracted significant attention.This brief article summarizes and discusses the use of Chinese medicine in the management of new and emerging infectious diseases.

Role of calcium in polycystic kidney disease:From signaling to pathology

Autosomal dominant polycystic kidney disease （ADPKD） is the most common inherited monogenic kidney disease. Characterized by the development and growth of cysts that cause progressive kidney enlargement, it ultimately leads to end-stage renal disease. Approximately 85% of ADPKD cases are caused by mutations in the PKD1 gene, while mutations in the PKD2 gene account for the remaining 15% of cases. The PKD1 gene encodes for polycystin-1 （PC1）, a large multi-functional memb-rane receptor protein able to regulate ion channel complexes, whereas polycystin-2 （PC2）, encoded by the PKD2 gene, is an integral membrane protein that functions as a calcium-permeable cation channel, located mainly in the endoplasmic reticulum （ER）. In the primary cilia of the epithelial cells, PC1 interacts with PC2 to form a polycystin complex that acts as a mechanosensor, regulating signaling pathways involved in the differentiation of kidney tubular epithelial cells. Despite progress in understanding the function of these proteins, the molecular mechanisms associated with the pathogenesis of ADPKD remain unclear. In this review we discuss how an imbalance between functional PC1 and PC2 proteins may disrupt calcium channel activities in the cilium, plasma membrane and ER, thereby altering intracellular calcium signaling and leading to the aberrant cell proliferation and apoptosis associated with the development and growth of renal cysts. Research in this feld could lead to the discovery of new molecules able to rebalance intracellular calcium, thereby normalizing cell proliferation and reducing kidney cyst progression.

Efficiency and safety of lamivudine therapy in patients with chronic HBV infection, dialysis or after kidney transplantation

AIM: To analyze the effectiveness and safety of lamivudine treatment in patients with chronic HBV infection undergoing hemodialysis or after kidney transplantation, and to study the frequency of tyrosine - methionine - aspartate - aspartate (YMDD) mutation occurrence after lamivudine treatment. METHODS: We analyzed 91 patients with chronic hepatitis B, among whom, 16 patients underwent hemodialysis, 7 patients had kidney transplantation and 68 patients had normal function of kidney. The hemodialysis patients were treated by lamivudine 300 mg/wk. patients after kidney transplantation and patiente with normal function of kidney were treated with lamivudine 100 mg/d. Therapy lasted for 12 mo. HBV-DNA, HBsAg, HBeAg and anti-HBe, and anti-HCV antibodies were assessed in sera of patients. The analysis was performed before and 6 mo after the end of lamivudine treatment. Before, during and after the lamivudine therapy, the number of erythrocytes, leukocytes, platelets and hemoglobin concentration, ALT and AST activity, as well as bilirubin, urea and creatinine concentrations were analyzed in sera from patients. RESULTS: After the 12-mo lamivudine treatment, elimination of HBV - DNA was observed in 56% patients undergoing hemodialysis and in 53% patients with normal kidney function. Only 1 from 7 (14%) kidney-transplanted patients eliminated HBV-DNA. Furthermore, HBeAg elimination was observed in 36% hemodialysis patients, in 51% patients with normal function of kidneys and in 43% kidney transplanted patients. Among the patients undergoing dialysis, no YMDD mutation was found after 12 mo of therapy, while it was detected in 9 patients (13%) with normal function of kidney and in 2 kidney-transplanted patients (29%, P<0.006). We did not observe significant side effecte of lamivudine treatment in studied patiente. CONCLUSION: Effectiveness of lamivudine therapy in dialysis patients is comparable with that in patiente with normal function of kidney. Lamivudine treatment is well tolerated and safe in patiente with renal insufficiency undergoing hemodialysis and kidney-transplantation. However, in the latter group, high incidence of YMDD mutation after lamivudine treatment was observed.

Old-age inflammatory bowel disease onset:A different problem?

Inflammatory bowel disease （IBD） in patients aged 60 accounts for 10%-15% of cases of the disease. Diganostic methods are the same as for other age groups. Care has to be taken to distinguish an IBD colitis from other forms of colitis that can mimick clinically, endoscopically and even histologically the IBD entity. The clinical pattern in ulcerative colitis （UC） is proctitis and left-sided UC, while granulomatous colitis with an inflammatory pattern is more common in Crohn’s disease （CD）. The treatment options are those used in younger patients, but a series of considerations related to potential pharmacological interactions and side effects of the drugs must be taken into account. The safety profile of conventional immunomodulators and biological therapy is acceptable but more data are required on the safety of use of these drugs in the elderly population. Biological therapy has risen question on the possibility of increased side effects, however this needs to be confirmed. Adherence to performing all the test prior to biologic treatment administration is very important. The overall response to treatment is similar in the different patient age groups but elderly patients have fewer recurrences. The number of hospitalizations in patients 65 years is greater than in younger group, accounting for 25% of all admissions for IBD. Mortality is similar in UC and slightly higher in CD, but significantly increased in hospitalized patients. Failure of medicaltreatment continues to be the most common indication for surgery in patients aged 60 years. Age is not considered a contraindication for performing restorative proctocolectomy with an ileal pouch-anal anastomosis. However, incontinence evaluation should be taken into account an individualized options should be considered

Recent advances in cytokines:Therapeutic implications for inflammatory bowel diseases

Inflammatory bowel diseases （IBDs） are complex and chronic disabling conditions resulting from a dysregulated dialogue between intestinal microbiota and components of both the innate and adaptive immune systems. Cytokines are essential mediators between activated immune and non-immune cells, including epithelial and mes- enchymal cells. They are immunomodulatory peptides released by numerous cells and these have significant effects on immune function leading to the differentiation and survival of T cells. The physiology of IBD is becom- ing a very attractive field of research for development of new therapeutic agents. These include cytokines involved in intestinal immune inflammation. This review will focus on mechanisms of action of oytokines involved in IBD and new therapeutic opportunities for these diseases.

Safety of anti-tumor necrosis factor therapy in inflammatory bowel disease

Inflammatory bowel disease (IBD), in particular Crohn's disease refractory to conventional therapy, fistulizing Crohn's disease and chronic active ulcerative colitis, generally respond well to anti-tumor necrosis factor (TNF) therapy. However, serious side effects do occur, necessitating careful monitoring of therapy. Potential side effects of anti-TNF therapy include opportunistic infections, which show a higher incidence when concomitant immunosuppression is used. Furthermore, antibody formation against anti-TNF is associated with decreased efficacy and an increased frequency of infusion reactions. The hypothesis of a slightly increased risk of lymphomas in IBD patients treated with anti TNF-therapy is debatable, since most studies lack the specific design to properly address this issue. Alarmingly, the occurrence of hepatosplenic T-cell lymphomas coincides with combined immunosuppressive therapy. Despite the potential serious side effects, anti-TNF therapy is an effective and relatively safe treatment option for refractory IBD. Future research is needed to answer important questions, such as the long-term risk of malignancies, safety during pregnancy, when to discontinue and when to switch anti-TNF therapy, as well as to determine the balance between therapeutic and toxic effects.

New SLC12A3 disease causative mutation of Gitelman's syndrome

Gitelman's syndrome(GS) is a salt-losing tubulopathy with an autosomal recessive inheritance caused by mutations of SLC12A3, which encodes for the thiazidesensitive Na Cl cotransporter. In this study we report a new mutation of SLC12A3 found in two brothers affected by GS. Hypokalemia, hypocalciuria and hyperreninemia were present in both patients while hypomagnesemia was detected only in one. Both patients are compound heterozygotes carrying one well known GS associated mutation(c.2581 C > T) and a new one(c.283 del C) in SLC12A3 gene. The new mutation results in a possible frame-shift with a premature stopcodon(pG ln95 Argfs X19). The parents of the patients, heterozygous carriers of the mutations found in SLC12A3, have no disease associated phenotype. Therefore, the new mutation is causative of GS.

Combined therapeutic approach:Inflammatory bowel diseases and peripheral or axial arthritis

Inflammatory bowel diseases(IBDs), particularly Crohn's disease(CD) and ulcerative colitis(UC), are associated with a variety of extra-intestinal manifestations(EIMs).About 36% of IBD patients have at least one EIM, which most frequently affect the joints, skin, eyes and the biliary tract.The EIMs associated with IBD have a negative impact on patients with UC and CD, and the resolution of most of them parallels that of the active IBD in terms of timing and required therapy;however, the clinical course of EIMs such as axial arthritis, pyoderma gangrenosum, uveitis, and primary sclerosing cholangitis is independent of IBD activity.The peripheral and axial arthritis associated with IBD have traditionally been treated with simple analgesics, non-steroidal anti-inflammatory drugs, steroids, sulfasalazine, methotrexate, local steroid injections and physiotherapy, but the introduction of biological response modifi ers such as tumor necrosis factor-α blockers, has led to further improvements.

单核细胞增多在儿童流感病毒及肺炎支原体感染中的意义及其免疫功能变化的对照分析

目的探讨单核细胞增多在儿童流感病毒及肺炎支原体感染中的意义及免疫功能变化，为早期临床诊治提供依据。 方法 本研究对发热〉3d患儿进行研究，对确诊为肺炎支原体感染102例（肺炎支原体组）、流感病毒感染124例（流感病毒组）和同期90名健康体检儿童（正常对照组）分别检测血WBC、RBC、PLT、N（%）、L（%）、单核细胞（MONO）、CRP、IgG、IgA、IgM、C3及C4水平，比较各组患儿外周血象等指标及相关免疫指标变化的相似点及差异。结果 两组患儿单核细胞均增多，且显著高于正常对照组（P〈0.05）。流感病毒组WBC显著低于肺炎支原体组（P〈0.05），而肺炎支原体组CRP明显高于流感病毒组（P〈0.05），但两组血象的其它项目比较差异均无统计学意义（P〉0.05）。流感病毒组免疫球蛋白IgA降低阳性率高于肺炎支原组（P〈0.05），肺炎支原体组IgM升高阳性率明显高于流感病毒组（P〈0.05）。结论 流感病毒及肺炎支原体感染儿童，具有反复发热、血象不高、单核细胞均增多和免疫功能变化的特点，如患儿WBC下降更明显，IgA降低明显，CRP稍高于正常值应考虑流感病毒感染；若患儿WBC值正常，以CRP显著升高，IgA降低不明显，而IgM升高应考虑肺炎支原体感染。此特点对上述疾病具有鉴别意义，可避免滥用抗菌药物。