• Pediatric Gastroenterology, Hepatology & Nutrition
• /
• 제9권2호
• /
• pp.129-138
• /
• 2006

Lots of cases relating Helicobacter pylori infection to iron-deficiency anemia have been described in the literature and H. pylori infection has emerged as a cause of refractory iron-deficiency anemia which is unresponsive to oral iron therapy. H. pylori-associated iron-deficiency anemia can be treated by H. pylori eradication. It is not thought to be attributable to gastrointestinal blood loss, such as duodenal ulcer. The mechanism by which H. pylori infection contributes to iron-deficiency anemia remains unclear. However, four possible explanations can be posited for this relationship; occult blood loss secondary to chronic gastritis, reduced iron absorption due to hypo- or achlorhydria, increased iron consumption by H. pylori, and iron sequestration in gastric mucosa. H. pylori-associated iron-deficiency anemia seems to develop in populations at increased risk for iron depletion. When pubescent girls, including athletes, are found to have iron-deficiency anemia refractory to iron administration, they should be evaluated for H. pylori infection.

• Clinical and Experimental Pediatrics
• /
• 제55권10호
• /
• pp.367-370
• /
• 2012

Urinary tract infection (UTI) is a common bacterial illness in children. Acute pyelonephritis in children may lead to renal scarring with the risk of later hypertension, preeclampsia during pregnancy, proteinuria, and renal insufficiency. Until now, vesicoureteral reflux (VUR) has been considered the most important risk factor for post-UTI renal scar formation in children. VUR predisposes children with UTI to pyelonephritis, and both are associated with renal scarring. However, reflux nephropathy is not always acquired; rather, it reflects reflux-associated congenital dysplastic kidneys. The viewpoint that chronic kidney disease results from renal maldevelopment-associated VUR has led to questioning the utility of any regimen directed at identifying or treating VUR. Despite the recognition that underlying renal anomalies may be the cause of renal scarring that was previously attributed to infection, the prevention of renal scarring remains the goal of all therapies for childhood UTI. Therefore, children at high risk of renal scar formation after UTI should be treated and investigated until a large clinical study and basic research give us more information.

• The Korean journal of internal medicine
• /
• 제33권6호
• /
• pp.1070-1078
• /
• 2018

Vibrio vulnificus is a gram-negative bacterium that can cause serious, potentially fatal infections. V. vulnificus causes three distinct syndromes: an overwhelming primary septicemia caused by consuming contaminated seafood, wound infections acquired when an open wound is exposed to contaminated warm seawater, and gastrointestinal tract-limited infections. Case-fatality rates are higher than 50% for primary septicemia, and death typically occurs within 72 hours of hospitalization. Risk factors for V. vulnificus infection include chronic liver disease, alcoholism, and hematological disorders. When V. vulnificus infection is suspected, appropriate antibiotic treatment and surgical interventions should be performed immediately. Third-generation cephalosporin with doxycycline, or quinolone with or without third-generation cephalosporin, may be potential treatment options for patients with V. vulnificus infection.

• Journal of Gastric Cancer
• /
• 제2권2호
• /
• pp.73-80
• /
• 2002

In spite the fact that H. pylori infection might be the causative organisms of acute and chronic gastritis, peptic ulcer diseases and the definition as the class I carcinogen by WHO IARC, still debates exist about the relationship between H. pylori and gastric carcinogenesis. Epidemiological and animal studies demonstrated a link between gastric cancer and chronic infection with H, pylori, but the exact mechanism responsible for the development of gastric cancer in H. pylori-infected patients still remain obscure. In order to declare the clear association, definate evidences like that decrement in the incidence of gastric cancer after the eradication of H. pylori in designated area compared to noneradicated region or the blockade of specific mechanism acting on the carcinogenesis by H. pylori infection. The other way is to identify the upregulating oncogenes or downregulating tumor suppressor genes specifically invovled in H. pylori-associated carcinogenesis. For that, we established the animal models using C57BL/6 mice strain. Already gastric carcinogenesis was developed in Mongolian gerbils infected with H. pylori, but there has been no development of gastric cancer in mice model infected with H. pylori after long-term evaluation. Significant changes such as atrophic gastritis were observed in mice model. However, we could observe the development of mucosal carcinoma in the stomach of transgenic mice featuring the loss of TGF-beta sig naling by the expressions of dominant negative forms of type II receptor specifically in the stomach. Moreover, the incidence of gastric adenocarcinoma was significantly increased in group administered with both MNU and H. pylori infection than MNU alone, signifying that H. pylori promoted the gastric carcinogenesis and there might be host susceptibility genes in H. pylori-associated gastric carcinogenesis. Based on the assumption that chronic, uncontrolled inflammation might predispose to carcinogenesis, there have been several evidences showing chronic atrophic gastritis predisposed to gastric carcinogenesis in H. pylori infection. Although definite outcome of chemoprevention was not drawn after the longterm administration of anti-inflammatory drug in H. pylori infection, the actual incidence of atrophic gastritis and molecular evidence of chemoprevention could be obtained. Selective COX-2 inhibitor was effective in decreasing the development of gastric carcinogenesis provoked by H. pylori infection and carcinogen like in chemoprevention of colon carcinogenesis.

• BMB Reports
• /
• 제44권4호
• /
• pp.217-231
• /
• 2011

T cell exhaustion develops under conditions of antigen-persistence caused by infection with various chronic pathogens, such as human immunodeficiency virus (HIV) and myco-bacterium tuberculosis (TB), or by the development of cancer. T cell exhaustion is characterized by stepwise and progressive loss of T cell function, which is probably the main reason for the failed immunological control of chronic pathogens and cancers. Recent observations have detailed some of the intrinsic and extrinsic factors that influence the severity of T cell exhaustion. Duration and magnitude of antigenic activation of T cells might be associated with up-regulation of inhibitory receptors, which is a major intrinsic factor of T cell exhaustion. Extrinsic factors might include the production of suppressive cytokines, T cell priming by either non-professional antigenpresenting cells (APCs) or tolerogenic dendritic cells (DCs), and alteration of regulatory T (Treg) cells. Further investigation of the cellular and molecular processes behind the development of T cell exhaustion can reveal therapeutic targets and strategies for the treatment of chronic infections and cancers. Here, we report the properties and the mechanisms of T cell exhaustion in a chronic environment.

• Clinical and Experimental Pediatrics
• /
• 제54권5호
• /
• pp.197-200
• /
• 2011

Respiratory syncytial virus (RSV) is a major cause of respiratory infection in children. Most of the pediatric population have RSV infection before the age of 2, and recurrent infections are common even within one season. Chronic lung disease, prematurity, along with congenital heart disease (CHD) are major risk factors in severe lower respiratory infection. In hemo-dynamically significant CHD patients with RSV infection, hospitalization is usually needed and the possibility of treatment in intensive care unit and the use of mechanical ventilator support are known to increase. Therefore the prevention of RSV infection in CHD patients is mandatory. The current standard for RSV prevention is immunoprophylaxis by palivizumab. Immunoprophylaxis is recommended monthly in hemodynamically significant CHD patients, up to 5 months. Motabizumab, a second generation drug and newly developing RSV vaccines are also expected to play a key role in RSV prevention in the future. The prophylaxis of RSV infection in CHD patients is cost-effective in both the medical aspect of the patients as well as the socio-economic aspect. Therefore an effort to promote prevention should be made by not only the family of the patients but also by the government.

• Applied Microscopy
• /
• 제45권2호
• /
• pp.80-88
• /
• 2015

The structural change and distribution of mitochondrial enzyme (ATPase, cytochrome-c-oxidase), cell proliferation (proliferating cell nuclear antigen, PCNA), cell death (caspase-3) and cell growth factor (fibroblast growth factor 8, FGF-8) in the Sprague-Dawley rat bile duct during Clonorchis sinensis infection was investigated. Experimental groups were divided into C. sinensis infection, superinfection and reinfection of C. sinensis after 'praziquantel' treatment group. As a result, C. sinensis infected rat bile ducts showed the features of chronic clonorchiasis, i.e., connective tissue thickening, ductal fibrosis and epithelial tissue dilatation. PCNA for cell proliferation increased in the infection group, and decreased after praziquantel treatment. Caspase-3 was distributed in reinfection group only. FGF-8 was distributed in the rat bile duct after praziquantel treatment but not distributed in infection and reinfection group. Overall, C. sinensis infection causes physical and chemical irritations and then brings on the abnormalities of intracellular energy metabolism and cellular growth factors, which hinders bile duct tissue from functioning properly, and resultingly, fibrosis occurs and epithelial cells dilated abnormally. More intense infection makes tissue fibrosis chronical and activates apoptosis factors.

• Asian Pacific Journal of Cancer Prevention
• /
• 제17권4호
• /
• pp.1631-1635
• /
• 2016

Helicobacter pylori infection plays an important role in the pathogenesis of chronic gastritis, peptic ulcer disease and gastric malignancy. A diagnosis of infection is thus an important part of a treatment strategy of many gastrointestinal tract diseases. Many diagnostic tests are available but all have some limitations in different clinical situations and laboratory settings. A single gold standard cannot available, but be used for diagnosis of Helicobacter pylori infection in daily clinical practice in all areas, so several techniques have been developed to give reliable results, especially focusing on real time endoscopic features. The narrow band imaging system (NBI) and high resolution endoscopy are imaging techniques for enhanced visualization of infected mucosa and premalignant gastric lesions. The aim of this article is to review the current diagnostic options and possible future developments detection of Helicobacter pylori infection.

• 가정간호학회지
• /
• 제21권1호
• /
• pp.69-78
• /
• 2014

Purpose: This study aimed at providing guidelines and educational manuals on infection control for the home care environment, by assessing the knowledge and performance among the caregivers in home care. Methods: Data were collected from January to March 2013. Participants were 172 caregivers who were registered in the home nursing center of university hospitals. Results: The total score on the level of knowledge of infection control was 13.28 points (${\pm}3.49$) out of 20 points. Secondly, 4.15 points were obtained for individual hygiene management, 4.14 points for hand wash, and 3.86 points for environment management. Lastly, the relationship between the knowledge and performance of infection control showed a significant positive correlation (r=0.37, p<.001). Conclusion: In many instances, the caregivers in the home environment provide nursing care for patients with chronic diseases and make use of various invasive devices. This study recommends the development of a manual or educational guidelines on infection control that can be used by caregivers at the home.

• IMMUNE NETWORK
• /
• 제24권1호
• /
• pp.4.1-4.19
• /
• 2024

TNF, a pleiotropic proinflammatory cytokine, is important for protective immunity and immunopathology during Mycobacterium tuberculosis (Mtb) infection, which causes tuberculosis (TB) in humans. TNF is produced primarily by phagocytes in the lungs during the early stages of Mtb infection and performs diverse physiological and pathological functions by binding to its receptors in a context-dependent manner. TNF is essential for granuloma formation, chronic infection prevention, and macrophage recruitment to and activation at the site of infection. In animal models, TNF, in cooperation with chemokines, contributes to the initiation, maintenance, and clearance of mycobacteria in granulomas. Although anti-TNF therapy is effective against immune diseases such as rheumatoid arthritis, it carries the risk of reactivating TB. Furthermore, TNF-associated inflammation contributes to cachexia in patients with TB. This review focuses on the multifaceted role of TNF in the pathogenesis and prevention of TB and underscores the importance of investigating the functions of TNF and its receptors in the establishment of protective immunity against and in the pathology of TB. Such investigations will facilitate the development of therapeutic strategies that target TNF signaling, which makes beneficial and detrimental contributions to the pathogenesis of TB.