Chia Chang Chuang

Serum total antioxidant capacity reflects severity of illness in patients with severe sepsis.

IntroductionWe conducted the present study to evaluate the changes in serum total antioxidant capacity (TAC) in patients with severe sepsis and to investigate the association between serum TAC and clinical severity.MethodThis was a prospective observational study involving a sample of patients who met established criteria for severe sepsis and were admitted to the emergency department of a university teaching hospital. Serum TAC was determined using the total radical-trapping antioxidant parameter method. The levels of TAC, uric acid, albumin, and bilirubin in sera were obtained in the emergency department and evaluated to determine whether there were any correlations between the major antioxidant biomarkers and clinical severity of sepsis. The Acute Physiology and Chronic Health Evaluation (APACHE) II score was used for clinical evaluation of the severity of sepsis.ResultsA total of 73 patients with sepsis, with a mean (± standard deviation) APACHE II score of 23.2 ± 8.2 and a mortality rate of 26.0%, were included. Seventy-six healthy individuals served as control individuals. Among the patients, serum TAC levels correlated significantly with APACHE II scores. Patients who died also had higher TAC than did those who survived. Serum uric acid levels correlated significantly with serum TAC and APACHE II scores in patients with severe sepsis.ConclusionElevated serum TAC level may reflect clinical severity of sepsis. In addition, serum uric acid levels appear to contribute importantly to the higher TAC levels observed in patients with severe sepsis.

Prevalence study of thyroid dysfunction in the elderly of Taiwan

The present study was aimed at investigating the prevalence of thyroid dysfunction in the elderly, aged 65 years or older, in a community of southern Taiwan. By using the records of the local household registry, a sampling frame for the elderly population was constructed, and a sample of 1,400 subjects was drawn by simple random sampling. After the exclusion of nonresponse subjects, 917 subjects aged between 65 and 88 years (mean 71.9) were included in our survey. The serum thyrotropin levels of these participants were measured by monoclonal antibodies TSH immunoradiometric assays. A normal range, 0.45–4.65 µU/ml, was determined from the middle 95% of the TSH distribu- tion of 140 ‘disease-free’ subjects. By reference to the normal range, 23 (2.51%) participants had high (>4.65 µU/ml), and 41 (4.47%) had low (<0.46 µU/ml) TSH levels. The overall prevalence of thyroid dysfunction in the sample was 6.98%. Of the 23 participants with high TSH levels, 8 (34.8%) had low free T4 values (<1.21 ng/dl), so-called overt hypothyroidism, and of the 41 participants with low TSH levels, only 1 (2.4%) had high T3 values, so-called T3 thyrotoxicosis. Antithyroid antibodies were found in 56.5% of those with high TSH levels but only 12.2% of those with low TSH levels (odds ratio = 8.53, 95% confidence limits = 2.55–28.50, p < 0.001). This result indicates that autoimmune disease is still the major cause of hypothyroidism in aged people. However, the prevalence of subclinical hyperthyroidism is higher than that of subclinical hypothyroidism and it might relate to nonautoimmune factors.

Macrophage migration inhibitory factor regulates interleukin-6 production by facilitating nuclear factor-kappa B activation during Vibrio vulnificus infection.

BackgroundPatients infected with Vibrio vulnificus (V. vulnificus) show severe inflammatory responses characterised by the upregulation of proinflammatory cytokines. Macrophage migration inhibitory factor (MIF), an upstream proinflammatory regulator, increases the inflammation caused by sepsis. Whether MIF regulates responses to V. vulnificus infection and the actual mechanism by which V. vulnificus initiates these MIF-modulated proinflammatory cytokines remain unclear.ResultsMIF increased inflammation during V. vulnificus infection in vivo. In V. vulnificus-infected mice, MIF was produced earlier than tumour necrosis factor (TNF)-α and interleukin (IL)-6 and was expressed in a time-dependent manner. ISO-1 ((S, R)-3-(4-hydroxyphenyl)-4,5-dihydro-5-isoxazole acetic acid methyl ester), a small-molecule inhibitor of MIF, significantly decreased IL-6, IL-8, and TNF-α production in a time- and dose-dependent manner in human peripheral blood cells infected with V. vulnificus. The induction of IL-6, IL-8, and TNF-α production by V. vulnificus infection was mediated via the NF-κB- and p38 MAPK-regulated pathways but not via the Akt pathway. ISO-1-treated human peripheral blood cells showed lower V. vulnificus-induced NF-κB activation, IL-6 mRNA expression, and IκB phosphorylation, but they did not show lower p38 MAPK activation.ConclusionsWe conclude that MIF regulates V. vulnificus-induced IL-6 production via NF-κB activation and that p38 MAPK activation in V. vulnificus infection is not MIF dependent.

Impact of an outbreak of severe acute respiratory syndrome on a hospital in Taiwan, ROC

Study objective: To estimate the impact of the severe acute respiratory syndrome (SARS) outbreak in early 2003 on a tertiary care hospital in Taiwan, ROC. Methods: The study estimated the utilisation of resources related to infection control, SARS related medical services, and routine medical services, and SARS related medical outcomes at National Cheng Kung University Hospital (NCKUH) from 25 March to 16 June 2003 through a cross sectional survey of hospital records. Results: A mean of 5100 persons per day (95%CI 4580 to 5610) underwent fever screening at the outpatient and emergency department (ED) entrances to the hospital, of which 35 per day (95% CI 30 to 40) were referred for further evaluation for suspected or probable SARS. ED isolation surge capacity was created via 12 new beds outside the ED: eight for SARS assessment, three for patients awaiting inhospital bed assignment, and one for resuscitation. A total of 382 patients were fully evaluated for suspected or probable SARS outside the ED, of which 27 were admitted. The mean numbers of outpatient clinic patient visits, ED visits, ED trauma patient visits, ED admissions, hospital admissions, and operative procedures decreased during the outbreak. Thirty eight patients were hospitalised with suspected SARS, of which three received the final diagnosis of probable SARS. Two patients with probable SARS died. No cases of nosocomial SARS transmission occurred. Conclusions: This SARS outbreak was associated with substantial use of hospital and ED resources aimed at infection control, comparatively less use of resources related to the medical care of patients with suspected or probable SARS, and decreased use of routine medical services.

Implementation of the Hospital Emergency Incident Command System during an outbreak of severe acute respiratory syndrome (SARS) at a hospital in Taiwan, ROC.

Abstract We sought to describe the implementation of the Hospital Emergency Incident Command System (HEICS) at National Cheng Kung University Hospital (NCKUH) in Taiwan, ROC during the outbreak of severe acute respiratory syndrome (SARS) in early 2003. We administered a 14-question survey via structured interviews to individuals occupying activated HEICS leadership positions at NCKUH to identify the organization, structure, and function of the HEICS units and subunits they led and the job actions they performed from 25 March to 16 June 2003 Thirty-three of 38 persons (87%) occupying 39 of 44 (89%) activated HEICS leadership positions directly participated in the survey. The participants collectively reported: 1) the creation of four new HEICS unit leader positions and corresponding units during the outbreak, including the infection control officer (administrative section) and SARS assessment, isolation, and critical care unit leaders (operations section); 2) the creation of six new HEICS subunits, including functional areas for fever screening, SARS assessment, and resuscitation outside the hospital, and SARS patient care, SARS critical care, and employee isolation inside the hospital; and 3) the performance of new job actions related to infection control by all HEICS unit leaders. HEICS provides a flexible framework that seems to have assisted NCKUH in the organization of its emergency response to the SARS outbreak in Taiwan, ROC.

Inhibition of transforming growth factor-β-induced liver fibrosis by a retinoic acid derivative via the suppression of Col 1A2 promoter activity

Transforming growth factor-beta1 (TGF-beta1) mediates expression of collagen 1A2 (Col 1A2) gene via a synergistic cooperation between Smad2/Smad3 and Sp1, both act on the Col 1A2 gene promoter. In our previous study, we reported that a retinoic acid derivative obtained from Phellinus linteus (designated PL) antagonizes TGF-beta-induced liver fibrosis through regulation of ROS and calcium influx. In this continuing study we seek further the effect of PL on the Smad signaling pathway. We used a Col 1A2 promoter-luciferase construct to study the action of PL on Smad through TGF-beta. We found that PL decreases the promoter activity of Col 1A2, hinders the translocalization of phosphorylated Smad2/3-Smad 4 complex from cytosol into nucleus and inhibits Sp1 binding activity. These results suggest that PL inhibits TGF-beta1-induced Col 1A2 promoter activity through blocking ROS and calcium influx as well as impeding Sp1 binding and translocalization of pSmad 2/3-Smad4 complex into nucleus.

High concentrations of circulating macrophage migration inhibitory factor in patients with severe blunt trauma: Is serum macrophage migration inhibitory factor concentration a valuable prognostic factor?

ObjectiveTo determine serum concentrations of macrophage migration inhibitory factor and other cytokines in severe blunt trauma patients in critical settings and to evaluate their association with patient outcome. DesignProspective, observational study. SettingEmergency department and surgical intensive care unit of a university hospital. PatientsFifty-four severe blunt trauma patients with systemic inflammatory response syndrome requiring intensive care, emergency surgical intervention, or both were enrolled in the study. Forty-four patients with minor injuries were the controls. InterventionsSerum macrophage migration inhibitory factor concentrations were measured in the emergency department <4 hrs postinjury (day 1) and the surgical intensive care unit 24 hrs later (day 2). Blood samples for determination of tumor necrosis factor-&agr;, interleukin-6, interleukin-8, and interleukin-10 were measured both in patients with severe blunt trauma and in controls. The Acute Physiology and Chronic Health Evaluation II, Injury Severity Score, Revised Trauma Score, and Trauma Revised Injury Severity Score were used for clinical evaluation of trauma severity. Measurements and Main ResultsSerum macrophage migration inhibitory factor concentrations were higher in severe blunt trauma patients than in controls; were significantly correlated with Acute Physiology and Chronic Health Evaluation II, Revised Trauma Score, and Trauma Revised Injury Severity Score scores in severe blunt trauma patients but not in controls; and were higher in nonsurvivors than in survivors. ConclusionsOur data suggest that the serum macrophage migration inhibitory factor concentration is higher in severe blunt trauma and that it reflects the severity of trauma. The serum macrophage migration inhibitory factor concentration might be a valuable predictor for the outcome of severe blunt trauma.

Urinary Macrophage Migration Inhibitory Factor Serves as a Potential Biomarker for Acute Kidney Injury in Patients with Acute Pyelonephritis

Conventional markers of kidney function that are familiar to clinicians, including the serum creatinine and blood urea nitrogen levels, are unable to reveal genuine injury to the kidney, and their use may delay treatment. Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine, and the predictive role and pathogenic mechanism of MIF deregulation during kidney infections involving acute kidney injury (AKI) are not currently known. In this study, we showed that elevated urinary MIF levels accompanied the development of AKI during kidney infection in patients with acute pyelonephritis (APN). In addition to the MIF level, the urinary levels of interleukin (IL)-1β and kidney injury molecule (KIM)-1 were also upregulated and were positively correlated with the levels of urinary MIF. An elevated urinary MIF level, along with elevated IL-1β and KIM-1 levels, is speculated to be a potential biomarker for the presence of AKI in APN patients.

Hepatic portal venous gas induced by emphysematous pyelonephritis: a rare case in hemodialytic women

Hepatic portal venous gas (HPVG) became more easily diagnosed after the advent of abdominal computed tomography scan in the emergency department. However, the clinical significance of HPVG is popularly discussed; and its etiology remains uncertain. In this report, we present a 49- year-old diabetic, hemodialytic woman who presented with afebrile flank pain and a significant HPVG detected on abdominal computed tomography, which implied a unilateral perirenal abscess (so-called emphysematous pyelonephritis). This patient received percutaneous drainage and antibiotics therapy without emergency laparotomy intervention. No evidence of existing mesenteric infarction or bowel obstruction was detected during admission, and the patient was discharged with an uneventful outcome. To our knowledge, this is the first case of HPVG that originated from emphysematous pyelonephritis and was treated by successful emergency drainage.

Three Novel EXT1 and EXT2 Gene Mutations in Taiwanese Patients with Multiple Exostoses

Multiple osteochondromatosis, also known as hereditary multiple exostoses (HME), is an inherited autosomal dominant disorder characterized by the presence of multiple exostoses on the long bones. These exostoses are benign cartilaginous tumors (enchondromata). Three different exostosis (EXT) loci on chromosomes 8q (exostosin 1, EXT1), 11p (exostosin 2, EXT2) and 19p (exostosin 3, EXT3) have been reported. Recently, the EXT1 and EXT2 genes were identified by positional cloning. Using polymerase chain reaction and direct sequencing, we analyzed the EXT1 and EXT2 genes in three familial cases and one sporadic case of HME in Taiwanese patients. We found three novel mutations (S277X in the EXT1 gene, and G194X and 939+1G>A in the EXT2 gene) and a known mutation (Q172X in the EXT2 gene). Mutation analysis in families with HME allows for genetic counseling and prenatal diagnosis.