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Endoscopic sphincterotomy (EST), endoscopic papillary balloon dilation (EPBD), and endoscopic sphincterotomy plus balloon dilation (ESBD) are all techniques used to manage choledocholithiasis. We aim to analyze the efficacy and safety of these techniques for treating choledocholithiasis in patients undergoing hemodialysis (HD).We performed a retrospective study of 80 patients with end-stage renal disease (ESRD) on HD who underwent endoscopic retrograde cholangiopancreatography (ERCP) for choledocholithiasis management between August 1st, 2012, and December 31st, 2020, at a medical center in southern Taiwan. These patients were divided into three groups: EST (n = 21), EPBD (n = 28), and ESBD (n = 31). Post-ERCP complications, including pancreatitis, bleeding, cholangitis, and perforation, were reviewed for analysis.There were no significant among-group differences in the rate of complete stone clearance and hospitalization day after ERCP. Patients in the EST group had a higher post-ERCP complication rate than was the case in the other groups (p = 0.016). ESBD significantly reduced post-ERCP bleeding, compared with that occurring with EST (OR 0.07; 95% CI, 0.01-0.72, p = 0.026). There were no significant among-group differences in the rates of pancreatitis and cholangitis. There were no ERCP-related perforations or deaths in this study.EST, EPBD, and ESBD are efficient methods for treating choledocholithiasis in ESRD patients. ESBD was found to lead to a lower risk of bleeding than EST, and the rate of pancreatitis or cholangitis was comparable for EST and EPBD. Our results suggest that ESBD is the best choice of treatment of choledocholithiasis in patients with ESRD undergoing HD.

Clostridioides difficile is a major causative pathogen of nosocomial antibiotic-associated diarrhea and severe colitis. Despite the use of vancomycin and fidaxomicin as standard drugs for the treatment of C. difficile infection (CDI), clinical relapse rates remain high. Therefore, new alternative therapeutics to treat CDI are urgently required. The nuclear receptor, peroxisome proliferator-activated receptor-γ (PPAR-γ), is mainly expressed in the adipose tissue and modulates lipid metabolism and insulin sensitization. Previous studies have shown that PPAR-γ is highly expressed in colonic tissues and regulates tight junction function in epithelial cells. However, the role of PPAR-γ in CDI pathogenesis remains unclear. In this study, we used a mouse model of CDI and found that both expression levels of PPAR-γ and the tight junction protein, occludin, were decreased in colonic tissues. Furthermore, to investigate the role of PPAR-γ in CDI, we used PPAR-γ defective mice and found that intestinal permeability and bacterial dissemination in these mice were significantly higher than those in wild-type mice during CDI. Administration of the PPAR-γ agonist, pioglitazone, to activate PPAR-γ activity improved the phenotypes of CDI, including bodyweight loss, inflammation, and intestinal integrity. Taken together, these results demonstrate that PPAR-γ is a potential therapeutic target in CDI, as it modulates colonic inflammation and integrity.

Background Clostridium difficile is the leading cause of nosocomial infectious diarrhea. Hospitalized patients were at risk of C. difficile-associated diarrhea (CDAD). However the risk factors of CDAD in patients with different hospitalization period are not clear. Material and methods A prospective investigation was conducted in medical wards of a district hospital in southern Taiwan, from January 2011 to January 2013. We arbitrary divided patients into two groups: hospitalized for at most 14 days and 15–30 days, and analyzed their risk factors for CDAD. Results Overall 451 patients were enrolled. The multivariable analysis of 19 (8.0%) patients developing CDAD within 14 days' hospital stay and 216 patients hospitalized for ≤ 14 days without CDAD showed malignancy (odds ratio [OR] 7.15, 95% confidence interval [CI] 1.82–28.09; P = 0.005), prior cephalosporin (OR 10.8, 95% CI 1.3–93.9; P = 0.03) and proton pump inhibitor (PPI; OR 7.1, 95% CI 2.1–24.7; P = 0.002) therapy were independently related to CDAD (Table 3), but hypertension (OR 0.2, 95% CI 0.1–0.7; P = 0.01) was reversely related to CDAD. However, of 9 (4.2%) patients developing CDAD later (15–30 days' hospital stay) and 207 patients with longer hospitalization (15–30 days) but free of CDAD, malignancy (OR 14.0, 95% CI 1.6–124.9; P = 0.02) and underlying diabetes mellitus (OR 20.5, 95% CI 2.9–144.9; P = 0.002) were independent risk factors of CDAD. Conclusion Risk factors for CDAD among hospitalized patients varied by the duration of hospital stay. Intervention strategies to prevent CDAD may be different in terms of hospital stay duration.

Yuan-Pin Hung,1–3,* Pei-Jane Tsai,4,* Yuan-Ti Lee,5,6 Hung-Jen Tang,7 Hsiao-Ju Lin,1–3 Hsiu-Chuan Liu,1 Jen-Chieh Lee,2 Bo-Yang Tsai,4 Po-Ren Hsueh,8 Wen-Chien Ko2,9,10 1Department of Internal Medicine, Tainan Hospital, Ministry of Health and Welfare, Tainan, Taiwan; 2Department of Internal Medicine, National Cheng Kung University Hospital, Tainan, Taiwan; 3Graduate Institute of Clinical Medicine, National Cheng Kung University, Tainan, Taiwan; 4Department of Medical Laboratory Science and Biotechnology, College of Medicine, National Cheng Kung University, Tainan, Taiwan; 5Institute of Medicine and School of Medicine, Chung Shan Medical University, Taichung, Taiwan; 6Division of Infectious Diseases, Department of Internal Medicine, Chung Shan Medical University Hospital, Taichung, Taiwan; 7Department of Internal Medicine, Chi-Mei Hospital, Tainan, Taiwan; 8Departments of Laboratory Medicine and Internal Medicine, National Taiwan University Hospital, National Taiwan University College of Medicine, Taipei, Taiwan; 9Center of Infection Control, National Cheng Kung University Hospital, Tainan, Taiwan; 10Department of Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan *These authors contributed equally to this work Objectives: The information of antimicrobial susceptibility, toxin gene, and ribotype distribution of toxigenic Clostridium difficile isolates in Taiwan remain limited. Patients and methods: The study was conducted from January 2015 to December 2016 in 5 hospitals in Taiwan. Adults aged ≥20 years with a hospital stay for >5 days were included, and those with colectomy or intestinal infection due to other enteropathogens were excluded. Multiplex PCR was used to detect tcdA, tcdB, cdtA, cdtB, and tcdC deletions, and antimicrobial susceptibility for metronidazole, vancomycin, doxycycline, and tigecycline was investigated. Ribotypes of those isolates with tcdC deletion and tcdA+/tcdB+ were determined. Results: Of 1112 C. difficile isolates collected from adults at 5 hospitals, 842 were toxigenic, including 749 (89.0%) tcdA+/tcdB+ isolates and 93 (11.0%) tcdA−/tcdB+. Of the toxigenic isolates, 76 (9.0%) had a tcdC deletion and were cdtA+/cdtB+, indicative of hypervirulence, and RT078 lineage, including RT126, RT127, and RT078, predominated (n=53, 76.3%). Similar to the susceptibility data in Asia countries, metronidazole or vancomycin resistance was rare, noted in 1.2% or 2.1%, respectively. Reduced doxycycline susceptibility (minimum inhibitory concentration [MIC] of ≥8 mg/L) was more common among RT078 lineage than non-RT078 lineage (75.9%, 44/58 vs 6.0%, 47/784; P

Objectives The information of antimicrobial susceptibility, toxin gene, and ribotype distribution of toxigenic Clostridium difficile isolates in Taiwan remain limited. Patients and methods The study was conducted from January 2015 to December 2016 in 5 hospitals in Taiwan. Adults aged ≥20 years with a hospital stay for >5 days were included, and those with colectomy or intestinal infection due to other enteropathogens were excluded. Multiplex PCR was used to detect tcdA, tcdB, cdtA, cdtB, and tcdC deletions, and antimicrobial susceptibility for metronidazole, vancomycin, doxycycline, and tigecycline was investigated. Ribotypes of those isolates with tcdC deletion and tcdA+/tcdB+ were determined. Results Of 1112 C. difficile isolates collected from adults at 5 hospitals, 842 were toxigenic, including 749 (89.0%) tcdA+/tcdB+ isolates and 93 (11.0%) tcdA−/tcdB+. Of the toxigenic isolates, 76 (9.0%) had a tcdC deletion and were cdtA+/cdtB+, indicative of hypervirulence, and RT078 lineage, including RT126, RT127, and RT078, predominated (n=53, 76.3%). Similar to the susceptibility data in Asia countries, metronidazole or vancomycin resistance was rare, noted in 1.2% or 2.1%, respectively. Reduced doxycycline susceptibility (minimum inhibitory concentration [MIC] of ≥8 mg/L) was more common among RT078 lineage than non-RT078 lineage (75.9%, 44/58 vs 6.0%, 47/784; P

Clostridium difficile infection (CDI) is known to be associated with prior exposure to many classes of antibiotics. Standard therapy for CDI (i.e., metronidazole and vancomycin) is associated with high recurrence rates. Although tetracycline derivatives such as tetracycline, doxycycline or tigecycline are not the standard therapeutic choices for CDI, they may serve as an alternative or a component of combination therapy. Previous tetracycline or doxycycline usage had been shown to have less association with CDI development. Tigecycline, a broad-spectrum glycylcycline with potency against many gram-positive or gram-negative pathogens, had been successfully used to treat severe or refractory CDI. The in vitro susceptibility of C. difficile clinical isolates to tigecycline in many studies showed low minimal inhibitory concentrations. Tigecycline can suppress in vitro toxin production in both historical and hypervirulent C. difficile strains and reduce spore production in a dose-dependent manner. Tetracycline compounds such as doxycycline, minocycline, and tigecycline possess anti-inflammatory properties that are independent of their antibiotic activity and may contribute to their therapeutic effect for CDI. Although clinical data are limited, doxycycline is less likely to induce CDI, and tigecycline can be considered one of the therapeutic choices for severe or refractory CDI.

Clostridium difficile can cause antibiotic-associated diarrhea in hospitalized patients. Asymptomatic colonization by C. difficile is common during the neonatal period and early infancy, ranging from 21% to 48%, and in childhood. The colonization rate of C. difficile in adult hospitalized patients shows geographic variation, ranging from 4.4% to 23.2%. Asymptomatic carriage in neonates caused no further disease in many studies, whereas adult patients colonized with toxigenic C. difficile were prone to the subsequent development of C. difficile-associated diarrhea (CDAD). However, the carriage of nontoxigenic C. difficile strains appears to prevent CDAD in hamsters and humans. Risk factors for C. difficile colonization include recent hospitalization, exposure to antimicrobial agents or gastric acid-suppressing drugs (such as proton-pump inhibitors and H2 blockers), a history of CDAD or cytomegalovirus infection, the presence of an underlying illness, receipt of immunosuppressants, the presence of antibodies against toxin B, and Toll-like receptor 4 polymorphisms. Asymptomatic C. difficile carriers are associated with significant skin and environmental contamination, similar to those with CDAD, and contact isolation and hand-washing practices should therefore be employed as infection control policies for the prevention of C. difficile spread. Treating patients with asymptomatic C. difficile colonization with metronidazole or vancomycin is not suggested by the currently available evidence. In conclusion, asymptomatic C. difficile colonization may lead to skin and environmental contamination by C. difficile, but more attention should be paid to the clinical impact of those with C. difficile colonization.

BACKGROUND Clostridium difficile is currently the leading cause of infectious diarrhea in hospitalized patients. In addition to the infection due to toxigenic C. difficile in the gastrointestinal tract of susceptible hosts, other predisposing factors for C. difficile infection (CDI) are identified, including advanced age, a prolonged hospital stay, and use of acid-suppressive drugs. Of note, exposure to gastric acid-reducing agents, such as H2 blockers and proton pump inhibitors (PPIs), remains a controversial risk factor, and has been associated with CDI in some studies but not in others. A mouse model of antibiotic-associated clostridial colitis was established to examine the role of PPIs for CDI. MATERIALS AND METHODS A mouse model of antibiotic-associated clostridial colitis was set up. NF-κB reporter mice were used to address the in vivo spatial and temporal inflammatory patterns of C. difficile-associated colitis. Serum levels of lipopolysaccharide and dextran-FITC were measured to reflect the barrier permeability of affected intestines. RESULTS Mice with CDI that were exposed to PPI exhibited greater losses of stool consistency and body and cecal weights than those that were not exposed to PPI. Further, more neutrophilic infiltrations, epithelial damage, and inflammatory cytokine expression were noted in colon specimens of the mice with PPI exposure. More-evident inflammatory responses were detected by in vivo imaging of NF-κB reporter mice with CDI that were exposed to PPI. Gut barrier permeability was increased to a greater extent, as reflected by higher serum levels of lipopolysaccharide and dextran-FITC in mice with CDI that were exposed to PPI. CONCLUSIONS Our mouse model demonstrates that PPI exposure increases the severity of intestinal inflammation in mice with C. difficile-associated colitis.

An 85 year-old male initially admitted for septic shock due to urinary tract infection experienced Clostridium difficile-associated diarrhea during hospitalization and was treated by oral vancomycin. His clinical course was complicated by cytomegalovirus colitis and then vancomycin-resistant Clostridium innocuum bacteremia, which was cured by uneventfully parenteral piperacillin-tazobactam therapy.

Background High Clostridium difficile colonization and infection rates among hospitalized patients had been noted in Taiwan. Nevertheless, the cognition about clinical diagnosis and management of CDI among infection control professionals in Taiwan is not clear. Material and methods A 24-item survey questionnaire about the diagnosis, therapy, or infection control policies toward CDI was distributed in the annual meeting of the Infectious Disease Society of Taiwan (IDST) in October 2015 and Infectious Control Society of Taiwan (ICST) in April 2016. Results Totally 441 individuals responded to the survey, and 280 (63.5%) participants would routinely monitor the prevalence of CDI and 347 (78.7%) reported the formulation of infection control policies of CDI in their hospital, including contact precaution (75.7%), wearing gloves (88.9%) or dressing (80.0%) at patient care, single room isolation (49.7%), preference of soap or disinfectant-based sanitizer (83.2%) and avoidance of alcohol-based sanitizer (63.3%), and environmental disinfection with 1000 ppm bleach (87.1%). For the timing of contact precaution discontinuation isolation for CDI patients, most (39.9%) participants suggested the time point of the absence of C. difficile toxin in feces. To treat mild CDI, most (61.9%) participants preferred oral metronidazole, and for severe CDI 26.1% would prescribe oral vancomycin as the drug of choice. Conclusion There were substantial gaps in infection control polices and therapeutic choices for CDI between international guidelines and the perceptions of medical professionals in Taiwan. Professional education program and the setup of guideline for CDI should be considered in Taiwan.

Critical patients are susceptible to Clostridium difficile infections (CDIs), which cause significant morbidity and mortality in the hospital. In Taiwan, the epidemiology of CDI in intensive care units (ICUs) is not well understood. This study was aimed to describe the incidence and the characteristics of CDI in the ICUs of a medical center in southern Taiwan. Adult patients with diarrhea but without colostomy/colectomy or laxative use were enrolled. Stool samples were collected with or without 5 ml alcohol and were plated on cycloserine-cefoxitin-fructose agar. C. difficile identification was confirmed by polymerase chain reaction. There were 1,551 patients admitted to ICUs, 1,488 screened, and 145 with diarrhea. A total of 75 patients were excluded due either to laxative use, a lack of stool samples, or refusal. Overall, 70 patients were included, and 14 (20%) were diagnosed with CDI, with an incidence of 8.8 cases per 10,000 patient-days. The incidence of CDI was found to be highest in March 2013 and lowest in the last quarter of 2013. The cases were categorized as the following: 5 severe, complicated, 5 severe, and 4 mild or moderate diseases. Among the 14 cases of CDI, the median patient age was 74 (range: 47–94) years, and the median time from admission to diarrhea onset was 16.5 (4–53) days. Eight cases received antimicrobial treatment (primarily metronidazole), and the time to diarrheal resolution was 11.5 days. Though 6 cases were left untreated, no patients died of CDI. The in-hospital mortality of CDI cases was 50%, similar to that of patients without CDI (46.4%; P = 1.0). We concluded that the overall incidence of CDI in our medical ICUs was low and there were variable seasonal incidences and disease severities of CDI.

From dyadic perspectives, this study explores the effect of market orientation on relationship learning and relationship performance and the moderating effect of relationship quality in Taiwan manufacturing industry. The results reveal that: (1) both customer market orientation and supplier market orientation are positively related to relationship learning; (2) relationship learning is positively related to relationship performance; (3) both customer and supplier market orientation has positively interaction effect on shared information and negatively interaction effect on sense-making activities; and (4) trust of relationship quality has moderating effect on the relationship between customer market orientation and relationship learning.

Drug-induced neuroadaptations within the medial prefrontal cortex (mPFC) are thought to underlie the development of cocaine sensitization. Here, we report that repeated cocaine administrationin vivoimpaired the long-term depression (LTD) induced by bath application of group II metabotropic glutamate receptor (mGluR) agonists DCG-IV [2S, 2′R, 3′R)-2-(2′, 3′-dicarboxycyclopropyl)glycine] or LY379268 [(1R,4R,5S,6R)-4-amino-2-oxabicyclo[3.1.0]hexane-4,6-dicarboxylic acid] at excitatory synapses onto layer V pyramidal neurons of rat mPFC. In contrast, this impairment was not found in slices from rats treated with saline or a single dose of cocaine. Such effect of cocaine was selectively prevented when cocaine was coadministered with the selective D1-like receptor antagonist SCH23390 [(R)-(+)-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine]. In slices from control rats, a brief application of either protein kinase C (PKC) activator phorbol-12,13-dibutyrute or adenosine A3receptor agonist 2-chloro-N6-(3-iodobenzyl)-adenosine-5-N-methyluronamide mimicked the effect of repeated cocaine treatment to impair the induction of LTD. Bilateral intra-mPFC infusion of PKC inhibitor bisindolylmaleimide I or adenosine A3receptor antagonist MRS1220 (N-[9-chloro-2-(2-furanyl)[1,2,4]-triazolo[1,5-c]quinazolin-5-benzeneacetamide) before cocaine injection prevented cocaine-induced impairment of LTD induction. Furthermore, endogenous adenosine tone is greater in slices from cocaine-treated rats than from the saline-treated controls. When the metabolism of cAMP to adenosine was blocked, the extent of LTD in slices from saline and cocaine-treated rats was similar. These results suggest that cocaine-induced impairment of group II mGluR-mediated LTD is caused, at least in part, by an increase in adenosine subsequent to the rise in cAMP after D1-like receptor activation, which leads to an adenosine A3receptor-mediated upregulation of PKC activity and thereby triggers an inhibition of group II metabotropic glutamate receptor function.

Although drug-induced adaptations in the prefrontal cortex (PFC) may contribute to several core aspects of addictive behaviors, it is not clear yet whether drugs of abuse elicit changes in synaptic plasticity at the PFC excitatory synapses. Here we report that, following repeated cocaine administration (15 mg/kg/day intraperitoneal injection for 5 consecutive days) with a 3-day withdrawal, excitatory synapses to layer V pyramidal neurons in rat medial prefrontal cortex (mPFC) become highly sensitive to the induction of long-term potentiation (LTP) by repeated correlated presynaptic and postsynaptic activity. This promoted LTP induction is caused by cocaine-induced reduction of gamma-aminobutyric acid (GABA)(A) receptor-mediated inhibition of mPFC pyramidal neurons. In contrast, in slices from rats treated with saline or a single dose of cocaine, the same LTP induction protocol did not induce significant LTP unless the blockade of GABA(A) receptors. Blockade of the D1-like receptors specifically prevented the cocaine-induced enhancement of LTP. Repeated cocaine exposure reduced the GABA(A) receptor-mediated synaptic currents in mPFC pyramidal neurons. Biotinylation experiments revealed a significant reduction of surface GABA(A) receptor alpha1 subunit expression in mPFC slices from repeated cocaine-treated rats. These findings support an important role for cocaine-induced enhancement of synaptic plasticity in the PFC in the development of drug-associated behavioral plasticity.

Objective Synthetic glucocorticoid dexamethasone (DEX) is frequently used as a therapeutic agent to lessen the morbidity of chronic lung disease in premature infants. Surprisingly, little is known about the long-term neurodevelopmental outcomes of this therapy. Methods Using a schedule of tapering doses of DEX similar to that used in premature infants, we examined the consequences of neonatal DEX treatment on hippocampal synaptic plasticity of infants and associative memory later in their lives. Results Neonatal DEX treatment changed the direction of synaptic plasticity, favoring low-frequency, stimulation-induced, long-term depression and opposing the induction of long-term potentiation by high-frequency stimulation in adolescent (5-week-old) rats, but these alterations disappeared in young adult (8-week-old) rats. The effects of DEX on long-term depression and long-term potentiation were found to correlate with an increase in the autophosphorylation of Ca2+/calmodulin-dependent protein kinase II and a decrease in the protein phosphatase 1 activity. Neonatal DEX treatment also disrupted memory retention in 5-week-old (but not 8-week-old) rats subjected to passive avoidance learning tasks. Interpretation: These results suggest that neonatal DEX treatment alters hippocampal synaptic plasticity and contextual fear memory formation in later life, but these impairments apparently are not permanent. Ann Neurol 2006;59:939-951

Background/PurposeThe prevalence of extended spectrum beta-lactamase (ESBL)-producing Enterobacteriaceae in nursing home residents has rarely been reported in Taiwan.MethodsA retrospective study was performed at medical wards of a district hospital at southern Taiwan between July 2009 and June 2011. Patients were included if they were older than 18 years, admitted via the emergency department, and their blood, sputum, or urine culture revealed the growth of Escherichia coli, Klebsiella pneumoniae, or Proteus mirabilis. From each patient only the first isolate from the infection site was included. Antimicrobial susceptibility was determined using the disc diffusion method.ResultsOverall, 827 patients were included, with 354 (42.8%) coming from the community and 473 (57.2%) referred from a nursing home. Of the isolates acquired in nursing home, 45.5% (215/473) harbored ESBL. By contrast, 20.6% (73) of 354 isolates acquired in the community exhibited the ESBL production phenotype (p 90% Enterobacteriaceae isolates, irrespective of ESBL production.ConclusionESBL production was common among clinical Enterobacteriaceae isolates, especially E. coli or those isolated from nursing home residents.

Introduction Several virulent Clostridium difficile clones, designated as polymerase chain reaction (PCR) ribotypes 017, 027, or 078, are well recognized in western countries. However, the ribotype distribution of clinical C. difficile isolates in Taiwan remains unclear. Method Between 2010 and 2012, we identified three patients with C. difficile- associated diarrhea (CDAD) at a hospital in southern Taiwan. The C. difficile strains isolated from these patients were further characterized by PCR detection of tcdA , tcdB , tcdC , cdtA , and cdtB , toxinotyping, multilocus sequence typing, ribotyping and repetitive-based PCR. Results Three C. difficile strains harbored tcdC Δ39 and belonged to multilocus sequence typing 11 (ST11), toxinotype V, and ribotype 126 (a ribotype 078-like clone). Notably, one patient developed pseudomembranous colitis and recurrent CDAD. These three isolates were noted between January 2012 and June 2012 and were identical, as evidenced by repetitive sequence-based PCR, suggestive of case clustering. Conclusion A hypervirulent C. difficile clone, ribotype 126, causing pseudomembranous colitis and recurrent CDAD, is present in southern Taiwan.

Background This study is to investigate the significance and risk factors of fecal toxigenic (tCdC) or non-toxigenic Clostridium difficile colonization (ntCdC) among hospitalized patients. Methods Adults admitted to medical wards in a district hospital between January 2011 and June 2012 were enrolled, and those with a history of colectomy, C. difficile fecal colonization or infection or receipt of either metronidazole or oral vancomycin within 3 months, were excluded. Stools collected within 48 hours after admission and every week during hospitalization were cultured for C. difficile. Findings Among the 441 enrolled patients, 84 (20.0%) had CdC at initial screening, including 58 (13.2%) with tCdC and 26 (6.8%) with ntCdC. Among patients with initial negative fecal screening for CdC, it took an average of 70.6 days or 66.5 days to develop tCdC or ntCdC during the study period. Finally 78 (17.7%) had tCdC and 34 (7.7%) had ntCdC. During the follow-up period, the patients with tCdC had a higher risk of CDAD (11/79, 14.1%) than those without CdC (3/328, 0.9%) and those with ntCdC (0/34, 0%) (P

BackgroundPPARγ and RBP4 are known to regulate lipid and glucose metabolism and insulin resistance. The influences of PPARγ (C1431T and Pro12Ala) and RBP4 (-803GA) polymorphisms on metabolic syndrome in HIV-infected patients receiving anti-retroviral therapy were examined in this study.Materials and methodsA cross-sectional study of HIV-1 infected adults with antiretroviral therapy for more than one year in the National Cheng Kung University Hospital was conducted. The gene polymorphisms were determined by quantitative PCR.ResultsNinety-one patients were included in the study. Eighty-two (90.1%) patients were males with a mean age of 44.4 years. For the C1431T polymorphism in PPARγ, while patients with the T allele (48.4%) had trends toward lower rate of hypertriglyceridemia, the borderline significance together with insignificant power did not support the protective effect of the T allele against development of hypertriglyceridemia. For the Pro12Ala polymorphism in PPARγ, although patients with the Pro/Ala genotype (8.8%) had a higher level of serum LDL (138.0 vs. 111.5 mg/dl, P = 0.04) and trends toward higher rates of hypercholesterolemia and serum LDL>110 mg/dl, these variables were found to be independent of the Pro/Ala genotype in the multivariate analysis. For the -803GA polymorphism in RBP4, patients with the A allele (23.1%) more often had insulin resistance (HOMA>3.8; 33.3 vs. 8.7%, P = 0.01) and more often received anti-hypoglycemic drugs (14.3 vs. 1.4%, P = 0.04). The detrimental effect of the A allele in RBP4 -803GA polymorphism on development of insulin resistance was supported by the multivariate analysis adjusting for covariates.ConclusionThe impacts of PPARγ C1431T and Pro12Ala polymorphisms on metabolism in HIV-infected patients are not significant. RBP4 -803GA polymorphism has increased risk of insulin resistance in HIV-infected patients with anti-retroviral therapy.

Background The impact of toxigenic Clostridium difficile colonization (tCDC) in hospitalized patients is not clear. Aim To study the significance of tCDC in hospitalized patients. Methods A prospective study in the medical wards of a regional hospital was performed from January to June 2011. Fecal samples collected from patients at the time of admission were tested for tcdB by real-time polymerase chain reaction (PCR) and cultured for C. difficile. The patients were followed up weekly or when they developed diarrhea during hospitalization. If C. difficile was isolated, tcdA and tcdB would be tested by multiplex PCR. The primary outcome was the development of C. difficile-associated diarrhea (CDAD). Findings Of 168 patients enrolled, females predominated (87, 51.8%), and the mean patient age was 75.4 years old. Approximately 70% of the patients were nursing home residents, and one third had a recent hospitalization within the prior three months. Twenty-eight (16.7%) patients had tCDC, including 16 (9.5%) patients with tCDC at the time of admission and 12 (7.2%) with tCDC during the follow-up period. With regard to the medications taken during hospitalization, the patients were more likely to have tCDC if they had received more than one class of antibiotics than if they had received monotherapy (odds ratio [OR] 6.67, 95% confidence interval [CI] 1.41–31.56, P = 0.01), particularly if they received a glycopeptide in combination with a cephalosporin or penicillin or a cephalosporin and a carbapenem. More patients with tCDC developed CDAD than those without tCDC (17.9%, 5/28 vs. 1.4%, 2/140, P = 0.002). Overall 7 (4.2%) of the 168 patients developed CDAD, and crude mortality rate of those with and without tCDC was similar (21.4%, 6/28 vs. 19.4%, 27/140, P = 0.79). Conclusion Recent use of glycopeptides and β-lactam antibiotics is associated with toxigenic C. difficile colonization, which is a risk factor for developing C. difficile-associated diarrhea.

Background Patients with toxigenic Clostridium difficile colonization (tCDC) are at risk of developing C. difficile -associated diarrhea (CDAD). However, the risk factors of hospitalized patients with tCDC developing CDAD are not clear. Methods We conducted an 18-month prospective study at a medical ward in a district hospital in southern Taiwan. Within 48 hours of admission, weekly stool samples from asymptomatic hospitalized patients were obtained to detect fecal CDC. A polymerase chain reaction for tcdB was performed to determine toxigenic isolates. CDAD was diagnosed if the patient had diarrhea and toxigenic C. difficile present in a stool sample. Results A total 483 patients with stool samples were eligible for the study. Eighty-six (17.8%) patients had tCDC after screening, of whom 14 (16.3%) developed CDAD during follow-up. Among those with tCDC, patients with subsequent CDAD were more likely to have diabetes mellitus ( p = 0.01) and to have received piperacillin–tazobactam ( p = 0.04), or proton-pump inhibitors (PPIs; p = 0.04) than those without developing CDAD. The variables were statistically significant as determined by multivariate analysis. However, the 60-day crude mortality rates among tCDC patients with and without subsequent development of CDAD were similar. Conclusion Diabetes mellitus and recent receipt of piperacillin–tazobactam or PPIs are independent risk factors for the development of CDAD among hospitalized patients with tCDC.

Background/Purpose(s) To identify the clinical characteristics of cytomegalovirus (CMV) disease in chronic kidney disease (CKD) patients. Methods Patients from two sources were reviewed: (1) a retrospective study of hospitalized patients admitted between January 1990 and February 2009 was performed at a tertiary hospital in Taiwan; (2) the English literature from 1990 to 2009 was reviewed for additional cases, and adults with CKD and histopathologically documented cytomegalovirus disease were included. Results Seven CKD patients from our hospital and seven from the literature were included. Nine (64.3%) patients were males, and the mean age was 66 years. Histopathologically proven CMV disease was present in the gastrointestinal (GI) tract of 13 (92.9%) and in the skin of one (7.1%) patient. GI symptoms included bleeding (78.6%), abdominal pain (35.7%), and diarrhea (28.6%).The most common comorbidities were diabetes mellitus (7, 50%) and hypertension (8, 57.1%). Thirteen patients had CMV GI disease. The endoscopic gross features of the GI tract lesions included single or multiple ulcers and a large polypoid or uneven surface mass. Of the seven cases with available data, a low body mass index (22.3 ± 1.3 kg/m 2 ) and hypoalbuminemia (25 ± 7.0 g/L) were noted. Twelve patients had received ganciclovir or valganciclovir therapy. Five (35.7%) patients died, and the death of two patients was directly related to bowel perforation caused by CMV colitis. Conclusion CMV disease may occur in CKD patients without the presence of overt immunodeficiency. The gastrointestinal tract is the most common site of involvement. Clinicians should be aware of this possibility in CKD patients who have GI symptoms.