209 research outputs found
sj-docx-1-dhj-10.1177_20552076231223811 - Supplemental material for Predicting delirium and the effects of medications in hospitalized COVID-19 patients using machine learning: A retrospective study within the Korean Multidisciplinary Cohort for Delirium Prevention (KoMCoDe)
No full textSupplemental material, sj-docx-1-dhj-10.1177_20552076231223811 for Predicting delirium and the effects of medications in hospitalized COVID-19 patients using machine learning: A retrospective study within the Korean Multidisciplinary Cohort for Delirium Prevention (KoMCoDe) by So Hee Lee, Hyun Jung Hur, Sung Nyun Kim, Jang Ho Ahn, Du Hyun Ro, Arum Hong, Hye Yoon Park, Pyoeng Gyun Choe, Back Kim and Hye Youn Park in DIGITAL HEALTH</p
Tuberculosis manifested by immune reconstitution inflammatory syndrome during HAART
No full textThe proportion of tuberculosis manifested by immune reconstitution inflammatory syndrome (IRIS) after HAART has not been established. We describe the incidence and clinical features of tuberculosis manifested by IRIS after HAART in an intermediate tuberculosis burden area. The findings suggest that a significant proportion of the tuberculosis occurring early after starting HAART is manifested by IRIS.Y
Immune reconstitution inflammatory syndrome in the first year after HAART: influence on long-term clinical outcome
No full textLittle is known about the effect of immune reconstitution inflammatory syndrome (IRIS) on the long-term clinical outcome. Of 52 opportunistic infections (OI) occurring within one year after the start of HAART in 387 HIV patients, 33 (63%) were classified as having IRIS. The patients with IRIS showed no significant difference in the AIDS event-free survival curve compared with the matched control group without OI and in contrast to non-IRIS OI.Y
Early modification of initial HAART regimen associated with poor clinical outcome in HIV patients
No full textAlthough the importance of the initial regimen in highly active antiretroviral therapy (HAART) has been emphasized, the effect on clinical outcome of early modification of the initial HAART regimen has not been well-defined. The analysis included antiretroviral-naive HIV patients who started HAART between 1999 and 2005 at a university hospital. Early modification was defined as any drug change within 2 months of starting HAART. The effect of early regimen modification on the occurrence of new AIDS-defining illness or death was assessed using Kaplan-Meier survival estimates, and hazard ratios were estimated using Cox's proportional hazards regression model. Of 398 patients beginning HAART, 21% experienced early modification of their regimen, the most common reason being gastrointestinal toxicity (49%). After adjusting for risk factors for occurrence of a new AIDS event or death, identified by univariate analysis, the hazards ratio contrasting early modification with maintenance of initial HAART regimen was 3.06 (95% confidence interval, 1.36-6.90; p = 0.007). There were significant differences between the AIDS event-free survival curves of patients in clinical categories B or C with or without early modification of initial HAART regimen (p = 0.0002), but no significant difference in patients in clinical category A (p = 0.706). A considerable proportion of patients who started HAART changed treatment regimen mainly due to intolerance early after start of HAART. Early modification of an initial HAART regimen was associated with poor clinical outcome in HIV patients in the advanced clinical categories.N
Emerg Infect Dis
No full textWe report a patient with human granulocytic anaplasmosis in South Korea. The patient had fever and thrombocytopenia. Human granulocytic anaplasmosis was confirmed by seroconversion, PCR, and sequence analysis for Anaplasma phagocytophilum. Morulae were observed in the cultured HL-60 cells inoculated with blood from the patient
Emerg Infect Dis
No full textWe report a retrospectively identified fatal case of severe fever with thrombocytopenia syndrome (SFTS) in South Korea from 2012. SFTS virus was isolated from the stored blood of the patient. Phylogenetic analysis revealed this isolate was closely related to SFTS virus strains from China and Japan
Genetic Factors Influencing Severe Atazanavir-Associated Hyperbilirubinemia in a Population with Low UDP-Glucuronosyltransferase 1A1*28 Allele Frequency
No full textBackground. High prevalence of severe atazanavir-associated hyperbilirubinemia in Asians with low prevalence of the UDP-glucuronosyltransferase (UGT)1A1*28 polymorphism suggests the importance of genetic factors other than UGT1A1*28 for atazanavir-associated hyperbilirubinemia in these populations. Methods. Serum bilirubin levels were measured in 129 Korean human immunodeficiency virus-infected patients 3 months after initiation of atazanavir (400 mg per day) with good adherence to medication. The multidrug resistance gene 1 (MDR1) C3435T and G2677T/A variations and UGT1A1*6 and *28 were examined by direct sequencing of DNA from peripheral whole blood samples. The associations between genetic polymorphisms and severe (grade 3-4) hyperbilirubinemia were evaluated using multivariate logistic regression analysis including demographic and clinical variables. Results. The median patient age was 39 years (interquartile range, 34-51 years), and 91% were men. At baseline, the median CD4 cell count was 261 cells/mu L (interquartile range, 181-405 cells/mu L). Severe hyperbilirubinemia was detected in 27 patients (21%). The independent risk factors for severe hyperbilirubinemia were low baseline CD4 cell count (adjusted odds ratio per 10 cells/mu L increase, 0.97; 95% confidence interval, 0.94-0.99), UGT1A1*28 (adjusted odds ratio, 4.15; 95% confidence interval, 1.46-11.84), and MDR1 G2677T/A (adjusted odds ratio, 9.65; 95% confidence interval, 1.09-85.61). Of 19 patients with wild-type alleles for both MDR1 2677 and UGT1A1*28, none developed severe hyperbilirubinemia. Conclusion. The MDR1 G2677T/A variation and UGT1A1*28 are independent risk factors for severe atazanavir-associated hyperbilirubinemia in Korean human immunodeficiency virus-infected patients.Hartkoorn RC, 2010, PHARMACOGENET GENOM, V20, P112, DOI 10.1097/FPC.0b013e328335b02dTorti C, 2009, INFECTION, V37, P244, DOI 10.1007/s15010-008-8010-6Siccardi M, 2008, CLIN INFECT DIS, V47, P1222, DOI 10.1086/592304Phillips EJ, 2008, CURR OPIN INFECT DIS, V21, P16Xu P, 2008, PHARMACOLOGY, V82, P221, DOI 10.1159/000156488CHOE PG, 2008, 15 INT S HIV EM INF, P37Ma Q, 2007, PHARMACOGENOMICS, V8, P227, DOI 10.2217/14622416.8.3.227Rodriguez-Novoa S, 2007, AIDS, V21, P41Lankisch TO, 2006, HEPATOLOGY, V44, P1324, DOI 10.1002/hep.21361Urawa N, 2006, ONCOL REP, V16, P801Boyd MA, 2006, PHARMACOGENET GENOM, V16, P321Kim YO, 2006, SEIZURE-EUR J EPILEP, V15, P67, DOI 10.1016/j.seizure.2005.11.001RODRIGUEZNOVOA S, 2006, CLIN INFECT DIS, V42, P291Rotger M, 2005, J INFECT DIS, V192, P1381Takeuchi K, 2004, J GASTROEN HEPATOL, V19, P1023, DOI 10.1111/j.1400-1746.2004.03370.xMarzolini C, 2004, CLIN PHARMACOL THER, V75, P13, DOI 10.1016/j.clpt.2003.09.012Ki CS, 2003, CLIN CHEM, V49, P2078, DOI 10.1373/clinchem.2003.024174Anglicheau D, 2003, J AM SOC NEPHROL, V14, P1889, DOI 10.1097/01.ASN.0000073901.74759.36Verstuyft C, 2003, EUR J CLIN PHARMACOL, V58, P809, DOI 10.1007/s00228-003-0567-5Chowbay B, 2003, PHARMACOGENETICS, V13, P89Siegmund W, 2002, CLIN PHARMACOL THER, V72, P572, DOI 10.1067/mcp.2002.127739Kurata Y, 2002, CLIN PHARMACOL THER, V72, P209, DOI 10.1067/mcp.2002.126177Tang K, 2002, PHARMACOGENETICS, V12, P437Nakamura T, 2002, CLIN PHARMACOL THER, V71, P297, DOI 10.1067/mcp.2002.122055Fellay J, 2001, LANCET, V358, P1322Kim RB, 2001, CLIN PHARMACOL THER, V70, P189, DOI 10.1067/mcp.2001.117412Duong M, 2001, CLIN INFECT DIS, V33, P386Tanabe M, 2001, J PHARMACOL EXP THER, V297, P1137Cascorbi I, 2001, CLIN PHARMACOL THER, V69, P169Maggiolo F, 2000, J ACQ IMMUN DEF SYND, V25, P36Hoffmeyer S, 2000, P NATL ACAD SCI USA, V97, P3473Akaba K, 1998, BIOCHEM MOL BIOL INT, V46, P21Beutler E, 1998, P NATL ACAD SCI USA, V95, P8170Yamamoto K, 1998, BBA-MOL BASIS DIS, V1406, P267BOSMA PJ, 1995, NEW ENGL J MED, V333, P1171
Intensive Care Unit Relocation and Its Effect on Multidrug-Resistant Respiratory Microorganisms
No full textBackground Infection by multidrug-resistant (MDR) pathogens leads to poor patient outcomes in intensive care units (ICUs). Contact precautions are necessary to reduce the transmission of MDR pathogens. However, the importance of the surrounding environment is not well known. We studied the effects of ICU relocation on MDR respiratory pathogen detection rates and patient outcomes. Methods Patients admitted to the ICU before and after the relocation were retrospectively analyzed. Baseline patient characteristics, types of respiratory pathogens detected, antibiotics used, and patient outcomes were measured. Results A total of 463 adult patients admitted to the ICU, 4 months before and after the relocation, were included. Of them, 234 were admitted to the ICU before the relocation and 229 afterward. Baseline characteristics, including age, sex, and underlying comorbidities, did not differ between the two groups. After the relocation, the incidence rate of MDR respiratory pathogen detection decreased from 90.0 to 68.8 cases per 1,000 patient-days, but that difference was statistically insignificant. The use of colistin was significantly reduced from 53.5 days (95% confidence interval [CI], 20.3 to 86.7 days) to 18.7 days (95% CI, 5.6 to 31.7 days). Furthermore, the duration of hospital stay was significantly reduced from a median of 29 days (interquartile range [IQR], 14 to 50 days) to 21 days (IQR, 11 to 39 days). Conclusions Incidence rates of MDR respiratory pathogen detection were not significantly different before and after ICU relocation. However, ICU relocation could be helpful in reducing the use of antibiotics against MDR pathogens and improving patient outcomes
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