The impact of diabetes mellitus medication on the incidence of endogenous endophthalmitis
Autoři:
Ke-Hung Chien aff001; Ke-Hao Huang aff001; Chi-Hsiang Chung aff004; Yun-Hsiu Hsieh aff001; Chang-Min Liang aff001; Yu-Hua Chang aff006; Tzu-Heng Weng aff001; Wu-Chien Chien aff004
Působiště autorů:
Department of Ophthalmology, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan
aff001; Institute of Pharmacology, National Yang-Ming University, Taipei, Taiwan
aff002; Department of Ophthalmology, Songshan Branch of Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan
aff003; School of Public Health, National Defense Medical Center, Taipei, Taiwan
aff004; Taiwanese Injury Prevention and Safety Promotion Association (TIPSPA), Taipei, Taiwan
aff005; Division of Colorectal Surgery, Department of Surgery, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan
aff006; Department of Medical Research, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan
aff007; Graduate Institute of Life Science, National Defense Medical Center, Taipei, Taiwan
aff008
Vyšlo v časopise:
PLoS ONE 15(1)
Kategorie:
Research Article
doi:
https://doi.org/10.1371/journal.pone.0227442
Souhrn
Purpose
This study aimed to evaluate the relationship between diabetic mellitus (DM) treatment and the incidence rate of endogenous endophthalmitis (EE).
Design
This study used a matched cohort design. We utilized the Longitudinal Health Insurance Database to identify outpatients and inpatients who were diagnosed with DM and treated with medication from 2000 to 2010.
Methods
Several factors and different DM medications were also investigated. The influence of DM medication on the incidence of EE was examined by using Cox proportional hazards regression models, and the hazard ratios and 95% confidence intervals were determined.
Results
The cumulative incidence of EE was lower in DM patients treated with medication than in subjects in the control group (P = 0.002). The adjusted hazard ratio (AHR) was 0.47-fold lower in the treatment group than in the control group (P = 0.004). With respect to DM medication, single-agent therapy with insulin, metformin, gliclazide, glimepiride, or repaglinide and combination therapy with glimepiride/metformin or repaglinide/metformin were associated with decreased AHRs (0.257–0.544, all P<0.05).
Conclusions
Diabetic patients treated with medication had lower AHRs than those in the control group. Further stratification indicated that liver abscess, liver disease DM patients who were treated with medication had a lower risk of developing EE. Several specific DM medications may decrease the incidence of EE.
Klíčová slova:
Abscesses – Cancer treatment – diabetes mellitus – Drug therapy – Gastroenterology and hepatology – Liver diseases – Oncology – Pneumonia
Zdroje
1. El-Mollayess GM, Saadeh JS, Salti HI. Exogenous endophthalmitis in diabetic patients: a systemic review. ISRN Ophthalmol. 2012;2012: 456209. doi: 10.5402/2012/456209 24555128
2. Kattan HM, Flynn HW, Pflugfelder SC, Robertson C, Forster RK. Nosocomial endophthalmitis survey. Current incidence of infection after intraocular surgery. Ophthalmology. 1991;98: 227–238. 2008282
3. May D, Peyman G. Endophthalmitis after vitrectomy. Am J Ophthalmol. 1976;81: 520–521. doi: 10.1016/0002-9394(76)90314-7 1083674
4. Durand ML. Endophthalmitis. Clin Microbiol Infect. 2013;19: 227–234. doi: 10.1111/1469-0691.12118 23438028
5. Sheu SJ. Endophthalmitis. Korean J Ophthalmol. 2017;31: 283–289. doi: 10.3341/kjo.2017.0036 28752698
6. Madu AA, Mayers M. Ocular manifestation of systemic infections. Curr Opin Ophthalmol. 1995;6: 88–91. doi: 10.1097/00055735-199512000-00015 10160425
7. Arevalo JF, Jap A, Chee SP, Zeballos DG. Endogenous endophthalmitis in the developing world. Int Ophthalmol Clin. 2010;50: 173–187. doi: 10.1097/IIO.0b013e3181d26dfc 20375870
8. Jackson TL, Paraskevopoulos T, Georgalas I. Systematic review of 342 cases of endogenous bacterial endophthalmitis. Surv Ophthalmol. 2014;59: 627–635. doi: 10.1016/j.survophthal.2014.06.002 25113611
9. Vaziri K, Pershing S, Albini TA, Moshfeghi DM, Moshfeghi AA. Risk factors predictive of endogenous endophthalmitis among hospitalized patients with hematogenous infections in the United States. Am J Ophthalmol. 2015;159: 498–504. doi: 10.1016/j.ajo.2014.11.032 25486541
10. Mowat A, Baum J. Chemotaxis of polymorphonuclear leukocytes from patients with diabetes mellitus. N Engl J Med. 1971;284: 621–627. doi: 10.1056/NEJM197103252841201 5545603
11. Alba-Loureiro TC, Munhoz CD, Martins JO, Cerchiaro GA, Scavone C, Curi R, et al. Neutrophil function and metabolism in individuals with diabetes mellitus. Braz J Med Biol Res. 2007;40: 1037–1044. doi: 10.1590/s0100-879x2006005000143 17665039
12. Saini JS, Khandalavla B. Corneal epithelial fragility in diabetes mellitus. Can J Ophthalmol. 1995;30: 142–146. 7627899
13. Friend J, Ishii Y, Thoft RA. Corneal epithelial changes in diabetic rats. Ophthalmic Res. 1982;14: 269–278. doi: 10.1159/000265202 7133621
14. Weng TH, Chang HC, Chung CH, Lin FH, Tai MC, Tsao CH, et al. Epidemiology and mortality-related prognostic factors in endophthalmitis. Invest Ophthalmol Vis Sci. 2018;59: 2487–2494. doi: 10.1167/iovs.18-23783 29847653
15. Han SH. Review of hepatic abscess from Klebsiella pneumoniae. An association with diabetes mellitus and septic endophthalmitis. West J Med. 1995;162: 220–224. 7725704
16. Schiedler V, Scott IU, Flynn HW, Davis JL, Benz MS, Miller D. Culture-proven endogenous endophthalmitis: clinical features and visual acuity outcomes. Am J Ophthalmol. 2004;137: 725–731. doi: 10.1016/j.ajo.2003.11.013 15059712
17. Wong JS, Chan TK, Lee HM, Chee SP. Endogenous bacterial endophthalmitis: an East Asian experience and a reappraisal of a severe ocular affliction. Ophthalmology. 2000;107: 1483–1491. doi: 10.1016/s0161-6420(00)00216-5 10919895
18. Weishaar PD, Flynn HW, Murray TG, Davis JL, Barr CC, Gross JG, et al. Endogenous aspergillus endophthalmitis. Clinical features and treatment outcomes. Ophthalmology. 1998;105: 57–65. doi: 10.1016/s0161-6420(98)71225-3 9442779
19. Michelson JB, Friedlaender MH. Endophthalmitis of drug abuse. Int Ophthalmol Clin. 1987;27: 120–126. doi: 10.1097/00004397-198702720-00009 3294704
20. Binder MI, Chua J, Kaiser PK, Procop GW, Isada CM. Endogenous endophthalmitis: an 18-year review of culture-positive cases at a tertiary care center. Medicine. 2003;82: 97–105. doi: 10.1097/00005792-200303000-00004 12640186
21. Okada AA, Johnson RP, Liles WC, D'Amico DJ, Baker AS. Endogenous bacterial endophthalmitis. Report of a ten-year retrospective study. Ophthalmology. 1994;101: 832–838. 8190467
22. Jackson TL, Eykyn SJ, Graham EM, Stanford MR. Endogenous bacterial endophthalmitis: a 17-year prospective series and review of 267 reported cases. Surv Ophthalmol. 2003;48: 403–423. doi: 10.1016/s0039-6257(03)00054-7 12850229
23. Leibovitch I, Lai T, Raymond G, Zadeh R, Nathan F, Selva D. Endogenous endophthalmitis: a 13-year review at a tertiary hospital in South Australia. Scand J Infect Dis. 2005;37: 184–189. doi: 10.1080/00365540410020965 15849050
24. Zhang H, Liu Z. Endogenous endophthalmitis: a 10-year review of culture-positive cases in Northern China. Ocul Immunol Inflamm. 2010;18: 133–138. doi: 10.3109/09273940903494717 20370344
25. Frank RN. The mechanism of blood-retinal barrier breakdown in diabetes. JAMA Ophthalmol. 1985;103: 1303–1304.
26. Zhang C, Wang H, Nie J, Wang F. Protective factors in diabetic retinopathy: focus on blood-retinal barrier. Discov Med. 2014;18: 105–112. 25227751
27. Cecilia O-M, José Alberto C-G, José N-P, Ernesto Germán C-M, Ana Karen L-C, Luis Miguel R-P, et al. Oxidative stress as the main target in diabetic retinopathy pathophysiology. J Diabetes Res. 2019;2019: 1–21.
28. Xu H-Z, Le Y-Z. Significance of outer blood–retina barrier breakdown in diabetes and ischemia. Invest Ophthalmol Vis Sci. 2011;52: 2160–2164. doi: 10.1167/iovs.10-6518 21178141
29. Xu KP, Li Y, Ljubimov AV, Yu FS. High glucose suppresses epidermal growth factor receptor/phosphatidylinositol 3-kinase/Akt signaling pathway and attenuates corneal epithelial wound healing. Diabetes. 2009;58: 1077–1085. doi: 10.2337/db08-0997 19188434
30. Xu K, Yu FS. Impaired epithelial wound healing and EGFR signaling pathways in the corneas of diabetic rats. Invest Ophthalmol Vis Sci. 2011;52: 3301–3308. doi: 10.1167/iovs.10-5670 21330660
31. Coburn PS, Wiskur BJ, Christy E, Callegan MC. The diabetic ocular environment facilitates the development of endogenous bacterial endophthalmitis. Invest Ophthalmol Vis Sci. 2012;53: 7426–7431. doi: 10.1167/iovs.12-10661 23036996
32. Gupta A, Gupta V, Gupta A, Dogra MR, Pandav SS, Ray P, et al. Spectrum and clinical profile of post cataract surgery endophthalmitis in North India. Indian J Ophthalmol. 2003;51: 139–145. 12831144
33. Keswani T, Ahuja V, Changulani M. Evaluation of outcome of various treatment methods for endogenous endophthalmitis. Indian J Med Sci. 2006;60: 454–460. doi: 10.4103/0019-5359.27972 17090866
34. Doft BH, Wisniewski SR, Kelsey SF, Groer-Fitzgerald S. Diabetes and postcataract extraction endophthalmitis. Curr Opin Ophthalmol. 2002;13: 147–151. doi: 10.1097/00055735-200206000-00003 12011682
35. Sheu SJ, Kung YH, Wu TT, Chang FP, Horng YH. Risk factors for endogenous endophthalmitis secondary to Klebsiella pneumoniae liver abscess: 20-year experience in Southern Taiwan. Retina. 2011;31: 2026–2031. doi: 10.1097/IAE.0b013e31820d3f9e 21499189
Článek vyšel v časopise
PLOS One
2020 Číslo 1
- Tisícileté topoly, mokří psi, stárnoucí kočky a ospalé octomilky – „jednohubky“ z výzkumu 2024/41
- Jaké jsou aktuální trendy v léčbě karcinomu slinivky?
- Může hubnutí souviset s vyšším rizikem nádorových onemocnění?
- Menstruační krev má značný diagnostický potenciál, mimo jiné u diabetu
- Metamizol jako analgetikum první volby: kdy, pro koho, jak a proč?
Nejčtenější v tomto čísle
- Severity of misophonia symptoms is associated with worse cognitive control when exposed to misophonia trigger sounds
- Chemical analysis of snus products from the United States and northern Europe
- Calcium dobesilate reduces VEGF signaling by interfering with heparan sulfate binding site and protects from vascular complications in diabetic mice
- Effect of Lactobacillus acidophilus D2/CSL (CECT 4529) supplementation in drinking water on chicken crop and caeca microbiome
Zvyšte si kvalifikaci online z pohodlí domova
Všechny kurzy