2. Flethcer EC, Chong NV. Retina. In: Riordan-Eva P, Whither JP (Eds) Vaughan & Asbury’s General Ophthalmology. 17th ed. London: McGraw Hill; 2007. chapter 10.
3. Fauci AS, Kasper DL, Longo DL, et al. Diabetes mellitus. In: Fauci AS, Kasper DL, Longo DL, Braunwald E, Hauser SL, Jameson Jl, et al. Harrison’s Principles of Internal Medicine. 17th ed. USA: The McGraw-Hill; 2008. chapter 338.
4. Vitreoretinal Division, Department of Ophthalmology, Faculty of Medicine, University of Indonesia. Prevalence of diabetic retinopathy. Unpublished raw data; 2013.
5. Limb GA, Webster L, Soomro H, Janikoun S, Shiling J. Platelet expression of tumour necrosis factor-alpha (TNF-a), TNF receptors and intercellular adhesion molecule-1 (ICAM-1) in patients with proliferative diabetic retinopathy. Clin Exp Immunol. 1999;118:213-218. https://www.ncbi.nlm.nih.gov/pubmed/10540181
6. Mroczek JA, Mlynczak JPO, Hojlo MM. Proliferative diabetic retinopathy—the influence of diabetes control on the activation of the intraocular molecule system. Diabetes Res Clin Pract. 2009;84:46-50. doi: 10.1016/j.diabres.2009.01.012
7. Zhang K, Ferreyra HA, Grob S, Bedell M, Zhang JJ. Diabetic retinopathy: genetics and etiologic mechanisms. In: Ryan SJ, et al. (Eds), Retina. 5th ed. Philadelphia: Elsevier; 2013:975-985. https://clinicalgate.com/diabetic-retinopathy-genetics-and-etiologic-mechanisms/
8. Mroczek JA, Mlynczak JO. Assessment of selected adhesion molecule and proinflammatory cytokine levels in the vitreous body of patients with type 2-diabetes role of the inflammatory immune process in the pathogenesis of proliferative diabetic retinopathy. Graefes Arch Clin Exp Ophthalmol. 2008;246:1665-1670. DOI: 10.1007/s00417-008-0868-6
9. Ghonaim MM, El-Edel RH. Circulating cell adhesion molecules (sICAM-1 and sVCAM-1) and microangiopathy in diabetes mellitus. Ibnosina J Med BS. 2015;7(6):211-218. http://journals.sfu.ca/ijmbs/index.php/ijmbs/article/view/522/1085
10. Joussen AM, Poulaki V, Le ML, et al. A central role for inflammation in the pathogenesis of diabetic retinopathy. FASEB J. 2004;18:1450-1452. doi: 10.1096/ij.03-1476fje
11. Yan Y, Zhu L, Hong L, Deng J, Song Y, Chen X. The impact of ranibizumab on the level of intercellular adhesion molecule type 1 in the vitreous of eyes with proliferative diabetic retinopathy. Acta Ophthalmol. 2016;94:358-364. DOI: 10.1111/aos.12806
12. El-Asrar AMA, Nawaz MI, Kangave D, et al. High-mobility group box-1 and biomarkers of inflammation in the vitreous from patients with proliferative diabetic retinopathy. Mol Vis. 2011;17:1829-1838. https://www.ncbi.nlm.nih.gov/pubmed/21850157
13. Ruszkowska-Ciastek B, Sokup A, Wernik T, et al. Effect of uncontrolled hyperglycemia on levels of adhesion molecules in patients with diabetes mellitus type 2. J Zhejiang Univ Sci B. 2015;16(5):355-361. doi: 10.1631/jzus.B1400218
14. Noda K, Nakao S, Zandi S, Sun D, Hayes KC, Hafezi-Moghadam A. Retinopathy in a novel model of metabolic syndrome and type 2 diabetes: new insight on the inflammatory paradigm. FASEB J. 2014;28(5):2038-2046. doi: 10.1096/fj.12-215715
15. Huang G, Gandhi JK, Zhong X, et al. TNF-a is required for late BRB breakdown in diabetic retinopathy, and its inhibition prevents leukostasis and protects vessels and neurons from apoptosis. 2011 Mar 10;52(3):1336-44. doi: 10.1167/iovs.10-5768. Print 2011 Mar.
16. Nagineni CN, Kutty RK, Detrick B, Hooks JJ. Inflammatory cytokine induce intercellular adhesion molecule-1 (ICAM-1) mRNA synthesis and protein secretion by human retinal pigment epithelial cell cultures. Cytokine. 1996 Aug; 8(8):622-630.
17. Qaum T, Xu Q, Joussen AM, et al. VEGF-initiated blood retinal barrier breakdown in early diabetes. Retina. 2001 Sept; 42(10):2408-2413.
18. King GL, Buzney SM, Kahn CR, et al. Differential responsiveness to insulin of endothelial and support cells from micro- and macrovessels. J Clin Invest. 1983;71:974-979. https://www.ncbi.nlm.nih.gov/pubmed/6339562
19. Jingi AM, Noubiap JJ, Essouma M, et al. Association of insulin treatment versus oral hypoglycemic agents with diabetic retinopathy and its severity in type 2 diabetes patients in Cameroon, sub-Saharan Africa. Ann Transl Med. 2016 Oct;4(20):395. DOI: 10.21037/atm.2016.08.42
20. Hirata F, Yoshida M, Niwa Y, et al. Insulin enhances leukocyte endothelial cell adhesion in the retinal microcirculation through surface expression of intercellular adhesion molecule-1. Microvasc Res. 2005;69:135-141. doi: 10.1016/j.mvr.2005.03.002
- Abstract viewed - 242 times
- 516 PDF downloaded - 78 times
License

This work is licensed under a Creative Commons Attribution 4.0 International License.
Copyright
© Andi Arus Victor, Tjahjono D. Gondhowiardjo, Rahayuningsih Dharma, Sri W. A. Jusman, Vivi R. Yandri, Ressa Yuneta, Rizky E. P. Yuriza, 2020
Affiliations
Andi A. Victor
Department of Ophthalmology, Cipto Mangunkusumo General Hospital, Faculty of Medicine Universitas Indonesia
Tjahjono D. Gondhowiardjo
Department of Ophthalmology, Faculty of Medicine, Universitas Indonesia
Rahayuningsih Dharma
Affiliation not stated
Sri W. A. Jusman
Affiliation not stated
Vivi R. Yandri
Affiliation not stated
Ressa Yuneta
Affiliation not stated
Rizky E. P. Yuriza
Affiliation not stated
How to Cite
Intercellular adhesive molecule-1 (ICAM-1) in proliferative diabetic retinopathy
- Andi A. Victor ,
- Tjahjono D. Gondhowiardjo ,
- Rahayuningsih Dharma ,
- Sri W. A. Jusman ,
- Vivi R. Yandri ,
- Ressa Yuneta ,
- Rizky E. P. Yuriza
Vol 17 No 1 (2019): Asian Journal of Ophthalmology
Submitted: Jan 22, 2018
Published: Jan 17, 2020
Abstract
Purpose: To determine the level of intercellular adhesion molecule-1 (ICAM-1) in vitreous fluid of patients with proliferative diabetic retinopathy (PDR) and its affecting factors including HbA1c level, duration of diabetes mellitus (DM) and insulin usage.
Methods: A cross-sectional study was conducted in Cipto Mangunkusumo National General Central Hospital, Jakarta, Indonesia from June 2015 to August 2016. Thirty-three consecutive vitreous samples harvested from PDR patients underwent vitrectomy. The level of vitreous ICAM-1 was determined by enzyme-linked immunosorbent assay.
Results: Based on the glycemic status, vitreous ICAM-1 level in the uncontrolled glycemic group (21.61 ng/ml) was lower than controlled glycemic group (24.20 ng/ml). Patients with DM for more than 10 years had higher level of vitreous ICAM-1 (26.30 ng/ml). Vitreous ICAM-1 level in DM patients with insulin was higher than those without insulin (27.07 ng/ml vs. 24.17 ng/ml). There was no statistically significant difference between vitreous ICAM-1 levels among all groups (p > 0.05).
Conclusion: The concentration of vitreous ICAM-1 may not be influenced by glucose control and conventional insulin therapy.