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PHOTO ESSAY
Year : 2015  |  Volume : 10  |  Issue : 4  |  Page : 493-494

Multiple retinal vein occlusions associated with anti-thrombin III deficiency


Ophthalmic Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran

Date of Submission06-Jul-2014
Date of Acceptance14-Mar-2015
Date of Web Publication18-Feb-2016

Correspondence Address:
Ramin Nourinia
Ophthalmic Research Center, Shahid Beheshti University of Medical Sciences, Boostan 9 St., Paidarfard St., Pasdaran Ave., Tehran 16666
Iran
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2008-322X.176906

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How to cite this article:
Nourinia R, Montahaei T, Behdad B, Aghajani A. Multiple retinal vein occlusions associated with anti-thrombin III deficiency. J Ophthalmic Vis Res 2015;10:493-4

How to cite this URL:
Nourinia R, Montahaei T, Behdad B, Aghajani A. Multiple retinal vein occlusions associated with anti-thrombin III deficiency. J Ophthalmic Vis Res [serial online] 2015 [cited 2020 Oct 23];10:493-4. Available from: https://www.jovr.org/text.asp?2015/10/4/493/176906


  Presentation Top


A 23-year-old man was presented with slowly progressive bilateral decreasing vision over the past 3 years. He had no remarkable medical, surgical or family history of ocular or systemic disease. Best-corrected visual acuity (BCVA) was 20/200 in both eyes with -1-0.75×90 and -1.50-0.50×90 correction in the right and left eyes, respectively. Anterior segment examination revealed diffuse neovascularization of iris (NVI) in both eyes [Figure 1]. Diffuse capillary non-perfused areas associated with occluded retinal vessels in both eyes, and fibrovascular membrane with traction on the macula in the left eye were present in dilated fundus examination [Figure 2] and [Figure 3]. Moreover, on wide field fluorescein angiography (FAG), extensive capillary non-perfused areas, occluded vessels, and retinal artery narrowing were observed [Figure 4] and [Figure 5]. A complete systemic workup including detailed thrombophilia factors was requested among which a reduced level of circulating anti-thrombin III was significant. The patient was managed by pan-retinal laser photocoagulation (PRP) bilaterally in addition to intravitreal bevacizumab injection in the right eye.
Figure 1. Slit lamp photography shows diffuse iris neovascularization around the pupil.

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Figures 2. Color fundus photograph of the right eye shows pale optic disc, severe arterial narrowing, occluded vessels, shunt vessels and mild fibrosis.

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Figures 3. Fundus photograph of the left eye shows a fibrovascular membrane on the optic disc with macular traction, retinal arterial narrowing occluded vessels, shunt vessels.

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Figures 4. Wide-field FAG of the right eye shows diffuse hypo fluorescence (capillary non-perfused area), occluded vessels and shunt vessels.

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Figures 5. Wide-field FAG of the left eye shows significant hypo fluorescence due to occluded vessels, disc leakage, peripapillary shunt and neovascular capillary networks.

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  Discussion Top


Anti-thrombin III is a potent inhibitor of reactions in the coagulation cascade. Its main duty is to virtually inhibit all coagulation enzymes to some extent. Congenital anti-thrombin III deficiency is an autosomal dominant disorder in which an individual inherits one copy of a defective gene. This condition leads to an increased risk of venous and arterial thrombosis with onset of clinical manifestations typically appearing in young adulthood.[1],[2] Acquired anti-thrombin III (AT III) deficiency has been reported in metabolic acidosis, hyper-lipoproteinemias, chronic liver diseases especially liver cirrhosis, active inflammatory bowel diseases, nephrotic syndrome, hemodialysis and disseminated intravascular coagulation.[3] Anti-thrombin deficiency is associated with a 5 to 50-fold increased risk for venous thrombosis.[4]

Since the average age in patients affected by retinal vein occlusion (RVO) is 65,[5] the majority of RVO cases are mainly secondary to underlying cardiovascular diseases.[6] Although there is no consensus, it seems rational to refer patients with central RVO for thrombophilia screening if they are younger than 50 years of age.[7]

Herein, we reported a patient with severe retinal ischemia secondary to multiple RVO with anti-thrombin III deficiency to emphasize the importance of detection of thrombophilia in cases of vein occlusion particularly in young subjects. Ophthalmologists play a key role in approaching such cases by uncovering systemic associations and preventing vision and life-threatening conditions.

 
  References Top

1.
Beauchamp NJ, Pike RN, Daly M, Butler L, Makris M, Dafforn TR, et al. Antithrombins Wibble and Wobble (T85M/K): Archetypal conformational diseases with in vivo latent-transition, thrombosis, and heparin activation. Blood 1998;92:2696-2706.  Back to cited text no. 1
    
2.
Kuhle S, Lane DA, Jochmanns K, Male C, Quehenberger P, Lechner K, et al. Homozygous antithrombin deficiency type II (99 Leu to Phe mutation) and childhood thromboembolism. Thromb Haemost 2001;86:1007-1011.  Back to cited text no. 2
    
3.
Müller G. Acquired antithrombin III deficiency. Z Gesamte Inn Med 1992;47:74-77.  Back to cited text no. 3
    
4.
Khor B, Van Cott EM. Laboratory tests for antithrombin deficiency. Am J Hematol 2010;85:947-950.  Back to cited text no. 4
    
5.
Hattenbach LO, Klais C, Scharrer I. Heparin cofactor II deficiency in central retinal vein occlusion. Acta Ophthalmol Scand 1998;76:758-759.  Back to cited text no. 5
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6.
Kuhli C, Hattenbach LO, Scharrer I, Koch F, Ohrloff C. High prevalence of resistance to APC in young patients with retinal vein occlusion. Graefes Arch Clin Exp Ophthalmol 2002;240:163-168.  Back to cited text no. 6
    
7.
Pierre-Filho Pde T, Pierre AM, Nascimento MA, Marcondes AM. Central retinal vein prethrombosis as an initial manifestation of protein S deficiency. Sao Paulo Med J 2004;122:134-135.  Back to cited text no. 7
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]



 

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