Central retinal vein and branch artery occlusion associated with inherited plasminogen deficiency and high lipoprotein(a) levels: A case report

Tavola, Alessandra; D'Angelo, S Vigano; Bandello, Francesco; Brancato, Rosario; Parlavecchia, Mariella; Safa, Omid; D’Angelo, Armando

doi:10.1016/0049-3848(95)00183-r

Cited by 25 publications

(32 citation statements)

References 10 publications

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“…In addition, inherited plasminogen deficiency has also been reported in such patients. 36 However, other prothrombotic factors, such as antiphospholipid antibodies37 and hyperhomocysteinaemia,38 have been less commonly reported in retinal vein occlusion or retinal artery occlusion.…”

Section: Discussionmentioning

confidence: 99%

Abnormalities in haemorheological factors and lipoprotein (a) in retinal vascular occlusion: Implications for increased vascular risk

Lip¹,

Blann

Jones

et al. 1998

Eye

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Section: Discussionmentioning

confidence: 99%

Abnormalities in haemorheological factors and lipoprotein (a) in retinal vascular occlusion: Implications for increased vascular risk

Lip¹,

Blann

Jones

et al. 1998

Eye

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“…1 The underlying conditions in the previously reported single cases with simultaneous central retinal vein and branch retinal artery occlusion were inherited plasminogen deficiency and high lipoprotein (a) levels, systemic lupus erythematosus, and antiphospholipid antibodies. [3][4][5] This unusual combination has not been reported with other thrombophilic disorders.…”

Section: Commentmentioning

confidence: 86%

“…[1][2][3][4][5] Branch retinal artery obstruction is again a rare event, even less common than central retinal artery obstruction overall. Branch retinal artery obstruction is, however, more prevalent than central retinal artery obstruction in young patients as our cases.…”

Section: Commentmentioning

confidence: 99%

“…[1][2] Simultaneous occlusion of central retinal vein and artery is much rare in young adults, and information regarding risk factors in this group is scant. [1][2][3][4][5] Elevated plasma homocysteine is a recently recognized vascular risk factor for thrombosis and vascular diseases. [6][7] It is also shown to be a significant risk factor for retinal vascular occlusions.…”

Section: Introductionmentioning

confidence: 99%

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Simultaneous central retinal vein and retinal artery branch occlusions in two patients with homocystinaemia

Özdek

Yülek

Güreli̇k

et al. 2004

Eye

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“…Indeed, congenital hypoplasminogenemia and high plasma levels of Lp(a) were recently associated with thrombosis. 58 In addition, it has recently been demonstrated that plasminogen deficiency greatly accelerates the formation of intimal lesions in transgenic hypercholesterolemic apo E-deficient mice. 59 Furthermore, it has been shown that modification of apo(a) lysinebinding sites reduces atherosclerosis in transgenic mice.…”

Section: Discussionmentioning

confidence: 99%

Effect of Individual Plasma Lipoprotein(a) Variations In Vivo on Its Competition With Plasminogen for Fibrin and Cell Binding

Soulat

Loyau

Baudouin

et al. 2000

ATVB

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Abstract-Simultaneous natural changes in lipoprotein(a) [Lp(a)] and plasminogen occur in the nephrotic syndrome and offer a unique opportunity to investigate their effects on plasminogen activation under conditions fashioned in vivo. Plasminogen, Lp(a), and apolipoprotein(a) in plasma were characterized, and their competitive binding to carboxyterminal lysine residues of fibrin and cell membrane proteins was determined in nephrotic children during a flare-up of the disease (61 cases) and after 6 weeks (33 cases) and 6 months (42 cases) of remission. Low plasminogen concentrations (median 1.34 mol/L, range 0.39 to 1.96 mol/L) and high Lp(a) levels (median 0.27 g/L, range 0.07 to 2.57 g/L) were detected at flare-up. These changes were associated with an increased Lp(a) binding ratio onto fibrin (3.13Ϯ0.48) and cells (1.53Ϯ0.24) compared with binding ratios of control children (1.31Ϯ0.19 and 1.05Ϯ0.07, respectively) with normal plasminogen and low Lp(a) (median 0.071 g/L). After 6 weeks and 6 months of remission, the values for net decrease in Lp(a) binding to fibrin were 1.7Ϯ0.22 (after 6 weeks) and 1.88Ϯ0.38 (after 6 months) and were correlated with low Lp(a) concentrations (median 0.2 g/L, range 0.07 to 0.8 g/L; and median 0.12 g/L, range 0.07 to 1.34 g/L) and inversely associated with increased plasminogen levels (median 1.82 mol/L, range 1.4 to 2.1 mol/L; and median 1.58 mol/L, range 1.1 to 2.1 mol/L). These studies provide the first quantitative evidence that binding of Lp(a) to lysine residues of fibrin and cell surfaces is directly related to circulating levels of both plasminogen and Lp(a) and that these glycoproteins may interact as competitive ligands for these biological surfaces in vivo. This mechanism may be of relevance to the atherothrombotic role of Lp(a), particularly in nephrotic patients.

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Central retinal vein and branch artery occlusion associated with inherited plasminogen deficiency and high lipoprotein(a) levels: A case report

Cited by 25 publications

References 10 publications

Abnormalities in haemorheological factors and lipoprotein (a) in retinal vascular occlusion: Implications for increased vascular risk

Abnormalities in haemorheological factors and lipoprotein (a) in retinal vascular occlusion: Implications for increased vascular risk

Simultaneous central retinal vein and retinal artery branch occlusions in two patients with homocystinaemia

Effect of Individual Plasma Lipoprotein(a) Variations In Vivo on Its Competition With Plasminogen for Fibrin and Cell Binding

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